DatabaseID	StudyType	PubMedID	Author	Title	Journal	PublishDate	Chromosome	Disease	Technology	Species	CaseID	Platform	CNA	Connection	Gene	Affiliation	Abstract	GenomeAssembly	GEO	dbGaP	ENA	IsCancer	FusionGene
CTDB0001	Research	24440784	Paolo Fontana, Rita Genesio, Alberto Casertano, Gerarda Cappuccio, Angela Mormile, Lucio Nitsch, Achille Iolascon, Generoso Andria, Daniela Melis	Loeys-Dietz syndrome type 4, caused by chromothripsis, involving the TGFB2 gene	Gene	2014 Jan	1,9,21	Loeys-Dietz syndrome	Array CGH	Homo sapiens	24440784_1	NimbleGen CGX-6 PKI Array	chr1:212338589-217573448:-1;chr1:236581779-237907878:-1;chr21:34848660-35675464:-1;chr9:485809-644518:-1		CENPF;CHRM3;CLIC6;ESRRG;KANK1;KCNK2;KCTD3;PTPN14;RCAN1;RRP15;RUNX1;SMYD2;SPATA17;TGFB2;USH2A	Department of Molecular Medicine and Medical Biotechnology, Federico II University, Naples, Italy	The TGF-beta signaling pathway controls cellular proliferation, growth and differentiation and regulates several functions of the connective tissue. Disruption of genes coding for components of the TGF-beta signaling pathway or its interactors, such as fibrillin-1, has been shown to cause several human pathologies. Large deletions and non-sense mutations in TGFB2 gene have been recently described in patients with aortic aneurysm, scoliosis, arachnodactyly, chest deformities, joint hyper-flexibility, and mild intellectual disability; this condition has been called Loeys-Dietz syndrome, type 4. In this paper we describe an 18-year-old girl with borderline mental impairment, seizures, retinal degeneration, short stature, congenital hip dysplasia, severe and worsening joint hypermobility, scoliosis, progressive deformation of the long bones, aortic dilatation and platelet disorder. Molecular study of DNA by Array CGH demonstrated four de novo microdeletions: TGFB2 is among the genes deleted and we consider it the obvious candidate for the clinical phenotype. The multiple chromosomal rearrangements detected in the current patient can be ascribed to an event of constitutional chromothripsis.	NCBI 36/hg18				No	NA
CTDB0002	Research	24462510	Julio Fernandez-Banet, Nikki P. Lee, Kin Tak Chan, Huan Gao, Xiao Liu, Wing-Kin Sung,Winnie Tan, Sheung Tat Fan, Ronnie T. Poon, Shiyong Li, Keith Ching, Paul A. Rejto, Mao Mao, Zhengyan Kan	Decoding complex patterns of genomic rearrangement in hepatocellular carcinoma 	Genomics	2014 Jan	1	Hepatocellular carcinoma	Next Generation Sequencing	Homo sapiens	117T	Illumina HiSeq 2000	chr10:77254129-77359565:-1;chr11:65195677-65195803:-1;chr12:68486967-69618037:1;chr12:7093691-25298569:-1;chr13:24949808-24951540:1;chr16:25832301-25833569:-1;chr18:69827554-69829289:-1;chr18:77317033-77317075:1;chr19:45434282-45435022:-1;chr1:151216266-183227564:1;chr1:151216545-226557614:1;chr1:151216692-197000991:-1;chr1:153707307-226558570:-1;chr1:153827733-212908203:1;chr1:153829027-212908199:-1;chr1:154422953-197657552:-1;chr1:156419438-183174553:1;chr1:156419724-193352718:1;chr1:156539673-183228294:1;chr1:156539677-156660305:1;chr1:156539750-166055253:-1;chr1:156539796-162087621:-1;chr1:156540190-196263378:1;chr1:156540308-183191885:-1;chr1:156546546-226257332:1;chr1:156659962-197702859:1;chr1:156660385-159852249:1;chr1:156660627-193373804:1;chr1:157104393-159971005:-1;chr1:157105087-196464550:1;chr1:159851334-161972637:1;chr1:161349421-244937596:1;chr1:161998837-162225053:-1;chr1:162087993-226609105:-1;chr1:162361758-207117521:1;chr1:166138797-193352167:-1;chr1:168684997-183320210:-1;chr1:174008782-207113572:1;chr1:174036961-213142231:-1;chr1:179158752-203172242:-1;chr1:179252913-201536915:-1;chr1:183174569-226558257:-1;chr1:183181774-204188039:1;chr1:183188743-197001349:1;chr1:183191112-202900543:1;chr1:183217871-226558409:-1;chr1:183222686-212517877:1;chr1:183222884-197702104:-1;chr1:183226816-193373821:1;chr1:183227084-197658068:1;chr1:183227173-197658591:1;chr1:183228110-197658472:-1;chr1:183229493-193348141:-1;chr1:183320100-197702226:-1;chr1:190542073-205723232:-1;chr1:193240589-197002565:1;chr1:193329541-203172404:1;chr1:193329654-196876022:-1;chr1:193352659-212908317:1;chr1:193352728-197657694:-1;chr1:193372405-196263839:1;chr1:193373290-248071857:1;chr1:193373636-226558697:-1;chr1:193382469-226558514:1;chr1:193383174-208121707:-1;chr1:196263326-197658056:1;chr1:196263595-197658404:-1;chr1:196263694-197001376:1;chr1:196608183-202900385:1;chr1:197001051-203912534:-1;chr1:197001199-197659148:1;chr1:197001378-226558324:-1;chr1:197001415-226558398:-1;chr1:197657765-226558358:1;chr1:197657765-226558369:1;chr1:197657875-197658960:-1;chr1:197658517-213262561:1;chr1:197659157-226558564:-1;chr1:197668357-208168692:1;chr1:202900485-213262283:-1;chr1:203008523-209973625:-1;chr1:205298940-242014388:1;chr1:206887324-224549492:1;chr1:211809174-242013705:-1;chr1:221673283-221833746:-1;chr20:51623677-51623894:-1;chr2:38225978-38229325:-1;chr2:79763416-79985150:-1;chr4:39868393-40938932:1;chr4:85233794-85234156:-1;chr6:94769059-94769762:-1;chr7:86853240-144987383:-1	hs1:31893066-31893066,hs13:24788007-24788007;hs1:31893220-31893220,hs13:24949935-24949935;hs1:86002715-86002715,hs1:161998892-161998892;hs1:144836511-144836511,hs1:167412963-167412963;hs1:145486380-145486380,hs1:155179290-155179290;hs1:153829409-153829409,hs1:197000979-197000979;hs1:153829454-153829454,hs1:156539869-156539869;hs1:155880732-155880732,hs1:234376099-234376099;hs1:156539908-156539908,hs1:197657683-197657683;hs1:156540972-156540972,hs1:193373640-193373640;hs1:156660640-156660640,hs1:203912330-203912330;hs1:156660699-156660699,hs1:153829470-153829470;hs1:159851559-159851559,hs1:183136169-183136169;hs1:161701440-161701440,hs1:197882253-197882253;hs1:162358626-162358626,hs1:221611488-221611488;hs1:162362049-162362049,hs1:212908096-212908096;hs1:174071175-174071175,hs1:168622854-168622854;hs1:178667640-178667640,hs1:182956851-182956851;hs1:179081472-179081472,hs1:150792743-150792743;hs1:179149797-179149797,hs1:213323192-213323192;hs1:183191318-183191318,hs1:193372991-193372991;hs1:183191784-183191784,hs1:196263932-196263932;hs1:183227161-183227161,hs1:213262709-213262709;hs1:183227308-183227308,hs1:156660585-156660585;hs1:183227545-183227545,hs1:212516825-212516825;hs1:183229139-183229139,hs1:183259106-183259106;hs1:183229559-183229559,hs1:226558226-226558226;hs1:193241084-193241084,hs1:197658450-197658450;hs1:193241377-193241377,hs1:197001350-197001350;hs1:193331467-193331467,hs1:211853286-211853286;hs1:193348537-193348537,hs1:213263243-213263243;hs1:193348571-193348571,hs1:197668535-197668535;hs1:193352916-193352916,hs1:156419876-156419876;hs1:193372542-193372542,hs1:226558773-226558773;hs1:196263828-196263828,hs1:226558512-226558512;hs1:196576981-196576981,hs1:149986788-149986788;hs1:196961522-196961522,hs1:200079749-200079749;hs1:196972484-196972484,hs1:193382384-193382384;hs1:197001192-197001192,hs1:193352966-193352966;hs1:197657412-197657412,hs1:183230803-183230803;hs1:197658450-197658450,hs1:197001745-197001745;hs1:197658633-197658633,hs1:226558388-226558388;hs1:197666994-197666994,hs1:202900278-202900278;hs1:197702311-197702311,hs1:183228283-183228283;hs1:202900543-202900543,hs1:226558531-226558531;hs1:203180459-203180459,hs1:211853103-211853103;hs1:205299279-205299279,hs1:207105285-207105285;hs1:206974277-206974277,hs1:183224796-183224796;hs1:211740833-211740833,hs1:215718327-215718327;hs1:211809133-211809133,hs1:156540136-156540136;hs1:212517898-212517898,hs1:197001401-197001401;hs1:212908006-212908006,hs1:156539639-156539639;hs1:212908093-212908093,hs1:197001055-197001055;hs1:212908221-212908221,hs1:156660329-156660329;hs1:213262521-213262521,hs1:162358375-162358375;hs1:213262560-213262560,hs1:193348554-193348554;hs1:213353881-213353881,hs1:159851641-159851641;hs1:220858213-220858213,hs1:168122089-168122089;hs1:221611428-221611428,hs1:212517702-212517702;hs1:226558310-226558310,hs1:161971847-161971847;hs1:226558375-226558375,hs1:212517723-212517723;hs1:226558433-226558433,hs1:203770824-203770824;hs1:226558462-226558462,hs1:153707151-153707151;hs1:226558483-226558483,hs1:183227229-183227229;hs1:229318979-229318979,hs1:165739180-165739180;hs1:235588314-235588314,hs1:193792362-193792362;hs1:237894639-237894639,hs10:135333128-135333128;hs10:53668488-53668488,hs16:20411364-20411364;hs12:32492419-32492419,hs12:28489853-28489853;hs14:25715713-25715713,hs14:25837291-25837291;hs5:62966392-62966392,hs18:51802022-51802022;hs8:32680009-32680009,hs3:132264991-132264991	ABL2;APBB2;APOC1P1;ARNT;BICD1;CASC1;CCDC19;CCDC91;CD247;CFHR4;CFHR5;CNIH4;CTNNA2;DDAH1;DENND1B;DPT;ETV3;EXO1;FAM78B;FAM82A1;GATAD2B;H3F3AP4;HS3ST4;IL19;IL6R;INTS3;IQGAP3;IRF6;KCNT2;LAMC2;LHX9;LIX1L;LPCAT3;MAPKAPK2;MTX1;NMNAT2;NOS1AP;NR5A2;NSL1;OLFML2B;PARP1;PDILT;PDS5A;PIGR;PIP5K1A;PLEKHA6;POLI;PPP2R5A;PRKG1;RIT1;RPS6KC1;RYR2;SERINC2;SLC35F3;SPATA13;TBCE;TSHZ2;VASH2;ZC3H11A	Pfizer Oncology, San Diego, CA, USA	Elucidating the molecular basis of hepatocellular carcinoma (HCC) is crucial to developing targeted diagnostics and therapies for this deadly disease. The landscape of somatic genomic rearrangements (GRs), which can lead to oncogenic gene fusions, remains poorly characterized in HCC. We have predicted 4314 GRs including large-scale insertions, deletions, inversions and translocations based on the whole-genome sequencing data for 88 primary HCC tumor/non-tumor tissues. We identified chromothripsis in 5 HCC genomes (5.7%) recurrently affecting chromosomal arms 1q and 8q. Albumin (ALB) was found to harbor GRs, deactivating mutations and deletions in 10% of cohort. Integrative analysis identified a pattern of paired intra-chromosomal translocations flanking focal amplifications and asymmetrical patterns of copy number variation flanking breakpoints of translocations. Furthermore, we predicted 260 gene fusions which frequently result in aberrant over-expression of the 3' genes in tumors and validated 18 gene fusions, including recurrent fusion (2/88) of ABCB11 and LRP2.	GRCh37/hg19	GSE25097		ERP001196	Yes	CASC1,LPCAT3;CCDC19,OLFML2B;CNIH4,MAPKAPK2;DENND1B,KCNT2;DENND1B,NMNAT2;DENND1B,PARP1;ETV3,KCNT2;FAM78B,IQGAP3;GATAD2B,NSL1;IL19,NMNAT2;IQGAP3,KCNT2;IQGAP3,NMNAT2;KCNT2,DENND1B;LAMC2,KCNT2;NMNAT2,DENND1B;NMNAT2,DPT;NSL1,GATAD2B;PARP1,DENND1B;PARP1,INTS3;PARP1,NMNAT2;PARP1,PPP2R5A;PDS5A,APBB2;PPP2R5A,NMNAT2;RPS6KC1,ABL2;RPS6KC1,CCDC19;RPS6KC1,NMNAT2;SLC35F3,RIT1;ZC3H11A,PARP1
CTDB0003	Research	24462510	Julio Fernandez-Banet, Nikki P. Lee, Kin Tak Chan, Huan Gao, Xiao Liu, Wing-Kin Sung,Winnie Tan, Sheung Tat Fan, Ronnie T. Poon, Shiyong Li, Keith Ching, Paul A. Rejto, Mao Mao, Zhengyan Kan	Decoding complex patterns of genomic rearrangement in hepatocellular carcinoma 	Genomics	2014 Jan	1	Hepatocellular carcinoma	Next Generation Sequencing	Homo sapiens	206T	Illumina HiSeq 2000	chr10:101134331-101134374:-1;chr10:101143033-101145802:-1;chr11:122149898-134092564:-1;chr11:65590381-76540398:-1;chr11:68444454-124736618:-1;chr11:73128420-80752310:1;chr11:74323445-79732185:1;chr1:146576320-159118830:-1;chr1:146736676-171678710:1;chr1:149235223-220750399:-1;chr1:150459539-152261925:1;chr1:150827918-216172237:-1;chr1:151465603-159352265:-1;chr1:151614533-229423173:1;chr1:151863833-205365371:-1;chr1:152631890-242335715:1;chr1:152742746-230381514:1;chr1:159461183-204755475:1;chr1:159902366-181056554:-1;chr1:163661169-227774749:1;chr1:163693223-192049853:-1;chr1:163783040-216170571:1;chr1:164712917-182996551:1;chr1:166905347-178313768:1;chr1:169336909-209391679:1;chr1:171519238-173839298:-1;chr1:174229440-178282824:-1;chr1:174805655-174820281:-1;chr1:179374223-192310590:-1;chr1:181745502-189398493:-1;chr1:184254352-229426177:-1;chr1:185935455-227264899:-1;chr1:187068878-238083701:1;chr1:189356056-196610462:-1;chr1:192553897-215691503:1;chr1:192989501-223497448:1;chr1:193192583-194601401:1;chr1:193192583-194601409:1;chr1:193751148-194040887:-1;chr1:194549288-232942000:-1;chr1:195032033-199886834:1;chr1:196393448-203706783:1;chr1:197849228-242306806:1;chr1:200472535-220406759:1;chr1:201233402-208011691:1;chr1:204457776-215758989:1;chr1:205528016-248863405:-1;chr1:216238536-227544390:1;chr1:219793875-226007670:-1;chr1:220245564-238320629:1;chr1:222290954-243306461:1;chr1:222761439-231572578:-1;chr1:224705899-248169258:1;chr1:232315322-238325295:-1;chr1:232759584-232761882:-1;chr1:234517585-234526972:-1;chr1:234873722-235522758:1;chr1:237348463-248094735:1;chr1:241007437-242757695:1;chr1:241762174-247076107:-1;chr1:242641679-243582764:-1;chr1:243309074-245820476:1;chr4:181109427-181110424:-1;chr5:178764778-178764984:1;chr5:178764786-178764984:1;chr5:33973937-33973978:-1;chr7:79115004-79205821:1;chr8:134955565-134955612:1;chr9:116780725-116801090:-1;chrX:133328467-133487475:1	hs1:111896187-111896187,hs11:65217853-65217853;hs1:146818500-146818500,hs1:200328646-200328646;hs1:146863053-146863053,hs1:232081753-232081753;hs1:149153301-149153301,hs1:145391889-145391889;hs1:149164820-149164820,hs1:179380983-179380983;hs1:150062567-150062567,hs1:215667836-215667836;hs1:150402990-150402990,hs1:243612759-243612759;hs1:150601833-150601833,hs1:150601903-150601903;hs1:151764005-151764005,hs1:165321241-165321241;hs1:154577448-154577448,hs1:225884334-225884334;hs1:155066707-155066707,hs1:155066796-155066796;hs1:155869389-155869389,hs1:162715340-162715340;hs1:158447506-158447506,hs1:235449737-235449737;hs1:159458286-159458286,hs1:178276568-178276568;hs1:161720490-161720490,hs1:161303252-161303252;hs1:162050228-162050228,hs1:179375991-179375991;hs1:162698316-162698316,hs1:161063421-161063421;hs1:163326962-163326962,hs1:181751146-181751146;hs1:165763955-165763955,hs1:202770635-202770635;hs1:168808434-168808434,hs1:196692913-196692913;hs1:171186678-171186678,hs1:182132210-182132210;hs1:178016006-178016006,hs1:154383252-154383252;hs1:178321060-178321060,hs1:191871196-191871196;hs1:179014260-179014260,hs1:159192967-159192967;hs1:179329259-179329259,hs1:193670940-193670940;hs1:181049481-181049481,hs1:201262059-201262059;hs1:183470358-183470358,hs1:171459756-171459756;hs1:183496068-183496068,hs1:248862991-248862991;hs1:187064952-187064952,hs1:163778920-163778920;hs1:188389276-188389276,hs1:219312420-219312420;hs1:188514228-188514228,hs1:209753183-209753183;hs1:192714059-192714059,hs1:147105620-147105620;hs1:193673677-193673677,hs1:196139605-196139605;hs1:194087018-194087018,hs1:220403200-220403200;hs1:199402572-199402572,hs1:206813601-206813601;hs1:200078852-200078852,hs1:208060345-208060345;hs1:200078920-200078920,hs1:180739519-180739519;hs1:201744318-201744318,hs1:159347886-159347886;hs1:203932050-203932050,hs1:221949487-221949487;hs1:205042012-205042012,hs1:212532087-212532087;hs1:205463738-205463738,hs1:205798201-205798201;hs1:206974257-206974257,hs1:242316699-242316699;hs1:207558305-207558305,hs1:201747590-201747590;hs1:210964274-210964274,hs1:235467231-235467231;hs1:212518361-212518361,hs1:199673532-199673532;hs1:214240872-214240872,hs1:215668677-215668677;hs1:215659601-215659601,hs1:151471494-151471494;hs1:216613413-216613413,hs1:248206843-248206843;hs1:219045452-219045452,hs1:234752056-234752056;hs1:219549963-219549963,hs1:186085962-186085962;hs1:219706673-219706673,hs1:184079100-184079100;hs1:220241414-220241414,hs1:246862847-246862847;hs1:221564763-221564763,hs1:246317011-246317011;hs1:221610982-221610982,hs1:240336663-240336663;hs1:222510946-222510946,hs1:241471857-241471857;hs1:226497591-226497591,hs1:165076945-165076945;hs1:226561606-226561606,hs1:206272659-206272659;hs1:227469535-227469535,hs1:196658686-196658686;hs1:227782654-227782654,hs1:227547446-227547446;hs1:229632434-229632434,hs1:153174214-153174214;hs1:230392560-230392560,hs1:146719451-146719451;hs1:232037074-232037074,hs1:243578878-243578878;hs1:232317217-232317217,hs1:208040318-208040318;hs1:234280579-234280579,hs1:220409874-220409874;hs1:234487961-234487961,hs1:173835909-173835909;hs1:235841129-235841129,hs1:237580068-237580068;hs1:242761494-242761494,hs1:189254341-189254341;hs1:245172709-245172709,hs1:193598317-193598317;hs1:246026360-246026360,hs1:188830278-188830278;hs1:248318267-248318267,hs1:193549573-193549573;hs11:116595859-116595859,hs11:120900807-120900807;hs11:120884215-120884215,hs11:122150331-122150331;hs18:48198026-48198026,hs4:54769265-54769265;hs2:42035919-42035919,hs5:58684453-58684453;hs2:192440470-192440470,hs11:56401950-56401950;hs20:26220634-26220634,hs19:33444268-33444268;hs21:38472500-38472500,hs5:165406325-165406325;hs3:22107821-22107821,hs9:88214033-88214033;hs5:94059708-94059708,hs1:75213827-75213827;hs6:65458491-65458491,hs6:65456526-65456526	ADAMTS2;ADAR;AGTPBP1;AHCTF1;ARID4B;ARNT;ATP2B4;AXDND1;C1orf186;C1orf31;C1orf98;CACNA1E;CD34;CDC42BPA;CDC73;CEP170;CEP89;CFH;CHD1L;CNNM1;CNTN2;DDR2;DISC1;DUSP12;DYRK3;EFCAB2;ENSA;EPHX1;EYS;FAM168A;FAM20B;FMN2;GALNT2;GAS5;HMCN1;IGSF9;IL19;IL6R;ILDR2;KCNH1;KCNT2;KCTD3;KDM5B;KIAA1383;KIF26B;LAMC1;LEMD1;LMX1A;LOC100130331;LOC100289211;LOC643723;LYST;MAPK4;MARK1;MCTP1;MIR548F1;NAV1;NCAPD3;NME7;NOS1AP;NR5A2;NUP133;OPN3;OR2L13;OR8U8;PARP1;PBX1;PDE4D;PIK3C2B;PKP1;PLD5;PM20D1;POLD3;PPP2R5A;PRRC2C;RAB3GAP2;RAB4A;RABGAP1L;RASAL2;RGS21;RGS7;RIT1;RNU5F-1;ROBO3;RPRD2;RYR2;SDCCAG8;SDHC;SLC35F3;SLC45A2;SMG7;SMYD3;SNX27;SUSD4;TAF1A;TBCEL;THEM4;TTC3;TYW3;UCHL5;USH2A;VAMP4;VPS45;XPR1;ZBTB37;ZNF618;ZNF678	Pfizer Oncology, San Diego, CA, USA	Elucidating the molecular basis of hepatocellular carcinoma (HCC) is crucial to developing targeted diagnostics and therapies for this deadly disease. The landscape of somatic genomic rearrangements (GRs), which can lead to oncogenic gene fusions, remains poorly characterized in HCC. We have predicted 4314 GRs including large-scale insertions, deletions, inversions and translocations based on the whole-genome sequencing data for 88 primary HCC tumor/non-tumor tissues. We identified chromothripsis in 5 HCC genomes (5.7%) recurrently affecting chromosomal arms 1q and 8q. Albumin (ALB) was found to harbor GRs, deactivating mutations and deletions in 10% of cohort. Integrative analysis identified a pattern of paired intra-chromosomal translocations flanking focal amplifications and asymmetrical patterns of copy number variation flanking breakpoints of translocations. Furthermore, we predicted 260 gene fusions which frequently result in aberrant over-expression of the 3' genes in tumors and validated 18 gene fusions, including recurrent fusion (2/88) of ABCB11 and LRP2.	GRCh37/hg19	GSE25097		ERP001196	Yes	AHCTF1,OPN3;AXDND1,RGS21;CD34,NR5A2;CDC42BPA,CFH;DDR2,RIT1;LAMC1,PBX1;LEMD1,THEM4;LOC100289211,DISC1;LYST,RYR2;MCTP1,TYW3;PLD5,IL19;PRRC2C,ZBTB37;RAB3GAP2,SLC35F3;RAB4A,SNX27;RABGAP1L,RASAL2;UCHL5,SUSD4;USH2A,ARNT
CTDB0004	Research	24462510	Julio Fernandez-Banet, Nikki P. Lee, Kin Tak Chan, Huan Gao, Xiao Liu, Wing-Kin Sung,Winnie Tan, Sheung Tat Fan, Ronnie T. Poon, Shiyong Li, Keith Ching, Paul A. Rejto, Mao Mao, Zhengyan Kan	Decoding complex patterns of genomic rearrangement in hepatocellular carcinoma 	Genomics	2014 Jan	6,8,13	Hepatocellular carcinoma	Next Generation Sequencing	Homo sapiens	39T	Illumina HiSeq 2000	chr12:24645563-24738879:1;chr12:78169609-88786765:1;chr13:23912324-80201009:1;chr13:24443145-80055872:-1;chr13:65105106-66024797:-1;chr13:65939359-81547930:1;chr13:67613309-80940102:-1;chr13:79973005-80575107:-1;chr15:101236855-101240400:-1;chr15:61676817-61747812:-1;chr18:55243248-55251507:-1;chr1:12558131-12558872:-1;chr1:223588075-223655247:-1;chr20:42848008-42848137:1;chr2:125777393-164375256:-1;chr2:31558963-40628785:1;chr3:158988279-159870359:-1;chr6:33505941-40678634:1;chr6:35648993-40896804:-1;chr6:37384613-45069916:-1;chr6:40904604-40906513:1;chr6:41991234-42958247:-1;chr6:80825114-80825236:1;chr7:13697734-26238926:-1;chr8:10234784-11761656:-1;chr8:105320972-105659217:-1;chr8:105525208-117004096:-1;chr8:113771527-114762074:-1;chr8:113932031-114766291:1;chr8:114762169-114874375:-1;chr8:114785424-115394094:1;chr8:115323285-143937031:1;chr8:135318272-142160228:1;chr8:4588141-26742571:1;chr8:77924322-113737213:-1;chr8:96560827-108645368:-1	hs1:189940250-189940250,hs1:189953149-189953149;hs1:196679980-196679980,hs8:113109783-113109783;hs1:231932112-231932112,hs2:204851845-204851845;hs1:248324102-248324102,hs1:248518578-248518578;hs1:248436061-248436061,hs1:248218582-248218582;hs13:24303841-24303841,hs15:61664000-61664000;hs13:26867891-26867891,hs13:65652586-65652586;hs13:26870274-26870274,hs13:81128755-81128755;hs13:64573583-64573583,hs13:80434629-80434629;hs13:64583126-64583126,hs16:81911913-81911913;hs13:65652518-65652518,hs13:23914529-23914529;hs13:65939451-65939451,hs16:80340949-80340949;hs13:65988378-65988378,hs13:81576181-81576181;hs13:79972927-79972927,hs13:64575180-64575180;hs13:79979513-79979513,hs13:65178178-65178178;hs13:80050432-80050432,hs13:80050486-80050486;hs13:80205805-80205805,hs13:24410396-24410396;hs13:80316638-80316638,hs13:80154870-80154870;hs13:80434702-80434702,hs13:24413912-24413912;hs13:80550064-80550064,hs13:80933817-80933817;hs13:81537261-81537261,hs13:80316551-80316551;hs13:81545032-81545032,hs13:81587298-81587298;hs13:81582445-81582445,hs13:79899143-79899143;hs13:81612188-81612188,hs13:24301682-24301682;hs15:61539678-61539678,hs15:61548443-61548443;hs15:61591460-61591460,hs13:64502324-64502324;hs15:61727064-61727064,hs13:25553931-25553931;hs16:80151163-80151163,hs13:80380806-80380806;hs2:111440809-111440809,hs2:183197424-183197424;hs2:183668080-183668080,hs2:183653531-183653531;hs2:183694977-183694977,hs6:46515027-46515027;hs4:153834036-153834036,hsM:14100-14100;hs6:7276363-7276363,hs17:9269015-9269015;hs6:36093582-36093582,hs6:45878184-45878184;hs6:36968553-36968553,hs11:101860408-101860408;hs6:38077296-38077296,hs6:38079360-38079360;hs6:40846035-40846035,hs6:40972867-40972867;hs6:40896748-40896748,hs6:40888377-40888377;hs6:40898405-40898405,hs1:223656150-223656150;hs6:40900111-40900111,hs6:40901312-40901312;hs6:40901675-40901675,hs6:40904967-40904967;hs6:40901675-40901675,hs6:40904968-40904968;hs6:41331902-41331902,hs6:35802864-35802864;hs6:41958640-41958640,hs6:40707988-40707988;hs6:45076739-45076739,hs6:39788433-39788433;hs6:46527072-46527072,hs6:46528998-46528998;hs6:57624207-57624207,hs6:57620145-57620145;hs6:112243271-112243271,hs22:24195877-24195877;hs8:77980613-77980613,hs8:77557676-77557676;hs8:98170895-98170895,hs8:105237233-105237233;hs8:105239259-105239259,hs8:98168374-98168374;hs8:105953917-105953917,hs8:117005433-117005433;hs8:110328750-110328750,hs8:105211082-105211082;hs8:111541912-111541912,hs8:114361923-114361923;hs8:111633152-111633152,hs8:113219005-113219005;hs8:112615866-112615866,hs8:114353024-114353024;hs8:112617449-112617449,hs8:113222570-113222570;hs8:112741096-112741096,hs8:96550449-96550449;hs8:113300228-113300228,hs8:113399774-113399774;hs8:113763157-113763157,hs8:113219003-113219003;hs8:113764541-113764541,hs8:113770774-113770774;hs8:113810966-113810966,hs8:113390335-113390335;hs8:113811794-113811794,hs8:114879628-114879628;hs8:114762149-114762149,hs8:113202250-113202250;hs8:114784427-114784427,hs8:113525004-113525004;hs8:114801509-114801509,hs8:113810997-113810997;hs8:114801509-114801509,hs8:113810990-113810990;hs8:115422856-115422856,hs8:113419285-113419285;hsY:4972219-4972219,hsY:7366508-7366508	BCKDHB;CCND3;CDK8;CFH;CLIC5;CSMD1;CSMD3;CYP39A1;DAAM2;DENND3;FECH;FKBP5;HNRNPA2B1;IQCJ-SCHIP1;KIAA1377;LOC100192378;LOC100505783;LOC100616530;LRP12;MIPEP;MSRA;NDFIP2;NUDCD1;OR2L13;PCDH11Y;PCDH9;PDE1A;PLCG2;PPP2R5D;RBM26;RIMS2;SACS;SLC8A1;SOX5;SRPK1;STX8;SUPT3H;TSNAX-DISC1;VPS13D;XDH;ZFAND3	Pfizer Oncology, San Diego, CA, USA	Elucidating the molecular basis of hepatocellular carcinoma (HCC) is crucial to developing targeted diagnostics and therapies for this deadly disease. The landscape of somatic genomic rearrangements (GRs), which can lead to oncogenic gene fusions, remains poorly characterized in HCC. We have predicted 4314 GRs including large-scale insertions, deletions, inversions and translocations based on the whole-genome sequencing data for 88 primary HCC tumor/non-tumor tissues. We identified chromothripsis in 5 HCC genomes (5.7%) recurrently affecting chromosomal arms 1q and 8q. Albumin (ALB) was found to harbor GRs, deactivating mutations and deletions in 10% of cohort. Integrative analysis identified a pattern of paired intra-chromosomal translocations flanking focal amplifications and asymmetrical patterns of copy number variation flanking breakpoints of translocations. Furthermore, we predicted 260 gene fusions which frequently result in aberrant over-expression of the 3' genes in tumors and validated 18 gene fusions, including recurrent fusion (2/88) of ABCB11 and LRP2.	GRCh37/hg19	GSE25097		ERP001196	Yes	NUDCD1,RIMS2;SUPT3H,DAAM2;XDH,SLC8A1
CTDB0005	Research	24462510	Julio Fernandez-Banet, Nikki P. Lee, Kin Tak Chan, Huan Gao, Xiao Liu, Wing-Kin Sung,Winnie Tan, Sheung Tat Fan, Ronnie T. Poon, Shiyong Li, Keith Ching, Paul A. Rejto, Mao Mao, Zhengyan Kan	Decoding complex patterns of genomic rearrangement in hepatocellular carcinoma 	Genomics	2014 Jan	4,8	Hepatocellular carcinoma	Next Generation Sequencing	Homo sapiens	64T	Illumina HiSeq 2000	chr11:81895173-81911689:-1;chr12:100380237-100380309:1;chr14:106465634-106465776:-1;chr16:71944843-72006656:1;chr19:34673545-34709430:-1;chr1:215839087-215841241:-1;chr1:239438785-239633471:-1;chr2:11932745-11933488:1;chr3:193693498-193711106:-1;chr4:102549929-172081640:1;chr4:103409918-124865736:-1;chr4:106592727-170879794:1;chr4:109495142-174565906:-1;chr4:109495203-146836679:1;chr4:109565065-131888870:-1;chr4:111356876-174566198:1;chr4:113579060-124869332:1;chr4:121603891-125359396:1;chr4:124869276-175779672:1;chr4:132387940-146109529:1;chr4:147217604-175456604:-1;chr4:156397009-170879851:-1;chr4:172086657-178228788:-1;chr4:174566176-185501895:1;chr5:105255679-105258762:1;chr6:40965786-40965834:-1;chr7:41670302-41671109:-1;chr8:103195676-133607161:-1;chr8:103597286-103777796:-1;chr8:114439123-130455247:1;chr8:116385448-136103421:-1;chr8:117859836-118936351:1;chr8:122849206-129962339:1;chr8:124332270-125052786:-1;chr8:128894210-130370996:-1;chr8:129521077-135933749:-1;chr8:134777811-135512849:-1;chr8:137370708-138347859:-1;chr8:37876634-43614284:-1;chr8:48261425-49309404:1;chr8:48547636-49746817:-1;chr8:56847967-56952661:-1;chr8:65089340-75699428:-1;chr8:74072815-137398911:1;chr8:75492808-77422181:-1;chr8:77421600-91690139:-1;chr8:79228371-81714172:1;chr8:95027444-117688871:-1;chr8:98797220-127675980:-1;chr8:99718262-125906991:1;chr9:135687892-135687950:1	hs1:36303339-36303339,hs1:36281525-36281525;hs2:164288513-164288513,hs14:82326148-82326148;hs4:106021401-106021401,hs4:150134375-150134375;hs4:143752099-143752099,hs4:136925771-136925771;hs4:172461695-172461695,hs4:147039565-147039565;hs4:174566383-174566383,hs4:147217604-147217604;hs8:56490078-56490078,hs8:37726767-37726767;hs8:68724742-68724742,hs8:68728980-68728980;hs8:69855876-69855876,hs8:69853896-69853896;hs8:77582980-77582980,hs8:80242614-80242614;hs8:77861557-77861557,hs8:77862675-77862675;hs8:79323100-79323100,hs8:79546151-79546151;hs8:79323411-79323411,hs8:79323674-79323674;hs8:101095006-101095006,hs8:134405629-134405629;hs8:101717551-101717551,hs8:131949480-131949480;hs8:103002232-103002232,hs8:131946810-131946810;hs8:103112358-103112358,hs10:901103-901103;hs8:103245907-103245907,hs8:118855185-118855185;hs8:103586116-103586116,hs8:103586304-103586304;hs8:103778146-103778146,hs8:117937970-117937970;hs8:104332473-104332473,hs8:104333412-104333412;hs8:116201762-116201762,hs8:103095381-103095381;hs8:118867203-118867203,hs8:118865816-118865816;hs8:119143960-119143960,hs10:900860-900860;hs8:127012676-127012676,hs8:99186903-99186903;hs8:129961177-129961177,hs8:129694309-129694309;hs8:130381233-130381233,hs8:126390246-126390246;hs8:130390627-130390627,hs8:98846696-98846696;hs8:130461838-130461838,hs8:136239100-136239100;hs8:131583499-131583499,hs8:130381878-130381878;hs8:133409994-133409994,hs8:138635123-138635123;hs8:135719141-135719141,hs8:136228459-136228459;hs8:136103597-136103597,hs8:136104889-136104889;hs8:137172350-137172350,hs8:94648196-94648196;hs10:900860-900860,hs8:119143960-119143960;hs10:11382639-11382639,hs8:130365555-130365555;hs10:11740121-11740121,hs10:11741973-11741973;hs10:12301195-12301195,hs10:1059278-1059278;hs11:12316286-12316286,hs1:31033224-31033224;hs12:106109871-106109871,hs1:27064182-27064182;hs16:13956409-13956409,hs9:79921336-79921336;hs16:32146478-32146478,hs16:26669738-26669738;hs19:18099404-18099404,hs19:18097016-18097016;hs19:18807594-18807594,hs19:18818887-18818887;hs19:19561653-19561653,hs19:19562727-19562727;hs19:19611425-19611425,hs19:19614380-19614380;hs19:19655285-19655285,hs19:19657425-19657425;hs19:21085362-21085362,hs19:21084072-21084072;hs21:23284828-23284828,hs7:46116145-46116145	ADCY8;AK8;ARHGEF38;ARID1A;ATAD2;CILP2;CRTC1;CSMD3;EIF2C4;EIF3H;EXT1;FER1L6;FZD6;GATAD2A;GTPBP4;INPP4B;IST1;KCNN1;KCNQ3;KIAA0146;LAPTM4B;LARP4B;LOC100192378;LOC100505545;LOC100505718;LOC100506085;LOC285456;LOC642924;LOC647323;LPIN1;LRRC6;LSM14A;LYN;MICALCL;NCALD;PABPC1;PKD1L3;PVT1;RAB11FIP1;RAD21;RGS22;RRM2B;SLC10A7;STK3;USH2A;VPS13A;ZFAT;ZNF704;ZNF827	Pfizer Oncology, San Diego, CA, USA	Elucidating the molecular basis of hepatocellular carcinoma (HCC) is crucial to developing targeted diagnostics and therapies for this deadly disease. The landscape of somatic genomic rearrangements (GRs), which can lead to oncogenic gene fusions, remains poorly characterized in HCC. We have predicted 4314 GRs including large-scale insertions, deletions, inversions and translocations based on the whole-genome sequencing data for 88 primary HCC tumor/non-tumor tissues. We identified chromothripsis in 5 HCC genomes (5.7%) recurrently affecting chromosomal arms 1q and 8q. Albumin (ALB) was found to harbor GRs, deactivating mutations and deletions in 10% of cohort. Integrative analysis identified a pattern of paired intra-chromosomal translocations flanking focal amplifications and asymmetrical patterns of copy number variation flanking breakpoints of translocations. Furthermore, we predicted 260 gene fusions which frequently result in aberrant over-expression of the 3' genes in tumors and validated 18 gene fusions, including recurrent fusion (2/88) of ABCB11 and LRP2.	GRCh37/hg19	GSE25097		ERP001196	Yes	FER1L6-AS1,ATAD2;LARP4B,NCALD;LOC285456,ZNF827;RAD21,EXT1
CTDB0006	Research	24462510	Julio Fernandez-Banet, Nikki P. Lee, Kin Tak Chan, Huan Gao, Xiao Liu, Wing-Kin Sung,Winnie Tan, Sheung Tat Fan, Ronnie T. Poon, Shiyong Li, Keith Ching, Paul A. Rejto, Mao Mao, Zhengyan Kan	Decoding complex patterns of genomic rearrangement in hepatocellular carcinoma 	Genomics	2014 Jan	5,6,8	Hepatocellular carcinoma	Next Generation Sequencing	Homo sapiens	172T	Illumina HiSeq 2000	chr10:10051003-10052023:1;chr11:41512269-41733251:1;chr11:88223296-88228599:1;chr12:92625984-92627496:1;chr13:94471716-94967268:1;chr14:35009793-36335438:1;chr14:45077719-45084845:1;chr15:89972297-89972392:1;chr17:63340100-63356474:1;chr18:2365198-2366710:1;chr18:23937090-23937284:1;chr18:26455189-26455568:1;chr18:27107918-27110932:1;chr18:8534188-8550686:1;chr20:14837336-15068900:1;chr21:38898415-38903014:1;chr21:40789981-40790716:1;chr2:1865608-1865769:1;chr2:44435710-44598872:1;chr2:55935032-56004654:1;chr2:57031863-57032517:1;chr3:100097590-100150293:1;chr3:188304251-188556373:1;chr3:237018-237452:1;chr3:59804088-59804159:1;chr3:9375294-9491177:1;chr4:138014618-141690684:1;chr4:2429134-2429236:1;chr4:42592600-42592708:1;chr5:10213227-10213392:1;chr5:11015881-11019157:1;chr5:11564826-14457566:1;chr5:12543675-12544226:1;chr5:1396087-1616608:1;chr5:14189219-14809528:1;chr5:14220006-19542336:1;chr5:14334754-23640791:1;chr5:1477839-22967118:1;chr5:1622046-5767200:1;chr5:16571082-28963504:1;chr5:180044484-180045491:1;chr5:19563981-23546575:1;chr5:23597185-23720076:1;chr5:305672-10355780:1;chr5:464224-10255486:1;chr5:4893853-24001982:1;chr5:5328131-5862262:1;chr5:5663477-13320272:1;chr5:5758896-23718587:1;chr5:6755464-19607989:1;chr5:7886969-14827491:1;chr5:795023-1543664:1;chr5:8443743-9062774:1;chr5:9080504-22968161:1;chr6:11618091-11777956:1;chr6:43532095-43535523:1;chr6:5449672-5454059:1;chr6:5458546-6111528:1;chr6:5462364-11699345:1;chr6:5468965-7835514:1;chr6:5956210-11695773:1;chr6:5956210-11695823:1;chr6:6107798-7872067:1;chr6:6340781-11781130:1;chr6:65440058-67675963:1;chr6:7917744-11779800:1;chr8:17440427-30390723:1;chr8:18105994-29827622:1;chr8:23943758-29423238:1;chr8:30321556-30322484:1;chr8:38023193-39300280:1;chr8:70728634-140423708:1;chr8:73298385-125801646:1;chr9:114358123-114398971:1;chrX:19848352-20220688:1;chrX:39125286-39126165:1;chrX:76085104-76085876:1;chrX:96343876-96344599:1	hs10:32936400-32936400,hs1:171667047-171667047;hs10:50262499-50262499,hs6:134043724-134043724;hs11:18920395-18920395,hs11:18919178-18919178;hs11:18979009-18979009,hs11:18981385-18981385;hs11:98229200-98229200,hs11:123802464-123802464;hs11:123802223-123802223,hs11:98229225-98229225;hs13:54689582-54689582,hs5:26511-26511;hs14:38975592-38975592,hs14:38972823-38972823;hs14:86463888-86463888,hs6:38300981-38300981;hs17:28721365-28721365,hs17:28555875-28555875;hs17:45721478-45721478,hsX:39125375-39125375;hs18:50513688-50513688,hs18:27068052-27068052;hs19:19165634-19165634,hs19:19163503-19163503;hs5:26527-26527,hs13:54689564-54689564;hs5:253701-253701,hs5:16540536-16540536;hs5:671403-671403,hs5:256527-256527;hs5:2334545-2334545,hs5:4506713-4506713;hs5:5856154-5856154,hs5:5753910-5753910;hs5:5877309-5877309,hs5:8439829-8439829;hs5:5888559-5888559,hs5:6450687-6450687;hs5:6753770-6753770,hs5:6784796-6784796;hs5:6784791-6784791,hs5:6784605-6784605;hs5:6964269-6964269,hs5:16900080-16900080;hs5:7654115-7654115,hs5:15283661-15283661;hs5:7656828-7656828,hs5:5945436-5945436;hs5:9465754-9465754,hs5:6602002-6602002;hs5:11565776-11565776,hs5:20231496-20231496;hs5:13316329-13316329,hs5:9462770-9462770;hs5:14456164-14456164,hs5:16098130-16098130;hs5:15288863-15288863,hs5:14843739-14843739;hs5:19179321-19179321,hs5:1402045-1402045;hs5:19247108-19247108,hs5:28368087-28368087;hs5:23570650-23570650,hs5:6018136-6018136;hs5:23604532-23604532,hs5:5767990-5767990;hs5:28369940-28369940,hs5:1544551-1544551;hs5:61454023-61454023,hs5:61449963-61449963;hs6:5449718-5449718,hs6:5450171-5450171;hs6:5465398-5465398,hs6:6350653-6350653;hs6:6106984-6106984,hs6:11616666-11616666;hs6:6106984-6106984,hs6:11616641-11616641;hs6:6106984-6106984,hs6:11616654-11616654;hs6:6342063-6342063,hs6:11825975-11825975;hs6:6351984-6351984,hs6:6343180-6343180;hs6:7875083-7875083,hs6:5462722-5462722;hs6:7893933-7893933,hs6:11790612-11790612;hs6:11559755-11559755,hs6:5468543-5468543;hs6:11560346-11560346,hs6:11828899-11828899;hs6:11616666-11616666,hs6:6106982-6106982;hs6:11784151-11784151,hs6:5450260-5450260;hs6:11793320-11793320,hs6:6111850-6111850;hs6:37615498-37615498,hs6:37597857-37597857;hs6:38300981-38300981,hs14:86463888-86463888;hs6:43495270-43495270,hs6:43489493-43489493;hs6:43984615-43984615,hs6:43987113-43987113;hs6:53494861-53494861,hs6:53495420-53495420;hs6:98473392-98473392,hs6:98473565-98473565;hs6:99000252-99000252,hs6:83983758-83983758;hs6:100946081-100946081,hs6:83982749-83982749;hs8:4686344-4686344,hs8:61983099-61983099;hs8:30044559-30044559,hs8:30130426-30130426;hs8:36661291-36661291,hs8:36639876-36639876;hs8:72164328-72164328,hs8:90634225-90634225;hs8:75136267-75136267,hs8:75138504-75138504;hs8:90634247-90634247,hs8:72164440-72164440;hsX:39125377-39125377,hs17:45721476-45721476	ADCY2;AHRR;ANKH;ARMC6;ATP8A1;BMP6;BRMS1L;BTBD9;C10orf68;C6orf105;CAMKMT;CCT5;CDH18;CPD;CSMD1;CTNND2;DCC;DIAPH2;DNAJC25;EXOC3;EYA1;EYS;FAM134B;FARS2;FHIT;FLT4;GPC6;KCNU1;LCA5L;LNP1;LOC402160;LOC728613;LOC729506;LPCAT1;LPP;LSM1;LY86-AS1;MACROD2;MDGA1;ME1;MIR548O2;MTRR;MUTED-TXNDC5;MYO10;MYT1L;NSUN2;PAPD7;PDGFRL;PPM1B;PTGR1;RBPMS;RPS6KA3;SDHA;SEMA5A;SETD5;SH3KBP1;SLC6A3;SLC6A4;SLCO5A1;TAF4B;TMEM170B;TOMM70A;TPPP;TRIO;UBE2QL1;VSTM4;XPO5	Pfizer Oncology, San Diego, CA, USA	Elucidating the molecular basis of hepatocellular carcinoma (HCC) is crucial to developing targeted diagnostics and therapies for this deadly disease. The landscape of somatic genomic rearrangements (GRs), which can lead to oncogenic gene fusions, remains poorly characterized in HCC. We have predicted 4314 GRs including large-scale insertions, deletions, inversions and translocations based on the whole-genome sequencing data for 88 primary HCC tumor/non-tumor tissues. We identified chromothripsis in 5 HCC genomes (5.7%) recurrently affecting chromosomal arms 1q and 8q. Albumin (ALB) was found to harbor GRs, deactivating mutations and deletions in 10% of cohort. Integrative analysis identified a pattern of paired intra-chromosomal translocations flanking focal amplifications and asymmetrical patterns of copy number variation flanking breakpoints of translocations. Furthermore, we predicted 260 gene fusions which frequently result in aberrant over-expression of the 3' genes in tumors and validated 18 gene fusions, including recurrent fusion (2/88) of ABCB11 and LRP2.	GRCh37/hg19	GSE25097		ERP001196	Yes	C6orf105,MUTED-TXNDC5;CAMKMT,PPM1B;CPD,SLC6A4;EXOC3,CCT5;FARS2,BMP6;FARS2,LY86-AS1;LOC729506,SEMA5A;MARCH6,PDCD6;RBPMS,PDGFRL;RPS6KA3,SH3KBP1;SDHA,FAM134B;SLC6A3,LOC728613;TPPP,SDHA;TRIO,MARCH11
CTDB0007	Research	23911237	Ruth N. MacKinnon, Lynda J. Campbell	Chromothripsis under the microscope: a cytogenetic perspective of two cases of AML with catastrophic chromosome rearrangement	Cancer Genet	2013 May	1,4,18	Acute myeloid leukemia		Homo sapiens	Case1	Illumina CytoSNP 12				Victorian Cancer Cytogenetics Service, St Vincent's Hospital Melbourne, Fitzroy, Australia	Chromothripsis is a recently described phenomenon identified in cancer cells that produces catastrophic chromosome reorganization of one or a small number of chromosomes. It has been proposed that the multiple breakage events occur at a single point in time. Here we introduce the term anachromosome to describe an abnormal chromosome produced by chromothripsis. We report two cases of acute myeloid leukemia matching the description of chromothripsis that illustrate different aspects of this phenomenon from a cytogenetic perspective. Fluorescence in situ hybridization (FISH) analyses, including multicolor FISH and FISH for repeat elements that are not present on microarrays and that are resistant to sequencing, helped interpret the rearrangements but did not reveal their level of complexity. The anachromosomes conformed to the normal constraints of chromosome structure by including segments that provide two telomeres and a centromere. In patient samples, there are mixtures of cells with and without deletions. The deletion B allele frequencies for heterozygous loci in a mixture of cells with and without the deletions create a distinctive array pattern that is consistent with all the deletions in the anachromosomes having occurred concurrently. This evidence supporting the single-event hypothesis for chromothripsis has not previously been highlighted, to our knowledge. In the context of exploring mechanisms for chromosome shattering, we discuss a possible connection between chromosome pulverization and fragile sites. Understanding chromothripsis in the context of chromosome biology will help us identify its causes and consequences.					Yes	NA
CTDB0008	Research	23911237	Ruth N. MacKinnon, Lynda J. Campbell	Chromothripsis under the microscope: a cytogenetic perspective of two cases of AML with catastrophic chromosome rearrangement	Cancer Genet	2013 May	1,5	Acute myeloid leukemia		Homo sapiens	Case2	Illumina CytoSNP 12				Victorian Cancer Cytogenetics Service, St Vincent's Hospital Melbourne, Fitzroy, Australia	Chromothripsis is a recently described phenomenon identified in cancer cells that produces catastrophic chromosome reorganization of one or a small number of chromosomes. It has been proposed that the multiple breakage events occur at a single point in time. Here we introduce the term anachromosome to describe an abnormal chromosome produced by chromothripsis. We report two cases of acute myeloid leukemia matching the description of chromothripsis that illustrate different aspects of this phenomenon from a cytogenetic perspective. Fluorescence in situ hybridization (FISH) analyses, including multicolor FISH and FISH for repeat elements that are not present on microarrays and that are resistant to sequencing, helped interpret the rearrangements but did not reveal their level of complexity. The anachromosomes conformed to the normal constraints of chromosome structure by including segments that provide two telomeres and a centromere. In patient samples, there are mixtures of cells with and without deletions. The deletion B allele frequencies for heterozygous loci in a mixture of cells with and without the deletions create a distinctive array pattern that is consistent with all the deletions in the anachromosomes having occurred concurrently. This evidence supporting the single-event hypothesis for chromothripsis has not previously been highlighted, to our knowledge. In the context of exploring mechanisms for chromosome shattering, we discuss a possible connection between chromosome pulverization and fragile sites. Understanding chromothripsis in the context of chromosome biology will help us identify its causes and consequences.					Yes	NA
CTDB0009	Research	23550136	Jonathan J. M. Landry, Paul Theodor Pyl, Tobias Rausch, Thomas Zichner, Manu M. Tekkedil, Adrian M. Stutz, Anna Jauch, Raeka S. Aiyar, Gregoire Pau, Nicolas Delhomme, Julien Gagneur, Jan O. Korbel, Wolfgang Huber, Lars M. Steinmetz	The Genomic and Transcriptomic Landscape of a HeLa Cell Line	G3 (Bethesda)	2013 Mar	5,11,19,X	Cervical cancer	Next Generation Sequencing	Homo sapiens	23550136_1	Illumina HiSeq 2000				European Molecular Biology Laboratory, Genome Biology Unit, 69117 Heidelberg, Germany, and University Hospital Heidelberg, Institute of Human Genetics, 69120 Heidelberg, Germany	HeLa is the most widely used model cell line for studying human cellular and molecular biology. To date, no genomic reference for this cell line has been released, and experiments have relied on the human reference genome. Effective design and interpretation of molecular genetic studies performed using HeLa cells require accurate genomic information. Here we present a detailed genomic and transcriptomic characterization of a HeLa cell line. We performed DNA and RNA sequencing of a HeLa Kyoto cell line and analyzed its mutational portfolio and gene expression profile. Segmentation of the genome according to copy number revealed a remarkably high level of aneuploidy and numerous large structural variants at unprecedented resolution. Some of the extensive genomic rearrangements are indicative of catastrophic chromosome shattering, known as chromothripsis. Our analysis of the HeLa gene expression profile revealed that several pathways, including cell cycle and DNA repair, exhibit significantly different expression patterns from those in normal human tissues. Our results provide the first detailed account of genomic variants in the HeLa genome, yielding insight into their impact on gene expression and cellular function as well as their origins. This study underscores the importance of accounting for the strikingly aberrant characteristics of HeLa cells when designing and interpreting experiments, and has implications for the use of HeLa as a model of human biology.	GRCh37/hg19		phs000643		Yes	NA
CTDB0010	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	2	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG014	Illumina HiSeq 2000	chr11:5741151-5765859:-1;chr12:65705844-65860964:1;chr12:81020356-81057622:1;chr2:170199813-170326345:-1;chr2:57315075-77261648:-1;chr2:58945897-64101169:1;chr2:59398168-62198357:1;chr2:61030770-64950932:1;chr2:61603741-64186434:1;chr2:61959737-65021132:-1;chr2:64107369-83051955:1;chr2:64110075-65196092:1;chr2:64113324-65011399:-1;chr2:65060073-83052605:1;chr2:79181777-83926268:-1;chr6:76460862-77861329:-1;chr6:76957466-76993247:1;chr8:129070957-129271216:1	hs17:25765380-25765380,hs2:176675354-176675354;hs17:48938937-48938937,hs2:119668564-119668564;hs17:48922187-48922187,hs2:119665556-119665556;hs2:35595408-35595408,hs2:117065447-117065447;hs2:82171889-82171889,hs2:83807361-83807361;hs2:79094169-79094169,hs2:83058298-83058298;hs2:60090711-60090711,hs2:62199561-62199561;hs2:65279526-65279526,hs2:65287675-65287675;hs2:64079006-64079006,hs2:64192609-64192609;hs2:77936878-77936878,hs2:84222375-84222375;hs2:83398215-83398215,hs6:136004781-136004781;hs2:60450993-60450993,hs2:60495932-60495932;hs2:83700519-83700519,hs2:84985328-84985328;hs2:61026746-61026746,hs2:65237642-65237642;hs2:64077491-64077491,hs2:65019980-65019980;hs2:60485726-60485726,hs2:61960697-61960697;hs4:43228837-43228837,hs17:49888087-49888087;hs6:75376489-75376489,hs6:76456545-76456545;hs6:75942261-75942261,hs6:76460877-76460877;hs6:41494848-41494848,hs6:69619654-69619654;hs6:75965673-75965673,hs6:118982169-118982169		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0011	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	1,2,9,17	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG028	Illumina HiSeq 2000	chr10:119070367-121619306:-1;chr11:35141779-35165434:-1;chr14:36701359-36840978:-1;chr14:72625917-72666602:-1;chr17:21644130-22782616:1;chr17:40668478-40735550:-1;chr18:51225332-51298777:-1;chr19:7005812-14457285:1;chr1:1297525-1346091:-1;chr1:152467650-152471574:-1;chr2:146440464-148588487:-1;chr3:189003121-189799358:-1;chr6:30004458-30022379:-1;chr6:31200494-32919822:-1;chr9:21854346-21958850:-1	hs1:56808946-56808946,hs6:106644529-106644529;hs1:56808986-56808986,hs6:106644512-106644512;hs1:204432648-204432648,hs1:210243172-210243172;hs17:24009064-24009064,hs17:36056640-36056640;hs19:54622010-54622010,hs19:63789465-63789465;hs19:62436306-62436306,hs2:146408009-146408009;hs2:113889788-113889788,hs4:191114592-191114592;hs4:49021102-49021102,hs1:141547959-141547959;hsX:136261018-136261018,hsX:153961240-153961240		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0012	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	6,9,13,15,18	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG034	Illumina HiSeq 2000	chr11:89591175-89603940:-1;chr19:10201579-10243189:-1;chr3:116907103-117124779:1;chr3:30882610-32919140:1;chr4:27509942-27522063:1;chr6:32556135-32787998:1;chr9:73648796-135984683:-1;chr9:74010545-122137819:1;chr9:74012466-135928486:-1	hs1:7917554-7917554,hs2:212411334-212411334;hs1:211480185-211480185,hs1:233469225-233469225;hs1:211480438-211480438,hs1:233470458-233470458;hs12:59079221-59079221,hs3:104717848-104717848;hs13:19333012-19333012,hs6:58448015-58448015;hs13:74231050-74231050,hs6:148187364-148187364;hs15:43161536-43161536,hs15:44265431-44265431;hs18:99044-99044,hsX:29179265-29179265;hs18:3223258-3223258,hs7:31794203-31794203;hs18:35202776-35202776,hs18:35963496-35963496;hs18:38646689-38646689,hs9:72929765-72929765;hs18:55281977-55281977,hs9:100213501-100213501;hs18:58944466-58944466,hs14:105453750-105453750;hs18:60448528-60448528,hs9:80921411-80921411;hs18:60448860-60448860,hs9:80920106-80920106;hs4:19855480-19855480,hs5:160965636-160965636;hs4:114010531-114010531,hs8:135704572-135704572;hs9:29523040-29523040,hs13:64616941-64616941;hs9:68504374-68504374,hs9:135678585-135678585;hs9:87562349-87562349,hs9:135983249-135983249;hsX:27045422-27045422,hs2:64728521-64728521		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0013	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	1	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG043	Illumina HiSeq 2000	chr11:48324097-48330277:-1;chr11:5741151-5765859:-1;chr11:5741151-5765859:-1;chr1:12250777-193382205:-1;chr1:213285864-213354216:-1;chr1:228454814-228632682:-1	hs1:6929266-6929266,hs1:223002855-223002855;hs1:9608555-9608555,hs1:17082878-17082878;hs1:16411862-16411862,hs1:204052851-204052851;hs1:41088909-41088909,hs1:211452286-211452286;hs1:193508150-193508150,hs1:197311616-197311616;hs1:209387883-209387883,hs1:215984986-215984986;hs18:58938257-58938257,hs14:105425455-105425455;hs20:28212606-28212606,hs3:84522975-84522975;hs3:80977085-80977085,hs1:158052243-158052243		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0014	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	6,8,12,15	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG065	Illumina HiSeq 2000	chr11:71343029-73802765:-1;chr12:68010736-68052393:1;chr13:49224823-50468703:-1;chr5:72192415-72193673:-1;chr6:105567621-132861645:-1;chr6:139952895-147336937:1;chr6:3009669-139952687:1	hs1:98275905-98275905,hs1:113273697-113273697;hs12:14506772-14506772,hs7:149989270-149989270;hs12:14514646-14514646,hs15:53207573-53207573;hs12:16829260-16829260,hs15:54045543-54045543;hs12:29522767-29522767,hs12:32709099-32709099;hs12:47646759-47646759,hs6:149700841-149700841;hs12:79781431-79781431,hs15:82417226-82417226;hs12:119440408-119440408,hs6:142993440-142993440;hs15:40231347-40231347,hs12:80162742-80162742;hs15:100006694-100006694,hs7:121288645-121288645;hs19:11504357-11504357,hs22:16500825-16500825;hs3:31670104-31670104,hs5:78448167-78448167;hs4:49021102-49021102,hs1:141547959-141547959;hs6:110462792-110462792,hs6:149748688-149748688;hs6:132761733-132761733,hs6:139232864-139232864;hs8:11037250-11037250,hs7:16958961-16958961;hs8:11613426-11613426,hs8:15450879-15450879;hs8:11631937-11631937,hs12:80817101-80817101;hs8:12284062-12284062,hs15:53985158-53985158;hs8:15450613-15450613,hs12:80256871-80256871;hs8:15554496-15554496,hs12:68010980-68010980;hs8:27950108-27950108,hs1:204062668-204062668		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0015	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	1,7	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG074	Illumina HiSeq 2000	chr1:161136806-164717238:-1;chr1:165516699-166573985:-1;chr1:165525571-166580798:1;chr1:169353666-169846970:1;chr1:169966121-171343966:-1;chr2:85107885-85109419:-1;chr7:105070585-106658688:-1;chr7:110440087-110968574:-1;chr7:85466212-104951519:1;chr7:87605427-106955682:-1;chr9:13774490-125208378:-1;chr9:22774444-125209873:1;chrX:151065582-151261917:-1	hs7:112055184-112055184,hs7:112094401-112094401;hs1:165837846-165837846,hs1:169870169-169870169;hs7:105066896-105066896,hs7:106645924-106645924;hs7:111796478-111796478,hs7:111806087-111806087;hs7:111916426-111916426,hs7:112093752-112093752;hs1:168679194-168679194,hs1:168895539-168895539;hs1:13101833-13101833,hs7:109944707-109944707;hsY:11929072-11929072,hs10:41706096-41706096;hs7:82539845-82539845,hs13:99069416-99069416;hs7:109852760-109852760,hs7:109873275-109873275;hs7:89334567-89334567,hs7:106168598-106168598;hs7:97968349-97968349,hs7:110474110-110474110;hs2:88942551-88942551,hs2:88978418-88978418;hs20:28252248-28252248,hs7:105752285-105752285;hs1:159430181-159430181,hs1:172193289-172193289;hs9:44010661-44010661,hs2:94838950-94838950;hs1:163359478-163359478,hs1:163382721-163382721;hs17:827988-827988,hs3:80842380-80842380;hs3:57430662-57430662,hs3:60881705-60881705		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0016	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	1,4,11,12	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG081	Illumina HiSeq 2000	chr10:135210223-135221652:-1;chr11:48324097-48330277:-1;chr11:77458412-77470894:-1;chr12:62518696-62526039:-1;chr15:42783127-42792027:-1;chr19:1839676-56743095:-1;chr19:57953041-61224839:-1;chr2:15290346-15403819:-1;chr2:228700177-228775363:-1;chr2:60515103-60536057:1;chr3:103031169-103221628:1;chr3:120755640-120766403:-1;chr5:77661760-77791264:-1;chr6:78415700-159397414:-1;chr7:31109735-31122428:1;chr8:59981864-60072798:-1;chr9:104534247-104552540:1	hs1:169413686-169413686,hs1:169451283-169451283;hs11:58248849-58248849,hs11:58291772-58291772;hs12:14067180-14067180,hs12:14086713-14086713;hs12:14076874-14076874,hs2:222123802-222123802;hs12:93617229-93617229,hs12:93641630-93641630;hs12:93624809-93624809,hs12:93640657-93640657;hs4:38520630-38520630,hs4:38536299-38536299;hs4:65363665-65363665,hs4:65373125-65373125;hs4:65364279-65364279,hs4:65411541-65411541		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0017	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	2,8	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG116	Illumina HiSeq 2000	chr10:37310572-59129250:-1;chr11:48324097-48330277:-1;chr12:126618424-126647066:1;chr13:18813546-53873925:-1;chr18:20509151-46914186:-1;chr1:237482552-237691235:1;chr1:3327087-8593408:-1;chr2:40798455-50552509:1;chr2:51424401-51528988:1;chr2:51425299-53158169:-1;chr3:1807114-3815014:1;chr6:109617475-110600692:1;chr6:109684178-109707834:1;chr6:109749781-109925749:1;chr6:136951284-139215017:-1;chr9:104573081-129090329:1;chrX:7327904-37082985:-1	hs10:109651099-109651099,hs10:109682554-109682554;hs10:127180408-127180408,hs10:127191092-127191092;hs14:86394108-86394108,hs14:99079370-99079370;hs14:105397889-105397889,hs3:189143698-189143698;hs14:105397897-105397897,hs3:189143731-189143731;hs2:53751682-53751682,hs7:158463320-158463320;hs22:15293067-15293067,hs6:165001564-165001564;hs3:2928142-2928142,hs3:5234158-5234158;hs3:3820714-3820714,hs3:5631812-5631812;hs3:5653917-5653917,hs3:5741494-5741494;hs3:23819256-23819256,hs3:23831402-23831402;hs3:26226052-26226052,hs3:28419205-28419205;hs3:27553307-27553307,hs2:34024816-34024816;hs3:156749177-156749177,hs3:192809310-192809310;hs3:178046832-178046832,hs3:192809461-192809461;hs5:2255807-2255807,hs20:51824061-51824061;hs6:108388775-108388775,hs6:110631606-110631606;hs6:109707669-109707669,hs6:109714992-109714992;hs6:109740948-109740948,hs6:109764520-109764520;hs6:109908135-109908135,hs4:150073818-150073818;hs6:109912609-109912609,hs6:109928181-109928181;hs6:112095624-112095624,hs6:114557104-114557104;hs8:4485226-4485226,hsX:57953555-57953555;hs8:19772839-19772839,hs8:137370851-137370851;hs9:5725249-5725249,hs8:121983547-121983547;		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0018	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	16,17,2,6,8,X	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG132	Illumina HiSeq 2000	chr16:28538120-29886949:-1;chr2:53036933-79163725:-1;chr2:59927998-114919109:1;chr2:66623177-84383564:-1;chr2:67023548-106133091:1;chr2:78392100-103293338:1;chr8:36998729-80575343:-1;chrX:33795147-34222789:1	hs17:21056252-21056252,hs17:21069872-21069872;hs17:21134312-21134312,hs10:41936522-41936522;hs2:50528422-50528422,hs2:103156366-103156366;hs2:67565481-67565481,hs2:94743186-94743186;hs2:99497033-99497033,hs2:106139452-106139452;hs6:58886185-58886185,hs13:106609271-106609271;hs8:2792863-2792863,hs8:43026187-43026187;hs8:29602247-29602247,hs8:30277494-30277494;hs8:36974639-36974639,hs8:36999408-36999408;hs8:40756189-40756189,hs8:56172812-56172812		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0019	Research	23699601	Ryan D. Morin, Karen Mungall, Erin Pleasance, Andrew J. Mungall, Rodrigo Goya, Ryan D. Huff, David W. Scott, Jiarui Ding, Andrew Roth, Readman Chiu, Richard D. Corbett, Fong Chun Chan, Maria Mendez-Lago, Diane L. Trinh, Madison Bolger-Munro, Greg Taylor, Alireza Hadj Khodabakhshi, Susana Ben-Neriah, Julia Pon, Barbara Meissner, Bruce Woolcock, Noushin Farnoud, Sanja Rogic, Emilia L. Lim, Nathalie A. Johnson, Sohrab Shah, Steven Jones, Christian Steidl, Robert Holt, Inanc Birol, Richard Moore, Joseph M. Connors, Randy D. Gascoyne, Marco A. Marra	Mutational and structural analysis of diffuse large B-cell lymphoma using whole-genome sequencing	Blood	2013 Aug	8,11,18	Diffuse large B-cell lymphoma	Next Generation Sequencing	Homo sapiens	RG138	Illumina HiSeq 2000	chr11:18716208-45329936:1;chr1:115502658-121186800:-1;chr1:6182243-95195626:-1;chr8:128525264-129544861:1;chr8:129282247-131956016:-1;chr8:50109248-70530204:1;chrX:152759760-153024102:1	hs8:50172131-50172131,hs8:70391059-70391059;hs2:4183144-4183144,hs2:4201354-4201354;hs6:58886798-58886798,hs6:75169496-75169496;hs11:45359344-45359344,hs11:46160005-46160005;hs17:21134312-21134312,hs10:41936522-41936522;hs3:183427260-183427260,hs3:183529139-183529139;hs4:105162145-105162145,hs4:106553660-106553660;hs4:105162153-105162153,hs4:105226236-105226236;hs19:1871143-1871143,hs19:2463361-2463361;hs6:58887071-58887071,hs6:76237245-76237245;hs18:35880144-35880144,hs18:55105867-55105867;hs22:15399058-15399058,hs12:120804324-120804324;hs8:37903757-37903757,hs4:190921474-190921474;hs8:50080227-50080227,hs8:70531495-70531495;hs18:35881611-35881611,hs18:52677321-52677321;hs18:36402620-36402620,hs18:54945798-54945798;hs18:36678172-36678172,hs18:52829615-52829615		Genome Sciences Centre, BC Cancer Agency, Vancouver, Canada	Diffuse large B-cell lymphoma (DLBCL) is a genetically heterogeneous cancer composed of at least 2 molecular subtypes that differ in gene expression and distribution of mutations. Recently, application of genome/exome sequencing and RNA-seq to DLBCL has revealed numerous genes that are recurrent targets of somatic point mutation in this disease. Here we provide a whole-genome-sequencing-based perspective of DLBCL mutational complexity by characterizing 40 de novo DLBCL cases and 13 DLBCL cell lines and combining these data with DNA copy number analysis and RNA-seq from an extended cohort of 96 cases. Our analysis identified widespread genomic rearrangements including evidence for chromothripsis as well as the presence of known and novel fusion transcripts. We uncovered new gene targets of recurrent somatic point mutations and genes that are targeted by focal somatic deletions in this disease. We highlight the recurrence of germinal center B-cell-restricted mutations affecting genes that encode the S1P receptor and 2 small GTPases (GNA13 and GNAI2) that together converge on regulation of B-cell homing. We further analyzed our data to approximate the relative temporal order in which some recurrent mutations were acquired and demonstrate that ongoing acquisition of mutations and intratumoral clonal heterogeneity are common features of DLBCL. This study further improves our understanding of the processes and pathways involved in lymphomagenesis, and some of the pathways mutated here may indicate new avenues for therapeutic intervention.	NCBI 36/hg18		phs000532		Yes	NA
CTDB0020	Research	23915422	Rita Genesio, Valentina Ronga, Pia Castelluccio, Gennaro Fioretti, Angela Mormile, Graziella Leone, Anna Conti, Maria Luigia Cavaliere, Lucio Nitsch	Pure 16q21q22.1 deletion in a complex rearrangement possibly caused by a chromothripsis event	Mol Cytogenet	2013 Aug	12,16	Congenital heart defects	Array CGH	Homo sapiens	23915422_1	4x44 CytoChip array			HSD11B2		Background: Partial monosomies of chromosome 16q are rare and overlapping effects from complex chromosomal rearrangements often hamper genotype-phenotype correlations for such imbalances. Here, we report the clinical features of an isolated partial monosomy 16q21q22.1 in a boy with a complex de novo rearrangement possibly resulting from a chromothripsis event. Results: The patient presented with low birth weight, microcephaly, developmental delay, facial dysmorphisms, short stature, dysmorphic ears and cardiopathy. Standard and molecular cytogenetics showed a complex rearrangement characterised by a pericentromeric inversion in one of chromosomes 12 and an inverted insertional translocation of the 12q14q21.1 region, from the rearranged chromosome 12, into the q21q22.1 tract of a chromosome 16. Array CGH analysis unravelled a partial 16q21q22.1 monosomy, localised in the rearranged chromosome 16. Conclusions: The comparison of the present case to other 16q21q22 monosomies contributed to narrow down the critical region for cardiac anomalies in the 16q22 deletion syndrome. However, more cases, well characterised both for phenotypic signs and genomic details, are needed to further restrict candidate regions for phenotypic signs in 16q deletions. The present case also provided evidence that a very complex rearrangement, possibly caused by a chromothripsis event, might be hidden behind a classical phenotype that is specific for a syndrome.	GRCh37/hg19				No	NA
CTDB0021	Research	23615946	Teles Alves I, Hiltemann S, Hartjes T, van der Spek P, Stubbs A, Trapman J, Jenster G	Gene fusions by chromothripsis of chromosome 5q in the VCaP prostate cancer cell line	Hum Genet	2013 Apr	5	Prostate cancer	Next Generation Sequencing	Homo 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VCaP cell line is widely used in prostate cancer research as it is a unique model to study castrate resistant disease expressing high levels of the wild type androgen receptor and the TMPRSS2-ERG fusion transcript. Using next generation sequencing, we assembled the structural variations in VCaP genomic DNA and observed a massive number of genomic rearrangements along the q arm of chromosome 5, characteristic of chromothripsis. Chromothripsis is a recently recognized phenomenon characterized by extensive chromosomal shattering in a single catastrophic event, mainly detected in cancer cells. Various structural events identified on chromosome 5q of VCaP resulted in gene fusions. Out of the 18 gene fusion candidates tested, 15 were confirmed on genomic level. In our set of gene fusions, only rarely we observe microhomology flanking the breakpoints. On RNA level, only five transcripts were detected and NDUFAF2-MAST4 was the only resulting in an in-frame fusion transcript. Our data indicate that although a marker of genomic instability, chromothripsis might lead to only a limited number of functionally relevant fusion genes.	NCBI 36/hg18					CPLX2,UBXD8;EBF1,FBXL17;EBF1,FEM1C;EFNA5,PCDHB7;JMY,DMGDH;KCNN2,EBF1;LMAN2,AP3S1;NDUFAF2,MAST4;PDE4D,C5orf47;PDE4D,FAM172A;PDE4D,PPP2R2B;PDE8B,UIMC1;PPP2R2B,FAM172A;RASGRF2,RNF145;TMPRSS2,ERG;TRIM40,FBXO38;YTHDC2,PPP2R2B;ZFP62,RGNEF
CTDB0022	Research	23860044	Lusine Nazaryan, Eunice G Stefanou, Claus Hansen, Nadezda Kosyakova, Mads Bak, Freddie H Sharkey, Theodora Mantziou, Anastasios D Papanastasiou, Voula Velissariou, Thomas Liehr, Maria Syrrou, and Niels Tommerup	The strength of combined cytogenetic and mate-pair sequencing techniques illustrated by a germline chromothripsis rearrangement involving FOXP2	Eur J Hum Genet	2013 Jul	2,5,7,16	Developmental delay	Next Generation Sequencing	Homo sapiens	23860044_1	Roche- Nimblegen 12x135K wholegenome array + Illumina Genome Analyzer IIx	chr7:12814117-14251879:1;chr7:13505886-114129050:1	hs2:56842021-56843702,hs5:14939951-14942072;hs5:14937322-14939104,hs7:114129941-114130585;hs2:41655927-41657380,hs5:17605465-17606575;hs16:12911097-12911134,hs18:7850070-7850105;hs5:150566906-150566941,hs14:59017557-59017594;hs2:41654255-41655319,hs2:60301348-60302967;hs5:12445869-12447205,hs5:24398254-24399503;hs5:15076731-15078724,hs5:22227821-22229757;hs2:56844026-56845886,hs2:60304057-60305174;hs5:12444115-12445044,hs5:15074553-15076007;hs7:12810996-12811974,hs7:13503520-13504608;hs2:161019051-161022248,hs2:164128044-164131466	CDH12;DGKB;FOXP2	Wilhelm Johannsen Centre for Functional Genome Research, Department of Cellular and Molecular Medicine, Faculty of Health Science, University of Copenhagen, Copenhagen, Denmark	Next-generation mate-pair sequencing (MPS) has revealed that many constitutional complex chromosomal rearrangements (CCRs) are associated with local shattering of chromosomal regions (chromothripsis). Although MPS promises to identify the molecular basis of the abnormal phenotypes associated with many CCRs, none of the reported mate-pair sequenced complex rearrangements have been simultaneously studied with state-of-the art molecular cytogenetic techniques. Here, we studied chromothripsis-associated CCR involving chromosomes 2, 5 and 7, associated with global developmental and psychomotor delay and severe speech disorder. We identified three truncated genes: CDH12, DGKB and FOXP2, confirming the role of FOXP2 in severe speech disorder, and suggestive roles of CDH12 and/or DGKB for the global developmental and psychomotor delay. Our study confirmes the power of MPS for detecting breakpoints and truncated genes at near nucleotide resolution in chromothripsis. However, only by combining MPS data with conventional G-banding and extensive fluorescence in situ hybridizations could we delineate the precise structure of the derivative chromosomes.	GRCh37/hg19				No	NA
CTDB0040	Research	23716474	Iwakawa R, Takenaka M, Kohno T, Shimada Y, Totoki Y, Shibata T, Tsuta K, Nishikawa R, Noguchi M, Sato-Otsubo A, Ogawa S, Yokota J	Genome-wide identification of genes with amplification and/or fusion in small cell lung cancer	Genes Chromosomes Cancer	2013 May	1,20	Small cell lung cancer	SNP Array	Homo sapiens	H1963	Affymetrix human 250K Nsp SNP arrays			PPIE;BMP8B;TRIT1;MYCL1;MFSD2A;CAP1;PPT1;RLF;TMCO2;ZMPSTE24;COL9A2;SMAP2;ZNF643;ZNF642;DEM1;ZNF684;RIMS3	Division of Multistep Carcinogenesis, National Cancer Center Research Institute, Tokyo 104-0045, Japan	To obtain a landscape of gross genetic alterations in small cell lung cancer (SCLC), genome-wide copy number analysis and whole-transcriptome sequencing were performed in 58 and 42 SCLCs, respectively. Focal amplification of known oncogene loci, MYCL1 (1p34.2), MYCN (2p24.3), and MYC (8q24.21), was frequently and mutually exclusively detected. MYCL1 and MYC were co-amplified with other regions on either the same or the different chromosome in several cases. In addition, the 9p24.1 region was identified as being amplified in SCLCs without amplification of MYC family oncogenes. Notably, expression of the KIAA1432 gene in this region was significantly higher in KIAA1432 amplified cells than in non-amplified cells, and its mRNA expression showed strong correlations with the copy numbers. Thus, KIAA1432 is a novel gene activated by amplification in SCLCs. By whole-transcriptome sequencing, a total of 60 fusion transcripts, transcribed from 95 different genes, were identified as being expressed in SCLC cells. However, no in-frame fusion transcripts were recurrently detected in >=2 SCLCs, and genes in the amplified regions, such as PVT1 neighboring MYC and RLF in MYCL1 amplicons, were recurrently fused with genes in the same amplicons or with those in different amplicons on either the same or different chromosome. Thus, it was indicated that amplification and fusion of several genes on chromosomes 1 and 8 occur simultaneously but not sequentially through chromothripsis in the development of SCLC, and amplification rather than fusion of genes plays an important role in its development.					Yes	RLF,MYCL1;RLF,COL9A2;RLF,BCL2L1;RLF,HM13;RLF,SMAP2;TPX2,HM13;BCL2L1,HM13;BCL2L1,DEM1;BCL2L1,RIMS3;BCL2L1,ZNF684;ZMPSTE24,MFSD2A;SMAP2,MYCL1;BCL2L1,ZNF643;PPT1,BCL2L1;BCL2L1,BMP8B;BCL2L1,RLF
CTDB0041	Research	23991058	Valentina Boeva, Stephanie Jouannet, Romain Daveau, Valerie Combaret, Cecile Pierre-Eugene, Alex Cazes, Caroline Louis-Brennetot, Gudrun Schleiermacher, Sandrine Ferrand, Gaelle Pierron, Alban Lermine, Thomas Rio Frio, Virginie Raynal, Gilles Vassal, Emma	Breakpoint Features of Genomic Rearrangements in Neuroblastoma with Unbalanced Translocations and Chromothripsis	PLoS One	2013 Aug	2,3	Neuroblastoma	Next Generation Sequencing	Homo sapiens	CLB-Re	Illumina Genome Analyzer Iix + SOLiD 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821422-51822596;hs21:18662734-18664468,hs21:18664612-18666655;hs21:39430214-39431963,hs21:39432136-39433942;hs21:43347296-43350072,hs21:43353577-43356312;hs21:43895273-43896989,hs21:43897144-43899197;hs22:23475510-23478215,hs22:23479675-23482121;hs22:46864727-46865782,hs22:46865869-46866569;hsX:117451678-117454032,hsX:117455089-117457048;hsX:136091199-136092964,hsX:136093039-136094957;hsX:147660963-147662170,hsX:147663153-147664307	ACOT12;ADAM22;ADAMTS9;ADAMTS9-AS2;ADCY8;ADRA1A;AFF2;AK8;ALK;AMPH;ANK1;APBA1;APOLD1;ARHGAP21;ARHGEF10;ARHGEF33;ARL6IP5;ASAP2;ASPRV1;ATAD2B;ATIC;ATL2;ATP13A1;ATP9B;ATXN7;BBX;BCL2;BRE;BSND;C10orf76;C1orf127;C2CD2;C2orf44;C3orf64;C3orf67;C4orf51;C8orf12;C9orf139;C9orf96;CADPS;CAPN13;CBFA2T3;CCDC164;CCDC63;CCDC75;CCDC88C;CDA;CDK5RAP2;CELF4;CELSR1;CHST9;CIB4;CLIC6;CLPTM1L;CMIP;CNTN3;CNTN4;CNTNAP2;COL17A1;COLEC11;CPM;CRIM1;CSGALNACT1;CSMD3;CYB5B;DCDC1;DHX57;DLEC1;DNAJC24;DNAJC8;DNM2;DNMT3A;DOK6;DPP6;DPYSL5;DSCR4;DTNB;DTWD2;DYM;EFR3B;EML4;EML5;EPT1;ERBB2IP;ERC1;EVC2;FAM179A;FAM19A1;FAM59B;FAM84A;FBXL14;FEZ2;FGF12;FGGY;FHIT;FKBP5;FLJ33534;FLJ43663;FNIP2;FOXP1;FRAS1;FRMD4B;FSTL4;FSTL5;G2E3;GABBR2;GALNT13;GDA;GHR;GMDS;GMIP;GPR113;GREB1;GRINA;GSK3A;GXYLT2;HAAO;HDAC4;HEATR7A;HOMER2;HPCAL1;HS1BP3;HSPG2;ICA1;IFT52;IGF1;IRF2;ISPD;ITSN2;KCNK3;KIAA1797;KIF3B;KIF3C;KLHDC4;KLHL29;KRTCAP3;LARP7;LBP;LCE1E;LDLRAD3;LINC00339;LOC100128590;LOC100271832;LOC339788;LOC387647;LOC388942;LOC400950;LOC440970;LOC641365;LOC649133;LOC728730;LPA;LPPR2;LRFN2;LRP1;LRRFIP1;LRRTM4;LTBP1;LUZP2;MAGI1;MAN1B1;MAP4K3;ME1;MEMO1;MFSD2B;MGAT4C;MIR4757;MITF;MLF1IP;MPP3;MRPL42P5;MRPS9;MTA3;MTHFD1L;MYCN;MYCNOS;MYO10;MYOCD;MYOM2;MYT1L;NBAS;NCOA1;NEDD4L;NLN;NOL10;NTF3;NTM;ODZ4;OPCML;OR7A10;OTOF;PAIP1;PARP10;PCBP1-AS1;PDIA6;PDZRN3;PEPD;PGD;PIK3C2G;PIK3CD;PITPNC1;PKDCC;PLA2G2C;PLA2R1;PLB1;PLEKHH2;POU2F3;PPP1R1C;PPP4R2;PRICKLE2;PRKCZ;PRKG1;PSD2;PTPRG;PTPRN2;PTPRZ1;PTRHD1;PVRL1;QTRT1;RAB10;RAD52;RASGEF1C;RCAN2;ROBO1;ROBO2;RPRD2;RPS23;RPS6KA2;RSPH1;RTDR1;RUFY1;SBF2;SCARA5;SDK1;SEMA3A;SGCZ;SH3PXD2A;SHISA9;SLC20A1;SLC25A25;SLC25A26;SLC8A1;SLCO3A1;SLIT3;SLK;SMAD3;SMC6;SNTG2;SOS1;SPATA13;SPI1;SRRM1;STARD3;STOX2;SYNDIG1;TAF1B;TBC1D3;TDH;TDRD5;TECPR1;TG;THADA;THSD4;TLL2;TMCC2;TMEM105;TMEM163;TMEM18;TMTC1;TP53BP2;TPO;TRIB2;TRIM37;TRIM54;TRPM2;TSHZ2;TSSC1;TTC15;TTC27;UBE2QL1;UBE2U;UBXN2A;UIMC1;USP40;VIT;VWA3B;WNK2;XRCC3;XYLT2;YPEL5;ZBTB26;ZC3H12D;ZNF236;ZNF385D;ZNF521;ZNF79	Inserm, U900, Paris, France	Neuroblastoma is a pediatric cancer of the peripheral nervous system in which structural chromosome aberrations are emblematic of aggressive tumors. In this study, we performed an in-depth analysis of somatic rearrangements in two neuroblastoma cell lines and two primary tumors using paired-end sequencing of mate-pair libraries and RNA-seq. The cell lines presented with typical genetic alterations of neuroblastoma and the two tumors belong to the group of neuroblastoma exhibiting a profile of chromothripsis. Inter and intra-chromosomal rearrangements were identified in the four samples, allowing in particular characterization of unbalanced translocations at high resolution. Using complementary experiments, we further characterized 51 rearrangements at the base pair resolution that revealed 59 DNA junctions. In a subset of cases, complex rearrangements were observed with templated insertion of fragments of nearby sequences. Although we did not identify known particular motifs in the local environment of the breakpoints, we documented frequent microhomologies at the junctions in both chromothripsis and non-chromothripsis associated breakpoints. RNA-seq experiments confirmed expression of several predicted chimeric genes and genes with disrupted exon structure including ALK, NBAS, FHIT, PTPRD and ODZ4. Our study therefore indicates that both non-homologous end joining-mediated repair and replicative processes may account for genomic rearrangements in neuroblastoma. RNA-seq analysis allows the identification of the subset of abnormal transcripts expressed from genomic rearrangements that may be involved in neuroblastoma oncogenesis.	GRCh37/hg19			ERP001414;ERP001988	Yes	ALK,CNTN3;ALK,LTBP1;ARHGEF33,THADA;ASAP2,MAGI1;ASPRV1,PCBP1-AS1;ATAD2B,MITF;BRE,MAGI1;C3orf64,PPP4R2;C3orf67,ADAMTS9;CIB4,ALK;CRIM1,FHIT;DPYSL5,THADA;FAM179A,MAP4K3;FAM59B,SOS1;FAM84A,FHIT;FHIT,ROBO1;GREB1,ATAD2B;HPCAL1,FAM179A;ITSN2,LTBP1;KCNK3,ALK;KIF3C,EPT1;KLHL29,ROBO2;KRTCAP3,FOXP1;LTBP1,MITF;MYT1L,ATL2;MYT1L,FHIT;NBAS,MAGI1;PLB1,LTBP1;PRICKLE2,MAGI1;PTRHD1,LOC100128590;RAB10,ADAMTS9;RAB10,PLB1;SLC8A1,CNTN3;SLC8A1,MAGI1;SNTG2,PRICKLE2;SNTG2,SOS1;THADA,CADPS;THADA,FHIT;TPO,THADA;TRIM54,TTC27;TTC15,ATXN7
CTDB0042	Research	23991058	Valentina Boeva, Stephanie Jouannet, Romain Daveau, Valerie Combaret, Cecile Pierre-Eugene, Alex Cazes, Caroline Louis-Brennetot, Gudrun Schleiermacher, Sandrine Ferrand, Gaelle Pierron, Alban Lermine, Thomas Rio Frio, Virginie Raynal, Gilles Vassal, Emma	Breakpoint Features of Genomic Rearrangements in Neuroblastoma with Unbalanced Translocations and Chromothripsis	PLoS One	2013 Aug	1,2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	NB1141	Illumina Genome Analyzer Iix + SOLiD V4/5500	chr10:15529190-15534526:-1;chr10:82748693-82755344:-1;chr10:83881117-83891684:-1;chr11:11820549-11826177:-1;chr11:21844990-21851266:-1;chr11:80897522-80954853:-1;chr12:117084488-117091290:-1;chr12:59934068-59949389:-1;chr12:80154933-80162240:1;chr14:29115847-29121527:-1;chr14:41606973-41672179:-1;chr14:84040576-84053462:-1;chr15:44134089-44140792:-1;chr15:98839166-98846740:-1;chr16:19942815-19970111:-1;chr16:58671655-58679585:-1;chr16:8063663-8070034:-1;chr18:40051191-40060344:-1;chr19:1947496-1954243:-1;chr19:35358488-35364082:-1;chr19:57472684-57478735:-1;chr1:1008696-33428101:1;chr1:102981985-118210856:1;chr1:104333229-160069178:-1;chr1:10532535-52086062:-1;chr1:10593721-22544984:-1;chr1:11000544-210352595:-1;chr1:11168798-210037600:-1;chr1:150207282-216546090:-1;chr1:150262096-220965516:-1;chr1:150267833-187360931:1;chr1:153924857-168223449:-1;chr1:173971109-186325486:-1;chr1:176021366-244022618:-1;chr1:176027486-210743602:1;chr1:176232171-183415615:-1;chr1:176662006-197116025:1;chr1:177243880-247265613:1;chr1:182809129-186315259:-1;chr1:182814024-245905715:1;chr1:186233169-186321810:1;chr1:187242483-223923379:-1;chr1:192433020-211838849:1;chr1:193312809-244172296:1;chr1:198301572-198313291:-1;chr1:203535803-241184504:-1;chr1:203660375-207790855:1;chr1:203738238-241394532:1;chr1:205493732-206227778:-1;chr1:2068550-227749001:1;chr1:208061423-212065304:1;chr1:22539918-26402564:-1;chr1:24470636-65806923:1;chr1:26491823-48278955:-1;chr1:27818230-53385947:1;chr1:30854615-76564199:-1;chr1:32828029-223917154:1;chr1:33387731-222083256:-1;chr1:33392618-228002678:1;chr1:35206835-186228869:1;chr1:41732082-208440994:1;chr1:42174094-62123246:-1;chr1:43711284-172794913:-1;chr1:43715503-116711705:1;chr1:44021796-46794418:-1;chr1:46869357-110734126:-1;chr1:47080149-57895203:1;chr1:48268839-70823296:-1;chr1:53388571-203532748:1;chr1:65434646-214126453:1;chr1:68578726-236343140:-1;chr1:70600665-227181629:1;chr1:71544272-187249590:-1;chr1:78381334-174930142:1;chr1:78438651-247270878:-1;chr1:82290565-226955829:-1;chr1:85083954-93405396:-1;chr1:86677932-86684957:-1;chr1:88286998-211865281:-1;chr1:92136276-102979292:1;chr1:9383812-115549141:1;chr1:94361854-173979899:-1;chr1:9649603-11175913:-1;chr22:19098103-19103450:-1;chr22:19568850-19575804:-1;chr22:22703334-22752441:1;chr2:108852881-108859177:-1;chr2:140990927-140997449:-1;chr2:163663230-163668712:-1;chr2:16940093-16949702:-1;chr2:196169811-196176361:-1;chr2:38956022-38972572:1;chr3:131986063-131998357:-1;chr3:165038483-165086313:-1;chr3:189222922-189227688:-1;chr3:189734079-189743455:-1;chr3:26447844-26454823:-1;chr3:41086972-41147816:-1;chr3:53024162-53041943:-1;chr3:84102144-84110568:-1;chr3:89391108-89422305:-1;chr4:175622591-175629943:-1;chr4:64131648-64157031:-1;chr4:71192597-71202301:-1;chr4:77835705-77840925:-1;chr5:150788348-150795389:-1;chr5:170127275-170133922:-1;chr5:179273528-179279633:-1;chr5:82479176-82485709:-1;chr5:88039999-88046084:-1;chr6:110393354-110417123:-1;chr6:132704943-132715688:-1;chr6:67005854-67050972:-1;chr6:74610890-74623068:-1;chr6:77433996-77461537:-1;chr7:127212044-127220658:-1;chr7:157730840-157736827:-1;chr8:5592539-5607475:-1;chr8:63032223-63043589:-1;chr8:87185470-87196722:-1;chr9:35978649-35984566:-1;chrX:11950774-11961984:-1;chrX:19463498-19472538:-1;chrX:91675313-91682189:-1;chrY:15715619-15733808:-1	hs1:54948487-54951659,hs2:16471642-16474882;hs1:168420447-168423941,hs8:30104833-30105849;hs1:215363951-215367234,hs2:15382398-15385750;hs2:808016-810857,hs3:15938261-15938856;hs2:39633376-39636378,hs5:126611809-126614967;hs5:21901609-21902330,hs13:61461250-61462231;hs5:80098576-80099975,hsX:29351349-29353077;hs1:1004867-1007660,hs1:48276716-48279021;hs1:1685962-1688147,hs1:159504785-159507102;hs1:4202418-4204433,hs1:4204549-4206063;hs1:6408891-6411178,hs1:44046003-44049001;hs1:6853393-6855834,hs1:8436418-8438863;hs1:6859214-6861316,hs1:47451425-47453557;hs1:8713341-8715164,hs1:163725403-163727518;hs1:9653601-9656094,hs1:235001227-235003141;hs1:10538687-10541143,hs1:39547723-39550155;hs1:10598035-10600813,hs1:184466137-184469221;hs1:10706786-10709474,hs1:227749851-227752064;hs1:10975755-10978962,hs1:82296483-82299429;hs1:11008495-11010874,hs1:211841853-211844204;hs1:15062466-15065058,hs1:202893997-202896280;hs1:21891623-21894398,hs1:211855786-211858232;hs1:21959686-21962265,hs1:85009249-85011179;hs1:23243501-23245597,hs1:76492376-76494808;hs1:23291097-23294022,hs1:175245472-175247940;hs1:24465977-24468106,hs1:33167271-33169437;hs1:25156470-25158623,hs1:25161550-25164564;hs1:26395646-26398296,hs1:165169781-165172145;hs1:35005180-35006837,hs1:35007277-35009059;hs1:36639361-36641627,hs1:97428248-97430881;hs1:38973578-38975999,hs1:161359375-161361020;hs1:41406644-41408702,hs1:98932089-98934354;hs1:41475631-41478286,hs1:156479673-156482383;hs1:42178727-42181808,hs1:207549769-207552778;hs1:43279431-43282744,hs1:203732827-203736051;hs1:44198440-44200976,hs1:240852477-240854708;hs1:46810408-46813517,hs1:113418964-113421203;hs1:4686178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U900, Paris, France	Neuroblastoma is a pediatric cancer of the peripheral nervous system in which structural chromosome aberrations are emblematic of aggressive tumors. In this study, we performed an in-depth analysis of somatic rearrangements in two neuroblastoma cell lines and two primary tumors using paired-end sequencing of mate-pair libraries and RNA-seq. The cell lines presented with typical genetic alterations of neuroblastoma and the two tumors belong to the group of neuroblastoma exhibiting a profile of chromothripsis. Inter and intra-chromosomal rearrangements were identified in the four samples, allowing in particular characterization of unbalanced translocations at high resolution. Using complementary experiments, we further characterized 51 rearrangements at the base pair resolution that revealed 59 DNA junctions. In a subset of cases, complex rearrangements were observed with templated insertion of fragments of nearby sequences. Although we did not identify known particular motifs in the local environment of the breakpoints, we documented frequent microhomologies at the junctions in both chromothripsis and non-chromothripsis associated breakpoints. RNA-seq experiments confirmed expression of several predicted chimeric genes and genes with disrupted exon structure including ALK, NBAS, FHIT, PTPRD and ODZ4. Our study therefore indicates that both non-homologous end joining-mediated repair and replicative processes may account for genomic rearrangements in neuroblastoma. RNA-seq analysis allows the identification of the subset of abnormal transcripts expressed from genomic rearrangements that may be involved in neuroblastoma oncogenesis.	GRCh37/hg19			ERP001414;ERP001988	Yes	ANP32E,USH2A;ATP2B4,CR1;CDK18,AVPR1B;DFFA,OSBPL9;DHX9,TPR;FAAH,SLC6A17;IL22RA1,DNAJC6;KCNK2,NBAS;LAX1,RGS7;LOC388630,HHLA3;MIR548F1,TPR;MOB3C,DAB1;NEXN,RABGAP1L;PAPPA2,ASPM;RFWD2,HHAT;TMEM201,MTOR;TSSK3,CAPN2;WASF2,ECHDC2;WLS,GPR137B
CTDB0043	Research	23991058	Valentina Boeva, Stephanie Jouannet, Romain Daveau, Valerie Combaret, Cecile Pierre-Eugene, Alex Cazes, Caroline Louis-Brennetot, Gudrun Schleiermacher, Sandrine Ferrand, Gaelle Pierron, Alban Lermine, Thomas Rio Frio, Virginie Raynal, Gilles Vassal, Emma	Breakpoint Features of Genomic Rearrangements in Neuroblastoma with Unbalanced Translocations and Chromothripsis	PLoS One	2013 Aug	6,19	Neuroblastoma	Next Generation Sequencing	Homo sapiens	NB1142	Illumina Genome Analyzer Iix + SOLiD V4/5500	chr10:132985660-132995251:-1;chr10:1579059-1588908:-1;chr10:15954855-15968097:-1;chr10:71277735-71295026:-1;chr10:81721053-81731645:-1;chr11:124771072-124781839:-1;chr11:7807484-7837743:-1;chr12:56912991-56959884:1;chr13:106702169-106722732:-1;chr14:25905886-25916204:-1;chr16:52409891-52418832:-1;chr16:83667149-83679289:-1;chr17:69601715-69610672:-1;chr19:15539293-51327008:-1;chr19:19726050-33382212:-1;chr19:19730038-59064493:1;chr19:39272147-51322273:1;chr19:47844171-59068942:-1;chr19:54189926-55853550:1;chr19:562142-11115016:-1;chr19:781621-21513741:-1;chr1:155589112-155726967:1;chr1:199107104-199117349:-1;chr1:248150477-248159424:-1;chr1:60043981-60054277:-1;chr1:66020112-66033875:-1;chr20:12454760-12479026:-1;chr21:18101423-18108767:-1;chr21:25254696-25267775:-1;chr21:45615676-45624372:-1;chr2:143453088-143465894:-1;chr2:208347634-208363143:-1;chr2:227558825-227568040:-1;chr2:235838370-235846454:-1;chr2:35577680-35620309:-1;chr2:79330714-79343389:1;chr3:107034072-107044826:-1;chr3:196930241-196943330:-1;chr3:2023912-2032848:-1;chr3:25026175-25036053:-1;chr3:46791915-46854633:-1;chr4:115504089-115517922:-1;chr4:122279125-122293394:-1;chr4:164610228-164619218:-1;chr4:17198756-17207600:-1;chr4:32514066-32524007:-1;chr5:150877792-150886768:-1;chr5:26792444-26806239:-1;chr5:7639502-7649315:-1;chr5:86965343-86976794:-1;chr5:9896902-9928889:-1;chr6:100534810-100542871:-1;chr6:108911690-108920587:-1;chr6:126097658-150070724:1;chr6:136006752-170470886:-1;chr6:219613-107430301:1;chr6:23738625-23748789:-1;chr6:33736589-111279330:1;chr6:35335168-67817228:-1;chr6:35754594-35766766:1;chr6:39435171-108400197:-1;chr6:52174676-52932227:-1;chr6:52924112-87848352:-1;chr6:53924807-53938573:-1;chr6:62450477-159553363:1;chr6:73332512-160539393:1;chr6:99365311-168647732:1;chr7:13274204-13284668:-1;chr8:16259283-16277307:-1;chr8:2253552-2268331:1;chr9:96218633-96229100:-1;chrX:146034707-146045627:-1	hs2:138746679-138747353,hsX:76651556-76652306;hs6:215500-218685,hs19:55556975-55560020;hs6:35142422-35145938,hs19:55596935-55599944;hs6:37524902-37528250,hs19:55573613-55577027;hs6:45986874-45990519,hs19:55577842-55581128;hs6:125180750-125184366,hs19:55654991-55658179;hs6:136611902-136612700,hs19:55560202-55560883;hs6:152045747-152048420,hs19:55013679-55017070;hs6:157558280-157559463,hs19:55552600-55554363;hs6:157640190-157641292,hs19:55553991-55555948;hs6:160530367-160533917,hs19:55649962-55653924;hs17:21195702-21196569,hs18:15165041-15165590;hs1:3497291-3500128,hs1:3500363-3502804;hs1:28546763-28551211,hs1:28554059-28557093;hs1:106112685-106113998,hs1:106114598-106116634;hs1:113540719-113541837,hs1:113543186-113545023;hs1:219159258-219161464,hs1:219160830-219164490;hs1:227598318-227600253,hs1:227600264-227602390;hs1:246680458-246683437,hs1:246685322-246689142;hs2:71842780-71845722,hs2:71845556-71847897;hs2:104041156-104042668,hs2:104043987-104045472;hs2:108850805-108855426,hs2:108856247-108859628;hs2:166011059-166014630,hs2:166016836-166020285;hs2:180998391-181000046,hs2:181000523-181001747;hs2:194922032-194923154,hs2:194924830-194926182;hs2:195293240-195297166,hs2:195298592-195302232;hs3:3476764-3481012,hs3:3483369-3487391;hs3:18828208-18829399,hs3:18830672-18832075;hs3:22859858-22862035,hs3:22862828-22863813;hs3:32715304-32716156,hs3:32717142-32718337;hs3:39759108-39761179,hs3:39762318-39764259;hs3:42834260-42838401,hs3:42840869-42844527;hs3:174478186-174479914,hs3:174480147-174482224;hs3:183376919-183379044,hs3:183379086-183381759;hs4:1037556-1040435,hs4:1039753-1041425;hs4:10207226-10211271,hs4:10234580-10238735;hs4:19076032-19079475,hs4:19085750-19090524;hs4:137070698-137073394,hs4:137076171-137079269;hs4:152786696-152789884,hs4:152794800-152799109;hs4:189956531-189957543,hs4:189958600-189959209;hs5:21232204-21237237,hs5:21238515-21242985;hs5:109565750-109567478,hs5:109568734-109570623;hs5:114320517-114325263,hs5:114334985-114339220;hs6:35146380-35149594,hs6:71696846-71700967;hs6:35339473-35343551,hs6:52179146-52183214;hs6:37520118-37523236,hs6:108432031-108435299;hs6:39045094-39048407,hs6:62444279-62448067;hs6:39401847-39404731,hs6:160535975-160539067;hs6:49593450-49597312,hs6:170725950-170729952;hs6:52174742-52177612,hs6:64986030-64990307;hs6:64982285-64985665,hs6:126222575-126226244;hs6:64999063-65000516,hs6:65000972-65003277;hs6:67004893-67008689,hs6:67048927-67052957;hs6:67808955-67812730,hs6:95859383-95863573;hs6:71691783-71695322,hs6:122279176-122282712;hs6:73713582-73715765,hs6:73716078-73718288;hs6:73991925-73996338,hs6:126227352-126231084;hs6:84569987-84573247,hs6:90539496-90543057;hs6:87840419-87844059,hs6:99355361-99359121;hs6:90535144-90538047,hs6:99276177-99279776;hs6:95865284-95868629,hs6:159241278-159244471;hs6:99271810-99275631,hs6:126092793-126096866;hs6:108435896-108440138,hs6:111280630-111284071;hs6:109694349-109698659,hs6:156445677-156449341;hs6:151888147-151891900,hs6:168197596-168201129;hs6:160527913-160531976,hs6:170730583-170734012;hs7:23093513-23096892,hs7:23105700-23109552;hs7:89806779-89810419,hs7:89812589-89817401;hs8:4977765-4979757,hs8:4980529-4982653;hs8:16197107-16201271,hs8:16207525-16211327;hs8:20899338-20900657,hs8:20901268-20903383;hs8:87172224-87173897,hs8:87175253-87176798;hs8:109134409-109135774,hs8:109135988-109137515;hs8:131039045-131041191,hs8:131041638-131043476;hs8:133919998-133920718,hs8:133922004-133923155;hs9:1802653-1804668,hs9:1805774-1807266;hs9:6726101-6728026,hs9:6728674-6730171;hs9:17397400-17401383,hs9:17407033-17411101;hs9:20590634-20591705,hs9:20592586-20593798;hs9:22492851-22496249,hs9:22504340-22507637;hs9:35492814-35494813,hs9:35495808-35497072;hs9:138240701-138241833,hs9:138242008-138243104;hs9:139928004-139929109,hs9:139931191-139931918;hs10:12452751-12457959,hs10:12455503-12459309;hs10:65504243-65509088,hs10:65511385-65515104;hs10:94130431-94134544,hs10:94137823-94141682;hs10:121711462-121713232,hs10:121714452-121716243;hs11:12657307-12661483,hs11:12662483-12664084;hs11:18398708-18399786,hs11:18400400-18401844;hs11:29963166-29967574,hs11:29968718-29972808;hs11:31389408-31393799,hs11:31397791-31402349;hs11:35267273-35270363,hs11:35270272-35273033;hs11:41829657-41831543,hs11:41831921-41834084;hs11:47448092-47452190,hs11:47450993-47453769;hs11:60380863-60384604,hs11:60424422-60428555;hs11:66160946-66164420,hs11:66162090-66164415;hs11:78588395-78590314,hs11:78591095-78593463;hs11:102599019-102602022,hs11:102601578-102604617;hs12:13107584-13109278,hs12:13109781-13111872;hs12:25740157-25742633,hs12:25741010-25745706;hs12:33293303-33296552,hs12:33307675-33309156;hs12:72184687-72189140,hs12:72190579-72193446;hs12:75007328-75008701,hs12:75010204-75011759;hs12:121950420-121952916,hs12:121953040-121955408;hs12:132398693-132401848,hs12:132400522-132404849;hs13:99255912-99257184,hs13:99258928-99260132;hs13:108944261-108946841,hs13:108951780-108955425;hs14:34672092-34673914,hs14:34675174-34676937;hs14:65838664-65843138,hs14:65842788-65846787;hs14:86769656-86772801,hs14:86784991-86789162;hs14:89148654-89150216,hs14:89150865-89152505;hs15:59128046-59129248,hs15:59130206-59132032;hs15:99629234-99630148,hs15:99630360-99631834;hs15:100928509-100931556,hs15:100931318-100932355;hs16:87019239-87019956,hs16:87020696-87022476;hs17:2254327-2259504,hs17:2260492-2263649;hs17:7204607-7205843,hs17:7205999-7207026;hs17:28395571-28398084,hs17:28398425-28400597;hs17:51406845-51409338,hs17:51409729-51412054;hs17:54867150-54868893,hs17:54870207-54871705;hs17:75641693-75642704,hs17:75644358-75645659;hs17:79324700-79325820,hs17:79326896-79327785;hs18:54727608-54728861,hs18:54730491-54731891;hs18:69614804-69616515,hs18:69617466-69618256;hs19:568253-571413,hs19:47848514-47852973;hs19:785786-789292,hs19:43966380-43970074;hs19:15543728-15548327,hs19:43962211-43965834;hs19:18549935-18552093,hs19:18552794-18554984;hs19:33373668-33377310,hs19:39267187-39271185;hs20:8640806-8642403,hs20:8643720-8645207;hs20:15297703-15301746,hs20:15303839-15308063;hs20:46817371-46818628,hs20:46819137-46820358;hs20:56547335-56549934,hs20:56550007-56553092;hs21:27161687-27163437,hs21:27163613-27165657;hs21:31940863-31941546,hs21:31943899-31944758;hs21:46642249-46644429,hs21:46645270-46647624;hs22:27163628-27168056,hs22:27169893-27173887;hsX:77523668-77525048,hsX:77525576-77528157;hsX:81993917-81995014,hsX:81993861-81996861;hsX:106834525-106835691,hsX:106836039-106837415;hsX:111950965-111952863,hsX:111953697-111955739;hsX:121873675-121875935,hsX:121875797-121877521;hsX:136395767-136397144,hsX:136398768-136399997;hsX:147506452-147509429,hsX:147511230-147515724;hsX:152194567-152195283,hsX:152197532-152198274	ADARB1;ADARB2;ADCY2;BCLAF1;BEND3;C17orf67;C6orf127;C6orf97;C9orf139;CAMK1D;CASP8AP2;CD164;CDH13;CEP89;CHMP2A;CLIC5;CLPS;CNTLN;CYB5R4;DCDC1;DLG1;DNAJC24;DNAJC8;DYSF;EFCAB5;EML5;EPS8L1;ESR1;EYS;EZR;FAM120A;FAM63B;FAT2;FBXL4;FBXO9;FGGY;FOXO3;GLP1R;GON4L;GPR77;GTF3C6;HIGD1A;HNMT;ICK;IFLTD1;ISYNA1;KCNQ5;KDM2B;KDM4C;KHDC1;KHDRBS2;KIF6;KLHL24;KLK1;LEPR;LINC00271;LINC00301;LOC255654;LOC285692;LOC344595;LYPD3;MACROD2;MAP2K3;MARCH1;MEGF6;MIR1283-1;MIR4462;MLIP;MLLT3;NCOA7;NUP43;ODZ4;OR2L13;PBX4;PLCB1;PPARD;PSMC3;QRFPR;RBMS2;RDH13;RHAG;RUSC2;SCN3A;SGSM2;SMARCA4;TCERG1L;TG;TNFSF13B;TNNT1;TRIM28;ULK1;WIZ;ZNF708	Inserm, U900, Paris, France	Neuroblastoma is a pediatric cancer of the peripheral nervous system in which structural chromosome aberrations are emblematic of aggressive tumors. In this study, we performed an in-depth analysis of somatic rearrangements in two neuroblastoma cell lines and two primary tumors using paired-end sequencing of mate-pair libraries and RNA-seq. The cell lines presented with typical genetic alterations of neuroblastoma and the two tumors belong to the group of neuroblastoma exhibiting a profile of chromothripsis. Inter and intra-chromosomal rearrangements were identified in the four samples, allowing in particular characterization of unbalanced translocations at high resolution. Using complementary experiments, we further characterized 51 rearrangements at the base pair resolution that revealed 59 DNA junctions. In a subset of cases, complex rearrangements were observed with templated insertion of fragments of nearby sequences. Although we did not identify known particular motifs in the local environment of the breakpoints, we documented frequent microhomologies at the junctions in both chromothripsis and non-chromothripsis associated breakpoints. RNA-seq experiments confirmed expression of several predicted chimeric genes and genes with disrupted exon structure including ALK, NBAS, FHIT, PTPRD and ODZ4. Our study therefore indicates that both non-homologous end joining-mediated repair and replicative processes may account for genomic rearrangements in neuroblastoma. RNA-seq analysis allows the identification of the subset of abnormal transcripts expressed from genomic rearrangements that may be involved in neuroblastoma oncogenesis.	GRCh37/hg19			ERP001414;ERP001988	Yes	BCLAF1,RDH13;C6orf127,CLPS;CLIC5,RDH13;GPR77,CHMP2A;MIR4462,RDH13;PBX4,CEP89;PBX4,TRIM28;WIZ,KLK1
CTDB0044	Research	24143197	Heng Gu, Jian-hui Jiang, Jian-ying Li, Ya-nan Zhang, Xing-sheng Dong, Yang-yu Huang, Xinming Son, Xinyan Lu, Zheng Chen	A Familial Cri-du-Chat/5p Deletion Syndrome Resulted from Rare Maternal Complex Chromosomal Rearrangements (CCRs) and/or Possible Chromosome 5p Chromothripsis	PLoS One	2013 Oct	5	Cri-du-chat syndrome	Array CGH	Homo sapiens	mother	Agilent 4x180K array			LOC340094;ADAMTS16;KIAA0947;FLJ33360;MED10;UBE2QL1;LOC255167;NSUN2;SRD5A1;PAPD7;MIR4278	Department of Medical Genetics, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, PR China	Cri-du-Chat syndrome (MIM 123450) is a chromosomal syndrome characterized by the characteristic features, including cat-like cry and chromosome 5p deletions. We report a family with five individuals showing chromosomal rearrangements involving 5p, resulting from rare maternal complex chromosomal rearrangements (CCRs), diagnosed post- and pre-natally by comprehensive molecular and cytogenetic analyses. Two probands, including a four-and-half-year-old brother and his two-and-half-year-old sister, showed no diagnostic cat cry during infancy, but presented with developmental delay, dysmorphic and autistic features. Both patients had an interstitial deletion del(5)(p13.3p15.33) spanning about 26.22 Mb. The phenotypically normal mother had de novo CCRs involving 11 breakpoints and three chromosomes: ins(11;5) (q23;p14.1p15.31),ins(21;5)(q21;p13.3p14.1),ins(21;5)(q21;p15.31p15.33),inv(7)(p22q32)dn. In addition to these two children, she had three first-trimester miscarriages, two terminations due to the identification of the 5p deletion and one delivery of a phenotypically normal daughter. The unaffected daughter had the maternal ins(11;5) identified prenatally and an identical maternal allele haplotype of 5p. Array CGH did not detect any copy number changes in the mother, and revealed three interstitial deletions within 5p15.33-p13.3, in the unaffected daughter, likely products of the maternal insertions ins(21;5). Chromothripsis has been recently reported as a mechanism drives germline CCRs in pediatric patients with congenital defects. We postulate that the unique CCRs in the phenotypically normal mother could resulted from chromosome 5p chromothripsis, that further resulted in the interstitial 5p deletions in the unaffected daughter. Further high resolution sequencing based analysis is needed to determine whether chromothripsis is also present as a germline structural variation in phenotypically normal individuals in this family.	GRCh37/hg19				No	NA
CTDB0045	Research	24143197	Heng Gu, Jian-hui Jiang, Jian-ying Li, Ya-nan Zhang, Xing-sheng Dong, Yang-yu Huang, Xinming Son, Xinyan Lu, Zheng Chen	A Familial Cri-du-Chat/5p Deletion Syndrome Resulted from Rare Maternal Complex Chromosomal Rearrangements (CCRs) and/or Possible Chromosome 5p Chromothripsis	PLoS One	2013 Oct	5	Cri-du-chat syndrome	Array CGH	Homo sapiens	daughter	Agilent 4x180K array			LOC340094;ADAMTS16;KIAA0947;FLJ33360;MED10;UBE2QL1;LOC255167;NSUN2;SRD5A1;PAPD7;MIR4278	Department of Medical Genetics, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, PR China	Cri-du-Chat syndrome (MIM 123450) is a chromosomal syndrome characterized by the characteristic features, including cat-like cry and chromosome 5p deletions. We report a family with five individuals showing chromosomal rearrangements involving 5p, resulting from rare maternal complex chromosomal rearrangements (CCRs), diagnosed post- and pre-natally by comprehensive molecular and cytogenetic analyses. Two probands, including a four-and-half-year-old brother and his two-and-half-year-old sister, showed no diagnostic cat cry during infancy, but presented with developmental delay, dysmorphic and autistic features. Both patients had an interstitial deletion del(5)(p13.3p15.33) spanning about 26.22 Mb. The phenotypically normal mother had de novo CCRs involving 11 breakpoints and three chromosomes: ins(11;5) (q23;p14.1p15.31),ins(21;5)(q21;p13.3p14.1),ins(21;5)(q21;p15.31p15.33),inv(7)(p22q32)dn. In addition to these two children, she had three first-trimester miscarriages, two terminations due to the identification of the 5p deletion and one delivery of a phenotypically normal daughter. The unaffected daughter had the maternal ins(11;5) identified prenatally and an identical maternal allele haplotype of 5p. Array CGH did not detect any copy number changes in the mother, and revealed three interstitial deletions within 5p15.33-p13.3, in the unaffected daughter, likely products of the maternal insertions ins(21;5). Chromothripsis has been recently reported as a mechanism drives germline CCRs in pediatric patients with congenital defects. We postulate that the unique CCRs in the phenotypically normal mother could resulted from chromosome 5p chromothripsis, that further resulted in the interstitial 5p deletions in the unaffected daughter. Further high resolution sequencing based analysis is needed to determine whether chromothripsis is also present as a germline structural variation in phenotypically normal individuals in this family.	GRCh37/hg19				No	NA
CTDB0046	Research	23612016	Bassaganyas L, Bea S, Escaramis G, Tornador C, Salaverria I, Zapata L, Drechsel O, Ferreira PG, Rodriguez-Santiago B, Tubio JM, Navarro A, Martin-Garcia D, Lopez C, Martinez-Trillos A, Lopez-Guillermo A, Gut M, Ossowski S, Lopez-Otin C, Campo E, Estivill 	Sporadic and reversible chromothripsis in chronic lymphocytic leukemia revealed by longitudinal genomic analysis	Leukemia	2013 May	1,6,10,12	Chronic lymphocytic leukemia	Next Generation Sequencing	Homo sapiens	016-T02	Illumina HiSeq 2000 + Illumina Genome Analyzer Iix	chr1:158916616-162228238:-1;chr1:204884807-207098441:-1;chr1:245750841-245754210:1;chr2:57538505-57546240:-1;chr3:66307700-66848190:-1;chr4:92032232-92035673:-1;chr4:55259599-190916819:1;chr6:21165446-21202889:-1;chr6:42655943-44314131:-1;chr6:87787340-87937492:-1;chr6:87831293-92372455:-1;chr6:98726379-1009453032:-1;chr6:105121236-107322576:-1;chr6:135571668-137893724:-1;chr7:142493998-142495773:-1;chr9:19557108-19559274:-1;chr10:103329084-105060989:-1;chr12:6174700-8452800:-1;chr12:10781231-13107215:-1;chr14:106330475-107178831:-1;chr18:118560-14978275:-1	hs1:158895420-158895420,hs12:9009852-9009852;hs1:158895935-158895935,hs1:207100978-207100978;hs1:158908565-158908565,hs1:204868609-204868609;hs1:162273578-162273578,hs10:103313969-103313969;hs1:162299645-162299645,hs1:207110393-207110393;hs1:204873185-204873185,hs1:13128829-13128829;hs1:204884852-204884852,hs6:87790817,87790817;hs1:204885286-204885286,hs10:103311319-103311319;hs1:207109744-207109744,hs6:98720478-98720478;hs4:49275540-49275540,hs18:14983384-14983384;hs6:87823275-87823275,hs6:98688205-98688205;hs6:92369212-92369212,hs6:100987026-100987026;hs6:92405452-92405452,hs10:103302215-103302215;hs6:92106400-92406400,hs6:137889638-137889638;hs6:92407820-92407820,hs6:100973954-100973954;hs6:137871508-137871508,hs12:10749843-10749843;hs10:70172296-70172296,hs3:168885793-168885793;hs10:101290756-101290756,hs2:89132330-89132330;hs10:103308280-103308280,hs6:98688129-98688129;hs10:103310475-103310475,hs6:100949176-100949176;hs10:103328997-103328997,hs6:100987263-100987263;hs10:105080595-105080595,hs6:137868980-137868980;hs12:5988079-5988079,hs6:92374031-92374031;hs12:5998576-5998576,hs6:87786886-87786886;hs12:10749697-10749697,hs10:105073574-105073574;hs12:10766354-10766354,hs6:87823973-87823973;hs12:13102811-13102811,hs12:13123781-13123781;hs12:13127322-13127322,hs1:162299794;hs17:61565839-61565839,hs5:100389381	NFKB2;UBR2;SPATS1	Center for Genomic Regulation (CRG), Barcelona, Spain		GRCh37/hg19				Yes	UBR2,SPATS1
CTDB0047	Research	24304937	MA Jacoby, RE De Jesus Pizarro, J Shao, DC Koboldt, RS Fulton, G Zhou, RK Wilson, MJ Walter	The DNA double-strand break response is abnormal in myeloblasts from patients with therapy-related acute myeloid leukemia	Leukemia	2013 Dec	3,7	Acute myeloid leukemia	Array CGH	Homo sapiens	189941	NimbleGen custom 2x720K array	chr12:11708326-22796431:-1;chr17:7517325-7518692:-1;chr3:103782198-106696566:-1;chr3:11079219-12582443:-1;chr3:113846696-114463826:-1;chr3:123948788-124132968:-1;chr3:169461120-170271699:-1;chr3:170375166-171616698:-1;chr3:171702102-173816191:-1;chr4:12024504-13146333:-1;chr5:105204558-180814163:-1;chr5:94263666-103717142:-1;chr7:18448564-19027294:-1;chr7:26521475-56468938:-1;chr7:62090285-70977718:-1;chr7:78426592-81535151:-1;chr7:81940100-87814558:-1;chr7:89133633-158816035:-1		TP53	Department of Internal Medicine, Division of Oncology, Washington University School of Medicine, St Louis, MO, USA	The complex chromosomal aberrations found in therapy-related acute myeloid leukemia (t-AML) suggest that the DNA double-strand break (DSB) response may be altered. In this study we examined the DNA DSB response of primary bone marrow cells from t-AML patients and performed next-generation sequencing of 37 canonical homologous recombination (HR) and non-homologous end-joining (NHEJ) DNA repair genes, and a subset of DNA damage response genes using tumor and paired normal DNA obtained from t-AML patients. Our results suggest that the majority of t-AML patients (11 of 15) have tumor-cell intrinsic, functional dysregulation of their DSB response. Distinct patterns of abnormal DNA damage response in myeloblasts correlated with acquired genetic alterations in TP53 and the presence of inferred chromothripsis. Furthermore, the presence of trisomy 8 in tumor cells was associated with persistently elevated levels of DSBs. Although tumor-acquired point mutations or small indels in canonical HR and NHEJ genes do not appear to be a dominant means by which t-AML leukemogenesis occurs, our functional studies suggest that an abnormal response to DNA damage is a common finding in t-AML.		GSE53250		PRJEB8343	Yes	NA
CTDB0048	Research	24304937	MA Jacoby, RE De Jesus Pizarro, J Shao, DC Koboldt, RS Fulton, G Zhou, RK Wilson, MJ Walter	The DNA double-strand break response is abnormal in myeloblasts from patients with therapy-related acute myeloid leukemia	Leukemia	2013 Dec	3	Acute myeloid leukemia	Array CGH	Homo sapiens	530447	NimbleGen custom 2x720K array	chr21:31315314-46915712:1;chr22:14735065-49565939:1;chr3:142706131-150187585:-1;chr3:156299137-199381715:-1;chr3:20043408-31915861:-1;chr3:35197820-38538003:-1;chr3:41756417-48479360:-1;chr3:62156517-69781020:-1;chr3:69795134-75771557:-1;chr3:79933983-99089183:-1;chr5:55790692-67822695:-1;chr5:70841242-180593129:-1;chr7:22509353-57453201:-1;chr7:77985837-158816035:-1;chr9:28278165-29708951:-1		TP53	Department of Internal Medicine, Division of Oncology, Washington University School of Medicine, St Louis, MO, USA	The complex chromosomal aberrations found in therapy-related acute myeloid leukemia (t-AML) suggest that the DNA double-strand break (DSB) response may be altered. In this study we examined the DNA DSB response of primary bone marrow cells from t-AML patients and performed next-generation sequencing of 37 canonical homologous recombination (HR) and non-homologous end-joining (NHEJ) DNA repair genes, and a subset of DNA damage response genes using tumor and paired normal DNA obtained from t-AML patients. Our results suggest that the majority of t-AML patients (11 of 15) have tumor-cell intrinsic, functional dysregulation of their DSB response. Distinct patterns of abnormal DNA damage response in myeloblasts correlated with acquired genetic alterations in TP53 and the presence of inferred chromothripsis. Furthermore, the presence of trisomy 8 in tumor cells was associated with persistently elevated levels of DSBs. Although tumor-acquired point mutations or small indels in canonical HR and NHEJ genes do not appear to be a dominant means by which t-AML leukemogenesis occurs, our functional studies suggest that an abnormal response to DNA damage is a common finding in t-AML.		GSE53250		PRJEB8343	Yes	NA
CTDB0049	Research	24304937	MA Jacoby, RE De Jesus Pizarro, J Shao, DC Koboldt, RS Fulton, G Zhou, RK Wilson, MJ Walter	The DNA double-strand break response is abnormal in myeloblasts from patients with therapy-related acute myeloid leukemia	Leukemia	2013 Dec	8	Acute myeloid leukemia	Array CGH	Homo sapiens	377512	NimbleGen custom 2x720K array	chr11:128800686-130257349:1;chr11:94227338-94952730:1;chr15:18422770-22846333:-1;chr2:236856627-241034230:-1;chr5:55540994-56620186:-1;chr5:93926699-158579837:-1;chr7:100907744-158816035:-1;chr8:110969199-116510809:1;chr8:116520326-120009329:-1;chr8:120983709-128749745:1;chr8:128750703-129002866:-1;chr8:129007972-129285458:1;chr8:129221549-130450443:-1;chr8:130456187-133444071:1;chr8:133476865-142859461:-1;chr8:16975-32351253:1;chr8:80504328-80762667:-1;chr8:80768366-84206585:1;chr8:86369737-87949326:1;chr8:90475849-108195805:1		TP53	Department of Internal Medicine, Division of Oncology, Washington University School of Medicine, St Louis, MO, USA	The complex chromosomal aberrations found in therapy-related acute myeloid leukemia (t-AML) suggest that the DNA double-strand break (DSB) response may be altered. In this study we examined the DNA DSB response of primary bone marrow cells from t-AML patients and performed next-generation sequencing of 37 canonical homologous recombination (HR) and non-homologous end-joining (NHEJ) DNA repair genes, and a subset of DNA damage response genes using tumor and paired normal DNA obtained from t-AML patients. Our results suggest that the majority of t-AML patients (11 of 15) have tumor-cell intrinsic, functional dysregulation of their DSB response. Distinct patterns of abnormal DNA damage response in myeloblasts correlated with acquired genetic alterations in TP53 and the presence of inferred chromothripsis. Furthermore, the presence of trisomy 8 in tumor cells was associated with persistently elevated levels of DSBs. Although tumor-acquired point mutations or small indels in canonical HR and NHEJ genes do not appear to be a dominant means by which t-AML leukemogenesis occurs, our functional studies suggest that an abnormal response to DNA damage is a common finding in t-AML.		GSE53250		PRJEB8343	Yes	NA
CTDB0050	Research	23630094	Stefan Nagel, Corinna Meyer, Hilmar Quentmeier, Maren Kaufmann, Hans G. Drexler, Roderick A. F. MacLeod	Chromothripsis in Hodgkin Lymphoma	Genes Chromosomes Cancer	2013 Apr	3,9	Hodgkin lymphoma	SNP Array	Homo sapiens	L-1236	Affymetrix SNP 6.0			ABL1;SHOX2	Department of Human and Animal Cell Lines, Leibniz-Institute DSMZ-German Collection of Microorganisms and Cell Cultures, Braunschweig,Germany	Chromosomal rearrangements are common features of most cancers, where they contribute to deregulated gene expression. Chromothripsis is a recently described oncogenic mechanism whereby small genomic pieces originating from one chromosomal region undergo massive rearrangements in a single step. Here, we document chromothripsis in Hodgkin lymphoma (HL) cell lines by genomic profiling, showing alternating amplicons of defined chromosomal regions. In L-1236 cells, fluorescent in situ hybridization analyses identified aberrations affecting amplified chromosomal segments that derived from the long arm regions of chromosomes 3 and 9 and that colocalized to a derivative chromosome 6, indicating the cataclysmic origin of this mutation. The ABL1 gene at 9q34 was targeted by these rearrangements leading to its overexpression in L-1236 cells, correlating with pharmacological resistance to treatment with the kinase inhibitor dasatinib. Collectively, we identified and characterized chromothriptic rearrangements in HL cell lines to serve as models for analyzing this novel oncogenomic mechanism.		GSE15264			Yes	NA
CTDB0051	Research	23738515	Mehine M, Kaasinen E, Makinen N, Katainen R, Kampjarvi K, Pitkanen E, Heinonen HR, Butzow R, Kilpivaara O, Kuosmanen A, Ristolainen H, Gentile M, Sjoberg J, Vahteristo P, Aaltonen LA	Characterization of Uterine Leiomyomas by Whole-Genome Sequencing	N Engl J Med	2013 Jun	1,17	Uterine leiomyoma	Next Generation Sequencing	Homo sapiens	MY10m3	Illumina + Complete Genomics			TP53;NF1	Department of Medical Genetics, Genome-Scale Biology Research Program, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland	BACKGROUND: Uterine leiomyomas are benign but affect the health of millions of women. A better understanding of the molecular mechanisms involved may provide clues to the prevention and treatment of these lesions. METHODS: We performed whole-genome sequencing and gene-expression profiling of 38 uterine leiomyomas and the corresponding myometrium from 30 women. RESULTS: Identical variants observed in some separate tumor nodules suggested that these nodules have a common origin. Complex chromosomal rearrangements resembling chromothripsis were a common feature of leiomyomas. These rearrangements are best explained by a single event of multiple chromosomal breaks and random reassembly. The rearrangements created tissue-specific changes consistent with a role in the initiation of leiomyoma, such as translocations of the HMGA2 and RAD51B loci and aberrations at the COL4A5-COL4A6 locus, and occurred in the presence of normal TP53 alleles. In some cases, separate events had occurred more than once in single tumor-cell lineages. CONCLUSIONS: Chromosome shattering and reassembly resembling chromothripsis (a single genomic event that results in focal losses and rearrangements in multiple genomic regions) is a major cause of chromosomal abnormalities in uterine leiomyomas; we propose that tumorigenesis occurs when tissue-specific tumor-promoting changes are formed through these events. Chromothripsis has previously been associated with aggressive cancer; its common occurrence in leiomyomas suggests that it also has a role in the genesis and progression of benign tumors. We observed that multiple separate tumors could be seeded from a single lineage of uterine leiomyoma cells.	GRCh37/hg19			ERP004006	Yes	NA
CTDB0052	Research	23738515	Mehine M, Kaasinen E, Makinen N, Katainen R, Kampjarvi K, Pitkanen E, Heinonen HR, Butzow R, Kilpivaara O, Kuosmanen A, Ristolainen H, Gentile M, Sjoberg J, Vahteristo P, Aaltonen LA	Characterization of Uterine Leiomyomas by Whole-Genome Sequencing	N Engl J Med	2013 Jun	2,5,7,22,X	Uterine leiomyoma	Next Generation Sequencing	Homo sapiens	MY23m4	Illumina + Complete Genomics			COL4A5;COL4A6;CUX1	Department of Medical Genetics, Genome-Scale Biology Research Program, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland	BACKGROUND: Uterine leiomyomas are benign but affect the health of millions of women. A better understanding of the molecular mechanisms involved may provide clues to the prevention and treatment of these lesions. METHODS: We performed whole-genome sequencing and gene-expression profiling of 38 uterine leiomyomas and the corresponding myometrium from 30 women. RESULTS: Identical variants observed in some separate tumor nodules suggested that these nodules have a common origin. Complex chromosomal rearrangements resembling chromothripsis were a common feature of leiomyomas. These rearrangements are best explained by a single event of multiple chromosomal breaks and random reassembly. The rearrangements created tissue-specific changes consistent with a role in the initiation of leiomyoma, such as translocations of the HMGA2 and RAD51B loci and aberrations at the COL4A5-COL4A6 locus, and occurred in the presence of normal TP53 alleles. In some cases, separate events had occurred more than once in single tumor-cell lineages. CONCLUSIONS: Chromosome shattering and reassembly resembling chromothripsis (a single genomic event that results in focal losses and rearrangements in multiple genomic regions) is a major cause of chromosomal abnormalities in uterine leiomyomas; we propose that tumorigenesis occurs when tissue-specific tumor-promoting changes are formed through these events. Chromothripsis has previously been associated with aggressive cancer; its common occurrence in leiomyomas suggests that it also has a role in the genesis and progression of benign tumors. We observed that multiple separate tumors could be seeded from a single lineage of uterine leiomyoma cells.	GRCh37/hg19			ERP004006	Yes	COL4A5,COL4A6
CTDB0053	Research	23738515	Mehine M, Kaasinen E, Makinen N, Katainen R, Kampjarvi K, Pitkanen E, Heinonen HR, Butzow R, Kilpivaara O, Kuosmanen A, Ristolainen H, Gentile M, Sjoberg J, Vahteristo P, Aaltonen LA	Characterization of Uterine Leiomyomas by Whole-Genome Sequencing	N Engl J Med	2013 Jun	1,4,22	Uterine leiomyoma	Next Generation Sequencing	Homo sapiens	MY46m1	Illumina + Complete Genomics				Department of Medical Genetics, Genome-Scale Biology Research Program, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland	BACKGROUND: Uterine leiomyomas are benign but affect the health of millions of women. A better understanding of the molecular mechanisms involved may provide clues to the prevention and treatment of these lesions. METHODS: We performed whole-genome sequencing and gene-expression profiling of 38 uterine leiomyomas and the corresponding myometrium from 30 women. RESULTS: Identical variants observed in some separate tumor nodules suggested that these nodules have a common origin. Complex chromosomal rearrangements resembling chromothripsis were a common feature of leiomyomas. These rearrangements are best explained by a single event of multiple chromosomal breaks and random reassembly. The rearrangements created tissue-specific changes consistent with a role in the initiation of leiomyoma, such as translocations of the HMGA2 and RAD51B loci and aberrations at the COL4A5-COL4A6 locus, and occurred in the presence of normal TP53 alleles. In some cases, separate events had occurred more than once in single tumor-cell lineages. CONCLUSIONS: Chromosome shattering and reassembly resembling chromothripsis (a single genomic event that results in focal losses and rearrangements in multiple genomic regions) is a major cause of chromosomal abnormalities in uterine leiomyomas; we propose that tumorigenesis occurs when tissue-specific tumor-promoting changes are formed through these events. Chromothripsis has previously been associated with aggressive cancer; its common occurrence in leiomyomas suggests that it also has a role in the genesis and progression of benign tumors. We observed that multiple separate tumors could be seeded from a single lineage of uterine leiomyoma cells.	GRCh37/hg19			ERP004006	Yes	NA
CTDB0054	Research	23738515	Mehine M, Kaasinen E, Makinen N, Katainen R, Kampjarvi K, Pitkanen E, Heinonen HR, Butzow R, Kilpivaara O, Kuosmanen A, Ristolainen H, Gentile M, Sjoberg J, Vahteristo P, Aaltonen LA	Characterization of Uterine Leiomyomas by Whole-Genome Sequencing	N Engl J Med	2013 Jun	1,2,11,15,X	Uterine leiomyoma	Next Generation Sequencing	Homo sapiens	MY47m1	Illumina + Complete Genomics	chr1:215048026-223440603:1;chr1:31282315-44432520:1;chr22:42110013-42176601:-1;chr2:38218515-61540231:-1	hs1:19539160-19539160,hs2:217077076-217077076;hs1:31299824-31299824,hs11:118397268-118397268;hs1:32820625-32820625,hs11:114620180-114620180;hs1:33506263-33506263,hs1:44820517-44820517;hs1:33506872-33506872,hs1:220044420-220044420;hs1:52870556-52870556,hs6:151805925-151805925;hs1:52871037-52871037,hs11:12381161-12381161;hs1:67456934-67456934,hs11:17806872-17806872;hs1:93896730-93896730,hs1:97107552-97107552;hs1:97064269-97064269,hs6:161230570-161230570;hs1:97107169-97107169,hs5:6689935-6689935;hs1:100368634-100368634,hs15:86207345-86207345;hs1:100454228-100454228,hs2:63807137-63807137;hs1:114474067-114474067,hs2:12647369-12647369;hs1:145455240-145455240,hs1:156695207-156695207;hs1:145455307-145455307,hs1:150516696-150516696;hs1:145498335-145498335,hs1:168054990-168054990;hs1:145498420-145498420,hs1:150516666-150516666;hs1:145575509-145575509,hs1:156655269-156655269;hs1:145576476-145576476,hs1:156655352-156655352;hs1:150516666-150516666,hs1:150516747-150516747;hs1:151386388-151386388,hs22:42066919-42066919;hs1:220309075-220309075,hs2:61486886-61486886;hs2:3404675-3404675,hs2:62048799-62048799;hs2:5620094-5620094,hs2:62048871-62048871;hs2:5620209-5620209,hs2:5644328-5644328;hs2:5644274-5644274,hs2:28618421-28618421;hs2:12648413-12648413,hs2:15596270-15596270;hs2:17878699-17878699,hs2:61545621-61545621;hs2:17878813-17878813,hs2:64344610-64344610;hs2:28461740-28461740,hs15:86388593-86388593;hs2:28462611-28462611,hs15:86388847-86388847;hs2:28478069-28478069,hs11:118397907-118397907;hs2:61368528-61368528,hs2:61487406-61487406;hs2:61538447-61538447,hs2:64344463-64344463;hs2:61546020-61546020,hs2:63808163-63808163;hs2:217077076-217077076,hs11:65061312-65061312;hs2:217077154-217077154,hs15:57223400-57223400;hs6:137661579-137661579,hs22:19144224-19144224;hs6:161146302-161146302,hs6:161150567-161150567;hs8:75087899-75087899,hs8:75095377-75095377;hs11:1570862-1570862,hs11:1591488-1591488;hs11:12396199-12396199,hs11:65061640-65061640;hs11:17807056-17807056,hs11:28105191-28105191;hs11:17836821-17836821,hs11:28280080-28280080;hs11:18046070-18046070,hs11:28165047-28165047;hs11:18058151-18058151,hs11:18099512-18099512;hs11:18058423-18058423,hs11:28369161-28369161;hs11:18101635-18101635,hs11:20655414-20655414;hs11:18168973-18168973,hs11:28164502-28164502;hs11:18169076-18169076,hs11:28650047-28650047;hs11:69240671-69240671,hs15:86472754-86472754;hs11:85367580-85367580,hs11:85368252-85368252;hs11:85367591-85367591,hs11:85367851-85367851;hs11:113178251-113178251,hs15:86471229-86471229;hs21:46222881-46222881,hs22:24203554-24203554;hs22:43084148-43084148,hs22:43087160-43087160;hsX:10879936-10879936,hsX:107677238-107677238;hsX:10880027-10880027,hsX:107743206-107743206;hsX:10944804-10944804,hsX:107743234-107743234;hsX:10944950-10944950,hsX:107726147-107726147	COL4A5;COL4A6;CCND1	Department of Medical Genetics, Genome-Scale Biology Research Program, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland	BACKGROUND: Uterine leiomyomas are benign but affect the health of millions of women. A better understanding of the molecular mechanisms involved may provide clues to the prevention and treatment of these lesions. METHODS: We performed whole-genome sequencing and gene-expression profiling of 38 uterine leiomyomas and the corresponding myometrium from 30 women. RESULTS: Identical variants observed in some separate tumor nodules suggested that these nodules have a common origin. Complex chromosomal rearrangements resembling chromothripsis were a common feature of leiomyomas. These rearrangements are best explained by a single event of multiple chromosomal breaks and random reassembly. The rearrangements created tissue-specific changes consistent with a role in the initiation of leiomyoma, such as translocations of the HMGA2 and RAD51B loci and aberrations at the COL4A5-COL4A6 locus, and occurred in the presence of normal TP53 alleles. In some cases, separate events had occurred more than once in single tumor-cell lineages. CONCLUSIONS: Chromosome shattering and reassembly resembling chromothripsis (a single genomic event that results in focal losses and rearrangements in multiple genomic regions) is a major cause of chromosomal abnormalities in uterine leiomyomas; we propose that tumorigenesis occurs when tissue-specific tumor-promoting changes are formed through these events. Chromothripsis has previously been associated with aggressive cancer; its common occurrence in leiomyomas suggests that it also has a role in the genesis and progression of benign tumors. We observed that multiple separate tumors could be seeded from a single lineage of uterine leiomyoma cells.	GRCh37/hg19			ERP004006	Yes	COL4A5,COL4A6
CTDB0055	Research	23738515	Mehine M, Kaasinen E, Makinen N, Katainen R, Kampjarvi K, Pitkanen E, Heinonen HR, Butzow R, Kilpivaara O, Kuosmanen A, Ristolainen H, Gentile M, Sjoberg J, Vahteristo P, Aaltonen LA	Characterization of Uterine Leiomyomas by Whole-Genome Sequencing	N Engl J Med	2013 Jun	6,8,12,14	Uterine leiomyoma	Next Generation Sequencing	Homo sapiens	MY64m1	Illumina + Complete Genomics		hs1:15735163-15735163,hs3:194489954-194489954;hs1:194721032-194721032,hs1:196290033-196290033;hs1:215599195-215599195,hs1:215599663-215599663;hs3:33644813-33644813,hs19:12274466-12274466;hs3:49074459-49074459,hs10:80831180-80831180;hs3:52745459-52745459,hs22:39922071-39922071;hs3:180156793-180156793,hs3:180157535-180157535;hs3:194490234-194490234,hs3:194493153-194493153;hs4:6584525-6584525,hs4:34998329-34998329;hs6:1943008-1943008,hs6:2489341-2489341;hs6:11156592-11156592,hs7:84183676-84183676;hs6:31058593-31058593,hs6:31059135-31059135;hs6:53137916-53137916,hs6:53201720-53201720;hs6:53145310-53145310,hs6:53203374-53203374;hs6:66868428-66868428,hs6:66870032-66870032;hs6:70162245-70162245,hs6:99829857-99829857;hs6:70175391-70175391,hs6:99787202-99787202;hs6:76745802-76745802,hs6:76746261-76746261;hs6:81852454-81852454,hs6:128469968-128469968;hs6:88875408-88875408,hs12:25545729-25545729;hs6:109995770-109995770,hs6:109996343-109996343;hs6:112035549-112035549,hs6:113078054-113078054;hs6:112036919-112036919,hs6:113841690-113841690;hs6:112419542-112419542,hs6:114208063-114208063;hs6:131747203-131747203,hs6:131794379-131794379;hs7:83853697-83853697,hs7:83854456-83854456;hs7:112249350-112249350,hs7:113118707-113118707;hs7:112249511-112249511,hs7:113124180-113124180;hs7:113923991-113923991,hs7:113924617-113924617;hs7:117113777-117113777,hs7:117114825-117114825;hs7:122019607-122019607,hs7:122019982-122019982;hs7:136616071-136616071,hs7:136658639-136658639;hs7:148391040-148391040,hs7:148550062-148550062;hs8:93147079-93147079,hs8:94323704-94323704;hs8:93534914-93534914,hs6:88875071-88875071;hs8:93535474-93535474,hs12:92634896-92634896;hs8:93978876-93978876,hs14:89023605-89023605;hs11:24998979-24998979,hs11:25993614-25993614;hs12:25545779-25545779,hs12:48018996-48018996;hs12:65562575-65562575,hs8:93149069-93149069;hs12:66627402-66627402,hs12:66653581-66653581;hs12:92419990-92419990,hs12:92420090-92420090;hs12:92634041-92634041,hs14:93599917-93599917;hs14:68772909-68772909,hs12:65992890-65992890;hs14:68921193-68921193,hs12:67255815-67255815;hs14:97338363-97338363,hs14:97338802-97338802;hsX:83913042-83913042,hsX:98148639-98148639	RAD51B;HMGA2;CUL1;EZH2	Department of Medical Genetics, Genome-Scale Biology Research Program, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland	BACKGROUND: Uterine leiomyomas are benign but affect the health of millions of women. A better understanding of the molecular mechanisms involved may provide clues to the prevention and treatment of these lesions. METHODS: We performed whole-genome sequencing and gene-expression profiling of 38 uterine leiomyomas and the corresponding myometrium from 30 women. RESULTS: Identical variants observed in some separate tumor nodules suggested that these nodules have a common origin. Complex chromosomal rearrangements resembling chromothripsis were a common feature of leiomyomas. These rearrangements are best explained by a single event of multiple chromosomal breaks and random reassembly. The rearrangements created tissue-specific changes consistent with a role in the initiation of leiomyoma, such as translocations of the HMGA2 and RAD51B loci and aberrations at the COL4A5-COL4A6 locus, and occurred in the presence of normal TP53 alleles. In some cases, separate events had occurred more than once in single tumor-cell lineages. CONCLUSIONS: Chromosome shattering and reassembly resembling chromothripsis (a single genomic event that results in focal losses and rearrangements in multiple genomic regions) is a major cause of chromosomal abnormalities in uterine leiomyomas; we propose that tumorigenesis occurs when tissue-specific tumor-promoting changes are formed through these events. Chromothripsis has previously been associated with aggressive cancer; its common occurrence in leiomyomas suggests that it also has a role in the genesis and progression of benign tumors. We observed that multiple separate tumors could be seeded from a single lineage of uterine leiomyoma cells.	GRCh37/hg19			ERP004006	Yes	NA
CTDB0056	Research	23738515	Mehine M, Kaasinen E, Makinen N, Katainen R, Kampjarvi K, Pitkanen E, Heinonen HR, Butzow R, Kilpivaara O, Kuosmanen A, Ristolainen H, Gentile M, Sjoberg J, Vahteristo P, Aaltonen LA	Characterization of Uterine Leiomyomas by Whole-Genome Sequencing	N Engl J Med	2013 Jun	1,5,14	Uterine leiomyoma	Next Generation Sequencing	Homo sapiens	MY18m3	Illumina + Complete Genomics	chr14:63744555-68216937:-1;chr19:27681783-141213431:-1;chr1:882685-29447281:-1;chr4:1-49660117:-1;chr5:149752077-158199892:-1	hs1:882685-882685,hs1:31085347-31085347;hs1:29447281-29447281,hs20:34130261-34130261;hs1:31085225-31085225,hs2:27270624-27270624;hs1:87129957-87129957,hs1:87131702-87131702;hs5:98538029-98538029,hs5:98780516-98780516;hs5:98774085-98774085,hs5:100605647-100605647;hs5:98780238-98780238,hs5:99577432-99577432;hs5:100534516-100534516,hs5:149570825-149570825;hs5:100607932-100607932,hs5:158551243-158551243;hs5:100611427-100611427,hs5:158199892-158199892;hs5:100881397-100881397,hs5:100882761-100882761;hs5:107392713-107392713,hs5:149752077-149752077;hs8:29056894-29056894,hs8:29049690-29049690;hs12:66200468-66200468,hs14:69025073-69025073;hs12:66336514-66336514,hs12:66336991-66336991;hs12:121190353-121190353,hs12:121190839-121190839;hs14:19162878-19162878,hs14:69524710-69524710;hs14:24720540-24720540,hs14:75769241-75769241;hs14:39424193-39424193,hs14:63744555-63744555;hs14:43740449-43740449,hs14:69021171-69021171;hs14:69020643-69020643,hs12:66201378-66201378;hs14:69025181-69025181,hs14:92959674-92959674;hs14:69524711-69524711,hs14:68216937-68216937;hs14:69624170-69624170,hs14:93149131-93149131;hs14:69624603-69624603,hs14:93160067-93160067;hs14:92957591-92957591,hs14:24720863-24720863;hs20:34130689-34130689,hs2:27316575-27316575	RAD51B;HMGA2	Department of Medical Genetics, Genome-Scale Biology Research Program, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland	BACKGROUND: Uterine leiomyomas are benign but affect the health of millions of women. A better understanding of the molecular mechanisms involved may provide clues to the prevention and treatment of these lesions. METHODS: We performed whole-genome sequencing and gene-expression profiling of 38 uterine leiomyomas and the corresponding myometrium from 30 women. RESULTS: Identical variants observed in some separate tumor nodules suggested that these nodules have a common origin. Complex chromosomal rearrangements resembling chromothripsis were a common feature of leiomyomas. These rearrangements are best explained by a single event of multiple chromosomal breaks and random reassembly. The rearrangements created tissue-specific changes consistent with a role in the initiation of leiomyoma, such as translocations of the HMGA2 and RAD51B loci and aberrations at the COL4A5-COL4A6 locus, and occurred in the presence of normal TP53 alleles. In some cases, separate events had occurred more than once in single tumor-cell lineages. CONCLUSIONS: Chromosome shattering and reassembly resembling chromothripsis (a single genomic event that results in focal losses and rearrangements in multiple genomic regions) is a major cause of chromosomal abnormalities in uterine leiomyomas; we propose that tumorigenesis occurs when tissue-specific tumor-promoting changes are formed through these events. Chromothripsis has previously been associated with aggressive cancer; its common occurrence in leiomyomas suggests that it also has a role in the genesis and progression of benign tumors. We observed that multiple separate tumors could be seeded from a single lineage of uterine leiomyoma cells.	GRCh37/hg19			ERP004006	Yes	RAD51B,HMGA2
CTDB0058	Research	24469795	Morrison CD, Liu P, Woloszynska-Read A, Zhang J, Luo W, Qin M, Bshara W, Conroy JM, Sabatini L, Vedell P, Xiong D, Liu S, Wang J, Shen H, Li Y, Omilian AR, Hill A, Head K, Guru K, Kunnev D, Leach R, Eng KH, Darlak C, Hoeflich C, Veeranki S, Glenn S, You M	Whole-genome sequencing identifies genomic heterogeneity at a nucleotide and chromosomal level in bladder cancer	PNAS	2014 Jan	4,5,6	Bladder cancer	Next Generation Sequencing	Homo sapiens	18195	Illumina HiSeq 2000	chr12:15868221-15869407:-1;chr13:25958271-25982948:-1;chr13:47357937-47895151:-1;chr13:50576609-51283899:-1;chr16:89347877-89355605:-1;chr17:15396178-15984150:-1;chr18:8064603-8079939:-1;chr2:141248335-141377828:-1;chr2:141682019-142033558:-1;chr2:141800301-141865698:-1;chr2:166207909-166746319:-1;chr2:212365974-212497679:-1;chr2:55702844-57945495:-1;chr2:76235801-76236576:-1;chr3:60647686-61150861:-1;chr4:143858104-150512751:-1;chr5:24639248-24829428:-1;chr7:51514678-51523200:-1;chr7:78339452-78352430:-1;chr9:13417895-14381409:-1	hs1:189182665-189182665,hs2:4522643-4522643;hs4:123484083-123484083,hs6:24118632-24118632;hs4:123561315-123561315,hs6:24122385-24122385;hs4:124664946-124664946,hs6:10407849-10407849;hs4:125115818-125115818,hs4:169013589-169013589;hs4:128690025-128690025,hs4:128690444-128690444;hs4:143860688-143860688,hs6:10407009-10407009;hs4:145338318-145338318,hs4:151076217-151076217;hs4:169007852-169007852,hs5:40050668-40050668;hs4:169014029-169014029,hs6:20697120-20697120;hs4:185413107-185413107,hs6:50112900-50112900;hs4:185717832-185717832,hs6:49786067-49786067;hs4:185720119-185720119,hs5:41232937-41232937;hs4:185727981-185727981,hs6:49787649-49787649;hs4:185879694-185879694,hs6:10408205-10408205;hs5:14499897-14499897,hs6:10400566-10400566;hs5:14503114-14503114,hs5:24902285-24902285;hs5:14511701-14511701,hs6:24347839-24347839;hs5:24625080-24625080,hs13:50006548-50006548;hs5:25237830-25237830,hs5:40040222-40040222;hs5:29690933-29690933,hs6:49784660-49784660;hs5:37251584-37251584,hs6:10424400-10424400;hs5:37295108-37295108,hs6:49782746-49782746;hs5:40062440-40062440,hs6:20736167-20736167;hs6:24325453-24325453,hs6:49597606-49597606;hs6:37516484-37516484,hs6:37530727-37530727;hs12:63150384-63150384,hs12:63602159-63602159;hs13:25957850-25957850,hs13:25961756-25961756;hs13:25963023-25963023,hs13:25984817-25984817	CDH10;CAB39L	Center for Personalized Medicine and Departments of Pharmacology and Therapeutics, Cancer Genetics, Biostatistics and Bioinformatics, Pathology, Urology, Molecular and Cellular Biology, and Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263.	Using complete genome analysis, we sequenced five bladder tumors accrued from patients with muscle-invasive transitional cell carcinoma of the urinary bladder (TCC-UB) and identified a spectrum of genomic aberrations. In three tumors, complex genotype changes were noted. All three had tumor protein p53 mutations and a relatively large number of single-nucleotide variants (SNVs; average of 11.2 per megabase), structural variants (SVs; average of 46), or both. This group was best characterized by chromothripsis and the presence of subclonal populations of neoplastic cells or intratumoral mutational heterogeneity. Here, we provide evidence that the process of chromothripsis in TCC-UB is mediated by nonhomologous end-joining using kilobase, rather than megabase, fragments of DNA, which we refer to as stitchers, to repair this process. We postulate that a potential unifying theme among tumors with the more complex genotype group is a defective replication-licensing complex. A second group (two bladdertumors) had no chromothripsis, and a simpler genotype, WT tumor protein p53, had relatively few SNVs (average of 5.9 per megabase) and only a single SV. There was no evidence of a subclonal population of neoplastic cells. In this group, we used a preclinical model of bladder carcinoma cell lines to study a unique SV (translocation and amplification) of the gene glutamate receptor ionotropic N-methyl D-aspertate as a potential new therapeutic target in ladder cancer.	NCBI 36/hg18			ERP004006	Yes	CDH10,CAB39L
CTDB0059	Research	24469795	Morrison CD, Liu P, Woloszynska-Read A, Zhang J, Luo W, Qin M, Bshara W, Conroy JM, Sabatini L, Vedell P, Xiong D, Liu S, Wang J, Shen H, Li Y, Omilian AR, Hill A, Head K, Guru K, Kunnev D, Leach R, Eng KH, Darlak C, Hoeflich C, Veeranki S, Glenn S, You M	Whole-genome sequencing identifies genomic heterogeneity at a nucleotide and chromosomal level in bladder cancer	PNAS	2014 Jan	11,12,17	Bladder cancer	Next Generation Sequencing	Homo sapiens	18698	Illumina HiSeq 2000	chr11:66504877-68461658:-1;chr12:46214421-47093283:-1;chr17:36915522-37804427:-1;chr1:47231278-87529442:-1;chr9:21868718-24184888:-1	hs1:105326347-105326347,hs1:105326669-105326669;hs3:13593328-13593328,hs3:21559260-21559260;hs3:18242480-18242480,hs3:18256751-18256751;hs4:180787743-180787743,hs4:181469774-181469774;hs7:107728025-107728025,hs7:115159186-115159186;hs8:34012822-34012822,hs17:37894488-37894488;hs11:69603563-69603563,hs11:71258963-71258963;hs11:119315586-119315586,hs12:47939157-47939157;hs12:46210326-46210326,hs12:46211370-46211370;hs12:47797901-47797901,hs12:47801447-47801447;hs13:22319164-22319164,hs13:22331301-22331301;hs17:36656397-36656397,hs17:36658640-36658640;hs17:59424176-59424176,hs17:59623009-59623009;hs18:27135323-27135323,hs18:28064691-28064691;hs18:29094661-29094661,hs18:29095531-29095531		Center for Personalized Medicine and Departments of Pharmacology and Therapeutics, Cancer Genetics, Biostatistics and Bioinformatics, Pathology, Urology, Molecular and Cellular Biology, and Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263.	Using complete genome analysis, we sequenced five bladder tumors accrued from patients with muscle-invasive transitional cell carcinoma of the urinary bladder (TCC-UB) and identified a spectrum of genomic aberrations. In three tumors, complex genotype changes were noted. All three had tumor protein p53 mutations and a relatively large number of single-nucleotide variants (SNVs; average of 11.2 per megabase), structural variants (SVs; average of 46), or both. This group was best characterized by chromothripsis and the presence of subclonal populations of neoplastic cells or intratumoral mutational heterogeneity. Here, we provide evidence that the process of chromothripsis in TCC-UB is mediated by nonhomologous end-joining using kilobase, rather than megabase, fragments of DNA, which we refer to as stitchers, to repair this process. We postulate that a potential unifying theme among tumors with the more complex genotype group is a defective replication-licensing complex. A second group (two bladdertumors) had no chromothripsis, and a simpler genotype, WT tumor protein p53, had relatively few SNVs (average of 5.9 per megabase) and only a single SV. There was no evidence of a subclonal population of neoplastic cells. In this group, we used a preclinical model of bladder carcinoma cell lines to study a unique SV (translocation and amplification) of the gene glutamate receptor ionotropic N-methyl D-aspertate as a potential new therapeutic target in ladder cancer.	NCBI 36/hg18				Yes	NA
CTDB0060	Research	24469795	Morrison CD, Liu P, Woloszynska-Read A, Zhang J, Luo W, Qin M, Bshara W, Conroy JM, Sabatini L, Vedell P, Xiong D, Liu S, Wang J, Shen H, Li Y, Omilian AR, Hill A, Head K, Guru K, Kunnev D, Leach R, Eng KH, Darlak C, Hoeflich C, Veeranki S, Glenn S, You M	Whole-genome sequencing identifies genomic heterogeneity at a nucleotide and chromosomal level in bladder cancer	PNAS	2014 Jan	2,4,5,6,10,18,19	Bladder cancer	Next Generation Sequencing	Homo sapiens	19685	Illumina HiSeq 2000	chr13:21067952-42227057:-1;chr13:46269197-70851443:-1;chr14:102894735-102918992:-1;chr14:41437002-41437905:-1;chr15:89778081-89851425:-1;chr17:47113498-47114554:-1;chr19:14031700-16386190:-1;chr19:14038991-14211307:-1;chr19:18740629-19009858:-1;chr19:28721949-31837160:-1;chr21:27419049-30352374:-1;chr21:27494111-31693492:-1;chr2:142808431-142817549:-1;chr2:194004736-201221178:-1;chr2:62687819-97678586:-1;chr4:19934716-19936610:-1;chr4:81774226-87306782:-1;chr4:87310129-99601329:-1;chr5:142492704-142543234:-1;chr5:31171782-31261268:-1;chr5:33835925-33841123:-1;chr5:61432448-160401023:-1;chr5:62106393-140375046:-1;chr6:20062895-20063651:-1;chr6:49699773-49701405:-1;chr6:62545122-66578795:-1;chr7:120306456-120308862:-1;chr7:44924241-46068829:-1;chr8:140348207-140367209:-1;chr8:141005164-141024666:-1;chr9:89734221-89750048:-1;chrX:24535818-24536939:-1	hs2:74496729-74496729,hs2:88536586-88536586;hs2:84278098-84278098,hs13:74531816-74531816;hs2:177602102-177602102,hs2:180425416-180425416;hs2:177850934-177850934,hs4:134021859-134021859;hs3:2231340-2231340,hs5:163882786-163882786;hs3:2239599-2239599,hs21:31420630-31420630;hs3:2271739-2271739,hs5:163488040-163488040;hs4:80876697-80876697,hs4:90969695-90969695;hs4:88965722-88965722,hs5:159136178-159136178;hs4:90784690-90784690,hs4:111017791-111017791;hs4:98230738-98230738,hs4:98298792-98298792;hs4:110318503-110318503,hs4:115783941-115783941;hs4:114352224-114352224,hs5:53118673-53118673;hs4:117358105-117358105,hs4:118357230-118357230;hs4:137613428-137613428,hs4:139064982-139064982;hs4:179409744-179409744,hs4:183350902-183350902;hs4:190851149-190851149,hs4:190852682-190852682;hs4:190864028-190864028,hs4:190864840-190864840;hs5:29794592-29794592,hs5:39986499-39986499;hs5:44712327-44712327,hs22:44760032-44760032;hs5:159938168-159938168,hs5:159939342-159939342;hs5:163482561-163482561,hs21:30411608-30411608;hs5:163862906-163862906,hs21:31057408-31057408;hs5:163930283-163930283,hs21:14760263-14760263;hs6:38642057-38642057,hs6:123531219-123531219;hs6:95495247-95495247,hs6:95507186-95507186;hs6:123664417-123664417,hs6:168228563-168228563;hs7:39122539-39122539,hs7:43488983-43488983;hs7:51782883-51782883,hs14:49749698-49749698;hs8:54044492-54044492,hs8:54056801-54056801;hs10:14590169-14590169,hs10:17339901-17339901;hs10:14920218-14920218,hs10:19462426-19462426;hs10:20488666-20488666,hs10:82241782-82241782;hs10:77971215-77971215,hs10:77972984-77972984;hs10:81226556-81226556,hs10:81227461-81227461;hs10:82529858-82529858,hs10:82531949-82531949;hs11:6055332-6055332,hs11:30222215-30222215;hs11:39205130-39205130,hs11:46336487-46336487;hs13:25465821-25465821,hs13:25482780-25482780;hs16:33611973-33611973,hs16:33614235-33614235;hs18:24946647-24946647,hs18:24946982-24946982;hs18:26240178-26240178,hs18:57422314-57422314;hs18:34109579-34109579,hs18:58799580-58799580;hs18:57416350-57416350,hs18:58358748-58358748;hs19:17136916-17136916,hs19:17348961-17348961;hs19:46716153-46716153,hs19:50384324-50384324;hs20:44543514-44543514,hs20:44545696-44545696		Center for Personalized Medicine and Departments of Pharmacology and Therapeutics, Cancer Genetics, Biostatistics and Bioinformatics, Pathology, Urology, Molecular and Cellular Biology, and Medicine, Roswell Park Cancer Institute, Buffalo, NY 14263.	Using complete genome analysis, we sequenced five bladder tumors accrued from patients with muscle-invasive transitional cell carcinoma of the urinary bladder (TCC-UB) and identified a spectrum of genomic aberrations. In three tumors, complex genotype changes were noted. All three had tumor protein p53 mutations and a relatively large number of single-nucleotide variants (SNVs; average of 11.2 per megabase), structural variants (SVs; average of 46), or both. This group was best characterized by chromothripsis and the presence of subclonal populations of neoplastic cells or intratumoral mutational heterogeneity. Here, we provide evidence that the process of chromothripsis in TCC-UB is mediated by nonhomologous end-joining using kilobase, rather than megabase, fragments of DNA, which we refer to as stitchers, to repair this process. We postulate that a potential unifying theme among tumors with the more complex genotype group is a defective replication-licensing complex. A second group (two bladdertumors) had no chromothripsis, and a simpler genotype, WT tumor protein p53, had relatively few SNVs (average of 5.9 per megabase) and only a single SV. There was no evidence of a subclonal population of neoplastic cells. In this group, we used a preclinical model of bladder carcinoma cell lines to study a unique SV (translocation and amplification) of the gene glutamate receptor ionotropic N-methyl D-aspertate as a potential new therapeutic target in ladder cancer.	NCBI 36/hg18				Yes	NA
CTDB0061	Research	25799107	de Pagter MS, van Roosmalen MJ, Baas AF, Renkens I, Duran KJ, van Binsbergen E, Tavakoli-Yaraki M, Hochstenbach R, van der Veken LT, Cuppen E, Kloosterman WP	Chromothripsis in healthy individuals affects multiple protein-coding genes and can result in severe congenital abnormalities in offspring	Am J Hum Genet	2015 Apr	9,10,14,16	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Mother1	AB SOLiD 4 System		hs9:10640282-10641388,hg9:12067163-12069048;hs10:85708440-85709723,hs16:62811907-62813013;hs9:10643066-10645130,hs14:87959160-87960589;hs9:9874447-9875887,hs9:10397725-10400216;hs9:9877636-9880121,hs9:10184962-10187413;hs16:62814654-62819507,hs16:62837225-62840110;hs9:9039041-9043602,hs9:12069501-12073773;hs9:633474-636448,hs9:9043966-9046015;hs9:9043986-9045832,hs10:84550840-84554624;hs10:85704055-85707766,hs16:62832514-62837165;hs14:87956251-87957402,hs9:630972-632755;hs10:84549834-84549834,hs9:9048033-9048033;hs9:10182312-10184604,hs9:10400974-10404035	PTPRD;KANK1;NRG3	Department of Medical Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht 3584 CG, the Netherlands	Chromothripsis represents an extreme class of complex chromosome rearrangements (CCRs) with major effects on chromosomal architecture. Although recent studies have associated chromothripsis with congenital abnormalities, the incidence and pathogenic effects of this phenomenon require further investigation. Here, we analyzed the genomes of three families in which chromothripsis rearrangements were transmitted from a mother to her child. The chromothripsis in the mothers resulted in completely balanced rearrangements involving 8-23 breakpoint junctions across three to five chromosomes. Two mothers did not show any phenotypic abnormalities, although 3-13 protein-coding genes were affected by breakpoints. Unbalanced but stable transmission of a subset of the derivative chromosomes caused apparently de novo complex copy-number changes in two children. This resulted in gene-dosage changes, which are probably responsible for the severe congenital phenotypes of these two children. In contrast, the third child, who has a severe congenital disease, harbored all three chromothripsis chromosomes from his healthy mother, but one of the chromosomes acquired de novo rearrangements leading to copy-number changes. These results show that the human genome can tolerate extreme reshuffling of chromosomal architecture, including breakage of multiple protein-coding genes, without noticeable phenotypic effects. The presence of chromothripsis in healthy individuals affects reproduction and is expected to substantially increase the risk of miscarriages, abortions, and severe congenital disease.	GRCh37/hg19	GSE65454			No	NA
CTDB0062	Research	25799107	de Pagter MS, van Roosmalen MJ, Baas AF, Renkens I, Duran KJ, van Binsbergen E, Tavakoli-Yaraki M, Hochstenbach R, van der Veken LT, Cuppen E, Kloosterman WP	Chromothripsis in healthy individuals affects multiple protein-coding genes and can result in severe congenital abnormalities in offspring	Am J Hum Genet	2015 Apr	6,7,9,10,12	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Mother2	AB SOLiD 4 System		hs7:36718108-36721671,hs12:99787831-99790893;hs9:11739802-11742710,hs9:31460247-31463007;hs9:11758195-11759972,hs12:110263742-110266538;hs9:7104763-7106960,hs12:103464346-103466774;hs9:12236188-12238989,hs9:26965673-26968013;hs9:13236665-13239425,hs12:101859464-101861141;hs6:123750357-123752276,hs9:11743072-11746336;hs6:123765872-123766384,hs12:101856510-101856537;hs9:31433337-31436333,hs9:31463517-31465231;hs9:31471300-31473229,hs12:99435218-99436825;hs6:123748945-123750012,hs6:123768304-123769906;hs10:66227201-66230197,hs12:99785257-99787355;hs9:8118030-8119888,hs10:65848657-65850658;hs7:36714976-36717979,hs12:103467238-103470137;hs9:7107641-7109780,hs9:35723601-35726283;hs9:13334672-13337076,hs9:31473792-31476201;hs9:13240004-13241557,hs9:26962041-26964677;hs9:7116561-7120299,hs9:31436447-31440029;hs9:8121313-8122780,hs9:11760865-11763707;hs9:12233990-12236078,hs12:99431406-99434124;hs9:7113602-7116395,hs12:110267135-110269429;hs9:13337440-13340068,hs12:99636114-99638904;hs10:65844061-65847557,hs10:66230913-66234003;hs12:99634461-99634461,hs9:35727377-35727377	AOAH;ANKS1B;TRPV4;KDM4C;MPDZ;IFT74;TRDN;TLN1;CREB3	Department of Medical Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht 3584 CG, the Netherlands	Chromothripsis represents an extreme class of complex chromosome rearrangements (CCRs) with major effects on chromosomal architecture. Although recent studies have associated chromothripsis with congenital abnormalities, the incidence and pathogenic effects of this phenomenon require further investigation. Here, we analyzed the genomes of three families in which chromothripsis rearrangements were transmitted from a mother to her child. The chromothripsis in the mothers resulted in completely balanced rearrangements involving 8-23 breakpoint junctions across three to five chromosomes. Two mothers did not show any phenotypic abnormalities, although 3-13 protein-coding genes were affected by breakpoints. Unbalanced but stable transmission of a subset of the derivative chromosomes caused apparently de novo complex copy-number changes in two children. This resulted in gene-dosage changes, which are probably responsible for the severe congenital phenotypes of these two children. In contrast, the third child, who has a severe congenital disease, harbored all three chromothripsis chromosomes from his healthy mother, but one of the chromosomes acquired de novo rearrangements leading to copy-number changes. These results show that the human genome can tolerate extreme reshuffling of chromosomal architecture, including breakage of multiple protein-coding genes, without noticeable phenotypic effects. The presence of chromothripsis in healthy individuals affects reproduction and is expected to substantially increase the risk of miscarriages, abortions, and severe congenital disease.	GRCh37/hg19	GSE65454			No	NA
CTDB0063	Research	25799107	de Pagter MS, van Roosmalen MJ, Baas AF, Renkens I, Duran KJ, van Binsbergen E, Tavakoli-Yaraki M, Hochstenbach R, van der Veken LT, Cuppen E, Kloosterman WP	Chromothripsis in healthy individuals affects multiple protein-coding genes and can result in severe congenital abnormalities in offspring	Am J Hum Genet	2015 Apr	1,3,5	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Mother3	AB SOLiD 4 System		hs3:158384939-158388876,hs3:195632595-195635632;hs1:154441965-154444308,hs3:195630328-195631725;hs1:154445895-154448216,hs3:156530510-156533437;hs1:153155549-153158347,hs5:29436496-29438223;hs1:151021102-151023743,hs5:29433067-29436167;hs3:128911732-128913422,hs3:156534632-156536932;hs1:153746565-153748730,hs3:158389428-158392531;hs1:151018679-151020295,hs1:153151785-153154013	GFM1;LXN;TNK2;SHE;IL6R;C1orf56;BNIPL;CDC42SE1;MLLT11;LEKR1;PA2G4P4;SLC27A3;INTS3	Department of Medical Genetics, Center for Molecular Medicine, University Medical Center Utrecht, Utrecht 3584 CG, the Netherlands	Chromothripsis represents an extreme class of complex chromosome rearrangements (CCRs) with major effects on chromosomal architecture. Although recent studies have associated chromothripsis with congenital abnormalities, the incidence and pathogenic effects of this phenomenon require further investigation. Here, we analyzed the genomes of three families in which chromothripsis rearrangements were transmitted from a mother to her child. The chromothripsis in the mothers resulted in completely balanced rearrangements involving 8-23 breakpoint junctions across three to five chromosomes. Two mothers did not show any phenotypic abnormalities, although 3-13 protein-coding genes were affected by breakpoints. Unbalanced but stable transmission of a subset of the derivative chromosomes caused apparently de novo complex copy-number changes in two children. This resulted in gene-dosage changes, which are probably responsible for the severe congenital phenotypes of these two children. In contrast, the third child, who has a severe congenital disease, harbored all three chromothripsis chromosomes from his healthy mother, but one of the chromosomes acquired de novo rearrangements leading to copy-number changes. These results show that the human genome can tolerate extreme reshuffling of chromosomal architecture, including breakage of multiple protein-coding genes, without noticeable phenotypic effects. The presence of chromothripsis in healthy individuals affects reproduction and is expected to substantially increase the risk of miscarriages, abortions, and severe congenital disease.	GRCh37/hg19	GSE65454			No	NA
CTDB0064	Research	25662009	McDermott DH, Gao JL, Liu Q, Siwicki M, Martens C, Jacobs P, Velez D, Yim E, Bryke CR, Hsu N, Dai Z, Marquesen MM, Stregevsky E, Kwatemaa N, Theobald N, Long Priel DA, Pittaluga S, Raffeld MA, Calvo KR, Maric I, Desmond R, Holmes KL, Kuhns DB, Balabanian 	Chromothriptic cure of WHIM syndrome	Cell	2015 Feb	2	WHIM syndrome	Next Generation Sequencing	Homo sapiens	WHIM-09	Illumina HiSeq 2000	chr2:9500000-22000000:-1;chr2:24000000-26000000:-1;chr2:102000000-106000000:-1;chr2:132000000-133500000:-1;chr2:134000000-137000000:-1;chr2:155000000-157000000:-1;chr2:158000000-165000000:-1	hs2:9650469-9650469,hs2:92323543-92323543,HH;hs2:26227289-26227289,hs2:102167978-102167978,TT;hs2:102168450-102168450,hs2:156704625-156704625,HT;hs2:157479872-157479872,hs2:134383040-134383040,HH;hs2:134379440-134379440,hs2:18013669-18013669,TT;hs2:18014058-18014058,hs2:137413687-137413687,HH;hs2:137402471-137402471,hs2:155186295-155186295,TH;hs2:137413696-137413696,hs2:134383068-134383068,TT;hs2:134384129-134384129,hs2:134208472-134208472,HH;hs2:133712996-133712996,hs2:132361705-132361705,TH;hs2:106220579-106220579,hs2:24238501-24238501,TH;hs2:22647206-22647206,hs2:137344145-137344145,TT;hs2:137350425-137350425,hs2:92314297-92314297,HT;hs2:102176282-102176282,hs2:13364053-13364053,HH;hs2:13332820-13332820,hs2:133689046-133689046,TT;hs2:133712975-133712975,hs2:134248797-134248797,HH;hs2:134208529-134208529,hs2:164835205-164835205,TT	ACMSD;ACVR1;ACVR1C;ADAM17;ADCY3;ANKRD30BL;APOB;ASXL2;ATP6V1C2;BAZ2B;C2orf27A;C2orf27B;C2orf43;C2orf44;C2orf48;C2orf49;C2orf50;C2orf84;CCDC148;CCNT2;CD302;CENPO;CXCR4;CYS1;CYTIP;DAPL1;DARS;DDX1;DNAJC27;DNAJC27-AS1;DNMT3A;DPP4;DTNB;E2F6;EFR3B;ERMN;FAM49A;FAM84A;FAP;FHL2;FIGN;FKBP1B;FLJ12334;FLJ33534;GALNT13;GALNT5;GCA;GCG;GDF7;GEN1;GPR39;GPR45;GREB1;GRHL1;HPCAL1;HS1BP3;IFIH1;IL18R1;IL18RAP;IL1R1;IL1R2;IL1RL1;IL1RL2;ITGB6;ITSN2;KCNF1;KCNH7;KCNJ3;KCNS3;KIF3C;KLF11;LAPTM4A;LCT;LOC100129961;LOC100144595;LOC100287010;LOC100506421;LOC100506474;LOC100507600;LOC150568;LOC284998;LOC285000;LOC375190;LOC554201;LOC645949;LPIN1;LY75;LY75-CD302;LYPD1;MAP4K4;MARCH7;MATN3;MCM6;MFSD2B;MFSD9;MGAT5;MIR128-1;MIR1301;MIR3125;MIR3679;MIR4261;MIR4262;MIR4429;MIR4757;MIR4772;MIR4785;MIR663B;MRPS9;MSGN1;MYCN;MYCNOS;NBAS;NCKAP5;NCOA1;NOL10;NT5C1B;NT5C1B-RDH14;NTSR2;ODC1;OSR1;PDIA6;PFN4;PKP4;PLA2R1;POMC;POTEKP;POU3F3;PQLC3;PSMD14;PTRHD1;PUM2;R3HDM1;RAB3GAP1;RAD51AP2;RBMS1;RDH14;RHOB;ROCK2;RRM2;SDC1;SF3B14;SLC4A10;SLC9A2;SLC9A4;SMC6;SNORA80B;TAF1B;TANC1;TANK;TBR1;TGFBRAP1;TMEM163;TMEM182;TP53I3;TRIB2;TTC32;UBXN4;UPP2;VSNL1;WDR35;WDSUB1;YSK4;YWHAQ;ZRANB3	Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA	Chromothripsis is a catastrophic cellular event recently described in cancer in which chromosomes undergo massive deletion and rearrangement. Here, we report a case in which chromothripsis spontaneously cured a patient with WHIM syndrome, an autosomal dominant combined immunodeficiency disease caused by gain-of-function mutation of the chemokine receptor CXCR4. In this patient, deletion of the disease allele, CXCR4(R334X), as well as 163 other genes from one copy of chromosome 2 occurred in a hematopoietic stem cell (HSC) that repopulated the myeloid but not the lymphoid lineage. In competitive mouse bone marrow (BM) transplantation experiments, Cxcr4 haploinsufficiency was sufficient to confer a strong long-term engraftment advantage of donor BM over BM from either wild-type or WHIM syndrome model mice, suggesting a potential mechanism for the patient's cure. Our findings suggest that partial inactivation of CXCR4 may have general utility as a strategy to promote HSC engraftment in transplantation.	GRCh37/hg19				No	MFSD2B,LOC258000;POTEKP,NCKAP5
CTDB0065	Research	25517748	Garsed DW, Marshall OJ, Corbin VD, Hsu A, Di Stefano L, Schroder J, Li J, Feng ZP, Kim BW, Kowarsky M, Lansdell B, Brookwell R, Myklebost O, Meza-Zepeda L, Holloway AJ, Pedeutour F, Choo KH, Damore MA, Deans AJ, Papenfuss AT, Thomas DM	The Architecture and Evolution of Cancer Neochromosomes	Cancer Cell	2014 Nov	1,4,5,7,9,10,12,13,15,16,20,21,22	Liposarcoma	Next Generation Sequencing	Homo sapiens	778	Illumina HiSeq 2000				Cancer Genomics, Peter MacCallum Cancer Centre, East Melbourne, VIC 3002, Australia	We isolated and analyzed, at single-nucleotide resolution, cancer-associated neochromosomes from well- and/or dedifferentiated liposarcomas. Neochromosomes, which can exceed 600 Mb in size, initially arise as circular structures following chromothripsis involving chromosome 12. The core of the neochromosome is amplified, rearranged, and corroded through hundreds of breakage-fusion-bridge cycles. Under selective pressure, amplified oncogenes are overexpressed, while coamplified passenger genes may be silenced epigenetically. New material may be captured during punctuated chromothriptic events. Centromeric corrosion leads to crisis, which is resolved through neocentromere formation or native centromere capture. Finally, amplification terminates, and the neochromosome core is stabilized in linear form by telomere capture. This study investigates the dynamic mutational processes underlying the life history of a special form of cancer mutation.	GRCh37/hg19				Yes	YEATS4,TAF3
CTDB0066	Research	25517748	Garsed DW, Marshall OJ, Corbin VD, Hsu A, Di Stefano L, Schroder J, Li J, Feng ZP, Kim BW, Kowarsky M, Lansdell B, Brookwell R, Myklebost O, Meza-Zepeda L, Holloway AJ, Pedeutour F, Choo KH, Damore MA, Deans AJ, Papenfuss AT, Thomas DM	The Architecture and Evolution of Cancer Neochromosomes	Cancer Cell	2014 Nov	1,4,5,9,10,12,13,15,16,20,21	Liposarcoma	Next Generation Sequencing	Homo sapiens	449	Illumina HiSeq 2000				Cancer Genomics, Peter MacCallum Cancer Centre, East Melbourne, VIC 3002, Australia	We isolated and analyzed, at single-nucleotide resolution, cancer-associated neochromosomes from well- and/or dedifferentiated liposarcomas. Neochromosomes, which can exceed 600 Mb in size, initially arise as circular structures following chromothripsis involving chromosome 12. The core of the neochromosome is amplified, rearranged, and corroded through hundreds of breakage-fusion-bridge cycles. Under selective pressure, amplified oncogenes are overexpressed, while coamplified passenger genes may be silenced epigenetically. New material may be captured during punctuated chromothriptic events. Centromeric corrosion leads to crisis, which is resolved through neocentromere formation or native centromere capture. Finally, amplification terminates, and the neochromosome core is stabilized in linear form by telomere capture. This study investigates the dynamic mutational processes underlying the life history of a special form of cancer mutation.	GRCh37/hg19				Yes	NA
CTDB0067	Research	25517748	Garsed DW, Marshall OJ, Corbin VD, Hsu A, Di Stefano L, Schroder J, Li J, Feng ZP, Kim BW, Kowarsky M, Lansdell B, Brookwell R, Myklebost O, Meza-Zepeda L, Holloway AJ, Pedeutour F, Choo KH, Damore MA, Deans AJ, Papenfuss AT, Thomas DM	The Architecture and Evolution of Cancer Neochromosomes	Cancer Cell	2014 Nov	1,12,13,X	Liposarcoma	Next Generation Sequencing	Homo sapiens	GOT3	Illumina HiSeq 2000				Cancer Genomics, Peter MacCallum Cancer Centre, East Melbourne, VIC 3002, Australia	We isolated and analyzed, at single-nucleotide resolution, cancer-associated neochromosomes from well- and/or dedifferentiated liposarcomas. Neochromosomes, which can exceed 600 Mb in size, initially arise as circular structures following chromothripsis involving chromosome 12. The core of the neochromosome is amplified, rearranged, and corroded through hundreds of breakage-fusion-bridge cycles. Under selective pressure, amplified oncogenes are overexpressed, while coamplified passenger genes may be silenced epigenetically. New material may be captured during punctuated chromothriptic events. Centromeric corrosion leads to crisis, which is resolved through neocentromere formation or native centromere capture. Finally, amplification terminates, and the neochromosome core is stabilized in linear form by telomere capture. This study investigates the dynamic mutational processes underlying the life history of a special form of cancer mutation.	GRCh37/hg19				Yes	NA
CTDB0068	Research	25517748	Garsed DW, Marshall OJ, Corbin VD, Hsu A, Di Stefano L, Schroder J, Li J, Feng ZP, Kim BW, Kowarsky M, Lansdell B, Brookwell R, Myklebost O, Meza-Zepeda L, Holloway AJ, Pedeutour F, Choo KH, Damore MA, Deans AJ, Papenfuss AT, Thomas DM	The Architecture and Evolution of Cancer Neochromosomes	Cancer Cell	2014 Nov	2,10,12	Liposarcoma	Next Generation Sequencing	Homo sapiens	T1000	Illumina HiSeq 2000				Cancer Genomics, Peter MacCallum Cancer Centre, East Melbourne, VIC 3002, Australia	We isolated and analyzed, at single-nucleotide resolution, cancer-associated neochromosomes from well- and/or dedifferentiated liposarcomas. Neochromosomes, which can exceed 600 Mb in size, initially arise as circular structures following chromothripsis involving chromosome 12. The core of the neochromosome is amplified, rearranged, and corroded through hundreds of breakage-fusion-bridge cycles. Under selective pressure, amplified oncogenes are overexpressed, while coamplified passenger genes may be silenced epigenetically. New material may be captured during punctuated chromothriptic events. Centromeric corrosion leads to crisis, which is resolved through neocentromere formation or native centromere capture. Finally, amplification terminates, and the neochromosome core is stabilized in linear form by telomere capture. This study investigates the dynamic mutational processes underlying the life history of a special form of cancer mutation.	GRCh37/hg19				Yes	NA
CTDB0069	Research	25517748	Garsed DW, Marshall OJ, Corbin VD, Hsu A, Di Stefano L, Schroder J, Li J, Feng ZP, Kim BW, Kowarsky M, Lansdell B, Brookwell R, Myklebost O, Meza-Zepeda L, Holloway AJ, Pedeutour F, Choo KH, Damore MA, Deans AJ, Papenfuss AT, Thomas DM	The Architecture and Evolution of Cancer Neochromosomes	Cancer Cell	2014 Nov	1,2,3,5,7,8,9,12,14,15	Liposarcoma	Next Generation Sequencing	Homo sapiens	LPS141	Illumina HiSeq 2000				Cancer Genomics, Peter MacCallum Cancer Centre, East Melbourne, VIC 3002, Australia	We isolated and analyzed, at single-nucleotide resolution, cancer-associated neochromosomes from well- and/or dedifferentiated liposarcomas. Neochromosomes, which can exceed 600 Mb in size, initially arise as circular structures following chromothripsis involving chromosome 12. The core of the neochromosome is amplified, rearranged, and corroded through hundreds of breakage-fusion-bridge cycles. Under selective pressure, amplified oncogenes are overexpressed, while coamplified passenger genes may be silenced epigenetically. New material may be captured during punctuated chromothriptic events. Centromeric corrosion leads to crisis, which is resolved through neocentromere formation or native centromere capture. Finally, amplification terminates, and the neochromosome core is stabilized in linear form by telomere capture. This study investigates the dynamic mutational processes underlying the life history of a special form of cancer mutation.	GRCh37/hg19				Yes	NA
CTDB0070	Research	25517748	Garsed DW, Marshall OJ, Corbin VD, Hsu A, Di Stefano L, Schroder J, Li J, Feng ZP, Kim BW, Kowarsky M, Lansdell B, Brookwell R, Myklebost O, Meza-Zepeda L, Holloway AJ, Pedeutour F, Choo KH, Damore MA, Deans AJ, Papenfuss AT, Thomas DM	The Architecture and Evolution of Cancer Neochromosomes	Cancer Cell	2014 Nov	9,12	Liposarcoma	Next Generation Sequencing	Homo sapiens	ST059	Illumina HiSeq 2000				Cancer Genomics, Peter MacCallum Cancer Centre, East Melbourne, VIC 3002, Australia	We isolated and analyzed, at single-nucleotide resolution, cancer-associated neochromosomes from well- and/or dedifferentiated liposarcomas. Neochromosomes, which can exceed 600 Mb in size, initially arise as circular structures following chromothripsis involving chromosome 12. The core of the neochromosome is amplified, rearranged, and corroded through hundreds of breakage-fusion-bridge cycles. Under selective pressure, amplified oncogenes are overexpressed, while coamplified passenger genes may be silenced epigenetically. New material may be captured during punctuated chromothriptic events. Centromeric corrosion leads to crisis, which is resolved through neocentromere formation or native centromere capture. Finally, amplification terminates, and the neochromosome core is stabilized in linear form by telomere capture. This study investigates the dynamic mutational processes underlying the life history of a special form of cancer mutation.	GRCh37/hg19				Yes	NA
CTDB0071	Research	25517748	Garsed DW, Marshall OJ, Corbin VD, Hsu A, Di Stefano L, Schroder J, Li J, Feng ZP, Kim BW, Kowarsky M, Lansdell B, Brookwell R, Myklebost O, Meza-Zepeda L, Holloway AJ, Pedeutour F, Choo KH, Damore MA, Deans AJ, Papenfuss AT, Thomas DM	The Architecture and Evolution of Cancer Neochromosomes	Cancer Cell	2014 Nov	12	Liposarcoma	Next Generation Sequencing	Homo sapiens	ST079	Illumina HiSeq 2000				Cancer Genomics, Peter MacCallum Cancer Centre, East Melbourne, VIC 3002, Australia	We isolated and analyzed, at single-nucleotide resolution, cancer-associated neochromosomes from well- and/or dedifferentiated liposarcomas. Neochromosomes, which can exceed 600 Mb in size, initially arise as circular structures following chromothripsis involving chromosome 12. The core of the neochromosome is amplified, rearranged, and corroded through hundreds of breakage-fusion-bridge cycles. Under selective pressure, amplified oncogenes are overexpressed, while coamplified passenger genes may be silenced epigenetically. New material may be captured during punctuated chromothriptic events. Centromeric corrosion leads to crisis, which is resolved through neocentromere formation or native centromere capture. Finally, amplification terminates, and the neochromosome core is stabilized in linear form by telomere capture. This study investigates the dynamic mutational processes underlying the life history of a special form of cancer mutation.	GRCh37/hg19				Yes	NA
CTDB0072	Research	25756553	van Engen-van Grunsven AC, Baar MP, Pfundt R, Rijntjes J, Kusters-Vandevelde HV, Delbecq AL, Keunen JE, Klevering JB, Wesseling P, Blokx WA, Groenen PJ.	Whole-genome copy-number analysis identifies new leads for chromosomal aberrations involved in the oncogenesis and metastastic behavior of uveal melanomas.	Melanoma Res	2015 Jun	13	Uveal melanoma	Array CGH	Homo sapiens	UM11	Affymetrix OncoScan Array				Departments of aPathology bHuman Genetics cOphthalmology, Radboud University Medical Center dDepartment of Pathology, Canisius Wilhelmina Hospital, Nijmegen eDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands	To further elucidate the genetic underpinnings of uveal melanoma (UM) and identify new markers that correlate with disease outcome, archival formalin-fixed, paraffin-embedded enucleation specimens from 25 patients with UM and a mean follow-up of 14 years were analyzed for whole-genome copy-number alterations using OncoScan analysis. Copy-number alterations of chromosomes 1, 3, 6, and 8 were also analyzed in these tumors using multiplex ligation-dependent probe-amplification, and mutations in GNAQ, GNA11, and BAP1 were searched for by Sanger sequencing. Our study confirms the previously reported GNAQ and GNA11 mutation frequencies in UMs as well as the presence of monosomy 3 as a factor strongly indicating poor prognosis. Two cases with metastatic disease, but without monosomy of chromosome 3, showed loss of a small region in the distal part of chromosome 2p. Also, UMs leading to metastatic disease had more chromosomal aberrations than those without metastases. Three UMs lacking a GNAQ or a GNA11 mutation showed a gain of chromosome 8q; one of these cases showed extensive chromothripsis. Another case (with suspect lung metastasis) showed focal chromothripsis. Our whole-genome copy-number analysis shows that focal loss of chromosome 2p may be involved in the metastatic spread of UMs without monosomy 3; metastatic UMs carry more chromosomal aberrations than those without metastases; and chromothripsis may play a role in the oncogenesis of UMs, but does not necessarily indicate a poor prognosis. The clinical and particularly diagnostic utility of these findings needs to be corroborated in a larger set of patients with UM.	GRCh37/hg19				Yes	NA
CTDB0073	Research	25756553	van Engen-van Grunsven AC, Baar MP, Pfundt R, Rijntjes J, Kusters-Vandevelde HV, Delbecq AL, Keunen JE, Klevering JB, Wesseling P, Blokx WA, Groenen PJ.	Whole-genome copy-number analysis identifies new leads for chromosomal aberrations involved in the oncogenesis and metastastic behavior of uveal melanomas.	Melanoma Res	2015 Jun	1,3,6	Uveal melanoma	Array CGH	Homo sapiens	UM25	Affymetrix OncoScan Array				Departments of aPathology bHuman Genetics cOphthalmology, Radboud University Medical Center dDepartment of Pathology, Canisius Wilhelmina Hospital, Nijmegen eDepartment of Pathology, VU University Medical Center, Amsterdam, The Netherlands	To further elucidate the genetic underpinnings of uveal melanoma (UM) and identify new markers that correlate with disease outcome, archival formalin-fixed, paraffin-embedded enucleation specimens from 25 patients with UM and a mean follow-up of 14 years were analyzed for whole-genome copy-number alterations using OncoScan analysis. Copy-number alterations of chromosomes 1, 3, 6, and 8 were also analyzed in these tumors using multiplex ligation-dependent probe-amplification, and mutations in GNAQ, GNA11, and BAP1 were searched for by Sanger sequencing. Our study confirms the previously reported GNAQ and GNA11 mutation frequencies in UMs as well as the presence of monosomy 3 as a factor strongly indicating poor prognosis. Two cases with metastatic disease, but without monosomy of chromosome 3, showed loss of a small region in the distal part of chromosome 2p. Also, UMs leading to metastatic disease had more chromosomal aberrations than those without metastases. Three UMs lacking a GNAQ or a GNA11 mutation showed a gain of chromosome 8q; one of these cases showed extensive chromothripsis. Another case (with suspect lung metastasis) showed focal chromothripsis. Our whole-genome copy-number analysis shows that focal loss of chromosome 2p may be involved in the metastatic spread of UMs without monosomy 3; metastatic UMs carry more chromosomal aberrations than those without metastases; and chromothripsis may play a role in the oncogenesis of UMs, but does not necessarily indicate a poor prognosis. The clinical and particularly diagnostic utility of these findings needs to be corroborated in a larger set of patients with UM.	GRCh37/hg19				Yes	NA
CTDB0074	Research	25836623	Tan L, Xu LH, Liu HB, Yang SJ	Small lymphocytic lymphoma/chronic lymphocytic leukemia with chromothripsis in an old woman.	Chin Med J (Engl)	2015 Apr	8,9,11,13,17,19,X	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	25836623_1					Center of Oncology and Hematology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510230, China.	Cell karyotyping in patients with small lymphocytic lymphoma/chronic lymphocytic leukemia (SLL/CLL) is not easy to success, and small genomic lesions (<5 Mb) are not routinely detected by this method. It is likely that a complete genomic characterization of CLL requires a combination of fluorescence in situ hybridization (FISH), single nucleotide polymorphism (SNP) array profiling for comprehensive genome-wide analysis of acquired genomic copy number aberrations (aCNAs) and loss-of-heterozygosity (LOH) in dominant clones, and karyotyping for detection of balanced translocations, isochromosomes, and marker chromosomes. SNP array analysis can reveal chromothripsis, a phenomenon by which regions of the cancer genome are shattered and recombined to generate frequent oscillations between the lower and the higher DNA copy number states. This study provided cytogenetic findings in a CLL/SLL patient with v-myc avian myelocytomatosis viral oncogene homolog (C-MYC)-amplification by FISH, in which SNP arrays detected profound genomic upheaval due to chromothripsis that may lead to malignant transformation.	GRCh37/hg19				Yes	NA
CTDB0075	Research	25979483	Kim TM, Jung SH, An CH, Lee SH, Baek IP, Kim M, Park SW, Rhee JK, Lee SH, Chung YJ	Subclonal genomic architectures of primary and metastatic colorectal cancer based on intratumoral genetic heterogeneity.	Clin Cancer Res	2015 May	2	Colorectal cancer	Array CGH	Homo sapiens	CRC3	Agilent SurePrint G3 Human CGH Microarray 180K				Center for Cancer Evolution, Medical Research Center, The Catholic University of Korea	PURPOSE: The intratumoral heterogeneity (ITH) and the evolution of genomic architectures associated with the development of distant metastases are not well understood in colorectal cancers (CRCs). EXPERIMENTAL DESIGN: We performed multiregion biopsies of primary and liver metastatic regions from five CRCs with whole-exome sequencing and copy number profiling. RESULTS: In addition to a substantial level of genetic ITH, multiregion genetic profiling identifies the subclonal mutational architecture leading to the region-based or spatial categorization of somatic mutations and the inference of intratumoral evolutionary history of cancers. The universal mutations (those observed in all the regional biopsies) are enriched in known cancer genes such as APC and TP53 with distinct mutational spectra compared to biopsy- or region-specific mutations suggesting that major operative mutational mechanisms and their selective pressures are not constant across the metastatic progression. The phylogenies inferred from genomic data show branching evolutionary patterns where some primary biopsies are often segregated with metastastic lesions. Our analyses also revealed that copy number changes such as the chromosomal gains of c-MYC and chromothripsis can be region-specific and the potential source of genetic ITH. CONCLUSIONS: Our data shows that the genetic ITH is prevalent in CRC serving as a potential driving force to generate metastasis-initiating clones and also as a means to infer the intratumoral evolutionary history of cancers. The paucity of recurrent metastasis-clonal events suggests that CRC distant metastases may not follow a uniform course of genomic evolution, which should be considered in the genetic diagnosis and the selection of therapeutic targets for the advanced CRC.	GRCh37/hg19	GSE58512			Yes	NA
CTDB0076	Research	25979483	Kim TM, Jung SH, An CH, Lee SH, Baek IP, Kim M, Park SW, Rhee JK, Lee SH, Chung YJ	Subclonal genomic architectures of primary and metastatic colorectal cancer based on intratumoral genetic heterogeneity.	Clin Cancer Res	2015 May	16	Colorectal cancer	Array CGH	Homo sapiens	CRC5	Agilent SurePrint G3 Human CGH Microarray 180K				Center for Cancer Evolution, Medical Research Center, The Catholic University of Korea	PURPOSE: The intratumoral heterogeneity (ITH) and the evolution of genomic architectures associated with the development of distant metastases are not well understood in colorectal cancers (CRCs). EXPERIMENTAL DESIGN: We performed multiregion biopsies of primary and liver metastatic regions from five CRCs with whole-exome sequencing and copy number profiling. RESULTS: In addition to a substantial level of genetic ITH, multiregion genetic profiling identifies the subclonal mutational architecture leading to the region-based or spatial categorization of somatic mutations and the inference of intratumoral evolutionary history of cancers. The universal mutations (those observed in all the regional biopsies) are enriched in known cancer genes such as APC and TP53 with distinct mutational spectra compared to biopsy- or region-specific mutations suggesting that major operative mutational mechanisms and their selective pressures are not constant across the metastatic progression. The phylogenies inferred from genomic data show branching evolutionary patterns where some primary biopsies are often segregated with metastastic lesions. Our analyses also revealed that copy number changes such as the chromosomal gains of c-MYC and chromothripsis can be region-specific and the potential source of genetic ITH. CONCLUSIONS: Our data shows that the genetic ITH is prevalent in CRC serving as a potential driving force to generate metastasis-initiating clones and also as a means to infer the intratumoral evolutionary history of cancers. The paucity of recurrent metastasis-clonal events suggests that CRC distant metastases may not follow a uniform course of genomic evolution, which should be considered in the genetic diagnosis and the selection of therapeutic targets for the advanced CRC.	GRCh37/hg19	GSE58512			Yes	NA
CTDB0077	Research	25545346	Flynn A, Benn D, Clifton-Bligh R, Robinson B, Trainer AH, James P, Hogg A, Waldeck K, George J, Li J, Fox SB, Gill AJ, McArthur G, Hicks RJ, Tothill RW.	The genomic landscape of phaeochromocytoma.	J Pathol	2015 May	11	Pheochromocytomas and paragangliomas	Next Generation Sequencing	Homo sapiens	VCB02	Illumina HiSeq 2000	chr14:106073266-106536937:1;chr16:32843707-33814986:1;chr16:34440466-34755821:1;chr3:47685582-47872388:-1;chr11:98991024-99161979:-1;chr11:96533199-96762477:-1;chr11:95608563-95930305:-1;chr11:94508023-94620805:-1;chr11:94307510-94470779:-1;chr11:91797259-92155444:-1;chr11:9367219-10284338:-1;chr11:89776112-90024424:-1;chr11:88352253-89082537:-1;chr11:87583591-88289050:-1;chr11:87002361-87233478:-1;chr11:86345604-86675077:-1;chr11:85511021-86119818:-1;chr11:84890976-85330346:-1;chr11:84541817-84859310:-1;chr11:83416225-83537533:-1;chr11:82618413-82876242:-1;chr11:80420032-80813781:-1;chr11:8821443-9093570:-1;chr11:78267489-78438566:-1;chr11:77703696-77971664:-1;chr11:77064365-77691641:-1;chr11:76332168-76906676:-1;chr11:76016990-76326128:-1;chr11:75101844-75387629:-1;chr11:72882191-73393921:-1;chr11:71623012-72056717:-1;chr11:7463828-7804974:-1;chr11:69352173-69685706:-1;chr11:66183168-66518052:-1;chr11:62963964-63663990:-1;chr11:60593122-60974801:-1;chr11:6933054-7185996:-1;chr11:6435737-6649461:-1;chr11:55206501-55523703:-1;chr11:55069587-55197997:-1;chr11:50170917-50540673:-1;chr11:5211480-5537779:-1;chr11:49760742-50140507:-1;chr11:49106326-49447432:-1;chr11:47627919-47857470:-1;chr11:44274374-44448702:-1;chr11:43934914-44038206:-1;chr11:41696445-41903840:-1;chr11:41074754-41640927:-1;chr11:4168971-4605342:-1;chr11:39951150-40153990:-1;chr11:39468320-39783916:-1;chr11:38858882-39223893:-1;chr11:37909219-38828813:-1;chr11:36962252-37150275:-1;chr11:36545392-36799259:-1;chr11:35233704-35482228:-1;chr11:34492845-34892554:-1;chr11:33809471-33949500:-1;chr11:32688176-33049125:-1;chr11:32394861-32517997:-1;chr11:31725783-31818527:-1;chr11:30156932-30325711:-1;chr11:28785168-29567555:-1;chr11:28010301-28478523:-1;chr11:27710179-27970772:-1;chr11:25707061-26794036:-1;chr11:24135915-24462793:-1;chr11:23410862-23549584:-1;chr11:22777357-23389992:-1;chr11:21555509-21791071:-1;chr11:2650148-2933291:-1;chr11:17642611-18357493:-1;chr11:16243002-17578752:-1;chr11:15472498-15827879:-1;chr11:14594787-15204006:-1;chr11:134437948-134926782:-1;chr11:133071873-133246375:-1;chr11:132105242-132545127:-1;chr11:130733003-131076450:-1;chr11:13819290-14010113:-1;chr11:129654440-130335492:-1;chr11:128683914-128944858:-1;chr11:128339223-128598913:-1;chr11:128123675-128333668:-1;chr11:127405476-127711014:-1;chr11:126506756-126657319:-1;chr11:124752782-125485272:-1;chr11:123569106-123745280:-1;chr11:122925150-123310144:-1;chr11:122425497-122597421:-1;chr11:120880908-121286023:-1;chr11:120164785-120796581:-1;chr11:119720167-119923765:-1;chr11:118817151-119069474:-1;chr11:118459669-118693577:-1;chr11:118340500-118398791:-1;chr11:117458359-118135597:-1;chr11:116338431-116733451:-1;chr11:114695697-116321333:-1;chr11:114098413-114409606:-1;chr11:111769372-111988453:-1;chr11:111099717-111325362:-1;chr11:110864603-111041161:-1;chr11:109509515-109746772:-1;chr11:104114588-104696235:-1;chr11:102496184-102700504:-1;chr11:10522089-10694873:-1;chr11:1624627-1958705:-1		ADRBK1;ALDH3B2;AMBRA1;AMPD3;AP2A2;ARCN1;ARHGAP42;BARX2;C11orf49;C11orf75;C2CD3;CAPN1;CARS;CD44;COPB1;CTC-497E21.5;CTD-2313N18.2;CTD-2560E9.3;CTNND1;CWF19L2;DAGLA;DENND5A;FAT3;FCHSD2;GALNTL4;GRIK4;HYLS1;KIRREL3;LDHAL6A;LDLRAD3;MADD;NELL1;NOX4;PACS1;PDE2A;POLR2G;PSMD13;PUS3;RAB6A;RP11-295K3.1;RP11-406D1.2;RP11-563P16.1;RP11-660M18.2;RP11-676M6.1;RP11-770J1.3;RP5-1027O15.2;SLC22A18;SPCS2;SPI1;TEAD1;TRAF6	The Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia; The Department of Pathology, University of Melbourne, Parkville, VIC, Australia	Phaeochromocytomas (PCCs) and paragangliomas (PGLs) are rare neural crest-derived tumours originating from adrenal chromaffin cells or extra-adrenal sympathetic and parasympathetic tissues. More than a third of PCC/PGL cases are associated with heritable syndromes involving 13 or more known genes. These genes have been broadly partitioned into two groups based on pseudo-hypoxic and receptor tyrosine kinase (RTK) signalling pathways. Many of these genes can also become somatically mutated, although up to one third of sporadic cases have no known genetic driver. Furthermore, little is known of the genes that co-operate with known driver genes to initiate and drive tumourigenesis. To explore the genomic landscape of PCC/PGL, we applied exome sequencing, high-density SNP-array analysis, and RNA sequencing to 36 PCCs and four functional PGL tumours. All tumours displayed low mutation frequency, in contrast to frequent large segmental copy-number alterations, aneuploidy, and evidence for chromothripsis in one case. Multi-region sampling of one benign familial PCC tumour provided evidence for the timing of mutations during tumourigenesis and ongoing clonal evolution. Thirty-one of 40 (77.5%) cases could be explained by germline or somatic mutations or structural alterations affecting known PCC/PGL genes. Deleterious somatic mutations were also identified in known tumour-suppressor genes associated with genome maintenance and epigenetic modulation. A multitude of other genes were also found mutated that are likely important for normal neuroendocrine cell function. We revisited the gene-expression subtyping of PCC/PGL by integrating published microarray data with our RNA-seq data, enabling the identification of six robust gene-expression subtypes. The majority of cases in our cohort with no identifiable driver mutation were classified into a gene-expression subtype bearing similarity to MAX mutant PCC/PGL. Our data suggest there are yet unknown PCC/PGL cancer genes that can phenocopy MAX mutant PCC/PGL tumours. This study provides new insight into the molecular diversity and genetic origins of PCC/PGL tumours.	GRCh37/hg19	GSE61594			Yes	ADRBK1,TEAD1;AMBRA1,LDHAL6A;AMPD3,C11orf49;AP2A2,CTC-497E21.5;ARCN1,SLC22A18;C11orf49,AMPD3;C11orf75,RP11-660M18.2;CAPN1,SPI1;CARS,RP11-563P16.1;CD44,ARHGAP42;CD44,HYLS1;CD44,PUS3;COPB1,C2CD3;CWF19L2,RP11-676M6.1;CWF19L2,RP11-770J1.3;DAGLA,DENND5A;DENND5A,TRAF6;FAT3,GALNTL4;FCHSD2,CTD-2313N18.2;GRIK4,CTD-2560E9.3;MADD,NOX4;NELL1,BARX2;NOX4,LDLRAD3;PACS1,KIRREL3;PDE2A,ALDH3B2;PSMD13,SPCS2;RAB6A,RP5-1027O15.2;RP11-295K3.1,CTNND1;RP11-406D1.2,POLR2G
CTDB0078	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	6	Xenograft tumor	Array CGH	Mus musculus	103	NimbleGen Hubrecht Rat 2.1M HX1				Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0079	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	1	Xenograft tumor	Array CGH	Mus musculus	170	NimbleGen Hubrecht Rat 2.1M HX1			Myc	Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0080	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	10,13	Xenograft tumor	Array CGH	Mus musculus	153	NimbleGen Hubrecht Rat 2.1M HX1			Vegfa	Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0081	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	7	Xenograft tumor	Array CGH	Mus musculus	82	NimbleGen Hubrecht Rat 2.1M HX1				Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0082	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	3,8,10	Xenograft tumor	Array CGH	Mus musculus	97	NimbleGen Hubrecht Rat 2.1M HX1				Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0083	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	3,10	Xenograft tumor	Array CGH	Mus musculus	112	NimbleGen Hubrecht Rat 2.1M HX1			Mycn;Alk	Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0084	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	5	Xenograft tumor	Array CGH	Mus musculus	142	NimbleGen Hubrecht Rat 2.1M HX1			Vegfa	Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0085	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	10,17	Xenograft tumor	Array CGH	Mus musculus	202	NimbleGen Hubrecht Rat 2.1M HX1				Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0086	Research	25811670	Hermsen R, Toonen P, Kuijk E, Youssef SA, Kuiper R, van Heesch S, de Bruin A, Cuppen E, Simonis M	Lack of major genome instability in tumors of p53 null rats.	PLoS One	2015 Mar	6	Xenograft tumor	Array CGH	Mus musculus	9	NimbleGen Hubrecht Rat 2.1M HX1				Hubrecht Institute, KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, The Netherlands	Tumorigenesis is often associated with loss of tumor suppressor genes (such as TP53), genomic instability and telomere lengthening. Previously, we generated and characterized a rat p53 knockout model in which the homozygous rats predominantly develop hemangiosarcomas whereas the heterozygous rats mainly develop osteosarcomas. Using genome-wide analyses, we find that the tumors that arise in the heterozygous and homozygous Tp53C273X mutant animals are also different in their genomic instability profiles. While p53 was fully inactivated in both heterozygous and homozygous knockout rats, tumors from homozygous animals show very limited aneuploidy and low degrees of somatic copy number variation as compared to the tumors from heterozygous animals. In addition, complex structural rearrangements such as chromothripsis and breakage-fusion-bridge cycles were never found in tumors from homozygous animals, while these were readily detectable in tumors from heterozygous animals. Finally, we measured telomere length and telomere lengthening pathway activity and found that tumors of homozygous animals have longer telomeres but do not show clear telomerase or alternative lengthening of telomeres (ALT) activity differences as compared to the tumors from heterozygous animals. Taken together, our results demonstrate that host p53 status in this rat p53 knockout model has a large effect on both tumor type and genomic instability characteristics, where full loss of functional p53 is not the main driver of large-scale structural variations. Our results also suggest that chromothripsis primarily occurs under p53 heterozygous rather than p53 null conditions.	RGSC3.4	GSE55895			Yes	NA
CTDB0087	Research	25537021	Zhao X, Zhao YJ, Lin Q, Yu L, Liu Z, Lindsay H, Kogiso M, Rao P, Li XN, Lu X	Cytogenetic landscape of paired neurospheres and traditional monolayer cultures in pediatric malignant brain tumors.	Neuro Oncol	2015 Jul	2,3,8,10	Xenograft tumor	Array CGH	Mus musculus	IC-1227AA					Laboratory of Molecular Neuro-Oncology, Texas Children's Hospital, Baylor College of Medicine, Houston, Texas	BACKGROUND: New therapeutic targets are needed to eliminate cancer stem cells (CSCs). We hypothesize that direct comparison of paired CSCs and nonstem tumor cells (NSTCs) will facilitate identification of primary driver chromosomal aberrations that can serve as diagnostic markers and/or therapeutic targets. METHODS: We applied spectral karyotyping and G-banding to matched pairs of neurospheres (CSC-enriched cultures) and fetal bovine serum-based monolayer cultures (enriched with NSTCs) from 16 patient-derived orthotopic xenograft mouse models, including 9 medulloblastomas (MBs) and 7 high-grade gliomas (HGGs), followed by direct comparison of their numerical and structural abnormalities. RESULTS: Chromosomal aberrations were detected in neurospheres of all 16 models, and 82.0% numerical and 82.4% structural abnormalities were maintained in their matching monolayer cultures. Among the shared abnormalities, recurrent clonal changes were identified including gain of chromosomes 18 and 7 and loss of chromosome 10/10q (5/16 models), isochromosome 17q in 2 MBs, and a new breakpoint of 13q14 in 3 HGGs. Chromothripsis-like evidence was also observed in 3 HGG pairs. Additionally, we noted 20 numerical and 15 structural aberrations that were lost from the neurospheres and found 26 numerical and 23 structural aberrations that were only present in the NSTCs. Compared with MBs, the neurosphere karyotypes of HGG were more complex, with fewer chromosomal aberrations preserved in their matching NSTCs. CONCLUSION: Self-renewing CSCs in MBs and pediatric HGGs harbor recurrent numerical and structural aberrations that were maintained in the matching monolayer cultures. These primary chromosomal changes may represent new markers for anti-CSC therapies.					Yes	NA
CTDB0088	Research	25537021	Zhao X, Zhao YJ, Lin Q, Yu L, Liu Z, Lindsay H, Kogiso M, Rao P, Li XN, Lu X	Cytogenetic landscape of paired neurospheres and traditional monolayer cultures in pediatric malignant brain tumors.	Neuro Oncol	2015 Jul	12	Xenograft tumor	Array CGH	Mus musculus	IC-1502GBM					Laboratory of Molecular Neuro-Oncology, Texas Children's Hospital, Baylor College of Medicine, Houston, Texas	BACKGROUND: New therapeutic targets are needed to eliminate cancer stem cells (CSCs). We hypothesize that direct comparison of paired CSCs and nonstem tumor cells (NSTCs) will facilitate identification of primary driver chromosomal aberrations that can serve as diagnostic markers and/or therapeutic targets. METHODS: We applied spectral karyotyping and G-banding to matched pairs of neurospheres (CSC-enriched cultures) and fetal bovine serum-based monolayer cultures (enriched with NSTCs) from 16 patient-derived orthotopic xenograft mouse models, including 9 medulloblastomas (MBs) and 7 high-grade gliomas (HGGs), followed by direct comparison of their numerical and structural abnormalities. RESULTS: Chromosomal aberrations were detected in neurospheres of all 16 models, and 82.0% numerical and 82.4% structural abnormalities were maintained in their matching monolayer cultures. Among the shared abnormalities, recurrent clonal changes were identified including gain of chromosomes 18 and 7 and loss of chromosome 10/10q (5/16 models), isochromosome 17q in 2 MBs, and a new breakpoint of 13q14 in 3 HGGs. Chromothripsis-like evidence was also observed in 3 HGG pairs. Additionally, we noted 20 numerical and 15 structural aberrations that were lost from the neurospheres and found 26 numerical and 23 structural aberrations that were only present in the NSTCs. Compared with MBs, the neurosphere karyotypes of HGG were more complex, with fewer chromosomal aberrations preserved in their matching NSTCs. CONCLUSION: Self-renewing CSCs in MBs and pediatric HGGs harbor recurrent numerical and structural aberrations that were maintained in the matching monolayer cultures. These primary chromosomal changes may represent new markers for anti-CSC therapies.					Yes	NA
CTDB0089	Research	25537021	Zhao X, Zhao YJ, Lin Q, Yu L, Liu Z, Lindsay H, Kogiso M, Rao P, Li XN, Lu X	Cytogenetic landscape of paired neurospheres and traditional monolayer cultures in pediatric malignant brain tumors.	Neuro Oncol	2015 Jul	5,X	Xenograft tumor	Array CGH	Mus musculus	IC-3752GBM					Laboratory of Molecular Neuro-Oncology, Texas Children's Hospital, Baylor College of Medicine, Houston, Texas	BACKGROUND: New therapeutic targets are needed to eliminate cancer stem cells (CSCs). We hypothesize that direct comparison of paired CSCs and nonstem tumor cells (NSTCs) will facilitate identification of primary driver chromosomal aberrations that can serve as diagnostic markers and/or therapeutic targets. METHODS: We applied spectral karyotyping and G-banding to matched pairs of neurospheres (CSC-enriched cultures) and fetal bovine serum-based monolayer cultures (enriched with NSTCs) from 16 patient-derived orthotopic xenograft mouse models, including 9 medulloblastomas (MBs) and 7 high-grade gliomas (HGGs), followed by direct comparison of their numerical and structural abnormalities. RESULTS: Chromosomal aberrations were detected in neurospheres of all 16 models, and 82.0% numerical and 82.4% structural abnormalities were maintained in their matching monolayer cultures. Among the shared abnormalities, recurrent clonal changes were identified including gain of chromosomes 18 and 7 and loss of chromosome 10/10q (5/16 models), isochromosome 17q in 2 MBs, and a new breakpoint of 13q14 in 3 HGGs. Chromothripsis-like evidence was also observed in 3 HGG pairs. Additionally, we noted 20 numerical and 15 structural aberrations that were lost from the neurospheres and found 26 numerical and 23 structural aberrations that were only present in the NSTCs. Compared with MBs, the neurosphere karyotypes of HGG were more complex, with fewer chromosomal aberrations preserved in their matching NSTCs. CONCLUSION: Self-renewing CSCs in MBs and pediatric HGGs harbor recurrent numerical and structural aberrations that were maintained in the matching monolayer cultures. These primary chromosomal changes may represent new markers for anti-CSC therapies.					Yes	NA
CTDB0090	Research	25764012	Prabowo AS, van Thuijl HF, Scheinin I, Sie D, van Essen HF, Iyer AM, Spliet WG, Ferrier CH, van Rijen PC, Veersema TJ, Thom M, Schouten-van Meeteren AY, Reijneveld JC, Ylstra B, Wesseling P, Aronica E	Landscape of chromosomal copy number aberrations in gangliogliomas and dysembryoplastic neuroepithelial tumours.	Neuropathol Appl Neurobiol	2015 Mar	7	Dysembryoplastic neuroepithelial tumour	Next Generation Sequencing	Homo sapiens	25764012_1	Illumina HiSeq 2000				Department of (Neuro)Pathology, University of Amsterdam, Amsterdam, The Netherlands	AIM: Gangliogliomas (GGs) and dysembryoplastic neuroepithelial tumours (DNTs) represent the most common histological entities within the spectrum of glioneuronal tumours (GNTs). The wide variability of morphological features complicates histological classification, including discrimination from prognostically distinct diffuse low-grade astrocytomas (AIIs). This study was performed to increase our understanding of these tumours. METHODS: We studied chromosomal copy number aberrations (CNAs) by genome-wide sequencing in a large cohort of GNTs and linked these to comprehensive histological analysis and clinical characteristics. One hundred fourteen GNTs were studied: 50 GGs and 64 DNTs. Also, a data set of CNAs from 38 diffuse AIIs was included. RESULTS: The most frequent CNAs in both GGs and DNTs were gains at chromosomes 5 and 7, often concurrent, and gain at chromosome 6. None of the CNAs was linked to histological subtype, immunohistochemical features or to clinical characteristics. Comparison of AIIs and diffuse GNTs revealed that gain at whole chromosome 5 is only observed in GNTs. CNA patterns indicative of chromothripsis were detected in three GNTs. CONCLUSION: We conclude that GNTs with diverse morphologies share molecular features, and our findings support the need to improve classification and differential diagnosis of tumour entities within the spectrum of GNTs, as well as their distinction from other gliomas.				EGAS00001000831;EGAS00001000643	Yes	NA
CTDB0091	Research	25764012	Prabowo AS, van Thuijl HF, Scheinin I, Sie D, van Essen HF, Iyer AM, Spliet WG, Ferrier CH, van Rijen PC, Veersema TJ, Thom M, Schouten-van Meeteren AY, Reijneveld JC, Ylstra B, Wesseling P, Aronica E	Landscape of chromosomal copy number aberrations in gangliogliomas and dysembryoplastic neuroepithelial tumours.	Neuropathol Appl Neurobiol	2015 Mar	7	Dysembryoplastic neuroepithelial tumour	Next Generation Sequencing	Homo sapiens	25764012_2	Illumina HiSeq 2000				Department of (Neuro)Pathology, University of Amsterdam, Amsterdam, The Netherlands	AIM: Gangliogliomas (GGs) and dysembryoplastic neuroepithelial tumours (DNTs) represent the most common histological entities within the spectrum of glioneuronal tumours (GNTs). The wide variability of morphological features complicates histological classification, including discrimination from prognostically distinct diffuse low-grade astrocytomas (AIIs). This study was performed to increase our understanding of these tumours. METHODS: We studied chromosomal copy number aberrations (CNAs) by genome-wide sequencing in a large cohort of GNTs and linked these to comprehensive histological analysis and clinical characteristics. One hundred fourteen GNTs were studied: 50 GGs and 64 DNTs. Also, a data set of CNAs from 38 diffuse AIIs was included. RESULTS: The most frequent CNAs in both GGs and DNTs were gains at chromosomes 5 and 7, often concurrent, and gain at chromosome 6. None of the CNAs was linked to histological subtype, immunohistochemical features or to clinical characteristics. Comparison of AIIs and diffuse GNTs revealed that gain at whole chromosome 5 is only observed in GNTs. CNA patterns indicative of chromothripsis were detected in three GNTs. CONCLUSION: We conclude that GNTs with diverse morphologies share molecular features, and our findings support the need to improve classification and differential diagnosis of tumour entities within the spectrum of GNTs, as well as their distinction from other gliomas.				EGAS00001000831;EGAS00001000643	Yes	NA
CTDB0092	Research	25764012	Prabowo AS, van Thuijl HF, Scheinin I, Sie D, van Essen HF, Iyer AM, Spliet WG, Ferrier CH, van Rijen PC, Veersema TJ, Thom M, Schouten-van Meeteren AY, Reijneveld JC, Ylstra B, Wesseling P, Aronica E	Landscape of chromosomal copy number aberrations in gangliogliomas and dysembryoplastic neuroepithelial tumours.	Neuropathol Appl Neurobiol	2015 Mar	7	Ganglioglioma	Next Generation Sequencing	Homo sapiens	25764012_3	Illumina HiSeq 2000				Department of (Neuro)Pathology, University of Amsterdam, Amsterdam, The Netherlands	AIM: Gangliogliomas (GGs) and dysembryoplastic neuroepithelial tumours (DNTs) represent the most common histological entities within the spectrum of glioneuronal tumours (GNTs). The wide variability of morphological features complicates histological classification, including discrimination from prognostically distinct diffuse low-grade astrocytomas (AIIs). This study was performed to increase our understanding of these tumours. METHODS: We studied chromosomal copy number aberrations (CNAs) by genome-wide sequencing in a large cohort of GNTs and linked these to comprehensive histological analysis and clinical characteristics. One hundred fourteen GNTs were studied: 50 GGs and 64 DNTs. Also, a data set of CNAs from 38 diffuse AIIs was included. RESULTS: The most frequent CNAs in both GGs and DNTs were gains at chromosomes 5 and 7, often concurrent, and gain at chromosome 6. None of the CNAs was linked to histological subtype, immunohistochemical features or to clinical characteristics. Comparison of AIIs and diffuse GNTs revealed that gain at whole chromosome 5 is only observed in GNTs. CNA patterns indicative of chromothripsis were detected in three GNTs. CONCLUSION: We conclude that GNTs with diverse morphologies share molecular features, and our findings support the need to improve classification and differential diagnosis of tumour entities within the spectrum of GNTs, as well as their distinction from other gliomas.				EGAS00001000831;EGAS00001000643	Yes	NA
CTDB0093	Research	25506394	Holzmann C, Markowski DN, Koczan D, Kupker W, Helmke BM, Bullerdiek J	Cytogenetically normal uterine leiomyomas without MED12-mutations - a source to identify unknown mechanisms of the development of uterine smooth muscle tumors.	Mol Cytogenet	2014 Nov	2,5,11,18	Uterine leiomyoma	SNP Array	Homo sapiens	My708	Affymetrix CytoScan HD Array				Institute of Medical Genetics, University Rostock Medical Center, Ernst-Heydemann-Strasse 8, D-18057 Rostock, Germany	BACKGROUND: Recent findings on genetic changes in uterine leiomyomas suggest these benign tumors being a heterogeneous group of diseases in terms of molecular pathogenesis with those showing karyotype alterations as well as those characterized only by cytogenetically invisible mutations of mediator subcomplex 12 (MED12). Herein, five uterine leiomyomas (UL) with an apparently normal karyotype that lacked MED12-mutations were investigated by copy number variation arrays along with their matching myometrium to search for small genomic imbalances. RESULTS: Of five tumors one showed chromothripsis-like phenomena with numerous gains and losses of small segments mainly clustered to five chromosomal regions i.e. 2p14-2pter, 2q33.1-2q37.3, 5q31.3-5qter,11q14.1-11qter, and 18p11.21-18q2.3. Apparently, these cells had escaped detection by classical cytogenetics. Histologically, the tumor presented as a cellular leiomyoma with extended hyalinization. Of the remaining four tumors, one had a small intragenic deletion of the HMGA2 gene that was lacking in the corresponding myometrium. The other three tumors did not show relevant copy number alterations at all. CONCLUSIONS: Overall, the results suggest that leiomyomas with an apparently normal karyotype based on classical cytogenetics and lacking MED12 mutations represent a heterogeneous group of diseases. While the HMGA2 deletion detected in one of the tumors likely represents the driver mutation and, due to its size, has escaped detection by classical cytogenetics, the extended genomic imbalances detected in one of the other cases cannot be overlooked by this method suggesting an inability of the affected cells to divide in vitro. Of particular interest in that case is the occurrence of so-called chromothripsis or firestorms without involvement of the loci of common chromosomal rearrangements in UL, as e.g. 12q14~15 and 6p21. While chromothripsis was initially described as a hallmark of malignancy, the etiology and significance of this phenomenon in benign tumors still remain obscure. In uterine smooth muscle tumors, these changes per se do not indicate malignancy.	GRCh37/hg19				Yes	NA
CTDB0094	Research	25736334	Wang JC, Fisker T, Sahoo T	Constitutional chromothripsis involving chromosome 19 in a child with subtle dysmorphic features.	Am J Med Genet A	2015 Apr	19	Dysmorphia	Array CGH	Homo sapiens	25736334_1	4x180 k oligonucleotide array				Cytogenetics Laboratory, Hamilton Regional Laboratory Medicine Program, Hamilton Health Sciences, Ontario, Canada	Chromothripsis is defined as a single event wherein tens to hundreds of chromosomal rearrangements occur in a limited number of genomic regions, although the minimum threshold for the number of breaks and regions involved in chromothripsis has not been defined.	GRCh37/hg19				No	NA
CTDB0095	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	1,4,12,13,15	Chronic lymphocytic leukemia	Next Generation Sequencing	Homo sapiens	PD3172a	Illumina Genome Analyzer II		hs1:170758115-170758115,hs4:173998000-173998000;hs1:170822660-170822660,hs4:119852135-119852135;hs1:172107770-172107770,hs4:81649760-81649760;hs4:70257618-70257618,hs4:105957165-105957165;hs4:70261129-70261129,hs4:80291486-80291486;hs4:71223258-71223258,hs4:81652006-81652006;hs4:77014716-77014716,hs4:170643878-170643878;hs4:77030145-77030145,hs4:119951745-119951745;hs4:77030147-77030147,hs4:119849842-119849842;hs4:77037605-77037605,hs4:80293316-80293316;hs4:77040817-77040817,hs4:81648619-81648619;hs4:77040842-77040842,hs4:86837950-86837950;hs4:77042952-77042952,hs4:105696487-105696487;hs4:78650104-78650104,hs4:169386977-169386977;hs4:78651579-78651579,hs4:81649652-81649652;hs4:80226572-80226572,hs4:170624360-170624360;hs4:80226595-80226595,hs4:81313713-81313713;hs4:80287286-80287286,hs4:170642768-170642768;hs4:80291307-80291307,hs4:107243297-107243297;hs4:80467681-80467681,hs4:119852103-119852103;hs4:80506413-80506413,hs4:104234697-104234697;hs4:81648711-81648711,hs4:99640521-99640521;hs4:99639025-99639025,hs4:107217807-107217807;hs4:104243155-104243155,hs4:167629140-167629140;hs4:105652371-105652371,hs4:105957018-105957018;hs4:105652481-105652481,hs4:105967833-105967833;hs4:105662342-105662342,hs4:106201407-106201407;hs4:105700611-105700611,hs12:59712049-59712049;hs4:105739492-105739492,hs4:119952131-119952131;hs4:106197097-106197097,hs4:107243349-107243349;hs4:107216936-107216936,hs4:170645224-170645224;hs4:119501206-119501206,hs4:169381508-169381508;hs4:119956158-119956158,hs4:167620640-167620640;hs4:162402650-162402650,hs12:59468319-59468319;hs4:167620542-167620542,hs15:21792673-21792673;hs4:169386926-169386926,hs4:170642728-170642728;hs4:170624368-170624368,hs4:173997876-173997876;hs4:173959368-173959368,hs12:59539267-59539267;hs12:59707038-59707038,hs15:23138396-23138396;hs13:49474759-49474759,hs13:50488499-50488499;hs15:21280398-21280398,hs15:40811223-40811223;hs4:104234642-104234942,hs4:107217311-107217611;hs4:106199979-106200279,hs4:107220534-107220834;hs4:106201375-106201675,hs15:21786025-21786325;hs4:80506144-80506444,hs15:21280101-21280401	TBCK_HUMAN;NEK1;ZBTB37;C4orf22	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	ZBTB37,C4orf22;TBCK_HUMAN,NEK1
CTDB0096	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	4,9,13	Chronic lymphocytic leukemia	Next Generation Sequencing	Homo sapiens	PD3175a	Illumina Genome Analyzer II		hs4:99985365-99985365,hs10:102805821-102805821;hs4:169615303-169615303,hs9:21789308-21789308;hs4:169770605-169770605,hs9:21457739-21457739;hs4:99990414-99990714,hs9:21464986-21465286;hs9:20322528-20322528,hs13:47760651-47760651;hs9:21465000-21465000,hs13:47765821-47765821;hs9:22237156-22237156,hs13:50426343-50426343;hs11:79215247-79215247,hs11:126343811-126343811;hs13:47298401-47298401,hs13:50430220-50430220	CDKN2A;miR-15a/16-1	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	NA
CTDB0097	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	5	Renal cancer	Next Generation Sequencing	Homo sapiens	TK10	Illumina Genome Analyzer II		hs5:1391571-1391571,hs5:58882426-58882426;hs5:5997677-5997677,hs5:172885499-172885499;hs5:82591088-82591088,hs5:87333255-87333255;hs5:150892726-150892726,hs5:179506251-179506251;hs5:116036409-116036709,hs5:121979782-121980082;hs5:40837990-40837990,hs5:155087856-155087856;hs5:122724312-122724312,hs5:149292657-149292657;hs5:80245290-80245290,hs5:88043252-88043252;hs5:30903628-30903628,hs5:179575729-179575729;hs5:176692704-176693004,hs5:176849251-176849551;hs5:14835731-14836031,hs5:154507851-154508151;hs5:155231047-155231047,hs5:155239167-155239167;hs5:10681875-10681875,hs5:115348662-115348662;hs5:93783789-93783789,hs5:118735125-118735125;hs5:8009373-8009673,hs5:158710597-158710897;hs5:58427832-58427832,hs5:81386796-81386796;hs5:16203070-16203070,hs5:171178291-171178291;hs5:156463031-156463031,hs5:167283727-167283727;hs5:167251737-167251737,hs5:167283889-167283889;hs5:116036273-116036273,hs5:125175837-125175837;hs5:143377847-143377847,hs5:170778628-170778628;hs5:149360242-149360242,hs5:159241778-159241778;hs5:40069776-40069776,hs5:167246377-167246377;hs5:65989166-65989466,hs5:150893224-150893524;hs5:1391961-1391961,hs5:40252955-40252955;hs5:170777227-170777527,hs5:171176733-171177033;hs5:17269304-17269304,hs5:130533138-130533138;hs5:25833862-25833862,hs5:41970498-41970498;hs5:164531274-164531274,hs5:170030775-170030775;hs5:85333134-85333134,hs5:93781890-93781890;hs5:20868092-20868092,hs5:34407621-34407621;hs5:82594065-82594065,hs5:93387598-93387598;hs5:115347784-115347784,hs5:116728213-116728213;hs5:10639936-10639936,hs5:81385621-81385621;hs5:116145701-116145701,hs5:124097158-124097158;hs5:116728965-116729265,hs5:164535526-164535826;hs5:114877024-114877024,hs5:114913231-114913231;hs5:118734017-118734017,hs5:143377782-143377782;hs5:142741896-142741896,hs5:172986135-172986135;hs5:102946493-102946493,hs5:110916800-110916800;hs5:4254208-4254208,hs5:85333005-85333005;hs5:146248274-146248274,hs5:149293070-149293070;hs5:73700457-73700457,hs5:95495199-95495199;hs5:110989909-110989909,hs5:171901209-171901209;hs5:110918352-110918352,hs5:154476395-154476395;hs5:87574938-87574938,hs5:119641592-119641592;hs5:4253813-4253813,hs5:8009710-8009710;hs5:13558101-13558101,hs5:24794276-24794276;hs5:10705318-10705318,hs5:149360688-149360688;hs5:84038311-84038311,hs5:96658107-96658107;hs5:32281581-32281581,hs5:66102085-66102085;hs5:93386712-93386712,hs5:124097383-124097383;hs5:14231532-14231532,hs5:129092795-129092795;hs5:41971777-41971777,hs5:157749099-157749099;hs5:148091942-148091942,hs5:154506363-154506363	LMAN2;C5orf21;CCDC100;PDLIM7;ZNF608;PDE6A	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	C5orf21,ZNF608;CCDC100,PDE6A;LMAN2,PDLIM7
CTDB0098	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	3,4,7,8,9	Chordoma	Next Generation Sequencing	Homo sapiens	PD3808a	Illumina Genome Analyzer II		hs16:69265309-69265309,hs21:36237341-36237341;hs4:123124159-123124159,hs4:155159776-155159776;hs4:160244766-160244766,hs9:12975640-12975640;hs3:139340487-139340487,hs3:188568303-188568303;hs3:105009813-105009813,hs3:115981971-115981971;hs3:125751870-125751870,hs3:125997366-125997366;hs9:12406646-12406646,hs9:13055939-13055939;hs3:128893222-128893222,hs3:193227946-193227946;hs7:114409936-114409936,hs9:7316206-7316206;hs7:153836592-153836592,hs8:15649993-15649993;hs7:153199562-153199562,hs8:35945668-35945668;hs3:111440555-111440555,hs9:12598203-12598203;hs3:198269534-198269534,hs8:20151294-20151294;hs7:142008035-142008035,hs7:142194692-142194692;hs7:153541205-153541205,hs8:37921420-37921420;hs8:36069934-36069934,hs8:37943155-37943155;hs3:107391861-107391861,hs3:154927561-154927561;hs3:107458456-107458456,hs4:155589198-155589198;hs8:23182631-23182631,hs9:18177075-18177075;hs7:118260884-118260884,hs8:23089086-23089086;hs3:103437636-103437636,hs3:111344479-111344479;hs7:114353063-114353063,hs8:6297119-6297119;hs3:112126377-112126377,hs3:176209249-176209249;hs7:124797117-124797117,hs8:24255233-24255233;hs9:14680733-14680733,hs9:15703851-15703851;hs4:143617033-143617033,hs4:154386445-154386445;hs3:175287849-175287849,hs7:125094174-125094174;hs21:31753291-31753291,hs21:32980788-32980788;hs8:3380667-3380667,hs9:2183009-2183009;hs3:169305809-169305809,hs4:159579170-159579170;hs3:143632931-143632931,hs7:115987536-115987536;hs3:131029503-131029503,hs8:27510652-27510652;hs7:108221716-108221716,hs7:111876430-111876430;hs8:2259557-2259557,hs9:5099157-5099157;hs4:155125184-155125184,hs4:155164041-155164041;hs3:185109118-185109118,hs8:22917884-22917884;hs3:109188323-109188323,hs8:13206097-13206097;hs3:104112605-104112605,hs8:31816236-31816236;hs3:173006812-173006812,hs3:179412453-179412453;hs4:154567973-154568273,hs8:20975643-20975943;hs3:139342416-139342716,hs8:22732250-22732550;hs7:108220627-108220927,hs8:40732209-40732509;hs3:169230059-169230359,hs7:114812766-114813066;hs3:188647808-188648108,hs4:147925705-147926005;hs7:111428079-111428379,hs7:114488081-114488381;hs4:155825482-155825782,hs8:31903051-31903351;hs3:125730301-125730301,hs3:125985653-125985653;hs3:104685671-104685971,hs4:157499321-157499621;hs7:124355725-124356025,hs9:13630760-13631060;hs3:125262369-125262369,hs3:157388224-157388224;hs3:129206188-129206488,hs3:148104334-148104634;hs3:185809534-185809834,hs9:3851333-3851633;hs3:127741362-127741662,hs7:150238171-150238471;hs7:117939595-117939895,hs9:18090627-18090927;hs4:156554532-156554532,hs8:40025625-40025625;hs4:147352460-147352460,hs7:153709547-153709547;hs3:127952177-127952177,hs9:9227307-9227307;hs3:46413547-46413547,hs19:46781534-46781534;hs3:194586374-194586374,hs8:3671798-3671798;hs3:162491470-162491470,hs7:121614819-121614819;hs3:166314683-166314683,hs7:107455505-107455505;hs3:130680026-130680026,hs3:150022346-150022346;hs3:150022492-150022492,hs9:14521843-14521843;hs3:46414148-46414148,hs22:18459484-18459484;hs3:164420972-164420972,hs3:164591947-164591947;hs7:105982090-105982090,hs7:124219623-124219623;hs21:33477317-33477317,hs21:35741213-35741213;hs8:15518658-15518658,hs9:24805672-24805672;hs7:123687423-123687423,hs9:7745598-7745598;hs4:157378862-157378862,hs8:29283626-29283626;hs3:138664031-138664031,hs8:24040020-24040020;hs3:158987767-158987767,hs3:191886018-191886018;hs3:108235308-108235308,hs8:35956663-35956663;hs3:168438541-168438541,hs7:118533955-118533955;hs4:155594968-155594968,hs8:28111767-28111767;hs7:108225342-108225342,hs7:112844222-112844222;hs3:144533104-144533104,hs8:37921782-37921782;hs3:164360375-164360375,hs3:190445467-190445467;hs7:122617539-122617539,hs7:123024103-123024103;hs7:103750502-103750502,hs8:38708000-38708000;hs3:97874051-97874051,hs7:112292247-112292247;hs20:52206438-52206438,hs20:52208530-52208530;hs3:141643303-141643303,hs3:180957055-180957055;hs3:129207203-129207203,hs3:156247362-156247362;hs3:11862467-11862467,hs20:2071667-2071667;hs3:149087043-149087043,hs8:39311333-39311333;hs8:19904290-19904590,hs9:20235876-20236176;hs4:155970697-155970697,hs4:156555443-156555443;hs3:118147498-118147498,hs8:36363040-36363040;hs4:156544080-156544080,hs9:12947309-12947309;hs3:102910471-102910471,hs7:124918640-124918640;hs3:144477589-144477589,hs9:1779626-1779626;hs8:20056378-20056378,hs8:39016067-39016067;hs3:149088054-149088354,hs7:117440947-117441247;hs8:15503001-15503301,hs8:39740184-39740484;hs3:103438814-103439114,hs9:19858660-19858960;hs3:116916724-116917024,hs9:25264982-25265282;hs3:156286767-156287067,hs7:116119258-116119558;hs3:127951124-127951424,hs7:150837060-150837360;hs8:15525786-15526086,hs9:21422589-21422889;hs3:120930878-120931178,hs8:6347796-6348096;hs7:122408422-122408722,hs9:7744692-7744992;hs4:147347813-147348113,hs9:11837349-11837649;hs3:152844675-152844975,hs7:122408596-122408896;hs3:146637952-146638252,hs9:2207720-2208020;hs3:104155150-104155450,hs7:115370000-115370300;hs3:128284411-128284411,hs3:180373930-180373930;hs7:119836543-119836543,hs9:25500198-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Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	DPP6,TUSC3;KCND2,MLLT3;MDFIC,MCPH1;MME,MET;RHEB,PRKAG2;TMCC1,CLU
CTDB0099	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	1,3,8,14	Chordoma	Next Generation Sequencing	Homo sapiens	PD3807a	Illumina Genome Analyzer II		hs1:26979575-26979875,hs8:69957063-69957363;hs1:30245671-30245671,hs1:38399550-38399550;hs1:31899334-31899334,hs3:150466521-150466521;hs1:31940315-31940315,hs8:919665-919665;hs1:32720036-32720036,hs8:69724087-69724087;hs1:34451346-34451346,hs3:152144281-152144281;hs1:39264122-39264122,hs8:69723165-69723165;hs1:50992002-50992002,hs8:55720159-55720159;hs1:70901720-70902020,hs8:50147581-50147881;hs1:71137728-71137728,hs5:139904720-139904720;hs3:2601916-2601916,hs14:76184263-76184263;hs3:2610083-2610083,hs5:140127749-140127749;hs3:3416718-3416718,hs14:67892033-67892033;hs3:11255004-11255004,hs3:20403223-20403223;hs3:16643353-16643353,hs14:104931398-104931398;hs3:20085341-20085341,hs3:157751761-157751761;hs3:32621814-32621814,hs3:151850188-151850188;hs3:53410516-53410516,hs3:146734291-146734291;hs3:57325976-57325976,hs14:76400221-76400221;hs3:58931785-58931785,hs8:69681901-69681901;hs3:58938129-58938129,hs3:60835256-60835256;hs3:64565291-64565291,hs8:57311429-57311429;hs3:129929497-129929797,hs14:94268591-94268891;hs3:130245385-130245385,hs14:68408332-68408332;hs3:136003981-136003981,hs8:87003917-87003917;hs3:136449926-136449926,hs3:158026243-158026243;hs3:141305365-141305365,hs3:141412115-141412115;hs3:146735572-146735572,hs8:56175908-56175908;hs3:146736430-146736430,hs14:75887005-75887005;hs3:161812795-161812795,hs5:139768903-139768903;hs5:109933566-109933566,hs5:119200299-119200299;hs8:50147822-50147822,hs14:94729283-94729283;hs8:50489945-50489945,hs8:87018123-87018123;hs8:55439756-55439756,hs14:102320080-102320080;hs8:55723885-55723885,hs8:87283463-87283463;hs8:67128213-67128213,hs14:94141759-94141759;hs8:69722663-69722963,hs14:75864127-75864427;hs8:69945067-69945067,hs14:67894685-67894685;hs14:68271232-68271232,hs14:93541559-93541559;hs16:68497215-68497215,hs16:73317076-73317076;hs3:140998678-140998978,hs8:56176216-56176516;hs1:70998381-70998681,hs14:104931320-104931620;hs1:32719745-32720045,hs3:161742587-161742887	ARID1A	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	NA
CTDB0100	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	8	Small cell lung cancer	Next Generation Sequencing	Homo sapiens	SCLC-21H	Illumina Genome Analyzer II		hs8:11334999-11334999,hs8:66529146-66529146;hs8:127488904-127489204,hs8:128760986-128761286;hs8:90066845-90066845,hs8:128859930-128859930;hs8:11330938-11331238,hs8:116315947-116316247;hs8:29625873-29625873,hs8:127545025-127545025;hs8:40494959-40495259,hs8:63578821-63579121;hs8:84078541-84078541,hs8:128774769-128774769;hs1:1104523-1104523,hs8:11303277-11303277;hs8:66433321-66433321,hs8:99226664-99226664;hs8:41381707-41381707,hs8:55578459-55578459;hs8:63584884-63584884,hs8:128840413-128840413;hs8:84096378-84096678,hs8:99276752-99277052;hs8:40540106-40540106,hs8:41382086-41382086;hs8:40339604-40339604,hs8:63659251-63659251;hs1:13658511-13658511,hs8:99232476-99232476;hs8:84104510-84104510,hs8:99330308-99330308;hs8:89927992-89927992,hs8:116377775-116377775;hs8:90028640-90028640,hs8:128761665-128761665;hs8:63602392-63602692,hs8:84121444-84121744;hs8:55612264-55612264,hs8:63246121-63246121;hs8:66498393-66498393,hs8:99256919-99256919;hs8:66447224-66447224,hs8:127528434-127528434;hs8:40355992-40355992,hs8:66481086-66481086;hs8:11269759-11269759,hs8:89936178-89936178;hs8:89956203-89956203,hs8:128765822-128765822;hs8:10621584-10621884,hs8:49802227-49802527;hs8:99273289-99273289,hs8:99280579-99280579;hs8:89954833-89954833,hs8:116356805-116356805;hs8:76384607-76384907,hs8:134647332-134647632;hs8:1003824-1003824,hs8:141999833-141999833;hs8:99318074-99318074,hs8:116325324-116325324;hs8:29641114-29641414,hs8:90005403-90005703;hs8:91926266-91926266,hs8:135534499-135534499;hs8:11252027-11252027,hs8:112539264-112539264;hs8:11239955-11239955,hs8:136340239-136340239;hs8:121837279-121837279,hs8:123774622-123774622;hs8:6667546-6667546,hs8:140843361-140843361;hs8:53604722-53605022,hs8:119331475-119331775;hs8:12622845-12623145,hs8:37781847-37782147;hs8:69085526-69085526,hs8:72157502-72157502;hs8:5921124-5921124,hs8:37922786-37922786;hs8:63424515-63424515,hs8:128768887-128768887;hs8:66451200-66451200,hs8:89934797-89934797;hs8:73092898-73092898,hs8:75122245-75122245;hs8:5923169-5923169,hs8:37103136-37103136;hs8:42555739-42556039,hs8:53416356-53416656;hs8:40344813-40344813,hs8:63613246-63613246;hs8:135261511-135261511,hs8:135459132-135459132;hs8:11318167-11318167,hs8:11325275-11325275;hs8:137408686-137408986,hs8:138979784-138980084;hs8:81970352-81970352,hs8:133921212-133921212;hs8:5577388-5577388,hs8:103976608-103976608;hs8:10869550-10869850,hs8:137489525-137489825;hs8:22454965-22454965,hs8:133758654-133758654;hs8:30198404-30198404,hs8:87186559-87186559;hs8:81490029-81490329,hs8:82207940-82208240;hs8:101805541-101805541,hs8:137328228-137328228;hs8:87195716-87196016,hs8:124310623-124310923;hs8:20165449-20165449,hs8:137411964-137411964;hs8:20715579-20715579,hs8:63840620-63840620;hs8:19455939-19456239,hs8:139725272-139725572;hs8:1885157-1885157,hs8:110183787-110183787;hs8:6439903-6439903,hs8:30899422-30899422;hs8:41698217-41698517,hs8:49711469-49711769;hs8:41531133-41531133,hs8:119159124-119159124;hs1:13722829-13722829,hs8:3402262-3402262;hs8:16740459-16740759,hs8:42436126-42436426;hs8:48923911-48923911,hs8:122969508-122969508;hs8:57061907-57061907,hs8:129237641-129237641;hs8:58330935-58330935,hs8:82283446-82283446;hs8:6436982-6436982,hs8:41378046-41378046;hs8:41378099-41378099,hs8:108886771-108886771;hs8:53082840-53082840,hs8:78461441-78461441;hs8:116275853-116275853,hs8:128828742-128828742;hs8:15704777-15704777,hs8:134608299-134608299;hs8:63090960-63090960,hs8:135329445-135329445;hs8:13586559-13586559,hs8:41787159-41787159;hs8:54855118-54855118,hs8:99974406-99974406;hs8:123883526-123883826,hs8:140842856-140843156;hs8:82709329-82709329,hs8:97955601-97955601;hs8:72083508-72083508,hs8:85848430-85848430;hs8:34648964-34648964,hs8:48847974-48847974;hs8:36361896-36361896,hs8:138502485-138502485;hs8:66479937-66480237,hs8:128825952-128826252;hs8:5176476-5176776,hs8:10727886-10728186;hs8:35832972-35832972,hs8:91411528-91411528;hs8:4370669-4370669,hs8:13784748-13784748;hs8:93723994-93723994,hs8:128402490-128402490;hs8:56516542-56516842,hs8:136073825-136074125;hs8:41455693-41455693,hs8:100196980-100196980;hs8:10648768-10649068,hs8:10712705-10713005;hs8:92636326-92636326,hs8:138924823-138924823;hs8:114147202-114147202,hs8:137491376-137491376;hs8:78324898-78324898,hs8:109073814-109073814;hs8:73877924-73877924,hs8:91348505-91348505;hs8:91348628-91348628,hs8:74002719-74002719;hs8:68133797-68133797,hs8:109759771-109759771;hs8:53708080-53708080,hs8:56789717-56789717;hs8:33447354-33447654,hs8:102357702-102358002;hs8:33646395-33646395,hs8:123077634-123077634;hs8:66629238-66629238,hs8:97684801-97684801;hs8:66438322-66438322,hs8:66509837-66509837;hs8:116188868-116188868,hs8:116193675-116193675;hs8:20312061-20312061,hs8:23887740-23887740;hs8:42495902-42495902,hs8:52109083-52109083;hs8:11329042-11329342,hs8:90066559-90066859;hs8:3354213-3354213,hs8:114008570-114008570;hs8:104149665-104149665,hs8:131922039-131922039;hs8:65277352-65277352,hs8:66084082-66084082;hs8:66084167-66084167,hs8:95888502-95888502;hs8:16829036-16829336,hs8:135763578-135763878;hs8:2015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Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	GINS4,EXT1
CTDB0101	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	15	Colorectal cancer	Next Generation Sequencing	Homo sapiens	SNU-C1	Illumina Genome Analyzer 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Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	AVEN,PML;RORA,USP3;RYR3,PML;RYR3,TRIM69;SNURF,MTMR15;TCF12,CHD2;TCF12,Q6UXQ8_HUMAN
CTDB0102	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	9	Thyroid cancer	Next Generation Sequencing	Homo sapiens	8505C	Illumina Genome Analyzer II		hs9:7454833-7454833,hs9:23145010-23145010;hs9:33098663-33098663,hs9:33789560-33789560;hs9:1579757-1580057,hs9:4663106-4663406;hs9:8949468-8949768,hs9:15540871-15541171;hs9:228188-228188,hs9:20424814-20424814;hs9:12762732-12762732,hs9:25879584-25879584;hs9:28587314-28587314,hs9:28670841-28670841;hs9:24506875-24506875,hs9:25193632-25193632;hs9:2952298-2952298,hs9:10667039-10667039;hs9:20852311-20852311,hs9:29560127-29560127;hs9:17454719-17454719,hs9:26368791-26368791;hs9:29419040-29419340,hs9:29660189-29660489;hs9:21777176-21777176,hs9:29568922-29568922;hs9:13145539-13145539,hs9:14221818-14221818;hs9:7980862-7980862,hs9:9928692-9928692;hs9:21948858-21948858,hs9:33397652-33397652;hs9:20453319-20453319,hs9:27238725-27238725;hs9:5100371-5100371,hs9:29054311-29054311;hs9:5889794-5889794,hs9:26668518-26668518;hs9:4422090-4422090,hs9:5116722-5116722;hs9:2290544-2290544,hs9:4605611-4605611;hs9:7247919-7247919,hs9:9929564-9929564;hs9:13512666-13512666,hs9:27132324-27132324;hs9:25058453-25058753,hs9:26498004-26498304;hs9:6019406-6019706,hs9:28380386-28380686;hs9:10765455-10765455,hs9:13039192-13039192;hs9:5011921-5011921,hs9:7764091-7764091;hs9:15143749-15143749,hs9:28595214-28595214;hs9:4651767-4651767,hs9:20901921-20901921;hs9:12737450-12737450,hs9:13124848-13124848;hs9:9373024-9373024,hs9:10071146-10071146;hs9:2506342-2506342,hs9:2644653-2644653;hs9:17724585-17724585,hs9:24527845-24527845;hs9:16442087-16442087,hs9:26864075-26864075;hs9:6089120-6089120,hs9:14603695-14603695;hs9:19499041-19499041,hs9:20013757-20013757;hs9:5055620-5055620,hs9:6317157-6317157;hs9:2859316-2859316,hs9:8867751-8867751;hs9:4591795-4591795,hs9:27240863-27240863;hs9:2138307-2138307,hs9:2719580-2719580;hs9:2852906-2852906,hs9:19629264-19629264;hs9:14293226-14293226,hs9:14513741-14513741;hs9:14322415-14322415,hs9:23245395-23245395;hs9:7955237-7955237,hs9:24407743-24407743;hs9:10323697-10323697,hs9:14426915-14426915;hs9:3262095-3262095,hs9:27825635-27825635;hs9:9415390-9415390,hs9:10722575-10722575;hs9:6366290-6366290,hs9:10018277-10018277;hs9:29619486-29619486,hs9:29691381-29691381;hs9:402038-402038,hs9:7374557-7374557;hs9:11704731-11704731,hs9:14050724-14050724;hs9:10359747-10359747,hs9:12587433-12587433;hs9:16395062-16395062,hs9:25840571-25840571;hs9:17644515-17644515,hs9:19650991-19650991;hs9:21724873-21724873,hs9:27350365-27350365;hs9:10626472-10626472,hs9:21786655-21786655;hs9:22382260-22382260,hs9:27758579-27758579;hs9:5288498-5288498,hs9:21459325-21459325;hs9:12418901-12418901,hs9:13734730-13734730;hs9:19502794-19503094,hs9:20827418-20827718;hs9:3104534-3104534,hs9:24190526-24190526;hs9:8934538-8934538,hs9:15718673-15718673;hs9:4507322-4507322,hs9:6998862-6998862;hs9:8588558-8588558,hs9:10067086-10067086;hs9:4716993-4716993,hs9:27515861-27515861;hs9:21912699-21912699,hs9:23468883-23468883;hs9:5080122-5080122,hs9:28373207-28373207;hs9:28470952-28470952,hs9:29452159-29452159;hs9:10747464-10747464,hs9:15140890-15140890;hs9:2773503-2773503,hs9:2826002-2826002;hs9:5020641-5020641,hs9:22930579-22930579;hs9:21029705-21029705,hs9:30556083-30556083;hs9:12665566-12665566,hs9:13117644-13117644;hs9:17654237-17654237,hs9:19771070-19771070;hs9:10321434-10321434,hs9:29595452-29595452;hs9:19104394-19104394,hs9:27734756-27734756;hs9:26413453-26413453,hs9:26756213-26756213	C9orf68;CDKN2A;JAK2;JMJD2C;KCNV2;KIAA1797;MLLT3;MPDZ;NFIB;SLC1A1;SMARCA2;TPD52L3	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	C9orf68,KIAA1797;JAK2,TPD52L3;MPDZ,NFIB;SLC1A1,JMJD2C;SMARCA2,KCNV2
CTDB0103	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	1	Synovial sarcoma	Next Generation Sequencing	Homo sapiens	SW982	Illumina Genome Analyzer II				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	NA
CTDB0104	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	11	Melanoma	Next Generation Sequencing	Homo sapiens	SC32	Illumina Genome Analyzer II				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	NA
CTDB0105	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	16	Glioblastoma	Next Generation Sequencing	Homo sapiens	A172	Illumina Genome Analyzer II				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	NA
CTDB0106	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	1,4,10,14	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	PD3646a	Illumina Genome Analyzer II				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	NA
CTDB0107	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	12,20	Osteosarcoma	Next Generation Sequencing	Homo sapiens	PD3799a	Illumina Genome Analyzer II		hs12:58442187-58442187,hs12:57620230-57620230;hs12:57620497-57620497,hs12:58957976-58957976;hs20:7501303-7501303,hs20:43336042-43336042;hs12:57011311-57011311,hs12:57554249-57554249;hs12:67076643-67076943,hs12:67078090-67078390;hs20:2773550-2773550,hs20:23029205-23029205;hs20:17367251-17367251,hs20:21747854-21747854;hs12:64896001-64896001,hs12:67076811-67076811;hs12:66879952-66879952,hs12:73819282-73819282;hs12:59641861-59641861,hs12:59342711-59342711;hs12:59342779-59342779,hs12:68303999-68303999;hs12:37900026-37900026,hs12:57263787-57263787;hs12:38289239-38289239,hs12:38309029-38309029;hs20:25223958-25224258,hs20:52966624-52966924;hs20:52039440-52039440,hs20:60256737-60256737;hs12:65629910-65629910,hs12:66479252-66479252;hs12:66316446-66316446,hs12:74211707-74211707;hs12:67671294-67671294,hs12:69870130-69870130;hs20:21439646-21439946,hs20:22033696-22033996;hs20:17412002-17412002,hs20:50802396-50802396;hs12:58428539-58428839,hs12:66811518-66811818;hs12:65789899-65789899,hs12:73627618-73627618;hs12:58912619-58912619,hs12:66695126-66695126;hs12:56074829-56074829,hs12:66023883-66023883;hs12:57025231-57025231,hs12:70247750-70247750;hs12:55988628-55988628,hs12:58481314-58481314;hs12:57290916-57290916,hs12:69220231-69220231;hs12:68246320-68246320,hs12:65313009-65313009;hs12:65312973-65312973,hs12:68247450-68247450;hs20:34354393-34354393,hs20:43844955-43844955;hs12:66649897-66649897,hs12:70220390-70220390;hs12:39452938-39452938,hs12:67694878-67694878;hs12:55957687-55957687,hs12:67026716-67026716;hs12:65570296-65570296,hs12:67574938-67574938;hs20:59727255-59727255,hs20:59880825-59880825;hs20:47000736-47000736,hs20:55792873-55792873;hs12:39454856-39454856,hs12:56573381-56573381;hs20:7141982-7141982,hs20:31100556-31100556;hs12:60388899-60388899,hs12:66908919-66908919;hs12:65253483-65253483,hs12:67018446-67018446;hs12:69881026-69881026,hs12:70299595-70299595;hs12:64506231-64506531,hs12:70132255-70132555;hs12:64502447-64502747,hs12:67215504-67215804;hs12:37173408-37173408,hs12:57397386-57397386;hs12:57779502-57779502,hs12:73945700-73945700;hs12:37593874-37593874,hs12:58987651-58987651;hs12:59292511-59292511,hs12:67150585-67150585;hs12:60428880-60429180,hs12:69403640-69403940;hs12:67470416-67470716,hs12:67471539-67471839;hs12:60123239-60123239,hs12:66815116-66815116;hs20:23295971-23295971,hs20:43085308-43085308;hs12:40208112-40208112,hs12:55974495-55974495;hs12:39976799-39976799,hs12:65238670-65238670;hs20:20615726-20615726,hs20:38766439-38766439;hs12:66356997-66356997,hs12:67797477-67797477;hs12:39826082-39826082,hs12:65283127-65283127;hs12:66695545-66695545,hs12:67857536-67857536;hs12:59846330-59846330,hs12:68244402-68244402;hs12:40350865-40350865,hs12:66125080-66125080;hs12:56572643-56572643,hs12:57290007-57290007;hs12:40343752-40343752,hs12:66003117-66003117;hs12:40004615-40004615,hs12:73459440-73459440;hs12:56316123-56316123,hs12:59359795-59359795;hs12:57829380-57829380,hs12:66032035-66032035;hs12:67013937-67013937,hs12:73509415-73509415;hs12:56835299-56835299,hs12:58031479-58031479;hs12:57025146-57025446,hs12:70247553-70247853;hs20:48658235-48658235,hs20:59724130-59724130;hs12:66553441-66553441,hs12:69990363-69990363;hs20:34354352-34354652,hs20:43844786-43845086;hs12:40417611-40417611,hs12:68190511-68190511;hs12:37614161-37614161,hs12:65369721-65369721;hs12:64502447-64502747,hs12:67215504-67215804;hs12:75195155-75195155,hs12:75196750-75196750;hs12:57763521-57763521,hs12:68088382-68088382;hs20:44155408-44155408,hs20:46026329-46026329;hs12:66325398-66325398,hs12:67282959-67282959;hs12:66297342-66297342,hs12:68775855-68775855;hs20:17758396-17758396,hs20:61252776-61252776;hs12:37593936-37594236,hs12:58987599-58987899;hs12:38720447-38720447,hs12:67489340-67489340;hs12:57620431-57620431,hs12:58486346-58486346;hs12:57997044-57997044,hs12:67474026-67474026;hs20:52163530-52163530,hs20:53475058-53475058;hs20:12865832-12865832,hs20:52036066-52036066;hs12:38142661-38142661,hs12:38821302-38821302;hs12:57400320-57400320,hs12:74122877-74122877;hs20:2773142-2773442,hs20:23028901-23029201;hs12:65412680-65412680,hs12:67660836-67660836;hs20:17367052-17367352,hs20:21747809-21748109;hs12:60009145-60009145,hs12:66006029-66006029;hs12:64895742-64896042,hs12:67076821-67077121;hs12:57304371-57304371,hs12:65919665-65919665;hs12:39870405-39870405,hs12:74420235-74420235;hs12:55988642-55988642,hs12:58481060-58481360;hs12:56233854-56233854,hs12:68211530-68211530;hs20:59727302-59727602,hs20:59880557-59880857;hs20:7141866-7142166,hs20:31100419-31100719;hs12:64506231-64506531,hs12:70132255-70132555;hs12:59002439-59002439,hs12:69951395-69951395;hs20:38833017-38833017,hs20:45835704-45835704;hs12:56777639-56777639,hs12:57102652-57102652;hs12:37613230-37613230,hs12:70256621-70256621;hs12:70497500-70497500,hs12:73380213-73380213;hs12:67327766-67327766,hs12:73440723-73440723	GZF1;STK4	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	GZF1,STK4
CTDB0108	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	8,12,14	Osteosarcoma	Next Generation Sequencing	Homo sapiens	PD3786a	Illumina Genome Analyzer II		hs3:118093916-118093916,hs3:118426816-118426816;hs4:177436270-177436270,hs22:32553886-32553886;hs5:14715569-14715569,hs17:31949191-31949191;hs7:69644187-69644187,hs7:69876978-69876978;hs8:3168052-3168052,hs8:3939631-3939631;hs8:3583877-3583877,hs14:50924581-50924581;hs8:3603627-3603627,hs14:36679515-36679515;hs8:3685593-3685593,hs14:34524805-34524805;hs8:4167645-4167645,hs14:33699490-33699490;hs8:5868740-5868740,hs14:52866436-52866436;hs8:6133331-6133331,hs8:6251428-6251428;hs8:6135587-6135587,hs14:52515435-52515435;hs8:6494155-6494155,hs8:6515408-6515408;hs8:8909506-8909506,hs8:21278604-21278604;hs8:9789525-9789525,hs8:11858135-11858135;hs8:9817353-9817353,hs8:11469184-11469184;hs8:9834568-9834568,hs8:17016047-17016047;hs8:10383750-10383750,hs8:14278669-14278669;hs8:10388325-10388325,hs8:10493176-10493176;hs8:10416024-10416024,hs8:11104659-11104659;hs8:10422441-10422441,hs8:17483930-17483930;hs8:10626797-10626797,hs8:21210586-21210586;hs8:10920388-10920388,hs8:16882348-16882348;hs8:10925607-10925607,hs8:17536211-17536211;hs8:11115284-11115284,hs8:13237022-13237022;hs8:11342940-11342940,hs8:17601844-17601844;hs8:11625722-11625722,hs8:11862030-11862030;hs8:11627133-11627133,hs14:37796212-37796212;hs8:12460390-12460390,hs8:21613065-21613065;hs8:13207928-13207928,hs8:21227969-21227969;hs8:13210727-13210727,hs8:13275530-13275530;hs8:13268473-13268473,hs8:17496360-17496360;hs8:16875456-16875456,hs8:21215670-21215670;hs8:20331966-20331966,hs8:20393586-20393586;hs8:21302938-21302938,hs14:26558249-26558249;hs8:91341238-91341238,hs8:141775822-141775822;hs8:141571747-141571747,hs12:16046949-16046949;hs8:142747126-142747126,hs12:16430865-16430865;hs8:142747678-142747678,hs12:16603247-16603247;hs8:142845370-142845370,hs8:143474860-143474860;hs8:144181010-144181010,hs12:3880124-3880124;hs9:129999857-129999857,hs9:130014062-130014062;hs10:112373403-112373403,hs19:17271609-17271609;hs10:112373452-112373452,hs22:34941910-34941910;hs12:1815281-1815281,hs12:12569624-12569624;hs12:4316907-4316907,hs14:102135076-102135076;hs12:8757731-8757731,hs12:8847883-8847883;hs12:9411021-9411021,hs14:27661974-27661974;hs12:10980072-10980072,hs12:30029899-30029899;hs12:11027103-11027103,hs14:102139231-102139231;hs12:11366981-11366981,hs14:94525195-94525195;hs12:12573054-12573054,hs12:30002256-30002256;hs12:12586928-12586928,hs14:102111610-102111610;hs12:12597865-12597865,hs14:99429192-99429192;hs12:12687540-12687540,hs12:14245323-14245323;hs12:14117741-14117741,hs12:14185562-14185562;hs12:16049923-16049923,hs12:17462418-17462418;hs12:16051037-16051037,hs12:23459482-23459482;hs12:16051062-16051062,hs12:17462804-17462804;hs12:16054806-16054806,hs12:16463017-16463017;hs12:16433142-16433142,hs12:16466398-16466398;hs12:16436484-16436484,hs12:23822360-23822360;hs12:20337069-20337069,hs16:9621049-9621049;hs12:29963884-29963884,hs14:96813809-96813809;hs12:30014548-30014548,hs14:99450969-99450969;hs12:69443870-69443870,hs12:94616586-94616586;hs12:69528086-69528086,hs12:96433506-96433506;hs12:95629192-95629192,hs12:96135863-96135863;hs12:95909413-95909413,hs12:96157768-96157768;hs14:26550303-26550303,hs14:26587979-26587979;hs14:27664758-27664758,hs14:54170365-54170365;hs14:27671101-27671101,hs14:37793569-37793569;hs14:28723349-28723349,hs14:28745622-28745622;hs14:28743412-28743412,hs14:36721446-36721446;hs14:28753669-28753669,hs14:47494643-47494643;hs14:28767333-28767333,hs14:47493254-47493254;hs14:28957683-28957683,hs14:43733199-43733199;hs14:33697734-33697734,hs14:33700245-33700245;hs14:34525615-34525615,hs14:50800669-50800669;hs14:36632961-36632961,hs14:49464699-49464699;hs14:36752027-36752027,hs14:42844674-42844674;hs14:40070726-40070726,hs14:50931706-50931706;hs14:48806826-48806826,hs14:50956419-50956419;hs14:50974535-50974535,hs14:93501647-93501647;hs14:51140501-51140501,hs14:52932863-52932863;hs14:51343897-51343897,hs14:90906379-90906379;hs14:53076409-53076409,hs14:90957960-90957960;hs14:90870347-90870347,hs14:90957576-90957576;hs14:90906448-90906448,hs14:90906383-90906383;hs14:96798857-96798857,hs14:102080242-102080242;hs16:5520573-5520573,hs16:6093705-6093705;hs16:6184030-6184030,hs16:6185476-6185476;hs16:6244340-6244340,hs16:20556910-20556910;hs16:7089113-7089113,hs16:7739957-7739957;hs16:7906912-7906912,hs16:32551273-32551273;hs16:20340850-20340850,hs16:25864734-25864734;hs17:3356980-3356980,hs17:19605371-19605371;hs17:4646185-4646185,hs17:15822489-15822489;hs17:15819233-15819233,hs17:19182180-19182180;hs17:17634699-17634699,hs20:44505837-44505837;hs17:19604264-19604264,hs20:44548966-44548966;hs17:41558942-41558942,hs22:34941922-34941922;hs18:10824696-10824696,hs18:51654932-51654932;hs18:10824697-10824697,hs18:10824728-10824728;hs18:35339189-35339189,hs18:35392785-35392785;hs18:49622225-49622225,hs20:32287220-32287220;hs18:64755617-64755617,hs18:65131219-65131219;hs20:29299369-29299369,hs20:32231405-32231405;hs20:44418631-44418631,hs20:44545380-44545380;hs22:32554028-32554028,hs4:177585285-177585285;hsY:8187550-8187550,hsY:8189429-8189429;hs12:4357009-4357009,hs12:10955611-10955611;hs8:10630023-10630323,hs8:11595592-11595892;hs8:9790035-9790335,hs8:21229839-21230139;hs14:33108356-33108656,hs14:34528126-34528426;hs12:29986214-29986214,hs14:102097072-102097072;hs12:90631856-90632156,hs12:94612735-94613035	Q6ZP57_HUMAN;GFRA2	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	Q6ZP57_HUMAN,GFRA2
CTDB0109	Research	21215367	Stephens PJ, Greenman CD, Fu B, Yang F, Bignell GR, Mudie LJ, Pleasance ED, Lau KW, Beare D, Stebbings LA, McLaren S, Lin ML, McBride DJ, Varela I, Nik-Zainal S, Leroy C, Jia M, Menzies A, Butler AP, Teague JW, Quail MA, Burton J, Swerdlow H, Carter NP, M	Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development	Cell	2011 Jan	7,9,12,13	Osteosarcoma	Next Generation Sequencing	Homo sapiens	PD3791a	Illumina Genome Analyzer II		hs13:59499579-59499579,hs13:82915974-82915974;hs21:30622804-30622804,hs21:30634524-30634524;hs13:77097904-77097904,hs13:94876739-94876739;hs8:135611010-135611010,hs8:135762196-135762196;hs7:17553972-17553972,hs7:35734706-35734706;hs13:60955586-60955586,hs13:82714826-82714826;hs13:48205283-48205283,hs13:50150066-50150066;hs7:69785170-69785170,hs7:69874968-69874968;hs5:176893660-176893660,hs5:176952466-176952466;hs7:15578703-15578703,hs7:34543166-34543166;hs13:78597797-78597797,hs13:79236995-79236995;hs13:82714808-82714808,hs13:84088098-84088098;hs7:15570337-15570337,hs9:131506924-131506924;hs7:33158940-33158940,hs13:100442204-100442204;hs9:131022073-131022073,hs12:12982393-12982393;hs7:15568375-15568375,hs13:48072900-48072900;hs7:17553579-17553579,hs13:81855713-81855713;hs7:34373151-34373151,hs13:82810817-82810817;hs9:130352994-130352994,hs12:11686468-11686468;hs7:15578929-15578929,hs13:107501387-107501387;hs7:35987789-35987789,hs13:56881282-56881282;hs7:34005998-34005998,hs13:48900633-48900633;hs7:34317837-34317837,hs13:49109337-49109337;hs9:130949365-130949365,hs13:84216848-84216848;hs9:131526566-131526566,hs13:48780919-48780919;hs17:7835375-7835375,hs17:7848044-7848044;hs8:48530501-48530501,hs8:70657533-70657533;hs13:60925213-60925213,hs13:82968411-82968411;hs13:84755845-84755845,hs13:92223455-92223455;hs13:43974978-43974978,hs13:82820285-82820285;hs4:11022842-11022842,hs4:11336969-11336969;hs8:86571587-86571587,hs8:97625240-97625240;hs13:102720277-102720277,hs13:103442443-103442443;hs13:81765610-81765610,hs13:85422486-85422486;hs13:87073096-87073096,hs13:87597947-87597947;hs8:84069743-84069743,hs8:103185573-103185573;hs13:31438240-31438240,hs13:49129602-49129602;hs13:49121696-49121696,hs13:56881285-56881285;hs8:80283311-80283311,hs8:119951058-119951058;hs13:78986804-78986804,hs13:92854589-92854589;hs13:84223964-84223964,hs13:89446785-89446785;hs7:15392876-15392876,hs7:16002674-16002674;hs13:83182133-83182133,hs13:84909048-84909048;hs13:84211057-84211057,hs13:92634637-92634637;hs10:15522819-15522819,hs10:15581536-15581536;hs17:7816821-7816821,hs17:7871527-7871527;hs8:68122659-68122659,hs8:92203315-92203315;hs2:5785041-5785341,hs2:5864425-5864725;hs5:14646093-14646393,hs5:14855324-14855624;hs6:71196895-71196895,hs6:71233346-71233346;hs7:17128705-17129005,hs13:101720860-101721160;hs7:17545091-17545091,hs9:130959968-130959968;hs7:17561816-17562116,hs13:49038306-49038606;hs7:17715498-17715498,hs7:34743376-34743376;hs7:33166625-33166625,hs13:84769984-84769984;hs7:34318132-34318132,hs13:84082986-84082986;hs7:34435925-34435925,hs7:35821800-35821800;hs7:34445925-34445925,hs13:94901467-94901467;hs7:34751314-34751614,hs13:83387061-83387361;hs7:35452585-35452585,hs13:48086547-48086547;hs7:35461291-35461291,hs13:83511816-83511816;hs7:35821965-35821965,hs13:50109227-50109227;hs7:36323243-36323243,hs13:49415266-49415266;hs7:36325447-36325447,hs13:95750937-95750937;hs8:10319985-10319985,hs8:72336297-72336297;hs8:10627693-10627693,hs8:19900359-19900359;hs8:15264001-15264001,hs8:48514905-48514905;hs8:17254278-17254278,hs8:84925287-84925287;hs8:19935905-19935905,hs8:105748022-105748022;hs8:21975069-21975069,hs8:84528700-84528700;hs8:49662696-49662696,hs8:125935980-125935980;hs8:89617303-89617303,hs8:95342668-95342668;hs8:93948443-93948443,hs8:102986476-102986476;hs8:131065144-131065144,hs8:131216815-131216815;hs9:130948824-130948824,hs13:48089482-48089482;hs10:80680600-80680600,hs10:80806585-80806585;hs11:85062165-85062165,hs11:85134471-85134471;hs11:69623478-69623778,hs11:69805619-69805919;hs12:11668570-11668570,hs13:92225461-92225461;hs13:31438241-31438241,hs13:49121691-49121691;hs13:41774644-41774644,hs13:85405618-85405618;hs13:43965419-43965419,hs13:52397246-52397246;hs13:43974532-43974532,hs13:49312362-49312362;hs13:44454294-44454294,hs13:48921870-48921870;hs13:47966014-47966014,hs13:95733556-95733556;hs13:48093779-48093779,hs13:94426410-94426410;hs13:48780835-48781135,hs13:80597813-80598113;hs13:48900350-48900350,hs13:82993208-82993208;hs13:48982947-48982947,hs13:107521925-107521925;hs13:49000163-49000163,hs13:81941909-81941909;hs13:49067280-49067280,hs13:56844933-56844933;hs13:49129599-49129599,hs13:78642773-78642773;hs13:49420650-49420650,hs13:56903507-56903507;hs13:50149573-50149573,hs13:92024874-92024874;hs13:92024822-92024822,hs13:92024888-92024888;hs13:50554976-50554976,hs13:89486704-89486704;hs13:60895207-60895207,hs13:84029239-84029239;hs13:65952585-65952585,hs13:77959707-77959707;hs13:73123219-73123219,hs13:94769714-94769714;hs13:74562077-74562077,hs13:84886089-84886089;hs13:76772706-76772706,hs13:81872343-81872343;hs13:77076546-77076846,hs13:82934400-82934700;hs13:80570746-80570746,hs13:103342070-103342070;hs13:80600527-80600527,hs13:89064951-89064951;hs13:83830407-83830407,hs13:84046864-84046864;hs13:84046794-84046794,hs13:84881848-84881848;hs13:84773871-84773871,hs13:94876655-94876655;hs13:86636203-86636203,hs13:94901020-94901020;hs13:89050628-89050628,hs13:90372387-90372387;hs13:92186056-92186056,hs13:92272100-92272100;hs13:49020561-49020861,hs13:94460207-94460507;hs13:61466108-61466408,hs13:89045402-89045702;hs7:34050050-34050350,hs7:35417964-35418264;hs13:50146435-50146735,hs13:59499522-59499822	SPTAN1;ETV6	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, Cambridge CB10 1SA, UK	Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2%-3% of all cancers, across many subtypes, and is present in ~25% of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer.	NCBI 36/hg18				Yes	SPTAN1,ETV6
CTDB0110	Research	21925314	Liu P, Erez A, Nagamani SC, Dhar SU, Kolodziejska KE, Dharmadhikari AV, Cooper ML, Wiszniewska J, Zhang F, Withers MA, Bacino CA, Campos-Acevedo LD, Delgado MR, Freedenberg D, Garnica A, Grebe TA, Hernandez-Almaguer D, Immken L, Lalani SR, McLean SD, Nort	Chromosome Catastrophes Involve Replication Mechanisms Generating Complex Genomic Rearrangements	Cell	2011 Sep	9	Dysmorphia	Array CGH	Homo sapiens	BAB3103	Nimblegen 4.2M Array				Department of Molecular and Human Genetics	Complex genomic rearrangements (CGRs) consisting of two or more breakpoint junctions have been observed in genomic disorders. Recently, achromosome catastrophe phenomenon termed chromothripsis, in which numerous genomic rearrangements are apparently acquired in one single catastrophic event, was described in multiple cancers. Here, we show that constitutionally acquired CGRs share similarities with cancer chromothripsis. In the 17 CGR cases investigated, we observed localization and multiple copy number changes including deletions, duplications, and/or triplications, as well as extensive translocations and inversions. Genomic rearrangements involved varied in size and complexities; in one case, array comparative genomic hybridization revealed 18 copy number changes. Breakpoint sequencing identified characteristic features, including small templated insertions at breakpoints and microhomology at breakpoint junctions, which have been attributed to replicative processes. The resemblance between CGR and chromothripsis suggests similar mechanistic underpinnings. Such chromosome catastrophic events appear to reflect basic DNA metabolism operative throughout an organism's life cycle.	GRCh37/hg19				No	NA
CTDB0111	Research	21925314	Liu P, Erez A, Nagamani SC, Dhar SU, Kolodziejska KE, Dharmadhikari AV, Cooper ML, Wiszniewska J, Zhang F, Withers MA, Bacino CA, Campos-Acevedo LD, Delgado MR, Freedenberg D, Garnica A, Grebe TA, Hernandez-Almaguer D, Immken L, Lalani SR, McLean SD, Nort	Chromosome Catastrophes Involve Replication Mechanisms Generating Complex Genomic Rearrangements	Cell	2011 Sep	22	Dysmorphia	Array CGH	Homo sapiens	BAB3104	Nimblegen 4.2M Array				Department of Molecular and Human Genetics	Complex genomic rearrangements (CGRs) consisting of two or more breakpoint junctions have been observed in genomic disorders. Recently, achromosome catastrophe phenomenon termed chromothripsis, in which numerous genomic rearrangements are apparently acquired in one single catastrophic event, was described in multiple cancers. Here, we show that constitutionally acquired CGRs share similarities with cancer chromothripsis. In the 17 CGR cases investigated, we observed localization and multiple copy number changes including deletions, duplications, and/or triplications, as well as extensive translocations and inversions. Genomic rearrangements involved varied in size and complexities; in one case, array comparative genomic hybridization revealed 18 copy number changes. Breakpoint sequencing identified characteristic features, including small templated insertions at breakpoints and microhomology at breakpoint junctions, which have been attributed to replicative processes. The resemblance between CGR and chromothripsis suggests similar mechanistic underpinnings. Such chromosome catastrophic events appear to reflect basic DNA metabolism operative throughout an organism's life cycle.	GRCh37/hg19				No	NA
CTDB0112	Research	21925314	Liu P, Erez A, Nagamani SC, Dhar SU, Kolodziejska KE, Dharmadhikari AV, Cooper ML, Wiszniewska J, Zhang F, Withers MA, Bacino CA, Campos-Acevedo LD, Delgado MR, Freedenberg D, Garnica A, Grebe TA, Hernandez-Almaguer D, Immken L, Lalani SR, McLean SD, Nort	Chromosome Catastrophes Involve Replication Mechanisms Generating Complex Genomic Rearrangements	Cell	2011 Sep	9	Dysmorphia	Array CGH	Homo sapiens	BAB3105	Nimblegen 4.2M Array				Department of Molecular and Human Genetics	Complex genomic rearrangements (CGRs) consisting of two or more breakpoint junctions have been observed in genomic disorders. Recently, achromosome catastrophe phenomenon termed chromothripsis, in which numerous genomic rearrangements are apparently acquired in one single catastrophic event, was described in multiple cancers. Here, we show that constitutionally acquired CGRs share similarities with cancer chromothripsis. In the 17 CGR cases investigated, we observed localization and multiple copy number changes including deletions, duplications, and/or triplications, as well as extensive translocations and inversions. Genomic rearrangements involved varied in size and complexities; in one case, array comparative genomic hybridization revealed 18 copy number changes. Breakpoint sequencing identified characteristic features, including small templated insertions at breakpoints and microhomology at breakpoint junctions, which have been attributed to replicative processes. The resemblance between CGR and chromothripsis suggests similar mechanistic underpinnings. Such chromosome catastrophic events appear to reflect basic DNA metabolism operative throughout an organism's life cycle.	GRCh37/hg19				No	NA
CTDB0113	Research	22265402	Rausch T, Jones DT, Zapatka M, Stutz AM, Zichner T, Weischenfeldt J, Jager N, Remke M, Shih D, Northcott PA, Pfaff E, Tica J, Wang Q, Massimi L, Witt H, Bender S, Pleier S, Cin H, Hawkins C, Beck C, von Deimling A, Hans V, Brors B, Eils R, Scheurlen W, Bl	Genome Sequencing of Pediatric Medulloblastoma Links Catastrophic DNA Rearrangements with TP53 Mutations	Cell	2012 Jan	3,4,14	Sonic-Hedgehog medulloblastoma	Next Generation Sequencing	Homo sapiens	LFS-MB1	Illumina HiSeq 2000	chr1:63444401-63528602:-1;chr3:113498368-130583576:-1;chr4:124191414-164362015:-1;chr4:164458233-175842161:-1;chr8:3492450-3852149:-1;chr12:11191764-11292955:-1;chr12:33535367-33818924:-1;chr14:106815470-107130874:-1;chr4:124098068-124191394:1;chr4:159597606-159858310:1;chr4:164362032-164458144:1;chr4:170360650-170395000:1;chr4:171723347-171841028:1;chr4:175842203-176109339:1;chr14:20664952-20670397:1;chr14:22803240-22833959:1;chr14:79925792-80106000:1;chr14:80115001-80144983:1;chr14:80230194-80311870:1;chr2:14216912-16903663:1;chr3:112938115-113498342:1;chr3:130583569-131022000:1;chr3:139617001-141173250:1	hs4:159858310-159858310,hs14:79925792-79925792;hs4:170360650-170360650,hs14:22803240-22803240;hs4:176109339-176109339,hs14:80230194-80230194;hs4:171723347-171723347,hs14:20670397-20670397;hs11:38226283-38226283,hs17:16021393-16021393;hs13:50502098-50502098,hs18:70220182-70220182;hs1:179666590-179666590,hs1:182191375-182191375;hs2:14216833-14216833,hs2:16903720-16903720;hs2:115961657-115961657,hs2:120963994-120963994;hs2:116503651-116503651,hs2:207025403-207025403;hs2:120596559-120596559,hs2:122113238-122113238;hs2:120610969-120610969,hs2:183771998-183771998;hs2:121087792-121087792,hs2:121835816-121835816;hs2:183737296-183737296,hs2:200282232-200282232;hs3:112938044-112938044,hs3:141173305-141173305;hs3:131021629-131021629,hs3:139858259-139858259;hs3:139616963-139616963,hs3:139858020-139858020;hs4:116681164-116681164,hs4:127291493-127291493;hs4:116953341-116953341,hs4:164151091-164151091;hs4:124098007-124098007,hs4:170394907-170394907;hs4:124543475-124543475,hs4:164588491-164588491;hs4:128368058-128368058,hs4:170025020-170025020;hs4:159597587-159597587,hs4:171841070-171841070;hs4:164803329-164803329,hs4:170426855-170426855;hs7:64763921-64763921,hs7:66469133-66469133;hs10:13089870-13089870,hs10:50289722-50289722;hs10:29054168-29054168,hs10:62557463-62557463;hs10:48429595-48429595,hs10:49919974-49919974;hs11:38614205-38614205,hs11:38855827-38855827;hs11:38615134-38615134,hs11:41317169-41317169;hs11:41577279-41577279,hs11:43868468-43868468;hs14:20664900-20664900,hs14:80311910-80311910;hs16:21667732-21667732,hs16:24069189-24069189;hs22:21317195-21317195,hs22:21398564-21398564;hsX:49210465-49210465,hsX:49366877-49366877	ADAM29;ANAPC10;BOC;FBXW7;GAB1;GLI2;GRIA2;GYPA;GYPB;IL15;MYCN;NEK11;PPP2R2C;TRIM2;WDR17	European Molecular Biology Laboratory, Meyerhofstr. 1, 69117 Heidelberg, Germany	Genomic rearrangements are thought to occur progressively during tumor development. Recent findings, however, suggest an alternative mechanism, involving massive chromosome rearrangements in a one-step catastrophic event termed chromothripsis. We report the whole-genome sequencing-based analysis of a Sonic-Hedgehog medulloblastoma (SHH-MB) brain tumor from a patient with a germline TP53 mutation (Li-Fraumeni syndrome), uncovering massive, complex chromosome rearrangements. Integrating TP53 status with microarray and deep sequencing-based DNA rearrangement data in additional patients reveals a striking association between TP53 mutation and chromothripsis in SHH-MBs. Analysis of additional tumor entities substantiates a link between TP53 mutation and chromothripsis, and indicates a context-specific role for p53 in catastrophic DNA rearrangements. Among these, we observed a strong association between somatic TP53 mutations and chromothripsis in acute myeloid leukemia. These findings connect p53 status and chromothripsis in specific tumor types, providing a genetic basis for understanding particularly aggressive subtypes of cancer.	GRCh37/hg19	GSE14437;GSE32462;GSE19101;GSE23452;GSE34323;GSE34258		EGAS00001000085	Yes	NA
CTDB0114	Research	22265402	Rausch T, Jones DT, Zapatka M, Stutz AM, Zichner T, Weischenfeldt J, Jager N, Remke M, Shih D, Northcott PA, Pfaff E, Tica J, Wang Q, Massimi L, Witt H, Bender S, Pleier S, Cin H, Hawkins C, Beck C, von Deimling A, Hans V, Brors B, Eils R, Scheurlen W, Bl	Genome Sequencing of Pediatric Medulloblastoma Links Catastrophic DNA Rearrangements with TP53 Mutations	Cell	2012 Jan	3,8,17,X	Sonic-Hedgehog medulloblastoma	Next Generation Sequencing	Homo sapiens	LFS-MB2	Illumina HiSeq 2000	chr4:188409906-189503084:-1;chr5:5922885-14314337:-1;chr5:50792381-98447862:-1;chr6:29911431-30228533:-1;chr7:90522308-90588071:-1;chr7:90612330-92469025:-1;chr7:91376469-92127901:-1;chr8:1875838-10722429:-1;chr8:9629722-17109168:-1;chr11:23172601-24575386:-1;chr17:48871254-48940606:-1;chr18:45077868-56806980:-1;chr19:13623874-15447939:-1;chr19:16494334-16994600:-1;chrX:117637014-120303308:-1;chrX:121432913-130860060:-1	hs2:50943844-50943844,hs2:51065148-51065148;hs3:4984736-4984736,hs3:36349735-36349735;hs4:189232547-189232547,hs4:189534830-189534830;hs5:1410207-1410207,hs5:103772276-103772276;hs5:5889265-5889265,hs5:14348517-14348517;hs5:54107033-54107033,hs5:96117539-96117539;hs5:56540227-56540227,hs5:103054335-103054335;hs5:99317512-99317512,hs5:104095025-104095025;hs7:90471247-90471247,hs7:105787298-105787298;hs7:90560959-90560959,hs7:106086607-106086607;hs7:90640706-90640706,hs7:90768468-90768468;hs7:90715844-90715844,hs7:91497552-91497552;hs7:90724457-90724457,hs7:106482610-106482610;hs7:90998372-90998372,hs7:105987011-105987011;hs7:91026730-91026730,hs7:92130470-92130470;hs7:91560973-91560973,hs7:106105823-106105823;hs7:91663486-91663486,hs7:92128327-92128327;hs7:91778926-91778926,hs7:92229681-92229681;hs7:91791410-91791410,hs7:92473297-92473297;hs7:91803566-91803566,hs7:92030918-92030918;hs7:92351343-92351343,hs7:105896877-105896877;hs7:92381639-92381639,hs7:92557144-92557144;hs7:92845067-92845067,hs7:106761774-106761774;hs7:129677752-129677752,hs7:132312507-132312507;hs8:9650762-9650762,hs8:15733400-15733400;hs8:9695585-9695585,hs8:16544505-16544505;hs8:10501739-10501739,hs8:66488505-66488505;hs8:16553290-16553290,hs8:48957757-48957757;hs8:17075594-17075594,hs8:66502400-66502400;hs8:28076906-28076906,hs8:66479399-66479399;hs8:42678552-42678552,hs8:75717941-75717941;hs8:48957507-48957507,hs8:68047639-68047639;hs17:15853987-15853987,hs17:54957986-54957986;hs17:26743059-26743059,hs17:27067877-27067877;hs17:27079023-27079023,hs17:55022936-55022936;hs17:31921782-31921782,hs17:43403969-43403969;hs17:32772969-32772969,hs17:32879681-32879681;hs17:50402026-50402026,hs17:55210345-55210345;hs17:55164797-55164797,hs17:64399654-64399654;hs17:57571985-57571985,hs17:58356131-58356131;hs18:40529221-40529221,hs18:44778253-44778253;hs18:40723689-40723689,hs18:43436945-43436945;hs18:40845756-40845756,hs18:41443431-41443431;hs18:41968741-41968741,hs18:42887677-42887677;hs18:42896239-42896239,hs18:44486476-44486476;hs18:43443538-43443538,hs18:44140503-44140503;hs19:53362609-53362609,hs19:53969645-53969645;hsX:2833855-2833855,hsX:78605776-78605776;hsX:65918786-65918786,hsX:136944645-136944645;hsX:71079504-71079504,hsX:91194619-91194619;hsX:73782637-73782637,hsX:87033199-87033199;hsX:73825461-73825461,hsX:73890151-73890151;hsX:73833598-73833598,hsX:106515760-106515760;hsX:87062791-87062791,hsX:127534168-127534168;hsX:91212287-91212287,hsX:92107029-92107029;hsX:92000657-92000657,hsX:127505080-127505080;hsX:93878280-93878280,hsX:119920717-119920717;hsX:120424739-120424739,hsX:149004603-149004603;hsX:121407933-121407933,hsX:133389821-133389821;hs3:3865919-3865919,hsX:121844920-121844920;hs12:34841679-34841679,hs8:46872792-46872792;hs12:34841679-34841679,hs19:27752864-27752864;hs20:26318595-26318595,hs5:46346297-46346297;hs20:26318603-26318603,hsX:130893215-130893215;hsX:106556626-106556626,hs3:3588416-3588416;hsX:121804642-121804642,hs12:32269547-32269547;hsX:121947652-121947652,hs3:36334979-36334979;hsX:133358177-133358177,hs3:4932716-4932716	CDK6;DCX;DDX3X;GLI2;FOXO4;MAGEA1;MYCN;NAMPT;TAF1	European Molecular Biology Laboratory, Meyerhofstr. 1, 69117 Heidelberg, Germany	Genomic rearrangements are thought to occur progressively during tumor development. Recent findings, however, suggest an alternative mechanism, involving massive chromosome rearrangements in a one-step catastrophic event termed chromothripsis. We report the whole-genome sequencing-based analysis of a Sonic-Hedgehog medulloblastoma (SHH-MB) brain tumor from a patient with a germline TP53 mutation (Li-Fraumeni syndrome), uncovering massive, complex chromosome rearrangements. Integrating TP53 status with microarray and deep sequencing-based DNA rearrangement data in additional patients reveals a striking association between TP53 mutation and chromothripsis in SHH-MBs. Analysis of additional tumor entities substantiates a link between TP53 mutation and chromothripsis, and indicates a context-specific role for p53 in catastrophic DNA rearrangements. Among these, we observed a strong association between somatic TP53 mutations and chromothripsis in acute myeloid leukemia. These findings connect p53 status and chromothripsis in specific tumor types, providing a genetic basis for understanding particularly aggressive subtypes of cancer.	GRCh37/hg19	GSE14437;GSE32462;GSE19101;GSE23452;GSE34323;GSE34258		EGAS00001000085	Yes	NAMPT,CDK6
CTDB0115	Research	22265402	Rausch T, Jones DT, Zapatka M, Stutz AM, Zichner T, Weischenfeldt J, Jager N, Remke M, Shih D, Northcott PA, Pfaff E, Tica J, Wang Q, Massimi L, Witt H, Bender S, Pleier S, Cin H, Hawkins C, Beck C, von Deimling A, Hans V, Brors B, Eils R, Scheurlen W, Bl	Genome Sequencing of Pediatric Medulloblastoma Links Catastrophic DNA Rearrangements with TP53 Mutations	Cell	2012 Jan	3,15	Sonic-Hedgehog medulloblastoma	Next Generation Sequencing	Homo sapiens	LFS-MB3	Illumina HiSeq 2000	chr1:81896744-82117509:-1;chr1:145079866-145189859:-1;chr2:110109313-110251287:-1;chr2:149690639-149790578:-1;chr2:233210308-233318177:-1;chr3:129535039-142240426:-1;chr4:867271-1581792:-1;chr4:18285761-96336487:-1;chr4:18414602-28991025:-1;chr4:134478891-166432306:-1;chr5:180375000-180432033:-1;chr6:152778995-152955408:-1;chr7:2153486-15038940:-1;chr7:56564619-57477969:-1;chr8:35121733-35291026:-1;chr12:17722945-30145481:-1;chr13:114325887-114426023:-1;chr15:25626015-35404817:-1;chr15:27592310-88731192:-1;chr15:27592381-50831447:-1;chr15:27638165-65034324:-1;chr15:27692334-35404806:-1;chr15:27692341-34751965:-1;chr15:28025119-29058591:-1;chr15:29564215-31973108:-1;chr15:34028982-84374758:-1;chr15:34602258-66226936:-1;chr15:34752392-35404837:-1;chr15:35405071-47542305:-1;chr15:35405083-60559493:-1;chr15:35405921-89774781:-1;chr15:35405943-56590661:-1;chr15:35406062-47784193:-1;chr15:35406068-61425482:-1;chr15:36048000-38826328:-1;chr15:36079877-62499897:-1;chr15:36141398-77852311:-1;chr15:38019644-85778959:-1;chr15:38354283-38856739:-1;chr15:38963868-55081326:-1;chr15:41476300-54247872:-1;chr15:41612473-84028139:-1;chr15:43080211-81247110:-1;chr15:44785584-82339510:-1;chr15:45265673-51715441:-1;chr15:45497532-67049070:-1;chr15:47535310-96255463:-1;chr15:47676606-92567896:-1;chr15:47845948-55080236:-1;chr15:49628274-59475290:-1;chr15:50108383-87670940:-1;chr15:50798716-101663200:-1;chr15:50813733-66438292:-1;chr15:50824388-63715435:-1;chr15:50833651-88731133:-1;chr15:56406665-100282989:-1;chr15:56614544-62885408:-1;chr15:57103408-58691682:-1;chr15:58386821-84945701:-1;chr15:60122494-88782529:-1;chr15:62784551-69024995:-1;chr15:64448240-87886231:-1;chr15:65433008-101841362:-1;chr15:66242159-93836383:-1;chr15:66836685-86095274:-1;chr15:70301222-92712797:-1;chr15:73600835-100160977:-1;chr15:75498764-76064634:-1;chr15:89416605-91127851:-1;chr18:75721727-75772072:-1;chr21:41468328-44066701:-1;chr21:42955522-43005639:-1;chrY:14440191-15234430:-1;chr15:37593001-37809000:1;chr15:44509001-44786000:1;chr15:46078001-47139000:1;chr15:54279001-54476000:1;chr15:65861001-65933000:1;chr15:66497001-66691000:1;chr15:77636001-77848000:1;chr15:79825001-79979000:1;chr15:82339001-83057580:1;chr15:85315001-85611000:1;chr15:99055001-100149000:1;chr2:13598001-17621000:1	hs1:78170570-78170570,hs1:79568682-79568682;hs1:78990540-78990540,hs1:83363860-83363860;hs2:13598087-13598087,hs2:17620755-17620755;hs2:170355427-170355427,hs2:170478847-170478847;hs3:53898723-53898723,hs3:53981596-53981596;hs4:1600174-1600174,hs4:21569204-21569204;hs4:1648566-1648566,hs4:1772823-1772823;hs4:1759629-1759629,hs4:2041362-2041362;hs4:18415910-18415910,hs4:31101146-31101146;hs4:19044222-19044222,hs4:23704174-23704174;hs4:21765873-21765873,hs4:23062496-23062496;hs4:21807855-21807855,hs4:22714648-22714648;hs4:22617210-22617210,hs4:22715322-22715322;hs4:24718977-24718977,hs4:25400304-25400304;hs4:24732441-24732441,hs4:30095895-30095895;hs4:101974096-101974096,hs4:139906781-139906781;hs5:176195896-176195896,hs5:176406025-176406025;hs6:64338556-64338556,hs6:105479874-105479874;hs6:157609433-157609433,hs6:157691407-157691407;hs7:1146265-1146265,hs7:8133233-8133233;hs7:1149649-1149649,hs7:7800358-7800358;hs7:6529998-6529998,hs7:18228910-18228910;hs7:15171873-15171873,hs7:26191860-26191860;hs7:61056588-61056588,hs7:61675249-61675249;hs9:84926330-84926330,hs9:85100582-85100582;hs9:99381288-99381288,hs9:99638918-99638918;hs9:112209390-112209390,hs9:112344043-112344043;hs12:2387147-2387147,hs12:6705540-6705540;hs15:23291122-23291122,hs15:33806523-33806523;hs15:24850022-24850022,hs15:39119625-39119625;hs15:25312632-25312632,hs15:96150563-96150563;hs15:25625740-25625740,hs15:35406091-35406091;hs15:25990006-25990006,hs15:68635056-68635056;hs15:26026945-26026945,hs15:33183012-33183012;hs15:26031340-26031340,hs15:78474256-78474256;hs15:26129574-26129574,hs15:39873798-39873798;hs15:26683575-26683575,hs15:68950551-68950551;hs15:26941413-26941413,hs15:73072495-73072495;hs15:27176088-27176088,hs15:73397401-73397401;hs15:27475815-27475815,hs15:40752573-40752573;hs15:27692074-27692074,hs15:35406067-35406067;hs15:27692092-27692092,hs15:35404831-35404831;hs15:27692336-27692336,hs15:35406053-35406053;hs15:27829421-27829421,hs15:79452789-79452789;hs15:27910654-27910654,hs15:35427659-35427659;hs15:27911295-27911295,hs15:35405121-35405121;hs15:27987635-27987635,hs15:51025797-51025797;hs15:28262125-28262125,hs15:66438978-66438978;hs15:29363291-29363291,hs15:34721143-34721143;hs15:29932964-29932964,hs15:60131426-60131426;hs15:30357629-30357629,hs15:54269262-54269262;hs15:30935070-30935070,hs15:67256394-67256394;hs15:32195355-32195355,hs15:48516453-48516453;hs15:33145274-33145274,hs15:60373138-60373138;hs15:33153560-33153560,hs15:45617574-45617574;hs15:33814655-33814655,hs15:60454777-60454777;hs15:33840954-33840954,hs15:95576509-95576509;hs15:33987983-33987983,hs15:36878965-36878965;hs15:34082813-34082813,hs15:90796798-90796798;hs15:34154892-34154892,hs15:73178927-73178927;hs15:3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Molecular Biology Laboratory, Meyerhofstr. 1, 69117 Heidelberg, Germany	Genomic rearrangements are thought to occur progressively during tumor development. Recent findings, however, suggest an alternative mechanism, involving massive chromosome rearrangements in a one-step catastrophic event termed chromothripsis. We report the whole-genome sequencing-based analysis of a Sonic-Hedgehog medulloblastoma (SHH-MB) brain tumor from a patient with a germline TP53 mutation (Li-Fraumeni syndrome), uncovering massive, complex chromosome rearrangements. Integrating TP53 status with microarray and deep sequencing-based DNA rearrangement data in additional patients reveals a striking association between TP53 mutation and chromothripsis in SHH-MBs. Analysis of additional tumor entities substantiates a link between TP53 mutation and chromothripsis, and indicates a context-specific role for p53 in catastrophic DNA rearrangements. Among these, we observed a strong association between somatic TP53 mutations and chromothripsis in acute myeloid leukemia. These findings connect p53 status and chromothripsis in specific tumor types, providing a genetic basis for understanding particularly aggressive subtypes of cancer.	GRCh37/hg19	GSE14437;GSE32462;GSE19101;GSE23452;GSE34323;GSE34258		EGAS00001000085	Yes	NA
CTDB0116	Research	22265402	Rausch T, Jones DT, Zapatka M, Stutz AM, Zichner T, Weischenfeldt J, Jager N, Remke M, Shih D, Northcott PA, Pfaff E, Tica J, Wang Q, Massimi L, Witt H, Bender S, Pleier S, Cin H, Hawkins C, Beck C, von Deimling A, Hans V, Brors B, Eils R, Scheurlen W, Bl	Genome Sequencing of Pediatric Medulloblastoma Links Catastrophic DNA Rearrangements with TP53 Mutations	Cell	2012 Jan	2,12	Sonic-Hedgehog medulloblastoma	Next Generation Sequencing	Homo sapiens	LFS-MB4	Illumina HiSeq 2000	chr2:2074250-15913826:-1;chr2:14156532-91794235:-1;chr2:23727492-121124467:-1;chr2:110109209-110251278:-1;chr2:149690550-149790676:-1;chr4:2071045-33527520:-1;chr4:7250202-7366570:-1;chr4:53097786-54003362:-1;chr4:55196757-55277010:-1;chr4:56788702-57032247:-1;chr4:103168108-107714052:-1;chr5:155138565-155188667:-1;chr5:180374717-180432585:-1;chr11:69089751-69139794:-1;chr12:4512391-23390634:-1;chr12:7540228-32371383:-1;chr12:19854988-20369213:-1;chr13:114325864-114426002:-1;chr15:34034045-47295315:-1;chr18:75721852-75772156:-1;chr21:42955390-43005560:-1;chr2:1934384-2074250:1;chr2:15913826-16157942:1;chr2:23554909-23727492:1;chr2:48236089-48566218:1;chr2:56279625-56326244:1;chr2:114704001-115892335:1;chr2:119939305-120031183:1;chr2:121124467-121431476:1;chr2:121432593-123704028:1;chr2:152495756-152743190:1	hs1:91853138-91853138,hs11:85195217-85195217;hs1:91853163-91853163,hs17:33478114-33478114;hs1:156186643-156186643,hs21:9826979-9826979;hs1:156186648-156186648,hs2:133013270-133013270;hs1:156186652-156186652,hs16:33963032-33963032;hs17:33478369-33478369,hs21:9827543-9827543;hs20:29653973-29653973,hs9:68425913-68425913;hs21:9827569-9827569,hs11:85195007-85195007;hs2:1934384-1934384,hs2:120031183-120031183;hs2:16157942-16157942,hs2:48566218-48566218;hs2:23554909-23554909,hs2:48236089-48236089;hs2:56279625-56279625,hs2:123704028-123704028;hs2:56326244-56326244,hs2:152743190-152743190;hs2:85364248-85364248,hs2:88644722-88644722;hs2:114704412-114704412,hs2:152495756-152495756;hs2:115892335-115892335,hs2:121431476-121431476;hs2:119939305-119939305,hs2:121432593-121432593;hs4:38623762-38623762,hs4:41458623-41458623;hs4:56803911-56803911,hs4:56872432-56872432;hs6:157609435-157609435,hs6:157691649-157691649;hs12:2356776-2356776,hs12:2884168-2884168;hs12:2356986-2356986,hs12:2884265-2884265;hs12:3596541-3596541,hs12:21013620-21013620;hs12:3597143-3597143,hs12:21013616-21013616;hs12:4512436-4512436,hs12:19959311-19959311;hs12:5303246-5303246,hs12:22259157-22259157;hs12:11188586-11188586,hs12:29102643-29102643;hs12:19919957-19919957,hs12:20409715-20409715;hs12:19956957-19956957,hs12:20345242-20345242;hs12:19958257-19958257,hs12:23390562-23390562;hs12:20356483-20356483,hs12:23525091-23525091;hs12:20359046-20359046,hs12:23523379-23523379;hs12:20359221-20359221,hs12:23525579-23525579;hs12:20451650-20451650,hs12:22761890-22761890;hs12:22248606-22248606,hs12:22478408-22478408;hs12:22482795-22482795,hs12:23315033-23315033;hs12:23184210-23184210,hs12:23354948-23354948;hs12:23184480-23184480,hs12:23355160-23355160;hs12:31864190-31864190,hs12:32478301-32478301;hs14:26854924-26854924,hs14:30667922-30667922;hs17:41399870-41399870,hs17:41466036-41466036	ALK;FSHR;GIGYF2;GLI2;ITGAV;MSH2;MYCN;NDUFA10;NEB;TMSB10	European Molecular Biology Laboratory, Meyerhofstr. 1, 69117 Heidelberg, Germany	Genomic rearrangements are thought to occur progressively during tumor development. Recent findings, however, suggest an alternative mechanism, involving massive chromosome rearrangements in a one-step catastrophic event termed chromothripsis. We report the whole-genome sequencing-based analysis of a Sonic-Hedgehog medulloblastoma (SHH-MB) brain tumor from a patient with a germline TP53 mutation (Li-Fraumeni syndrome), uncovering massive, complex chromosome rearrangements. Integrating TP53 status with microarray and deep sequencing-based DNA rearrangement data in additional patients reveals a striking association between TP53 mutation and chromothripsis in SHH-MBs. Analysis of additional tumor entities substantiates a link between TP53 mutation and chromothripsis, and indicates a context-specific role for p53 in catastrophic DNA rearrangements. Among these, we observed a strong association between somatic TP53 mutations and chromothripsis in acute myeloid leukemia. These findings connect p53 status and chromothripsis in specific tumor types, providing a genetic basis for understanding particularly aggressive subtypes of cancer.	GRCh37/hg19	GSE14437;GSE32462;GSE19101;GSE23452;GSE34323;GSE34258		EGAS00001000085	Yes	ACTR3,NEB
CTDB0117	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	1,2,15	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient1_child	AB SOLiD 4 System	chr2:173635809-173636102:-1;chr2:178960434-178966476:-1;chr2:145581576-145599659:-1;chr2:128911531-129009714:-1;chr2:178122186-178703789:-1;chr2:143596932-144357565:-1;chr2:124075514-127121524:-1	hs1:243411172-243412608,hs2:146558384-146560016;hs1:243412915-243416373,hs2:124072892-124075186;hs1:247929824-247932508,hs2:145578477-145581427;hs1:247933718-247935923,hs2:173101937-173105197;hs2:127121662-127124079,hs2:178118299-178122101;hs2:128506785-128511173,hs2:128908136-128911334;hs2:128900068-128903965,hs15:27746706-27750284;hs2:128904215-128906395,hs2:129010017-129011058;hs2:128907892-128911115,hs2:145624203-145627873;hs2:143593314-143596595,hs2:144357834-144359901;hs2:145492925-145496715,hs2:173097546-173101766;hs2:145497032-145499296,hs2:178957564-178960096;hs2:145600136-145602568,hs2:145628493-145631256;hs2:146553193-146556447,hs2:173636118-173638697;hs2:148129150-148132374,hs2:174865844-174868962;hs2:148132740-148134862,hs2:174862474-174865044;hs2:173632317-173635702,hs15:27742915-27746403;hs2:178703965-178707145,hs2:178966636-178969213;hs2:128502732-128505748,hs2:128904203-128906409		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0118	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	2,8,13	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient2_child	AB SOLiD 4 System	chr8:47918851-47918854:-1;chr13:108222644-108222647:-1;chr2:147801056-147801060:-1;chr8:87670313-87670319:-1;chr13:106187424-106187431:-1;chr13:90127871-90127888:-1;chr8:115818900-115818963:-1;chr2:166014695-166016745:-1;chr13:108216350-108221577:-1;chr13:93370259-93604112:-1;chr2:191897300-194718047:-1;chr2:163141421-166011053:-1;chr2:166014625-166014621:1;chr8:47912515-47912514:1;chr2:148535082-148535082:1;chr13:111879781-111879781:1	hs2:147797698-147801010,hs8:116895627-116898981;hs13:108212580-108216229,hs13:111876035-111879588;hs2:148531325-148534948,hs8:115815125-115818679;hs2:153601572-153605077,hs2:160119416-160123210;hs8:115819103-115822070,hs8:116899526-116902647;hs2:147801050-147804745,hs2:148535258-148538722;hs8:87503991-87507681,hs13:93604139-93607506;hs13:90123892-90127819,hs13:93366610-93369965;hs8:47912597-47915396,hs8:87670525-87674663;hs8:87500983-87503861,hs8:87667009-87669639;hs2:163137520-163141373,hs2:166011421-166014559;hs8:84214080-84217369,hs13:106187688-106191123;hs13:90127935-90131228,hs13:106183766-106187365;hs2:153621846-153625100,hs2:160123294-160127003;hs8:48086057-48089296,hs8:84218139-84224980;hs8:47915790-47918709,hs8:48081547-48084526;hs2:166011148-166014091,hs2:166016838-166020383;hs13:108221815-108222565,hs13:108223657-108226429;hs13:108221938-108222608,hs13:111881628-111883998;hs8:47908213-47912432,hs8:47918838-47921877;hs2:191894679-191897220,hs2:194718106-194721516		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0119	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	1,3,7,12	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient3_child	AB SOLiD 4 System	chr3:71078624-71078621:1;chr7:19320228-19320226:1;chr1:97683903-97683903:1;chr7:19114083-19114085:-1;chr1:95146001-95146004:-1;chr12:63505335-63505338:-1;chr1:98219835-98219840:-1;chr7:19003340-19003351:-1;chr7:19512505-19512655:-1;chr3:75208212-76406934:-1;chr7:17140783-18519891:-1;chr7:13962633-15423145:-1;chr7:11404421-13612031:-1	hs1:95143545-95145948,hs1:97683941-97686445;hs1:95145998-95148623,hs3:76407425-76409115;hs1:97681880-97683714,hs7:19111398-19113904;hs1:98218036-98219533,hs7:17138240-17139361;hs1:98219971-98221877,hs7:13960228-13962541;hs3:71076114-71078531,hs3:75205169-75208143;hs3:71078896-71081154,hs7:19000359-19002911;hs7:11401791-11404374,hs7:13612118-13614548;hs7:15423540-15425193,hs12:63503287-63505156;hs7:18519927-18522879,hs7:19317299-19320055;hs7:19003349-19006274,hs7:19114152-19116699;hs7:19510153-19512405,hs12:63505521-63507172;hs7:19320391-19322797,hs7:19512771-19514425		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0120	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	2,14	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient4_child	AB SOLiD 4 System	chr14:79136538-79136534:-1;chr2:38345501-38345498:-1	hs2:38343343-38344883,hs14:79136761-79138412;hs2:38345670-38347441,hs14:79133248-79136149;hs14:71206391-71207960,hs14:82090896-82093332;hs14:71204258-71206114,hs14:82088671-82090688		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0121	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	6	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient5_child	AB SOLiD 4 System		hs6:49330690-49332603,hs6:53327091-53329211;hs6:49796631-49797278,hs6:84993583-84994052;hs6:50321779-50323964,hs6:54655468-54656553;hs6:53325481-53326844,hs6:84491467-84493206;hs6:50321549-50325789,hs6:54656373-54660096;hs6:51326650-51327743,hs6:54112015-54114279;hs6:52508434-52509910,hs6:54110260-54111080;hs6:50324379-50325713,hs6:54656663-54657903;hs6:84993447-84993553,hs6:96423936-96424166		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0122	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	4,8,10,20	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient6_child	AB SOLiD 4 System	chr4:143384762-143384754:1;chr4:122008061-122008054:1;chr4:107840276-107840271:1;chr4:101067666-101067665:1;chr8:128109303-128109303:1;chr10:119944963-119944963:1;chr10:114339361-114339363:-1;chr10:118655641-118655643:-1;chr20:54035355-54035360:-1;chr8:129667371-129667382:-1;chr4:151511931-151511954:-1;chr4:122008107-122008215:-1;chr4:145924134-145929741:-1;chr4:149770244-149791519:-1;chr4:102128766-104640057:-1;chr4:133136227-141993229:-1	hs4:133133185-133135891,hs4:141993252-141996399;hs4:107840319-107842965,hs4:109420612-109423628;hs4:143384774-143387425,hs8:128109571-128112100;hs4:102126233-102128515,hs10:114339489-114342403;hs4:101067986-101071278,hs10:118655643-118658576;hs10:114336536-114339269,hs10:118652430-118655577;hs4:143381854-143384534,hs8:129664308-129667155;hs4:104640064-104642992,hs10:119941564-119944894;hs4:145921501-145924066,hs4:151512450-151515461;hs4:143442035-143443751,hs4:151508728-151511721;hs4:143436471-143439781,hs4:149791618-149794448;hs4:101064731-101067581,hs20:54035382-54037608;hs10:119945272-119947416,hs20:54032823-54035270;hs4:122008261-122011624,hs4:149767569-149770139;hs8:128106730-128109078,hs8:129667834-129669812;hs4:122005620-122007883,hs4:145929750-145933090;hs4:107838052-107839780,hs10:111414267-111416948;hs4:143440657-143442989,hs4:143444329-143447036;hs4:109417384-109420398,hs10:111953671-111956270		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0123	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	6,7,9,10,12	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient7_mother	AB SOLiD 4 System		hs7:36718108-36721671,hs12:99787831-99790893;hs9:11739802-11742710,hs9:31460247-31463007;hs9:11758195-11759972,hs12:110263742-110266538;hs9:7104763-7106960,hs12:103464346-103466774;hs9:12236188-12238989,hs9:26965673-26968013;hs9:13236665-13239425,hs12:101859464-101861141;hs6:123750357-123752276,hs9:11743072-11746336;hs6:123765872-123766384,hs12:101856510-101856537;hs9:31433337-31436333,hs9:31463517-31465231;hs9:31471300-31473229,hs12:99435218-99436825;hs6:123748945-123750012,hs6:123768304-123769906;hs10:66227201-66230197,hs12:99785257-99787355;hs9:8118030-8119888,hs10:65848657-65850658;hs7:36714976-36717979,hs12:103467238-103470137;hs9:7107641-7109780,hs9:35723601-35726283;hs9:13334672-13337076,hs9:31473792-31476201;hs9:13240004-13241557,hs9:26962041-26964677;hs9:7116561-7120299,hs9:31436447-31440029;hs9:8121313-8122780,hs9:11760865-11763707;hs9:12233990-12236078,hs12:99431406-99434124;hs9:7113602-7116395,hs12:110267135-110269429;hs9:13337440-13340068,hs12:99636114-99638904;hs10:65844061-65847557,hs10:66230913-66234003		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0124	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	7,9,10,12	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient7_child	AB SOLiD 4 System	chr7:36718025-36718027:-1;chr9:11742848-11742851:-1;chr9:31463189-31463192:-1;chr9:31436412-31436439:-1;chr9:7107289-7107387:-1;chr6:123749994-123750143:-1;chr9:13239726-13239970:-1;chr12:99435034-99435026:1;chr9:31473570-31473563:1;chr12:103467187-103467181:1;chr9:12236168-12236165:1;chr9:11760434-11760433:1;chr9:26965302-26965301:1	hs7:36718108-36721671,hs12:99787831-99790893;hs9:11739802-11742710,hs9:31460247-31463007;hs9:11758195-11759972,hs12:110263742-110266538;hs6:123750357-123752276,hs9:11743072-11746336;hs10:66227201-66230197,hs12:99785257-99787355;hs9:8118030-8119888,hs10:65848657-65850658;hs7:36714976-36717979,hs12:103467238-103470137;hs9:7107641-7109780,hs9:35723601-35726283;hs9:13334672-13337076,hs9:31473792-31476201;hs9:13240004-13241557,hs9:26962041-26964677;hs9:7116561-7120299,hs9:31436447-31440029;hs9:8121313-8122780,hs9:11760865-11763707;hs9:12233990-12236078,hs12:99431406-99434124;hs9:7113602-7116395,hs12:110267135-110269429;hs9:13337440-13340068,hs12:99636114-99638904		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0125	Research	22813740	Kloosterman WP, Tavakoli-Yaraki M, van Roosmalen MJ, van Binsbergen E, Renkens I, Duran K, Ballarati L, Vergult S, Giardino D, Hansson K, Ruivenkamp CA, Jager M, van Haeringen A, Ippel EF, Haaf T, Passarge E, Hochstenbach R, Menten B, Larizza L, Guryev V,	Constitutional Chromothripsis Rearrangements Involve Clustered Double-Stranded DNA Breaks and Nonhomologous Repair Mechanisms	Cell Rep	2012 Jun	5	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Patient8_child	AB SOLiD 4 System	chr5:86073427-86073423:1;chr5:85951324-85951326:-1;chr5:87868638-87868756:-1;chr5:85892461-85893557:-1;chr5:158684536-158689801:-1;chr5:87426377-87433416:-1;chr5:85363334-85371155:-1;chr5:158690111-158698437:-1;chr5:86343836-86352568:-1;chr5:86811684-86832176:-1;chr5:158658171-158681667:-1;chr5:158607508-158657977:-1;chr5:85289234-85361626:-1;chr5:85991759-86069335:-1;chr5:158400232-158515794:-1;chr5:87869800-88154277:-1;chr5:87472658-87866129:-1	hs5:85288262-85289063,hs5:87471596-87472480;hs5:85361748-85363159,hs5:85986973-85988074;hs5:85362297-85363176,hs5:85949965-85951002;hs5:85371275-85372561,hs5:158398863-158400207;hs5:85891815-85892371,hs5:87433424-87434332;hs5:85893782-85894176,hs5:87869006-87869529;hs5:85951411-85952184,hs5:158698680-158700075;hs5:85988366-85989838,hs5:87866188-87867502;hs5:86072712-86073373,hs5:87867565-87868374;hs5:86073542-86074750,hs5:158681697-158682944;hs5:86342145-86343603,hs5:86832213-86833137;hs5:86699993-86701408,hs5:88154363-88155823;hs5:87425754-87426279,hs5:158606012-158607009;hs5:87868652-87869713,hs5:158682840-158684494;hs5:86810647-86811269,hs5:158516037-158517066;hs5:85948396-85949213,hs5:86069481-86070538;hs5:85893996-85894198,hs5:85990821-85991347		Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	Chromothripsis represents a novel phenomenon in the structural variation landscape of cancer genomes. Here, we analyze the genomes of ten patients with congenital disease who were preselected to carry complex chromosomal rearrangements with more than two breakpoints. The rearrangements displayed unanticipated complexity resembling chromothripsis. We find that eight of them contain hallmarks of multiple clustered double-stranded DNA breaks (DSBs) on one or more chromosomes. In addition, nucleotide resolution analysis of 98 breakpoint junctions indicates that break repair involves nonhomologous or microhomology-mediated end joining. We observed that these eight rearrangements are balanced or contain sporadic deletions ranging in size between a few hundred base pairs and several megabases. The two remaining complex rearrangements did not display signs of DSBs and contain duplications, indicative of rearrangement processes involving template switching. Our work provides detailed insight into the characteristics of chromothripsis and supports a role for clustered DSBs driving some constitutional chromothripsis rearrangements.	GRCh37/hg19			ERP001035	No	NA
CTDB0126	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	2	Multiple myeloma	SNP Array	Homo sapiens	MM_06358	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0127	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	1,3	Multiple myeloma	SNP Array	Homo sapiens	MM_07545	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0128	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	16,17	Multiple myeloma	SNP Array	Homo sapiens	MM_08186	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0129	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	3	Multiple myeloma	SNP Array	Homo sapiens	MM_09402	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0130	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	10,12	Multiple myeloma	SNP Array	Homo sapiens	MM_10217	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0131	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	8,18	Multiple myeloma	SNP Array	Homo sapiens	MM_10353	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0132	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	1	Multiple myeloma	SNP Array	Homo sapiens	MM_10389	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0133	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	16	Multiple myeloma	SNP Array	Homo sapiens	MM_11762	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0134	Research	21628407	Magrangeas F, Avet-Loiseau H, Munshi NC, Minvielle S	Chromothripsis identifies a rare and aggressive entity among newly diagnosed multiple myeloma patients	Blood	2011 Jul	16	Multiple myeloma	SNP Array	Homo sapiens	MM_06415	Affymetrix SNP6 Array				Inserm U892, Universite de Nantes, Nantes, France	Multiple myeloma (MM) develops from a premalignant plasma cell proliferative disorder, and with time can progress to a more aggressive disease in extramedullary locations. The gradually clinical evolution is supported by clonal expansion of cells that acquire genetic lesions over years. This model of cancer evolution based on ongoing genomic instability mechanism may apply to development of most MM cases. However, in a small fraction of newly diagnosed MM who relapse quickly and finally die within 2 years, the gradual model appears to be untenable. Analysis of high resolution copy number profiles obtained using single nucleotide polymorphism array data from 764 newly diagnosed MM identified large numbers of genomic rearrangements with the hallmarks of chromothripsis in 1.3% of samples. Moreover, this catastrophic event confers a poor outcome. Because chromothripsis appears to occur in a single crisis, our results suggest that high-risk MM patients use this novel way of cancer evolution.	GRCh37/hg19	GSE27560			Yes	NA
CTDB0135	Research	23271725	Hirsch D, Kemmerling R, Davis S, Camps J, Meltzer PS, Ried T, Gaiser T	Chromothripsis and Focal Copy Number Alterations Determine Poor Outcome in Malignant Melanoma	Cancer Res	2013 Mar	5,20	Melanoma	Next Generation Sequencing	Homo sapiens	case14	Illumina HiSeq 2000				Genetics Branch, Center for Cancer Research, National Cancer Institute/NIH, Bethesda, Maryland 20892, USA	Genetic changes during tumorigenesis are usually acquired sequentially. However, a recent study showed that in 2% to 3% of all cancers a single catastrophic event, termed chromothripsis, can lead to massive genomic rearrangements confined to one or a few chromosomes. To explore whether the degree of genomic instability and chromothripsis influences prognosis in cancer, we retrospectively applied array-comparative genomic hybridization (aCGH) to 20 malignant melanomas that showed, despite comparable conventional clinical and pathologic parameters, a profoundly different clinical course. We compared 10 patients who died of malignant melanoma 3.7 years (median, range 0.9-7.6 years) after diagnosis with 10 patients who survived malignant melanoma and had a median disease-free survival of 14.8 years (range 12.5-16.7 years; P = 0.00001). We observed a striking association between the degree of chromosomal instability, both numerical and structural, and outcome. Malignant melanomas associated with good prognosis showed only few chromosomal imbalances (mean 1.6 alterations per case), predominantly whole chromosome or chromosome arm gains and losses, whereas malignant melanomas with poor prognosis harbored significantly more chromosomal aberrations (13.9 per case; P = 0.008). Array-based CGH showed that these aberrations were mostly focal events, culminating in two cases in a pattern consistent with the phenomenon of chromothripsis, which was confirmed by paired-end sequencing. This is the first description of chromothripsis in primary malignant melanomas. Our study therefore links focal copy number alterations and chromothripsis with poor outcome in patients with malignant melanomas (P = 0.0002) and provides a genetic approach to predict outcome in malignant melanomas.	GRCh37/hg19				Yes	NA
CTDB0136	Research	23271725	Hirsch D, Kemmerling R, Davis S, Camps J, Meltzer PS, Ried T, Gaiser T	Chromothripsis and Focal Copy Number Alterations Determine Poor Outcome in Malignant Melanoma	Cancer Res	2013 Mar	5,15	Melanoma	Array CGH	Homo sapiens	case20	Agilent CGH Microarrays 4x180 K				Genetics Branch, Center for Cancer Research, National Cancer Institute/NIH, Bethesda, Maryland 20892, USA	Genetic changes during tumorigenesis are usually acquired sequentially. However, a recent study showed that in 2% to 3% of all cancers a single catastrophic event, termed chromothripsis, can lead to massive genomic rearrangements confined to one or a few chromosomes. To explore whether the degree of genomic instability and chromothripsis influences prognosis in cancer, we retrospectively applied array-comparative genomic hybridization (aCGH) to 20 malignant melanomas that showed, despite comparable conventional clinical and pathologic parameters, a profoundly different clinical course. We compared 10 patients who died of malignant melanoma 3.7 years (median, range 0.9-7.6 years) after diagnosis with 10 patients who survived malignant melanoma and had a median disease-free survival of 14.8 years (range 12.5-16.7 years; P = 0.00001). We observed a striking association between the degree of chromosomal instability, both numerical and structural, and outcome. Malignant melanomas associated with good prognosis showed only few chromosomal imbalances (mean 1.6 alterations per case), predominantly whole chromosome or chromosome arm gains and losses, whereas malignant melanomas with poor prognosis harbored significantly more chromosomal aberrations (13.9 per case; P = 0.008). Array-based CGH showed that these aberrations were mostly focal events, culminating in two cases in a pattern consistent with the phenomenon of chromothripsis, which was confirmed by paired-end sequencing. This is the first description of chromothripsis in primary malignant melanomas. Our study therefore links focal copy number alterations and chromothripsis with poor outcome in patients with malignant melanomas (P = 0.0002) and provides a genetic approach to predict outcome in malignant melanomas.	GRCh37/hg19				Yes	NA
CTDB0137	Research	22014273	Kloosterman WP, Hoogstraat M, Paling O, Tavakoli-Yaraki M, Renkens I, Vermaat JS, van Roosmalen MJ, van Lieshout S, Nijman IJ, Roessingh W, van 't Slot R, van de Belt J, Guryev V, Koudijs M, Voest E, Cuppen E	Chromothripsis is a common mechanism driving genomic rearrangements in primary and metastatic colorectal cancer	Genome Biol	2011 Oct	13	Colorectal cancer	Next Generation Sequencing	Homo sapiens	Patient1_primary	AB SOLiD 4 System	chr2:31723836-31729392:-1;chr2:127550647-150230976:-1;chr3:60289022-60685547:-1;chr4:63174-131357:-1;chr5:18617213-18636314:1;chr5:83668804-83692744:-1;chr7:111063176-111079612:-1;chr10:53184024-53263339:-1;chr13:35646108-82606079:-1;chr13:90427666-90443779:1;chr13:102099102-104364526:1;chr13:104305099-104350436:-1;chr16:6744233-6849498:-1;chrX:133946999-133992828:-1	hs2:92296807-92300718,hs6:61902091-61905238;hs3:30413558-30413724,hs6:58778533-58779075;hs13:23098059-23099917,hs13:78198552-78200182;hs13:35687182-35688469,hs22:36193835-36195196;hs13:36611703-36613693,hs22:19236041-19237588;hs13:59999473-60000660,hs13:105967363-105969749;hs13:68630924-68632686,hs13:77812859-77814463;hs13:68634580-68635862,hs13:90956865-90958345;hs13:71101674-71103995,hs13:90414536-90417027;hs13:90971334-90973021,hs13:92942702-92944416;hs13:101866858-101868336,hs13:102397259-102398969;hs17:20784424-20784934,hs4:33847085-33848798	CCDC144NL;CLTCL1;CTD;DCLK1;EDIL3;FAM122C;FGF14;FHIT;GPC5;IMMP2L;LYPD6;MYCBP2;NALCN;NBEA;PRKG1;RBFOX2;RP11;SCEL;SNORA15;ZNF595;ZNF718	Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584 CG, The Netherlands	Structural rearrangements form a major class of somatic variation in cancer genomes. Local chromosome shattering, termed chromothripsis, is a mechanism proposed to be the cause of clustered chromosomal rearrangements and was recently described to occur in a small percentage of tumors. The significance of these clusters for tumor development or metastatic spread is largely unclear. RESULTS: We used genome-wide long mate-pair sequencing and SNP array profiling to reveal that chromothripsis is a widespread phenomenon in primary colorectal cancer and metastases. We find large and small chromothripsis events in nearly every colorectal tumor sample and show that several breakpoints of chromothripsis clusters and isolated rearrangements affect cancer genes, including NOTCH2, EXO1 and MLL3. We complemented the structural variation studies by sequencing the coding regions of a cancer exome in all colorectal tumor samples and found somatic mutations in 24 genes, including APC, KRAS, SMAD4 and PIK3CA. A pairwise comparison of somatic variations in primary and metastatic samples indicated that many chromothripsis clusters, isolated rearrangements and point mutations are exclusively present in either the primary tumor or the metastasis and may affect cancer genes in a lesion-specific manner. CONCLUSIONS: We conclude that chromothripsis is a prevalent mechanism driving structural rearrangements in colorectal cancer and show that a complex interplay between point mutations, simple copy number changes and chromothripsis events drive colorectal tumor development and metastasis.	GRCh37/hg19	GSE32711		ERP000875	Yes	SCE,RNA.492;NBEA,RBFOX2;DCLK1,L77569.1;L77569.1,CLTCL1;CLTCL1,SNORA15.3;NALCN,FGF14
CTDB0138	Research	22014273	Kloosterman WP, Hoogstraat M, Paling O, Tavakoli-Yaraki M, Renkens I, Vermaat JS, van Roosmalen MJ, van Lieshout S, Nijman IJ, Roessingh W, van 't Slot R, van de Belt J, Guryev V, Koudijs M, Voest E, Cuppen E	Chromothripsis is a common mechanism driving genomic rearrangements in primary and metastatic colorectal cancer	Genome Biol	2011 Oct	13	Colorectal cancer	Next Generation Sequencing	Homo sapiens	Patient1_metastasis	AB SOLiD 4 System	chr2:31723836-31729392:-1;chr2:127550647-150230976:-1;chr4:63174-131357:-1;chr5:18617213-18636314:1;chr13:35646108-82606079:-1;chr13:102099102-104364526:1;chr13:104305099-104350436:-1;chrX:133946999-133992828:-1	hs2:92296807-92300718,hs6:61902091-61905238;hs13:23098059-23099917,hs13:78198552-78200182;hs13:35687182-35688469,hs22:36193835-36195196;hs13:36611703-36613693,hs22:19236041-19237588;hs13:59999473-60000660,hs13:105967363-105969749;hs13:68630924-68632686,hs13:77812859-77814463;hs13:68634580-68635862,hs13:90956865-90958345;hs13:71101674-71103995,hs13:90414536-90417027;hs13:90971334-90973021,hs13:92942702-92944416;hs13:101866858-101868336,hs13:102397259-102398969;hs17:20784424-20784934,hs4:33847085-33848798	CCDC144NL;CLTCL1;DCLK1;FAM122C;FGF14;GPC5;LYPD6;MYCBP2;NALCN;NBEA;RBFOX2;RP11;SCEL;SNORA15;ZNF595;ZNF718	Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584 CG, The Netherlands	Structural rearrangements form a major class of somatic variation in cancer genomes. Local chromosome shattering, termed chromothripsis, is a mechanism proposed to be the cause of clustered chromosomal rearrangements and was recently described to occur in a small percentage of tumors. The significance of these clusters for tumor development or metastatic spread is largely unclear. RESULTS: We used genome-wide long mate-pair sequencing and SNP array profiling to reveal that chromothripsis is a widespread phenomenon in primary colorectal cancer and metastases. We find large and small chromothripsis events in nearly every colorectal tumor sample and show that several breakpoints of chromothripsis clusters and isolated rearrangements affect cancer genes, including NOTCH2, EXO1 and MLL3. We complemented the structural variation studies by sequencing the coding regions of a cancer exome in all colorectal tumor samples and found somatic mutations in 24 genes, including APC, KRAS, SMAD4 and PIK3CA. A pairwise comparison of somatic variations in primary and metastatic samples indicated that many chromothripsis clusters, isolated rearrangements and point mutations are exclusively present in either the primary tumor or the metastasis and may affect cancer genes in a lesion-specific manner. CONCLUSIONS: We conclude that chromothripsis is a prevalent mechanism driving structural rearrangements in colorectal cancer and show that a complex interplay between point mutations, simple copy number changes and chromothripsis events drive colorectal tumor development and metastasis.	GRCh37/hg19	GSE32711		ERP000875	Yes	SCE,RNA.492;NBEA,RBFOX2;DCLK1,L77569.1;L77569.1,CLTCL1;CLTCL1,SNORA15.3;NALCN,FGF14
CTDB0139	Research	22014273	Kloosterman WP, Hoogstraat M, Paling O, Tavakoli-Yaraki M, Renkens I, Vermaat JS, van Roosmalen MJ, van Lieshout S, Nijman IJ, Roessingh W, van 't Slot R, van de Belt J, Guryev V, Koudijs M, Voest E, Cuppen E	Chromothripsis is a common mechanism driving genomic rearrangements in primary and metastatic colorectal cancer	Genome Biol	2011 Oct	15,20	Colorectal cancer	Next Generation Sequencing	Homo sapiens	Patient3_primary	AB SOLiD 4 System	chr1:14814740-14837528:1;chr1:15031539-15273710:-1;chr1:17007460-145382302:1;chr1:42674412-42678368:-1;chr1:56398185-56402750:-1;chr1:86004803-144852992:-1;chr1:184934740-184939911:-1;chr1:194448325-194456448:-1;chr1:217751488-217756636:-1;chr1:242179761-249188200:-1;chr2:1522850-1529807:-1;chr2:206313065-206438788:-1;chr3:60105265-60239906:-1;chr3:60363597-60561868:-1;chr3:60865696-61122653:-1;chr3:82933940-82939170:-1;chr3:145929303-145934420:-1;chr4:36840296-36845327:-1;chr4:49633669-49659602:1;chr4:75323719-75491808:1;chr4:86794119-86799131:-1;chr4:91056889-91200535:-1;chr4:91704626-91736224:-1;chr4:130588752-130593845:-1;chr4:184654896-184659606:-1;chr4:188133117-188138335:-1;chr5:26323330-26327548:-1;chr5:81007149-81011306:-1;chr5:153647671-153796489:-1;chr5:177717867-177723069:-1;chr6:1318456-1322407:-1;chr6:52624253-52710633:-1;chr6:85431705-86318651:-1;chr6:147953818-148039772:1;chr6:149726411-149730778:-1;chr6:162401020-162431070:-1;chr6:162485734-162668565:-1;chr6:162663669-162755553:-1;chr6:162740676-162878837:-1;chr7:40352652-40412225:-1;chr7:64036351-64040567:-1;chr7:110071797-110501925:-1;chr7:142028006-142047406:1;chr7:142454954-142486104:1;chr8:39921544-40184993:-1;chr8:90317285-90386350:-1;chr8:142949641-142954962:-1;chr9:88720666-88725802:-1;chr9:125486301-125515809:-1;chr10:6876069-6880506:-1;chr10:17776474-18026803:-1;chr10:52936928-53050809:-1;chr10:57700014-57705209:-1;chr10:82901884-82906910:-1;chr10:100308414-101176300:1;chr10:126712876-126841247:-1;chr10:127191066-127200309:-1;chr10:134583023-134588259:-1;chr11:18939188-18967485:-1;chr11:66308339-66312407:-1;chr11:98888241-98893290:-1;chr11:134032953-134040158:-1;chr12:11181077-11213498:1;chr12:11250873-11286738:1;chr12:12025612-12030748:-1;chr12:40005354-40010269:-1;chr12:74102385-74107503:-1;chr13:24443874-24449191:-1;chr13:72840317-72850196:-1;chr13:112866635-112871373:-1;chr14:107052457-107133257:1;chr15:27019444-27024926:-1;chr15:56400176-56404784:-1;chr15:71551381-71563088:-1;chr15:75865555-75870469:-1;chr15:91400441-91405105:-1;chr15:91985948-91989513:1;chr16:78637104-78648608:-1;chr16:78820304-78930279:-1;chr16:78937512-79181617:-1;chr17:36540631-36545397:-1;chr17:39387716-39402908:-1;chr18:66202618-66210911:-1;chr19:55202334-55208256:-1;chr20:14571097-14606960:-1;chr20:14776528-14798489:-1;chr20:14786171-15380112:-1;chr20:15191174-15304606:-1;chr20:17101708-17106960:-1;chr20:24901783-24907406:-1;chr20:26288924-26297497:-1;chr20:56391233-56408300:-1;chr20:56428388-56637463:-1;chr20:56613894-57087384:-1;chr21:10732815-10768194:-1;chr21:10759902-10766569:-1;chr21:43701876-43707064:-1;chrX:7328146-7465605:-1;chrX:136079797-136085054:-1	hs1:120600580-120604241,hs1:145220210-145223766;hs1:218631217-218631269,hs6:86025759-86026723;hs1:227777955-227779872,hs1:227831411-227833614;hs2:77396098-77396119,hs3:131669077-131669796;hs2:96517724-96518218,hs7:151926630-151926973;hs2:133024098-133032655,hs11:57222874-57222878;hs2:133026740-133026781,hs11:57222871-57222878;hs2:238517686-238517708,hsX:111772267-111773705;hs3:64980158-64983807,hs3:64986193-64989130;hs4:190190834-190191481,hs9:66454770-66458090;hs6:82992290-82995613,hs7:77506942-77509892;hs6:149225004-149227597,hs7:66030659-66033143;hs6:150084766-150087498,hs6:156637160-156640036;hs6:156634435-156636981,hs7:66461463-66463726;hs7:61783170-61787643,hs7:61803407-61804398;hs8:37418985-37421969,hs8:39900483-39903232;hs8:49949658-49950815,hs13:67503027-67503216;hs8:49955413-49955964,hs13:67503009-67503043;hs10:53515362-53516968,hs3:60538443-60539820;hs10:54712347-54712939,hs4:131717652-131717679;hs11:43653102-43653134,hs17:45212925-45214262;hs11:45848223-45848248,hs11:85195020-85195130;hs12:6108343-6109209,hs22:17161432-17161816;hs12:30402246-30403569,hs12:30499480-30501580;hs14:50896878-50897862,hs7:11557798-11558922;hs15:70210862-70213701,hs20:57469150-57471853;hs15:70216996-70219165,hs20:57131996-57134594;hs15:70226269-70228551,hs15:71505444-71507954;hs15:70233781-70236494,hs20:56438663-56441250;hs15:70529801-70532429,hs15:71634917-71637448;hs15:70796906-70799660,hs20:57147895-57150764;hs15:71202894-71205623,hs20:57069430-57072115;hs15:71322490-71324993,hs15:71325037-71327301;hs15:71750633-71752866,hs20:56183769-56186225;hs16:26346160-26348091,hs16:26349524-26351401;hs16:33982670-33983669,hs4:110818558-110818589;hs19:17140647-17140662,hs2:40777573-40778472;hs19:33444352-33444473,hs20:26211178-26212420;hs19:56558861-56558879,hs8:40312597-40313321;hs20:15083408-15086276,hs21:11181331-11184298;hs20:15084044-15085874,hs22:18886482-18889075;hs20:29637760-29638445,hs4:14424126-14424146;hs21:19938101-19940988,hs21:19940991-19943607;hs21:41398863-41400456,hs21:41403207-41404561;hsX:134755739-134758154,hsX:134801424-134803334;hsY:28578330-28585953,hsY:58968823-58975090	5S_rRNA;ABCD2;ABCG1;AC119751.7;ACTN3;APCDD1L;AREG;AREGB;ARHGAP24;C7orf10;CCDC123;CDC27;CNTN5;COL23A1;CPNE4;CTA;CTB;CTBP2;CTD;DDAH1;DLG2;DSCAM;EIF3FP1;ETV6;FAM129A;FAM190A;FHIT;FOXJ3;GABRB3;GALNT10;GNAS;GOT1;GPATCH2;GS1;GSTA2;GSTA5;HPSE2;HSD17B12;IMMP2L;INPP5A;KRTAP9;LILRP1;LRRC49;LRRTM4;MACROD2;MAP4K5;MIPEP;MLL3;MLLT10P1;MRGPRX1;NCAPD3;NCRNA00227;NLRP5;NOTCH2;NOTCH2NL;OR1L4;OR1L6;PARD3B;PARK2;PCDH9;PCMT1;PDE4DIP;PHTF2;PLSCR4;PRKG1;PRSS1;PTPN9;RFX7;RP1;RP11;RP5;SBDS;SLC8A1;SOCS7;SSBP2;SYNCRIP;TAB2;TAS2R14;TAS2R46;THSD4;THSD7A;TPO;TYW1;UST;VWF_KB;WWOX;ZBP1;ZDHHC24;ZNF678	Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584 CG, The Netherlands	Structural rearrangements form a major class of somatic variation in cancer genomes. Local chromosome shattering, termed chromothripsis, is a mechanism proposed to be the cause of clustered chromosomal rearrangements and was recently described to occur in a small percentage of tumors. The significance of these clusters for tumor development or metastatic spread is largely unclear. RESULTS: We used genome-wide long mate-pair sequencing and SNP array profiling to reveal that chromothripsis is a widespread phenomenon in primary colorectal cancer and metastases. We find large and small chromothripsis events in nearly every colorectal tumor sample and show that several breakpoints of chromothripsis clusters and isolated rearrangements affect cancer genes, including NOTCH2, EXO1 and MLL3. We complemented the structural variation studies by sequencing the coding regions of a cancer exome in all colorectal tumor samples and found somatic mutations in 24 genes, including APC, KRAS, SMAD4 and PIK3CA. A pairwise comparison of somatic variations in primary and metastatic samples indicated that many chromothripsis clusters, isolated rearrangements and point mutations are exclusively present in either the primary tumor or the metastasis and may affect cancer genes in a lesion-specific manner. CONCLUSIONS: We conclude that chromothripsis is a prevalent mechanism driving structural rearrangements in colorectal cancer and show that a complex interplay between point mutations, simple copy number changes and chromothripsis events drive colorectal tumor development and metastasis.	GRCh37/hg19	GSE32711		ERP000875	Yes	AL109840.2,GNAS;LRRC49,APCDD1L;THSD4,ZBP1;MACROD2,EIF3FP1
CTDB0140	Research	22014273	Kloosterman WP, Hoogstraat M, Paling O, Tavakoli-Yaraki M, Renkens I, Vermaat JS, van Roosmalen MJ, van Lieshout S, Nijman IJ, Roessingh W, van 't Slot R, van de Belt J, Guryev V, Koudijs M, Voest E, Cuppen E	Chromothripsis is a common mechanism driving genomic rearrangements in primary and metastatic colorectal cancer	Genome Biol	2011 Oct	1	Colorectal cancer	Next Generation Sequencing	Homo sapiens	Patient3_metastasis	AB SOLiD 4 System	chr1:17007460-145382302:1;chr1:42674412-42678368:-1;chr1:56398185-56402750:-1;chr1:86004803-144852992:-1;chr1:184934740-184939911:-1;chr1:190003041-190552912:-1;chr1:194448325-194456448:-1;chr1:217751488-217756636:-1;chr1:217818705-227823641:1;chr1:226091191-226105416:-1;chr1:237282826-242017394:1;chr1:239542567-242253680:1;chr1:242179761-249188200:-1;chr1:242254059-247564326:1;chr1:242310129-247199201:-1;chr1:246129179-248413010:-1;chr2:1522850-1529807:-1;chr2:187428095-187446066:1;chr2:206112463-206131247:-1;chr3:60105265-60239906:-1;chr3:60363597-60561868:-1;chr3:60865696-61122653:-1;chr3:60966536-60991147:1;chr3:82933940-82939170:-1;chr3:94485781-96367675:-1;chr3:145929303-145934420:-1;chr4:36840296-36845327:-1;chr4:49633669-49659602:1;chr4:75323719-75491808:1;chr4:86794119-86799131:-1;chr4:91056889-91200535:-1;chr4:91171322-91178782:-1;chr4:91704626-91736224:-1;chr4:91855206-91916366:-1;chr4:130588752-130593845:-1;chr4:184654896-184659606:-1;chr4:188133117-188138335:-1;chr5:26323330-26327548:-1;chr5:81007149-81011306:-1;chr5:177717867-177723069:-1;chr6:1318456-1322407:-1;chr6:52624253-52710633:-1;chr6:85431705-86318651:-1;chr6:162401020-162431070:-1;chr6:162485734-162668565:-1;chr6:162663669-162755553:-1;chr6:162740676-162878837:-1;chr6:162750455-163020567:-1;chr7:40352652-40412225:-1;chr7:64036351-64040567:-1;chr7:110985925-111198073:-1;chr7:142028006-142047406:1;chr7:142454954-142486104:1;chr8:39921544-40184993:-1;chr8:90108849-90598688:-1;chr8:90317285-90386350:-1;chr8:142949641-142954962:-1;chr9:88720666-88725802:-1;chr9:125486301-125515809:-1;chr10:6876069-6880506:-1;chr10:17776474-18026803:-1;chr10:52936928-53050809:-1;chr10:53304737-53345051:-1;chr10:53698895-53761643:-1;chr10:53837609-53882685:1;chr10:57700014-57705209:-1;chr10:82901884-82906910:-1;chr10:100308414-101176300:1;chr10:126712876-126841247:-1;chr10:127191066-127200309:-1;chr10:134583023-134588259:-1;chr11:18939188-18967485:-1;chr11:66308339-66312407:-1;chr11:84282887-84450219:-1;chr11:98888241-98893290:-1;chr11:134032953-134040158:-1;chr12:6366670-44077731:-1;chr12:11181077-11213498:1;chr12:11250873-11286738:1;chr12:12025612-12030748:-1;chr12:40005354-40010269:-1;chr12:74102385-74107503:-1;chr13:24443874-24449191:-1;chr13:72840317-72850196:-1;chr13:112866635-112871373:-1;chr14:81528339-81533309:-1;chr14:107052457-107133257:1;chr15:27019444-27024926:-1;chr15:56400176-56404784:-1;chr15:75865555-75870469:-1;chr15:91400441-91405105:-1;chr16:79029865-79114771:-1;chr17:36540631-36545397:-1;chr17:39387716-39402908:-1;chr18:66202618-66210911:-1;chr19:21748981-21754355:-1;chr19:55202334-55208256:-1;chr20:14571097-14606960:-1;chr20:14587575-14763788:-1;chr20:14667618-15219026:-1;chr20:14776528-14798489:-1;chr20:14786171-15380112:-1;chr20:14818777-15034313:-1;chr20:15060067-15185810:-1;chr20:15208210-15273809:-1;chr20:17101708-17106960:-1;chr20:24901783-24907406:-1;chr20:26288924-26297497:-1;chr21:10732815-10768194:-1;chr21:10759902-10766569:-1;chr21:43701876-43707064:-1;chrX:136079797-136085054:-1	hs1:120600580-120604241,hs1:145220210-145223766;hs1:205634139-205636828,hs1:224369508-224372694;hs1:218631217-218631269,hs6:86025759-86026723;hs1:223829777-223832364,hs1:242731112-242733271;hs1:227777955-227779872,hs1:227831411-227833614;hs1:239132977-239133973,hs1:241678276-241678997;hs1:242470743-242472150,hs1:246115529-246117842;hs1:244818903-244821597,hs1:245884999-245887839;hs1:248440300-248443266,hs1:249183012-249185678;hs2:77396098-77396119,hs3:131669077-131669796;hs2:96517724-96518218,hs7:151926630-151926973;hs2:133024098-133032655,hs11:57222874-57222878;hs2:133026740-133026781,hs11:57222871-57222878;hs2:238517686-238517708,hsX:111772267-111773705;hs3:60586434-60587759,hs3:60589085-60590958;hs3:64980158-64983807,hs3:64986193-64989130;hs4:190190834-190191481,hs9:66454770-66458090;hs6:82992290-82995613,hs7:77506942-77509892;hs6:149225004-149227597,hs7:66030659-66033143;hs6:150084766-150087498,hs6:156637160-156640036;hs6:156634435-156636981,hs7:66461463-66463726;hs7:61783170-61787643,hs7:61803407-61804398;hs8:37418985-37421969,hs8:39900483-39903232;hs8:49949658-49950815,hs13:67503027-67503216;hs8:49955413-49955964,hs13:67503009-67503043;hs10:38869743-38874720,hs20:26200325-26201937;hs10:53515362-53516968,hs3:60538443-60539820;hs10:54712347-54712939,hs4:131717652-131717679;hs11:6105038-6105599,hs21:42571840-42571848;hs11:43653102-43653134,hs17:45212925-45214262;hs11:45848223-45848248,hs11:85195020-85195130;hs12:6108343-6109209,hs22:17161432-17161816;hs12:30402246-30403569,hs12:30499480-30501580;hs12:54799942-54802056,hs3:144358420-144360269;hs14:50896878-50897862,hs7:11557798-11558922;hs15:70529801-70532429,hs15:71634917-71637448;hs16:26346160-26348091,hs16:26349524-26351401;hs16:33982670-33983669,hs4:110818558-110818589;hs19:17140647-17140662,hs2:40777573-40778472;hs19:33444352-33444473,hs20:26211178-26212420;hs19:56558861-56558879,hs8:40312597-40313321;hs20:15083408-15086276,hs21:11181331-11184298;hs20:15084044-15085874,hs22:18886482-18889075;hs20:29637760-29638445,hs4:14424126-14424146;hs20:29648025-29648884,hs5:151497083-151497087;hs21:19938101-19940988,hs21:19940991-19943607;hs21:41398863-41400456,hs21:41403207-41404561;hsY:28578330-28585953,hsY:58968823-58975090	5S_rRNA;ABCD2;ABCG1;ACTN3;AREG;AREGB;ARHGAP24;BACE2;C7orf10;CAPN8;CCDC123;CDC27;CNTN5;COL23A1;CPNE4;CTA;CTB;CTBP2;CTD;DDAH1;DEGS1;DLG2;DSCAM;EIF3FP1;ETV6;EXO1;FAM129A;FAM190A;FH;FHIT;FOXJ3;GABRB3;GOT1;GPATCH2;GS1;GSTA2;GSTA5;HPSE2;HSD17B12;IMMP2L;INPP5A;ITGA5;KB;KRTAP9;LEFTY1;LILRP1;LRRTM4;MACROD2;MAP4K5;MIPEP;MLL3;MLLT10P1;MRGPRX1;NCAPD3;NLRP5;NOTCH2;NOTCH2NL;OR1L4;OR1L6;PARD3B;PARK2;PCDH9;PCMT1;PDE4DIP;PHTF2;PLD5;PLSCR4;PPPDE1;PRKG1;PRSS1;PTPN9;PYCR2;RFX7;RP1;RP11;RYR2;SBDS;SLC45A3;SLC8A1;SMYD3;SNORA72;SOCS7;SPATA17;SSBP2;SYNCRIP;TAS2R14;TAS2R46;THSD4;THSD7A;TPO;TSHR;TYW1;U66061;UST;VWF;WWOX;ZDHHC24;ZNF678	Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584 CG, The Netherlands	Structural rearrangements form a major class of somatic variation in cancer genomes. Local chromosome shattering, termed chromothripsis, is a mechanism proposed to be the cause of clustered chromosomal rearrangements and was recently described to occur in a small percentage of tumors. The significance of these clusters for tumor development or metastatic spread is largely unclear. RESULTS: We used genome-wide long mate-pair sequencing and SNP array profiling to reveal that chromothripsis is a widespread phenomenon in primary colorectal cancer and metastases. We find large and small chromothripsis events in nearly every colorectal tumor sample and show that several breakpoints of chromothripsis clusters and isolated rearrangements affect cancer genes, including NOTCH2, EXO1 and MLL3. We complemented the structural variation studies by sequencing the coding regions of a cancer exome in all colorectal tumor samples and found somatic mutations in 24 genes, including APC, KRAS, SMAD4 and PIK3CA. A pairwise comparison of somatic variations in primary and metastatic samples indicated that many chromothripsis clusters, isolated rearrangements and point mutations are exclusively present in either the primary tumor or the metastasis and may affect cancer genes in a lesion-specific manner. CONCLUSIONS: We conclude that chromothripsis is a prevalent mechanism driving structural rearrangements in colorectal cancer and show that a complex interplay between point mutations, simple copy number changes and chromothripsis events drive colorectal tumor development and metastasis.	GRCh37/hg19	GSE32711		ERP000875	Yes	NOTCH2,NOTCH2NL;NOTCH2NL,RP11-458D21.5;SLC45A3,DEGS1;DEGS1,SNORA72.2;SPATA17,ZNF678;CAPN8,RP11-105I12.1;LEFTY1,PYCR2;RYR2,7SK.259;7SK.259,EXO1
CTDB0141	Research	22014273	Kloosterman WP, Hoogstraat M, Paling O, Tavakoli-Yaraki M, Renkens I, Vermaat JS, van Roosmalen MJ, van Lieshout S, Nijman IJ, Roessingh W, van 't Slot R, van de Belt J, Guryev V, Koudijs M, Voest E, Cuppen E	Chromothripsis is a common mechanism driving genomic rearrangements in primary and metastatic colorectal cancer	Genome Biol	2011 Oct	3,6,8	Colorectal cancer	Next Generation Sequencing	Homo sapiens	Patient4_primary	AB SOLiD 4 System	chr1:49802947-49923762:-1;chr2:17406991-17437065:1;chr3:56654445-56988107:-1;chr3:132691793-193107195:-1;chr3:136042870-146982165:1;chr3:148192293-148197662:-1;chr3:174594991-174678318:-1;chr4:53011264-53069377:-1;chr4:107181579-107216856:1;chr4:110618643-110685486:-1;chr5:55466078-55471432:-1;chr5:59214410-59731083:-1;chr6:25006753-97562883:1;chr6:49455879-97565723:-1;chr6:66166717-66625922:-1;chr6:162163387-162185974:-1;chr6:162353175-163192040:-1;chr6:162427029-162443266:-1;chr7:24233931-24239286:-1;chr7:50067894-50190561:-1;chr7:70490878-70500367:-1;chr8:36158315-43649207:-1;chr8:36158830-41285081:1;chr8:36358927-40926150:1;chr8:36440148-39379270:1;chr8:39144393-47113502:1;chr10:65861498-65876909:-1;chr11:62159412-63936774:-1;chr15:20935275-21939883:1;chr16:6248506-6380774:-1;chr16:6586750-6597999:1;chr16:79194156-79272292:-1;chr18:48040416-48170802:-1;chr20:14575911-15363677:-1;chr20:14674638-15391922:-1;chr20:30112996-30342757:1;chrX:6785822-6827028:-1;chrX:7079832-8085559:-1	hs1:163398379-163400456,hs1:203494249-203496422;hs1:163442290-163443321,hs1:203497211-203498241;hs3:96404490-96407077,hs3:96439770-96443240;hs3:96407234-96409302,hs3:96443905-96446423;hs3:116274800-116277310,hs6:62543759-62545039;hs3:116505890-116507162,hs6:72831657-72833123;hs3:119898040-119899910,hs5:53265083-53266766;hs3:121546534-121548528,hs3:140999180-141001121;hs3:121549168-121551138,hs6:8110882-8112019;hs3:133639033-133640150,hs3:150984044-150985508;hs3:136535377-136537190,hs6:100167056-100168340;hs3:136539077-136539760,hs6:72506993-72508522;hs3:143367862-143369638,hs3:162711293-162713354;hs3:146568386-146569737,hs3:167129548-167131401;hs3:146809618-146811762,hs3:192148789-192150935;hs3:153861563-153863907,hs6:7975227-7976587;hs3:161783696-161785511,hs6:100381073-100383094;hs3:165209653-165212672,hs6:24857255-24860048;hs3:165260710-165263099,hs5:53505897-53508673;hs3:165773176-165775886,hs6:25994741-25997121;hs3:166524585-166527014,hs6:48537273-48539587;hs3:167515728-167518568,hs3:192530891-192533361;hs3:190616878-190619384,hs3:191135633-191137944;hs3:191542736-191545061,hs6:48108422-48110492;hs3:191611575-191612274,hs6:97835272-97836598;hs3:192155007-192156944,hs6:96782363-96783869;hs3:192534485-192536549,hs6:9333886-9336407;hs5:42882085-42883238,hs6:8108078-8109181;hs5:43672276-43674850,hs9:111708726-111710521;hs6:30222990-30225620,hs6:62895896-62897791;hs6:49361807-49364428,hs6:97836756-97838746;hs6:98390444-98392418,hs9:111427832-111430237;hs6:170909787-170911773,hs13:115106076-115109812;hs8:34330731-34333534,hs8:36782127-36785088;hs8:34331178-34333393,hs8:36511593-36513948;hs8:36867812-36870275,hs8:37789646-37791368;hs8:36912234-36914139,hs8:47119771-47121748;hs8:37473964-37476378,hs8:39390152-39392532;hs11:28546711-28548304,hs6:156302660-156304279;hs11:57028414-57030219,hs11:62164189-62166303;hs11:57390222-57393033,hs21:16464636-16466584;hs12:6661831-6663841,hs12:11479949-11482679;hs12:22241562-22243488,hs12:23901258-23903320;hs12:23923589-23925428,hs6:7620692-7623368;hs12:25696603-25699039,hs3:190805806-190808367;hs12:26078257-26080398,hs3:161917893-161919793;hs14:107026331-107028138,hs17:50697866-50699916;hs15:74653331-74655310,hs17:77772433-77773698;hs20:5709889-5710952,hs20:5711237-5712971;hs20:42881540-42883261,hs20:44091225-44093313;hs20:43974701-43976700,hs20:45117980-45120314	ACPL2;ADAM32;ADAM3A;AGBL4;ANKRD55;ARHGEF26;ARHGEF3;ARL15;ASRGL1;C3orf59;C3orf63;C7orf72;C9orf6;CASP6;CBX1P5;CBX8;CCDC66;CENPQ;CFI;CTD;CTNNAL1;CYP11A1;EAF2;EYSPACRG;FAM65B;FGF12;GDAP1L1;GOT1L1;GPR156;HLA-L;HM13;IFFO1;IFLTD1;IQCB1;KCNU1;KHDRBS2;KLHL32;LSAMP;MACROD1;MACROD2;MAPK4;MCHR2;MED12L;MUTED;NAALADL2;NCRNA00227;NNT;NOP2;P2RY14;PARK2;PCCB;PDE4D;RIMS1;RP1;RP11;SDC4;SEPP1;SERPINI1;SLC9A9;SNORD65.4;SOX5;TBCK;TMEM22;TPX2;WWOX;ZNF840;ZPBP	Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584 CG, The Netherlands	Structural rearrangements form a major class of somatic variation in cancer genomes. Local chromosome shattering, termed chromothripsis, is a mechanism proposed to be the cause of clustered chromosomal rearrangements and was recently described to occur in a small percentage of tumors. The significance of these clusters for tumor development or metastatic spread is largely unclear. RESULTS: We used genome-wide long mate-pair sequencing and SNP array profiling to reveal that chromothripsis is a widespread phenomenon in primary colorectal cancer and metastases. We find large and small chromothripsis events in nearly every colorectal tumor sample and show that several breakpoints of chromothripsis clusters and isolated rearrangements affect cancer genes, including NOTCH2, EXO1 and MLL3. We complemented the structural variation studies by sequencing the coding regions of a cancer exome in all colorectal tumor samples and found somatic mutations in 24 genes, including APC, KRAS, SMAD4 and PIK3CA. A pairwise comparison of somatic variations in primary and metastatic samples indicated that many chromothripsis clusters, isolated rearrangements and point mutations are exclusively present in either the primary tumor or the metastasis and may affect cancer genes in a lesion-specific manner. CONCLUSIONS: We conclude that chromothripsis is a prevalent mechanism driving structural rearrangements in colorectal cancer and show that a complex interplay between point mutations, simple copy number changes and chromothripsis events drive colorectal tumor development and metastasis.	GRCh37/hg19	GSE32711		ERP000875	Yes	CCDC66,C3orf63;C3orf63,ARHGEF3;ARHGEF3,RP11-51O17.1;LSAMP,RP11-63L4.1;RP11-63L4.1,KHDRBS2;LSAMP,RIMS1;GPR156,ARL15;ARL15,AC034246.1;IQCB1,ACPL2;ACPL2,RP11-438D8.2;IQCB1,EAF2;MED12L,P2RY14;P2RY14,RP11-600P18.4;PCCB,RP11-649A16.1;RP11-649A16.1,FGF12;ARHGEF26,MUTED;RP11-85M11.2,FAM65B;RP11-85M11.2,ARL15;ARL15,AC034246.1;SERPINI1,C3orf59;NAALADL2,RP11-432A8.2;RP11-432A8.2,NAALADL2;NAALADL2,RP11-432A8.2;AL662795.3,AL662795.4;AL662795.4,HLA-L;HLA-L,KHDRBS2;CENPQ,KLHL32;RP11-962G15.1,RP1-155O2.1;RP1-155O2.1,ADAM3A;ADAM3A,AC123767.2
CTDB0142	Research	22014273	Kloosterman WP, Hoogstraat M, Paling O, Tavakoli-Yaraki M, Renkens I, Vermaat JS, van Roosmalen MJ, van Lieshout S, Nijman IJ, Roessingh W, van 't Slot R, van de Belt J, Guryev V, Koudijs M, Voest E, Cuppen E	Chromothripsis is a common mechanism driving genomic rearrangements in primary and metastatic colorectal cancer	Genome Biol	2011 Oct	8,17,21	Colorectal cancer	Next Generation Sequencing	Homo sapiens	Patient4_metastasis	AB SOLiD 4 System	chr1:162534083-162562304:-1;chr2:17406991-17437065:1;chr5:55466078-55471432:-1;chr6:87330569-114998264:-1;chr6:162353175-163192040:-1;chr6:162427029-162443266:-1;chr7:24233931-24239286:-1;chr8:39144393-47113502:1;chr9:96569412-100368804:-1;chr11:62159412-63936774:-1;chr14:64687236-64720590:1;chr15:20935275-21939883:1;chr16:6248506-6380774:-1;chr16:6586750-6597999:1;chr16:79194156-79272292:-1;chr17:32113189-60139461:-1;chr17:40814703-70143738:1;chr17:64277098-72940896:1;chr18:48040416-48170802:-1;chr18:76525020-76540965:-1;chrX:6785822-6827028:-1	hs1:163398379-163400456,hs1:203494249-203496422;hs1:163442290-163443321,hs1:203497211-203498241;hs1:208378873-208380330,hs18:29271081-29273046;hs3:96404490-96407077,hs3:96439770-96443240;hs3:96407234-96409302,hs3:96443905-96446423;hs3:136539077-136539760,hs6:72506993-72508522;hs3:165773176-165775886,hs6:25994741-25997121;hs3:191611575-191612274,hs6:97835272-97836598;hs6:170909787-170911773,hs13:115106076-115109812;hs8:34331178-34333393,hs8:36511593-36513948;hs8:36867812-36870275,hs8:37789646-37791368;hs15:74653331-74655310,hs17:77772433-77773698;hs17:32112860-32113771,hs21:36078807-36080162;hs17:34387513-34388512,hs17:69836276-69837799;hs17:36271457-36274015,hs17:69794557-69797324;hs17:60138913-60139352,hs21:47004072-47004879;hs17:61528927-61531431,hs21:44019447-44021284;hs17:69672120-69672487,hs21:47004076-47004243;hs17:69672131-69672690,hs21:36077556-36079034;hs20:5709889-5710952,hs20:5711237-5712971;hs20:42881540-42883261,hs20:44091225-44093313	ACCN1;ADAM32;ANKRD55;AP001626.1;ASRGL1;CBX8;CLIC6;CTD;CYP11A1;ESR2;GDAP1L1;GOT1L1;MACROD1;MAPK4;MED13;OTOP3;PACRG;PARK2;PLEKHH3;PLXNA2;RP11;SYNE2;TMEM22;TMOD1;TSTD2;TUBG2;UAP1;WWOX	Department of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584 CG, The Netherlands	Structural rearrangements form a major class of somatic variation in cancer genomes. Local chromosome shattering, termed chromothripsis, is a mechanism proposed to be the cause of clustered chromosomal rearrangements and was recently described to occur in a small percentage of tumors. The significance of these clusters for tumor development or metastatic spread is largely unclear. RESULTS: We used genome-wide long mate-pair sequencing and SNP array profiling to reveal that chromothripsis is a widespread phenomenon in primary colorectal cancer and metastases. We find large and small chromothripsis events in nearly every colorectal tumor sample and show that several breakpoints of chromothripsis clusters and isolated rearrangements affect cancer genes, including NOTCH2, EXO1 and MLL3. We complemented the structural variation studies by sequencing the coding regions of a cancer exome in all colorectal tumor samples and found somatic mutations in 24 genes, including APC, KRAS, SMAD4 and PIK3CA. A pairwise comparison of somatic variations in primary and metastatic samples indicated that many chromothripsis clusters, isolated rearrangements and point mutations are exclusively present in either the primary tumor or the metastasis and may affect cancer genes in a lesion-specific manner. CONCLUSIONS: We conclude that chromothripsis is a prevalent mechanism driving structural rearrangements in colorectal cancer and show that a complex interplay between point mutations, simple copy number changes and chromothripsis events drive colorectal tumor development and metastasis.	GRCh37/hg19	GSE32711		ERP000875	Yes	ACCN1,CLIC6;ACCN1,MED13;TUBG2,PLEKHH3;PLEKHH3,AC005152.2
CTDB0143	Research	25074542	Xiang DB, Wei B, Abraham SC, Huo L, Albarracin CT, Zhang H, Babiera G, Caudle AS, Akay CL, Rao P, Zhao YJ, Lu X, Wu Y	Molecular cytogenetic characterization of mammary neuroendocrine carcinoma.	Hum Pathol	2014 Sep	1,6,8,15	Neuroendocrine carcinoma	Array CGH	Homo sapiens	Case2	Chroma Technology				Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030	Primary mammary neuroendocrine carcinoma (NEC) is an uncommon entity that accounts for 2% to 5% of breast carcinomas. Recent reports have shown that NEC of the breast is an aggressive subtype of mammary carcinoma that is distinct from invasive ductal carcinoma, not otherwise specified, and have suggested that these tumors have a poorer prognosis than invasive ductal carcinoma, not otherwise specified. In this study, we provide the first cytogenetic characterization of mammary NEC using both conventional G-banding and spectral karyotype on a group of 7 tumors. We identified clonal chromosomal aberrations in 5 (71.4%) cases, with 4 of them showing complex karyotypes. Of these, recurrent numerical aberrations included gain of chromosome 7 (n = 2) and loss of chromosome 15 (n = 2). Recurrent clonal structural chromosomal aberrations involved chromosomes 1 (n = 3), 3 (n = 2), 6q (n = 3), and 17q (n = 3). Of the 4 (57.1%) cases with complex karyotypes, 2 showed evidence of chromothripsis, a phenomenon in which tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. One of these had evidence of chromothripsis involving chromosomes 1, 6, 8, and 15. The other also had evidence of chromosome 8 chromothripsis, making this a recurrent finding shared by both cases. We also found that mammary NEC shared some cytogenetic abnormalities--such as trisomy 7 and 12--with other neuroendocrine tumors in the lung and gastrointestinal tract, suggesting trisomy 7 and 12 as potential common molecular aberrations in neuroendocrine tumors. To our knowledge, this is the first report on molecular cytogenetic characterization of mammary NEC.					Yes	NA
CTDB0144	Research	25074542	Xiang DB, Wei B, Abraham SC, Huo L, Albarracin CT, Zhang H, Babiera G, Caudle AS, Akay CL, Rao P, Zhao YJ, Lu X, Wu Y	Molecular cytogenetic characterization of mammary neuroendocrine carcinoma.	Hum Pathol	2014 Sep	8	Neuroendocrine carcinoma	Array CGH	Homo sapiens	Case5	Chroma Technology				Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030	Primary mammary neuroendocrine carcinoma (NEC) is an uncommon entity that accounts for 2% to 5% of breast carcinomas. Recent reports have shown that NEC of the breast is an aggressive subtype of mammary carcinoma that is distinct from invasive ductal carcinoma, not otherwise specified, and have suggested that these tumors have a poorer prognosis than invasive ductal carcinoma, not otherwise specified. In this study, we provide the first cytogenetic characterization of mammary NEC using both conventional G-banding and spectral karyotype on a group of 7 tumors. We identified clonal chromosomal aberrations in 5 (71.4%) cases, with 4 of them showing complex karyotypes. Of these, recurrent numerical aberrations included gain of chromosome 7 (n = 2) and loss of chromosome 15 (n = 2). Recurrent clonal structural chromosomal aberrations involved chromosomes 1 (n = 3), 3 (n = 2), 6q (n = 3), and 17q (n = 3). Of the 4 (57.1%) cases with complex karyotypes, 2 showed evidence of chromothripsis, a phenomenon in which tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. One of these had evidence of chromothripsis involving chromosomes 1, 6, 8, and 15. The other also had evidence of chromosome 8 chromothripsis, making this a recurrent finding shared by both cases. We also found that mammary NEC shared some cytogenetic abnormalities--such as trisomy 7 and 12--with other neuroendocrine tumors in the lung and gastrointestinal tract, suggesting trisomy 7 and 12 as potential common molecular aberrations in neuroendocrine tumors. To our knowledge, this is the first report on molecular cytogenetic characterization of mammary NEC.					Yes	NA
CTDB0145	Research	24636338	Zemanova Z, Michalova K, Buryova H, Brezinova J, Kostylkova K, Bystricka D, Novakova M, Sarova I, Izakova S, Lizcova L, Ransdorfova S, Krejcik Z, Merkerova MD, Dohnalova A, Siskova M, Jonasova A, Neuwirtova R, Cermak J	Involvement of deleted chromosome 5 in complex chromosomal aberrations in newly diagnosed myelodysplastic syndromes (MDS) is correlated with extremely adverse prognosis.	Leuk Res	2014 May	2,14,17,18,19	Myelodysplastic syndrome	SNP Array	Homo sapiens	24636338_1	BlueGnome CytoChip Cancer SNP 180K + Illumina Human CytoSNP-12 array				Center of Oncocytogenetics, Institute of Medical Biochemistry and Laboratory Diagnostics, General University Hospital and First Faculty of Medicine, Charles University in Prague, Czech Republic	MDS with complex chromosomal aberrations (CCA) are characterized by short survival and a high rate of transformation to AML. A comprehensive genome-wide analysis of bone-marrow cells of 157 adults with newly diagnosed MDS and CCA revealed a large spectrum of nonrandom genomic changes related to the advanced stages of MDS. Chromosome shattering, probably resulting from chromothripsis, was found in 47% of patients. Deleted chromosome 5 was unstable and often involved in different types of cryptic unbalanced rearrangements. No true monosomy 5 was observed. Patients with CCA involving deleted chromosome 5 had an extremely poor prognosis (median overall survival, 2 months).					No	NA
CTDB0146	Research	25128687	Plaisancie J, Kleinfinger P, Cances C, Bazin A, Julia S, Trost D, Lohmann L, Vigouroux A	Constitutional chromoanasynthesis: description of a rare chromosomal event in a patient.	Eur J Med Genet	2014 Oct	18	Congenital abnormality	SNP Array	Homo sapiens	25128687_1	Affymetrix CytoscanHD Array	chr18:11585369-12482080:1;chr18:30852180-36260132:1;chr18:44426209-44898600:1;chr18:46076777-46787156:1;chr18:52567865-58008305:1;chr18:60595227-60819311:1;chr18:63614315-66856964:1;chr18:73554500-77125545:1			Service de Genetique Medicale, Hopital Purpan, CHU Toulouse, France	Structural alterations in chromosomes are a frequent cause of cancers and congenital diseases. Recently, the phenomenon of chromosome crisis, consisting of a set of tens to hundreds of clustered genomic rearrangements, localized in one or a few chromosomes, was described in cancer cells under the term chromothripsis. Better knowledge and recognition of this catastrophic chromosome event has brought to light two distinct entities, chromothripsis and chromoanasynthesis. The complexity of these rearrangements and the original descriptions in tumor cells initially led to the thought that it was an acquired anomaly. In fact, a few patients have been reported with constitutional chromothripsis or chromoanasynthesis. Using microarray we identified a very complex chromosomal rearrangement in a patient who had a cytogenetically visible rearrangement of chromosome 18. The rearrangement contained more than 15 breakpoints localized on a single chromosome. Our patient displayed intellectual disability, behavioral troubles and craniofacial dysmorphism. Interestingly, the succession of duplications and triplications identified in our patient was not clustered on a single chromosomal region but spread over the entire chromosome 18. In the light of this new spectrum of chromosomal rearrangements, this report outlines the main features of these catastrophic events and discusses the underlying mechanism of the complex chromosomal rearrangement identified in our patient, which is strongly evocative of a chromoanasynthesis.	GRCh37/hg19				No	NA
CTDB0147	Research	24957271	Sarova I, Brezinova J, Lhotska H, Berkova A, Ransdorfova S, Zemanova Z, Soukupova J, Michalova K	Jumping-like translocation-a rare chromosomal rearrangement in a patient with Burkitt lymphoma/leukemia.	Cancer Genet	2014 May	11,15	Burkitt lymphoma/leukemia	SNP Array	Homo sapiens	24957271_1	BlueGnome CytoChip Cancer SNP 4 180K	chr13:90000000-98200000:1;chr13:98200000-115169878:-1;chr11:43500000-48800000:-1;chr15:44800000-59100000:-1;chr15:59100000-63700000:-1			Institute of Hematology and Blood Transfusion, Prague, Czech Republic	Chromosomal translocations are acquired genetic rearrangements in human cancers. Jumping translocations are rare nonreciprocal rearrangements involving the same donor chromosome segment translocated to two or more recipient chromosomes. In this report, we describe a patient with Burkitt lymphoma/leukemia (BL) and a complex karyotype including a t(2;8)(p12;q24), copy-neutral loss of heterozygosity at 17p13.1-p13.3 and 19q13.1-q13.2, trisomy 20, and two uncommon chromosomal aberrations. The first uncommon aberration was a complex rearrangement of chromosome 15 (probably the consequence of chromothripsis) masked by an apparently balanced reciprocal translocation, t(11;15)(p11.2;q21). The second one was a special type of unbalanced vice versa jumping translocation, which involved the same acceptor chromosome arm (13q) and various donor chromosome segments. It is unclear whether both atypical rearrangements are the consequence of the TP53 alteration or whether assumed chromothripsis influenced the development of the jumping-like translocation. However, the presence of the t(11;15)(p11.2;q21) in all pathological cells suggests that it occurred in the early stage of the disease, whereas the jumping-like translocation, as an additional change, subsequently accelerated the progression of the disease.	GRCh37/hg19				Yes	NA
CTDB0148	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	7,11	Breast cancer	Array CGH	Homo sapiens	T61	Agilent 244K CGH array			CCND1	Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0149	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	6	Breast cancer	Array CGH	Homo sapiens	T23	Agilent 244K CGH array				Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0150	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	8,19	Breast cancer	Array CGH	Homo sapiens	T46	Agilent 244K CGH array				Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0151	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	11	Breast cancer	Array CGH	Homo sapiens	T147	Agilent 244K CGH array			CCND1	Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0152	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	9	Breast cancer	Array CGH	Homo sapiens	T190	Agilent 244K CGH array				Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0153	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	8	Breast cancer	Array CGH	Homo sapiens	T199	Agilent 244K CGH array			MYC;PVT1	Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	MYC,PVT1
CTDB0154	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	7	Breast cancer	Array CGH	Homo sapiens	T79	Agilent 244K CGH array				Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0155	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	6,8,17	Breast cancer	Array CGH	Homo sapiens	T333	Agilent 244K CGH array			ERBB2	Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0156	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	8,17	Breast cancer	Array CGH	Homo sapiens	T111	Agilent 244K CGH array			BCAS3;ERBB2	Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0157	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	17	Breast cancer	Array CGH	Homo sapiens	T207	Agilent 244K CGH array			ERBB2	Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0158	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	8,17,21	Breast cancer	Array CGH	Homo sapiens	T74	Agilent 244K CGH array			MYC	Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0159	Research	25011954	Przybytkowski E, Lenkiewicz E, Barrett MT, Klein K, Nabavi S, Greenwood CM, Basik M	Chromosome-breakage genomic instability and chromothripsis in breast cancer.	BMC Genomics	2014 Jul	17,21	Breast cancer	Array CGH	Homo sapiens	T64	Agilent 244K CGH array				Department of Oncology, Lady Davis Institute for Medical Research, McGill University, 3755 Cote Ste-Catherine Road, Montreal, Quebec H3T-1E2, Canada	BACKGROUND: Chromosomal breakage followed by faulty DNA repair leads to gene amplifications and deletions in cancers. However, the mere assessment of the extent of genomic changes, amplifications and deletions may reduce the complexity of genomic data observed by array comparative genomic hybridization (array CGH). We present here a novel approach to array CGH data analysis, which focuses on putative breakpoints responsible for rearrangements within the genome. RESULTS: We performed array comparative genomic hybridization in 29 primary tumors from high risk patients with breast cancer. The specimens were flow sorted according to ploidy to increase tumor cell purity prior to array CGH. We describe the number of chromosomal breaks as well as the patterns of breaks on individual chromosomes in each tumor. There were differences in chromosomal breakage patterns between the 3 clinical subtypes of breast cancers, although the highest density of breaks occurred at chromosome 17 in all subtypes, suggesting a particular proclivity of this chromosome for breaks. We also observed chromothripsis affecting various chromosomes in 41% of high risk breast cancers. CONCLUSIONS: Our results provide a new insight into the genomic complexity of breast cancer. Genomic instability dependent on chromosomal breakage events is not stochastic, targeting some chromosomes clearly more than others. We report a much higher percentage of chromothripsis than described previously in other cancers and this suggests that massive genomic rearrangements occurring in a single catastrophic event may shape many breast cancer genomes.	GRCh37/hg19				Yes	NA
CTDB0160	Research	24509483	McEvoy J, Nagahawatte P, Finkelstein D, Richards-Yutz J, Valentine M, Ma J, Mullighan C, Song G, Chen X, Wilson M, Brennan R, Pounds S, Becksfort J, Huether R, Lu C, Fulton RS, Fulton LL, Hong X, Dooling DJ, Ochoa K, Mardis ER, Wilson RK, Easton J, Zhang 	RB1 gene inactivation by chromothripsis in human retinoblastoma.	Oncotarget	2014 Jan	13	Retinoblastoma	Next Generation Sequencing	Homo sapiens	SJRB031	Illumina sequencing			CAB39L;DACH1;EBPL;ENOX1;KLHL1;LMO7;RB1	Departments of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN, USA	Retinoblastoma is a rare childhood cancer of the developing retina. Most retinoblastomas initiate with biallelic inactivation of the RB1 gene through diverse mechanisms including point mutations, nucleotide insertions, deletions, loss of heterozygosity and promoter hypermethylation. Recently, a novel mechanism of retinoblastoma initiation was proposed. Gallie and colleagues discovered that a small proportion of retinoblastomas lack RB1 mutations and had MYCN amplification. In this study, we identified recurrent chromosomal, regional and focal genomic lesions in 94 primary retinoblastomas with their matched normal DNA using SNP 6.0 chips. We also analyzed the RB1 gene mutations and compared the mechanism of RB1 inactivation to the recurrent copy number variations in the retinoblastoma genome. In addition to the previously described focal amplification of MYCN and deletions in RB1 and BCOR, we also identified recurrent focal amplification of OTX2, a transcription factor required for retinal photoreceptor development. We identified 10 retinoblastomas in our cohort that lacked RB1 point mutations or indels. We performed whole genome sequencing on those 10 tumors and their corresponding germline DNA. In one of the tumors, the RB1 gene was unaltered, the MYCN gene was amplified and RB1 protein was expressed in the nuclei of the tumor cells. In addition, several tumors had complex patterns of structural variations and we identified 3 tumors with chromothripsis at the RB1 locus. This is the first report of chromothripsis as a mechanism for RB1 gene inactivation in cancer.					Yes	NA
CTDB0161	Research	24509483	McEvoy J, Nagahawatte P, Finkelstein D, Richards-Yutz J, Valentine M, Ma J, Mullighan C, Song G, Chen X, Wilson M, Brennan R, Pounds S, Becksfort J, Huether R, Lu C, Fulton RS, Fulton LL, Hong X, Dooling DJ, Ochoa K, Mardis ER, Wilson RK, Easton J, Zhang 	RB1 gene inactivation by chromothripsis in human retinoblastoma.	Oncotarget	2014 Jan	13	Retinoblastoma	Next Generation Sequencing	Homo sapiens	SJRB039	Illumina sequencing			CAB39L;DIAPH3;ENOX1;GPC5;KLF12;PIBF1;RB1;SLC35F4;TBC1D4;TDRD3	Departments of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN, USA	Retinoblastoma is a rare childhood cancer of the developing retina. Most retinoblastomas initiate with biallelic inactivation of the RB1 gene through diverse mechanisms including point mutations, nucleotide insertions, deletions, loss of heterozygosity and promoter hypermethylation. Recently, a novel mechanism of retinoblastoma initiation was proposed. Gallie and colleagues discovered that a small proportion of retinoblastomas lack RB1 mutations and had MYCN amplification. In this study, we identified recurrent chromosomal, regional and focal genomic lesions in 94 primary retinoblastomas with their matched normal DNA using SNP 6.0 chips. We also analyzed the RB1 gene mutations and compared the mechanism of RB1 inactivation to the recurrent copy number variations in the retinoblastoma genome. In addition to the previously described focal amplification of MYCN and deletions in RB1 and BCOR, we also identified recurrent focal amplification of OTX2, a transcription factor required for retinal photoreceptor development. We identified 10 retinoblastomas in our cohort that lacked RB1 point mutations or indels. We performed whole genome sequencing on those 10 tumors and their corresponding germline DNA. In one of the tumors, the RB1 gene was unaltered, the MYCN gene was amplified and RB1 protein was expressed in the nuclei of the tumor cells. In addition, several tumors had complex patterns of structural variations and we identified 3 tumors with chromothripsis at the RB1 locus. This is the first report of chromothripsis as a mechanism for RB1 gene inactivation in cancer.					Yes	NA
CTDB0162	Research	24509483	McEvoy J, Nagahawatte P, Finkelstein D, Richards-Yutz J, Valentine M, Ma J, Mullighan C, Song G, Chen X, Wilson M, Brennan R, Pounds S, Becksfort J, Huether R, Lu C, Fulton RS, Fulton LL, Hong X, Dooling DJ, Ochoa K, Mardis ER, Wilson RK, Easton J, Zhang 	RB1 gene inactivation by chromothripsis in human retinoblastoma.	Oncotarget	2014 Jan	13	Retinoblastoma	Next Generation Sequencing	Homo sapiens	SJRB051	Illumina sequencing				Departments of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN, USA	Retinoblastoma is a rare childhood cancer of the developing retina. Most retinoblastomas initiate with biallelic inactivation of the RB1 gene through diverse mechanisms including point mutations, nucleotide insertions, deletions, loss of heterozygosity and promoter hypermethylation. Recently, a novel mechanism of retinoblastoma initiation was proposed. Gallie and colleagues discovered that a small proportion of retinoblastomas lack RB1 mutations and had MYCN amplification. In this study, we identified recurrent chromosomal, regional and focal genomic lesions in 94 primary retinoblastomas with their matched normal DNA using SNP 6.0 chips. We also analyzed the RB1 gene mutations and compared the mechanism of RB1 inactivation to the recurrent copy number variations in the retinoblastoma genome. In addition to the previously described focal amplification of MYCN and deletions in RB1 and BCOR, we also identified recurrent focal amplification of OTX2, a transcription factor required for retinal photoreceptor development. We identified 10 retinoblastomas in our cohort that lacked RB1 point mutations or indels. We performed whole genome sequencing on those 10 tumors and their corresponding germline DNA. In one of the tumors, the RB1 gene was unaltered, the MYCN gene was amplified and RB1 protein was expressed in the nuclei of the tumor cells. In addition, several tumors had complex patterns of structural variations and we identified 3 tumors with chromothripsis at the RB1 locus. This is the first report of chromothripsis as a mechanism for RB1 gene inactivation in cancer.					Yes	NA
CTDB0163	Research	25254125	Agrawal A, Modi A, Alagusundaramoorthy SS, Ghali W	Chromothripsis: Basis of a Concurrent Unusual Association between Myelodysplastic Syndrome and Primary Ciliary Dyskinesia.	Case Rep Hematol	2014 Sep	7	Myelodysplastic syndrome	Flow cytometry	Homo sapiens	25254125_1	Flow cytometry				Department of Internal Medicine, Monmouth Medical Center, Long Branch, NJ 07740, USA	A 20 year old male was initially diagnosed suffering from Primary ciliary dyskinesia with symptoms of bronchiectasis, severe frontal, maxillary and ethmoid sinus disease. At the age of 20, the patient was also diagnosed with Myelodysplastic syndrome requiring Bone marrow transplant due to the advanced stage at time of presentation. Primary ciliary dyskinesia and Myelodsyplastic syndrome are both rare clinical conditions found in the general population, especially in young adults. This rare combination of disorders has never been reported in literature to the best of the author's knowledge. The presence of an advanced cancer and a genetic abnormality due to two deletions occurring in two arms of the same chromosome can be explained on the base of chromothripsis. A number of evidences have been published in the literature, about multiple deletions in chromosome 5 and advanced stages of MDS being associated with chromothripsis however this is the first case report on two deletions in chromosome 7 giving rise to two different clinical entities requiring multiple modes of management.					No	NA
CTDB0164	Research	25144242	Kodama T, Motoi N, Ninomiya H, Sakamoto H, Kitada K, Tsukaguchi T, Satoh Y, Nomura K, Nagano H, Ishii N, Terui Y, Hatake K, Ishikawa Y	A novel mechanism of EML4-ALK rearrangement mediated by chromothripsis in a patient-derived cell line.	J Thorac Oncol	2014 Nov	2	Non Small-cell lung cancer	Array CGH	Homo sapiens	JFCR-LC649	Agilent SurePrint G3 1M CGH array			EML4;ALK	Department of Pathology, The Cancer Institute Hospital, Tokyo, Japan	INTRODUCTION: EML4-ALK is a driver oncogene in non-small-cell lung cancer (NSCLC) and has been developed into a promising molecular target for antitumor agents. Although EML4-ALK is reported to be formed by inversion of chromosome 2, other mechanisms of this gene fusion remain unknown. This study aimed to examine the mechanism of EML4-ALK rearrangement using a novel cell line with the EML4-ALK fusion gene. METHODS: An EML4-ALK-positive cell line, termed JFCR-LC649, was established from pleomorphic carcinoma, a rare subtype of NSCLC. We investigated the chromosomal aberrations using fluorescence in situ hybridization and comparative genomic hybridization (CGH). Alectinib/CH5424802, a selective ALK inhibitor, was evaluated in the antitumor activity against JFCR-LC649 in vitro and in vivo xenograft model. RESULTS: We established an EML4-ALK-positive cell line, termed JFCR-LC649, derived from a patient with NSCLC and revealed that the JFCR-LC649 cells harbor variant 3 of the EML4-ALK fusion with twofold copy number gain. Interestingly, comparative genomic hybridization and metaphase-fluorescence in situ hybridization analysis showed that in addition to two normal chromosome 2, JFCR-LC649 cells contained two aberrant chromosome 2 that were fragmented and scattered. These observations provided the first evidence that EML4-ALK fusion in JFCR-LC649 cells was formed in chromosome 2 by a distinct mechanism of genomic rearrangement, termed chromothripsis. Furthermore, a selective ALK inhibitor alectinib/CH5424802 suppressed tumor growth of the JFCR-LC649 cells through inhibition of phospho-ALK in vitro and in vivo in a xenograft model. CONCLUSION: Our results suggested that chromothripsis may be a mechanism of oncogenic rearrangement of EML4-ALK. In addition, alectinib was effective against EML4-ALK-positive tumors with ALK copy number gain mediated by chromothripsis.					Yes	EML4,ALK
CTDB0165	Research	25161957	Ambros IM, Brunner C, Abbasi R, Frech C, Ambros PF	Ultra-High Density SNParray in Neuroblastoma Molecular Diagnostics.	Front Oncol	2014 Aug	2	Neuroblastoma	SNP Array	Homo sapiens	25161957_1	Affymetrix CytoScan HD Array			MYCN;ALK;ATRX;ARID1A;ARID1B	Children's Cancer Research Institute, St. Anna Kinderkrebsforschung , Vienna , Austria	Neuroblastoma serves as a paradigm for applying tumor genomic data for determining patient prognosis and thus for treatment allocation. MYCN status, i.e., amplified vs. non-amplified, was one of the very first biomarkers in oncology to discriminate aggressive from less aggressive or even favorable clinical courses of neuroblastoma. However, MYCN amplification is by far not the only genetic change associated with unfavorable clinical courses. So called segmental chromosomal aberrations, (SCAs) i.e., gains or losses of chromosomal fragments, can also indicate tumor aggressiveness. The clinical use of these genomic aberrations has, however, been hampered for many years by methodical and interpretational problems. Only after reaching worldwide consensus on markers, methodology, and data interpretation, information on SCAs has recently been implemented in clinical studies. Now, a number of collaborative studies within COG, GPOH, and SIOPEN use genomic information to stratify therapy for patients with localized and metastatic disease. Recently, new types of DNA based aberrations influencing the clinical behavior of neuroblastomas have been described. Deletions or mutations of genes like ATRX and a phenomenon referred to as chromothripsis are all assumed to correlate with an unfavorable clinical behavior. However, these genomic aberrations need to be scrutinized in larger studies applying the most appropriate techniques. Single nucleotide polymorphism arrays have proven successful in deciphering genomic aberrations of cancer cells; these techniques, however, are usually not applied in the daily routine. Here, we present an ultra-high density (UHD) SNParray technique which is, because of its high specificity and sensitivity and the combined copy number and allele information, highly appropriate for the genomic diagnosis of neuroblastoma and other malignancies.					Yes	NA
CTDB0166	Research	25043231	Macera MJ, Sobrino A, Levy B, Jobanputra V, Aggarwal V, Mills A, Esteves C, Hanscom C, Pereira S, Pillalamarri V, Ordulu Z, Morton CC, Talkowski M, Warburton D	Prenatal diagnosis of chromothripsis, with nine breaks characterized by karyotyping, FISH, microarray and whole-genome sequencing.	Prenat Diagn	2015 Mar	3,5,7,9,18	Congenital abnormality	Next Generation Sequencing	Homo sapiens	DGAP259	Next Generation Sequencing			CNTN6;TBC1D5;CNTNAP2;PTPRD;L3MBTL4;LOC1001304840;WDR7	New York Presbyterian Hospital, Columbia University Medical Center, New York, NY, USA	Detection of de novo complex chromosomal rearrangements (CCRs) in prenatal testing is extremely rare.	GRCh37/hg19				No	NA
CTDB0167	Research	26040972	Gamba BF, Richieri-Costa A, Costa S, Rosenberg C, Ribeiro-Bicudo LA	Chromothripsis with at least 12 breaks at 1p36.33-p35.3 in a boy with multiple congenital anomalies.	Mol Genet Genomics	2015 Jun	1	Congenital abnormality	Array CGH	Homo sapiens	26040972_1	Oxford Gene Technology CytosureTM 4X180K array	chr1:1023846-2761528:-1;chr1:3696933-5200401:-1;chr1:6882352-7718050:-1;chr1:14012378-14992103:-1;chr1:17213968-20934341:-1;chr1:24146844-30208750:1			Department of Genetics, Institute of Biosciences, University of Sao Paulo State, Botucatu, SP, Brazil	Terminal deletion in the short arm of chromosome 1 results in a disorder described as 1p36 deletion syndrome. The resulting phenotype varies among patients including mental retardation, developmental delay, sensorineural hearing loss, seizures, heart defects, and distinct facies. In the present case, we performed array-comparative genomic hybridization in a boy with multiple congenital malformations presenting some features overlapping the 1p36 deletion phenotype for whom chromosomal analysis did not reveal a terminal deletion in 1p. Results showed complex chromosome rearrangements involving the 1p36.33-p35.3 region. While the mechanism of origin of these rearrangements is still unclear, chromothripsis-a single catastrophic event leading to shattering chromosomes or chromosome regions and rejoining of the segments-has been described to occur in a fraction of cancers. The presence of at least 12 clustered breaks at 1p and apparent lack of mosaicism in the present case suggests that a single event like chromothripsis occurred. This finding suggests that chromothripsis is responsible for some constitutive complex chromosome rearrangements.	GRCh37/hg19				No	NA
CTDB0168	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	11,X	Ependymoma	Next Generation Sequencing	Homo sapiens	ST1	Illumina 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Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C1orf95,RELA;HDHD1,MACROD1;PRG2,C11orf95
CTDB0169	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	1,11	Ependymoma	Next Generation Sequencing	Homo sapiens	ST2	Illumina HighSeq	chr1:10101-23950200:-1;chr1:24078468-24080192:-1;chr2:10001-44700:1;chr2:128536801-128537500:-1;chr9:10001-141108100:-1;chr11:133701-55365400:-1;chr11:55459601-55784390:-1;chr11:56496718-56497900:1;chr11:56498057-56498168:1;chr11:56498169-56498545:1;chr11:56498546-56498608:1;chr11:56663001-56677510:-1;chr11:57352433-57353960:-1;chr11:57533945-57537111:-1;chr11:59910169-59912939:-1;chr11:60691595-60693442:-1;chr11:60840946-61159547:-1;chr11:61316664-61318506:-1;chr11:61742963-61745364:-1;chr11:62310777-62312488:-1;chr11:62462371-62464600:-1;chr11:63532010-64841368:1;chr11:64841369-64842810:-1;chr11:64842811-65429800:1;chr11:65429801-65431371:-1;chr11:65431372-65962744:1;chr11:65962745-65964931:-1;chr11:65964932-66178051:1;chr11:66178052-66505173:-1;chr11:66505174-76257798:1;chr11:76257799-77208636:-1;chr11:77874774-77877400:-1;chr11:78148643-78151579:-1;chr11:79130183-79133520:-1;chr11:79133521-80288992:1;chr11:80288993-80290733:-1;chr11:82249727-82253741:-1;chr11:83112371-83115905:-1;chr11:83115906-84613700:1;chr11:84613701-85617848:-1;chr11:85617849-86132389:1;chr11:88973847-88973900:1;chr11:88974001-88974300:1;chr11:88974365-88974484:1;chr11:88974485-88975242:-1;chr11:90813909-90819550:-1;chr11:90819551-92388918:1;chr11:92388919-92390137:-1;chr11:92390138-93274768:1;chr11:93274769-93275375:-1;chr11:93275376-118523766:1;chr11:118523767-133075931:-1;chr11:133459430-133461682:-1;chr11:134929801-134946400:1	hs11:64983067-64983067,hs11:64983501-64983501;hs3:34432532-34432532,hs3:34433003-34433003;hs11:57352433-57352433,hs11:83112371-83112371;hs11:57353961-57353961,hs11:56898805-56898805;hs6:109203696-109203696,hs6:109202055-109202055;hs13:56880933-56880933,hs13:56881767-56881767;hs11:56498169-56498169,hs11:88973888-88973888;hs11:56498609-56498609,hs11:86132705-86132705;hs11:86133004-86133004,hs11:88973932-88973932;hs1:24078468-24078468,hs11:82249727-82249727;hs11:93274769-93274769,hs11:66505174-66505174;hs11:65962745-65962745,hs11:79133521-79133521;hs11:77874774-77874774,hs11:57537112-57537112;hs11:92390138-92390138,hs11:65964932-65964932;hs11:56498022-56498022,hs11:88974396-88974396;hs11:88671613-88671613,hs11:62464596-62464596;hs11:56498609-56498609,hs11:86132705-86132705;hs11:56498169-56498169,hs11:88973888-88973888;hs7:20016970-20016970,hs7:20018602-20018602;hs11:92390138-92390138,hs11:65964932-65964932;hs11:56498022-56498022,hs11:88974396-88974396;hs11:60691595-60691595,hs11:57467033-57467033;hs11:86133004-86133004,hs11:88973932-88973932;hs11:88974331-88974331,hs11:85617849-85617849;hs11:56498169-56498169,hs11:88973888-88973888;hs11:62462371-62462371,hs1:24080193-24080193;hs11:76257799-76257799,hs11:56496718-56496718;hs11:77877366-77877366,hs11:62312489-62312489;hs11:78148643-78148643,hs11:88974372-88974372;hs17:42676519-42676519,hs2:58227721-58227721;hs11:56498169-56498169,hs11:88973888-88973888;hs11:133075932-133075932,hs11:61318507-61318507;hs21:25629382-25629382,hs21:25633408-25633408;hs11:90819551-90819551,hs11:65431372-65431372;hs11:86133004-86133004,hs11:88973932-88973932;hs11:61742963-61742963,hs11:55784391-55784391;hs11:88974365-88974365,hs11:88973839-88973839;hs11:56498169-56498169,hs11:88973888-88973888;hs11:56498057-56498057,hs11:60840946-60840946;hs11:88974331-88974331,hs11:85617849-85617849;hs11:78148643-78148643,hs11:88974372-88974372;hs11:133459430-133459430,hs11:59912940-59912940;hs11:56498022-56498022,hs11:88974396-88974396;hs11:77874774-77874774,hs11:57537112-57537112;hs11:88974331-88974331,hs11:85617849-85617849;hs11:80290734-80290734,hs11:61159548-61159548;hs11:57467021-57467021,hs11:59910169-59910169;hs11:133475467-133475467,hs11:56677511-56677511;hs11:56498609-56498609,hs11:86132705-86132705;hs11:133475462-133475462,hs11:77208637-77208637;hs11:56498169-56498169,hs11:88973888-88973888;hs11:78148643-78148643,hs11:88974372-88974372;hs11:57533945-57533945,hs11:61745365-61745365;hs11:92388919-92388919,hs11:93275376-93275376;hs11:88671613-88671613,hs11:62464596-62464596;hs11:86133004-86133004,hs11:88973932-88973932;hs11:92388919-92388919,hs11:93275376-93275376;hs11:88974350-88974350,hs11:90813909-90813909;hs11:62310777-62310777,hs11:56529059-56529059;hs11:65962745-65962745,hs11:79133521-79133521;hs11:80288993-80288993,hs11:86132390-86132390;hs11:86133004-86133004,hs11:88973932-88973932;hs11:133075932-133075932,hs11:61318507-61318507;hs6:104439597-104439597,hs6:104440200-104440200;hs20:36718918-36718918,hs20:36718843-36718843;hs11:76257799-76257799,hs11:56496718-56496718;hs11:57533945-57533945,hs11:61745365-61745365;hs11:86133004-86133004,hs11:88973932-88973932;hs11:56498022-56498022,hs11:88974396-88974396;hs11:76257799-76257799,hs11:56496718-56496718;hs11:66178052-66178052,hs11:64842811-64842811;hs11:56498169-56498169,hs11:88973888-88973888;hs11:62462371-62462371,hs1:24080193-24080193;hs11:79130183-79130183,hs11:133461683-133461683;hs11:76257799-76257799,hs11:56496718-56496718;hs11:56498022-56498022,hs11:88974396-88974396;hs11:56498609-56498609,hs11:86132705-86132705;hs19:58477128-58477128,hs19:58476480-58476480;hs11:88974280-88974280,hs11:88973839-88973839;hs11:88974330-88974330,hs11:83115906-83115906;hs11:64841369-64841369,hs11:118523767-118523767;hs11:56498169-56498169,hs11:88973888-88973888;hs11:56498022-56498022,hs11:88974396-88974396;hs11:56498609-56498609,hs11:86132705-86132705;hs11:61223391-61223391,hs11:82253742-82253742;hs11:61316664-61316664,hs11:86989226-86989226;hs11:65429801-65429801,hs11:63532010-63532010;hs21:24828945-24828945,hs21:24829265-24829265;hs11:56498169-56498169,hs11:88973888-88973888	SLC22A20;ARMC2;CCDC81_NARS2;C11orf30;TCEB3;C11orf75;PACS1;CTNND1;FAT3;BSCL2_GRM5;CCDC81_TYR;OR8U8;TYR;ZDHHC5;CCDC81;CCDC83;AHNAK;TYR_NARS2;NARS2;SYT7;CCDC81_CCDC83;TMX2-CTNND1;TYR_CCDC83;C11orf30_OR8U8;HNRNPUL2-BSCL2_GRM5;ODZ4;OPCML;RPRD1B_RPRD1B;OR8U8_OR8U8;BSCL2;C19orf18;PHLDB1;TMEM135_SYT7;C11orf95_RELA	St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C1orf95,RELA;PACS1,ODZ4;PHLDB1,CDCA5
CTDB0170	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	11	Ependymoma	Next Generation Sequencing	Homo sapiens	ST3	Illumina HighSeq	chr1:67625082-83788300:-1;chr1:107215337-107219950:-1;chr1:143538601-249240500:1;chr2:188210554-188212008:-1;chr3:50004272-50005960:-1;chr3:182041516-182045507:-1;chr4:108875141-109373478:-1;chr4:109383708-109384629:-1;chr4:109384630-109385237:1;chr4:109385238-109386211:-1;chr4:109386212-109388977:1;chr4:109388978-109390580:1;chr4:109390581-109392568:-1;chr4:109392569-109393500:1;chr4:109393501-109511572:-1;chr4:109511573-151613043:1;chr4:151613044-151632069:-1;chr5:100307271-100307355:-1;chr9:4714201-21901594:-1;chr9:21901595-22025245:-1;chr9:22025246-24430712:-1;chr9:24430713-24432864:-1;chr9:24432865-29916900:-1;chr9:29916901-31587601:1;chr9:31587602-31587699:-1;chr10:79386572-113490323:-1;chr11:48669201-48670070:-1;chr11:57399735-57400563:-1;chr11:59439701-59440268:-1;chr11:60105782-60107379:-1;chr11:60375800-60377018:-1;chr11:60377019-60377260:1;chr11:60377261-60543559:-1;chr11:60543560-62531300:-1;chr11:62531401-62531825:-1;chr11:64184367-64185239:-1;chr11:64185240-64791300:-1;chr11:64791384-64791800:-1;chr11:64791901-64799860:-1;chr11:64799861-64802103:-1;chr11:64802104-65088994:-1;chr11:65088995-65254664:-1;chr11:65254665-72042700:-1;chr11:72042801-72043094:-1;chr11:78798885-81003016:-1;chr11:81003017-81637490:1;chr11:81637491-81637738:1;chr11:81637739-81637836:1;chr11:81637837-83173785:-1;chr11:83565352-83566601:-1;chr11:88046595-88047613:-1;chr11:89831401-92099860:-1;chr11:94887474-94887888:1;chr11:94887889-94888065:1;chr11:94888066-94888527:1;chr11:94888528-94889981:1;chr11:94889982-94890456:-1;chr11:94890457-94961146:1;chr11:94961147-94962333:-1;chr11:95544046-95545829:-1;chr11:107827417-107952854:-1;chr11:111488261-111489062:-1;chr11:112270860-112272265:-1;chr11:112272266-114186121:-1;chr11:114186122-114186599:-1;chr11:116176859-116177461:-1;chr11:118812654-118813863:-1;chr11:119214409-119214728:-1;chr11:119214729-119705794:-1;chr11:119705795-119707689:-1;chr11:119912269-119913412:-1;chr11:123281297-125461747:-1;chr11:126349249-126741155:-1;chr11:132339815-132341900:-1;chr13:24806253-24827234:-1;chr14:19000101-34303789:1;chr14:34303790-34757423:-1;chr16:7865401-21594700:-1;chr17:1-2032200:1;chr17:28952501-30579648:1;chr17:30579649-32071800:1;chr17:32071801-32101473:1;chr17:32101474-34968606:1;chr18:49080713-49080811:-1	hs7:142998405-142998405,hs15:72276914-72276914;hs1:107215337-107215337,hs1:107219951-107219951;hs1:67625082-67625082,hs1:83788301-83788301;hs11:114186122-114186122,hs11:114186600-114186600;hs11:48669026-48669026,hs11:48670071-48670071;hs7:142998405-142998405,hs15:72276914-72276914;hs9:3123766-3123766,hs9:3123836-3123836;hs4:108877071-108877071,hs4:109384630-109384630;hs15:72276908-72276908,hs7:142998123-142998123;hs11:119214729-119214729,hs11:88047614-88047614;hs11:81637739-81637739,hs11:119707690-119707690;hs9:132014196-132014196,hs9:133525332-133525332;hs11:94887474-94887474,hs11:60377019-60377019;hs2:38306620-38306620,hs2:46717347-46717347;hs11:72042738-72042738,hs11:83566602-83566602;hs11:60105782-60105782,hs11:83565352-83565352;hs11:95544046-95544046,hs11:116177462-116177462;hs2:188210554-188210554,hs2:188212009-188212009;hs18:49080713-49080713,hs18:49080812-49080812;hs6:74110830-74110830,hs2:24763984-24763984;hs11:119214729-119214729,hs11:88047614-88047614;hs11:132341901-132341901,hs11:65254665-65254665;hs11:123281297-123281297,hs11:126349249-126349249;hs11:64184367-64184367,hs11:65088995-65088995;hs19:45622885-45622885,hs19:45622982-45622982;hs4:109386212-109386212,hs4:109373479-109373479;hs4:109385238-109385238,hs4:109511573-109511573;hs11:81637837-81637837,hs11:67359965-67359965;hs15:72276908-72276908,hs7:142998123-142998123;hs11:118812654-118812654,hs11:118813864-118813864;hs9:24430713-24430713,hs9:24432865-24432865;hs5:57769180-57769180,hs5:59079665-59079665;hs11:71621464-71621464,hs11:112272266-112272266;hs11:94888600-94888600,hs11:119214409-119214409;hs3:50005961-50005961,hs17:34889458-34889458;hs14:37151721-37151721,hs14:37151782-37151782;hs9:31587602-31587602,hs9:31587700-31587700;hs17:45569813-45569813,hs8:11787247-11787247;hs10:79386572-79386572,hs10:113490324-113490324;hs11:57399735-57399735,hs11:57400564-57400564;hs11:107827417-107827417,hs11:83173786-83173786;hs11:64799861-64799861,hs11:81637491-81637491;hs11:62531311-62531311,hs11:72043095-72043095;hs3:110372617-110372617,hs3:110372657-110372657;hs11:94888600-94888600,hs11:119214409-119214409;hs11:59439608-59439608,hs11:59440269-59440269;hs9:21901595-21901595,hs9:22025246-22025246;hs9:133525306-133525306,hs2:29004208-29004208;hs11:39887039-39887039,hs11:39887269-39887269;hs17:30579649-30579649,hs17:28951909-28951909;hs7:142998395-142998395,hs15:72276914-72276914;hs12:122342961-122342961,hs12:57917215-57917215;hs11:62531311-62531311,hs11:72043095-72043095;hs3:182041516-182041516,hs3:182045508-182045508;hs3:77984982-77984982,hs3:77984926-77984926;hs2:24763977-24763977,hs6:74110832-74110832;hs10:90471894-90471894,hs10:90428535-90428535;hs11:107827417-107827417,hs11:83173786-83173786;hs11:112270860-112270860,hs11:64791849-64791849;hs13:24806253-24806253,hs13:24827235-24827235;hs11:64799861-64799861,hs11:81637491-81637491;hs11:125461748-125461748,hs11:60107380-60107380;hs2:106475471-106475471,hs4:75849999-75849999;hs11:64791384-64791384,hs11:64802104-64802104;hs11:94962334-94962334,hs11:92099861-92099861;hs4:108875141-108875141,hs4:109383708-109383708;hs11:78798885-78798885,hs11:94887531-94887531;hs7:142998113-142998113,hs7:142998403-142998403;hs11:88046595-88046595,hs11:111488261-111488261;hs12:122342961-122342961,hs12:57917215-57917215;hs11:94887827-94887827,hs11:107952855-107952855;hs11:119214729-119214729,hs11:88047614-88047614;hs11:60105782-60105782,hs11:83565352-83565352;hs4:151613044-151613044,hs4:151632070-151632070;hs11:94888066-94888066,hs11:64185240-64185240;hs11:119705795-119705795,hs11:81003017-81003017;hs3:85646546-85646546,hs3:69873613-69873613;hs7:142998405-142998405,hs15:72276914-72276914;hs11:119912269-119912269,hs11:126741156-126741156;hs11:116176859-116176859,hs11:111489063-111489063;hs5:27443337-27443337,hs5:27443440-27443440;hs11:67373086-67373086,hs11:95545830-95545830;hs22:33661576-33661576,hs22:33661660-33661660;hs11:107827417-107827417,hs11:83173786-83173786;hs4:109390581-109390581,hs4:109392569-109392569;hs11:94888016-94888016,hs11:107828960-107828960;hs11:94961147-94961147,hs11:65433038-65433038;hs5:100307271-100307271,hs5:100307356-100307356;hs11:94887889-94887889,hs11:64634423-64634423;hs17:34886656-34886656,hs3:50004272-50004272;hs14:34303790-34303790,hs14:34757424-34757424;hs11:132339815-132339815,hs11:119913413-119913413;hs3:85646546-85646546,hs3:69873613-69873613;hs15:72276908-72276908,hs7:142998123-142998123;hs16:7106321-7106321,hs16:7106231-7106231;hs12:125506321-125506321,hs12:125506720-125506720;hs11:125459685-125459685,hs11:107828724-107828724;hs11:94890457-94890457,hs11:62531826-62531826;hs11:63531205-63531205,hs11:60543560-60543560	CASP2;MYO9A;MYO9A_MYO9A;CTSC;DLG2_CLPB;MS4A6E_DLG2;CEP57;CALCRL;DDX43;MFRP;OPCML;KIRREL3;CDC42EP2;LOC285456;PDE4D;LOC100133315;MYO19_RBM6;MRPL45P2;KCNMA1;RAB39;ARL2-SNX15;CLPB;C1QTNF5;CDKN2B-AS1;PPP1CB;LRRC37BP1;MBD6;POLR2G;LIPF;SPATA13_SPATA13;SNX15;MS4A6E;NCK2;ARL2-SNX15_ARL2-SNX15;SESN3_FAT3;ODZ4;SIK2_CTSC;PSMD9;CUL5;CADM2;SIK2;DLG2;SESN3;EHD1;RBM6_MYO19;MITF	St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C1orf95,RELA;KIRREL3,RP11-831A10
CTDB0171	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	2,11	Ependymoma	Next Generation Sequencing	Homo sapiens	ST4	Illumina HighSeq	chr2:32150501-32200497:-1;chr2:32850983-32851536:-1;chr2:34130260-34135800:-1;chr2:34654993-34666613:-1;chr2:39763329-39763957:-1;chr3:60201-90391100:-1;chr3:192886401-197948400:-1;chr4:96418001-191043900:1;chr5:11701-45912900:-1;chr5:100762101-180785400:-1;chr6:90701-65194400:-1;chr6:65202301-171050900:-1;chr7:10001-19614100:1;chr8:33501-78414800:-1;chr8:78448301-146303800:-1;chr9:10001-6700600:-1;chr9:6711401-141108100:-1;chr11:50616101-59242474:1;chr11:59242475-59247917:-1;chr11:63613166-63613448:-1;chr11:64429398-64484187:-1;chr13:56114201-115109800:1;chr21:9411201-48119800:-1;chr22:16054601-51234500:-1	hs2:33528011-33528011,hs2:37546802-37546802;hs11:57080811-57080811,hs11:55701486-55701486;hs11:65431243-65431243,hs11:63532315-63532315;hs11:59242475-59242475,hs2:34837578-34837578;hs11:63613166-63613166,hs11:63613449-63613449;hs2:31455656-31455656,hs2:33529265-33529265;hs6:149019988-149019988,hs6:149020049-149020049;hs2:37555137-37555137,hs2:31463551-31463551;hs2:39763958-39763958,hs11:59236125-59236125;hs11:65432268-65432268,hs2:34135762-34135762;hs11:64429398-64429398,hs2:39763329-39763329;hs2:34654993-34654993,hs2:32394770-32394770;hs2:32389918-32389918,hs2:32851537-32851537;hs2:34130260-34130260,hs2:51175100-51175100;hs2:34902878-34902878,hs2:34666614-34666614;hs2:39347009-39347009,hs2:31457120-31457120;hs11:65096960-65096960,hs11:65097953-65097953;hs1:57176418-57176418,hs1:57176469-57176469;hs11:55691545-55691545,hs11:57080302-57080302;hs11:59237569-59237569,hs2:32150351-32150351;hs3:77239677-77239677,hs3:77239792-77239792;hs11:60192521-60192521,hs11:60193197-60193197;hs11:62923912-62923912,hs2:32200498-32200498;hs2:52223302-52223302,hs2:39349632-39349632;hs2:32850983-32850983,hs11:64484188-64484188;hs2:31462408-31462408,hs11:59247918-59247918	LTBP1;TNKS1BP1;C11orf95;EHD3;LOC728730;LOC728730_NRXN2;SLC30A6;NRXN1;SOS1_EHD3;PRKAA2_PRKAA2;MEMO1;NRXN2	St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C1orf95,RELA;
CTDB0172	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	6,8,11	Ependymoma	Next Generation Sequencing	Homo sapiens	ST5	Illumina HighSeq	chr1:120378803-120381148:-1;chr6:2150195-2172900:-1;chr6:2172901-2174800:-1;chr6:2174801-2180017:-1;chr6:3927080-3943200:-1;chr11:63476704-63532899:-1;chr11:65091865-65094547:-1;chrY:2649501-59033300:-1	hs6:2180018-2180018,hs11:65430730-65430730;hs1:120378803-120378803,hs1:120381149-120381149;hs11:63476704-63476704,hs11:65091865-65091865;hs6:3927080-3927080,hs6:3943206-3943206;hs6:2150195-2150195,hs11:65094548-65094548;hs11:63093918-63093918,hs8:50418821-50418821;hs11:65430619-65430619,hs11:63532900-63532900	GMDS;NBPF7_NBPF7;RTN3;C11orf95	St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C1orf95,RELA;
CTDB0173	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	11	Ependymoma	Next Generation Sequencing	Homo sapiens	ST6	Illumina HighSeq	chr1:10101-249240500:-1;chr2:92277301-243183600:-1;chr3:60201-197948400:-1;chr4:10501-191043900:-1;chr5:11701-180375000:1;chr5:180440901-180785400:1;chr6:90701-171050900:-1;chr7:61886701-159128500:-1;chr8:33501-146303800:-1;chr9:10001-141108100:-1;chr11:133701-59887975:-1;chr11:59889851-61609285:-1;chr11:61609694-62624514:-1;chr11:62625097-63993126:-1;chr11:63993645-65431302:-1;chr11:65432736-68208863:-1;chr11:68208864-69354214:-1;chr11:69354215-71247036:-1;chr11:71249201-77358825:-1;chr11:77359102-78565937:-1;chr11:79499844-80280500:-1;chr11:80281436-82077333:-1;chr11:82077540-85582709:-1;chr11:85584876-86883342:-1;chr11:86884365-90519953:-1;chr11:90521007-134926900:-1;chr14:19000101-107289500:-1;chr18:10001-78017200:-1;chr20:60001-62965000:-1;chr22:16054601-51234500:-1;chrX:2699501-154930300:-1	hs11:71247037-71247037,hs11:61609694-61609694;hs11:77358826-77358826,hs11:85584876-85584876;hs11:65431303-65431303,hs11:63532061-63532061;hs11:62624515-62624515,hs11:80280644-80280644;hs11:71249048-71249048,hs11:59889851-59889851;hs11:90521007-90521007,hs11:77359102-77359102;hs11:78565938-78565938,hs11:86883343-86883343;hs9:138166501-138166501,hs9:138166442-138166442;hs11:63528854-63528854,hs11:86884365-86884365;hs22:49276093-49276093,hs22:49275975-49275975;hs11:82077540-82077540,hs11:80281436-80281436;hs19:21005728-21005728,hs19:21005944-21005944;hs11:63993127-63993127,hs11:62123694-62123694;hs11:79499844-79499844,hs11:69354215-69354215;hs5:70763497-70763497,hs5:70764157-70764157;hs11:59887976-59887976,hs11:85582710-85582710;hs5:91502446-91502446,hs5:91502530-91502530;hs11:62123343-62123343,hs11:82077334-82077334;hs11:68208864-68208864,hs11:90519954-90519954;hs11:63993127-63993127,hs11:62123694-62123694;hs11:65432736-65432736,hs11:63993645-63993645;hs11:61609286-61609286,hs11:62625097-62625097	sFADS2;CCDC83;C11orf95;SLC3A2;TMEM135_ODZ4;TMEM135;ASRGL1;BDP1;LRP5;TRPT1;FADS2_SLC3A2	St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C1orf95,RELA;
CTDB0174	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	6,11	Ependymoma	Next Generation Sequencing	Homo sapiens	ST7	Illumina HighSeq	chr2:61586301-61779500:-1;chr3:97275094-97283404:-1;chr4:63432036-63432100:1;chr5:164888567-164995689:-1;chr7:79979905-79979984:1;chr7:159103401-159128500:1;chr9:21333545-24963469:-1	hs11:62493322-62493322,hs11:65384107-65384107;hs11:54928254-54928254,hs11:54929101-54929101;hs9:21333545-21333545,hs9:24963470-24963470;hs3:97275094-97275094,hs3:97283405-97283405;hs11:65384119-65384119,hs6:3457860-3457860;hs11:62493322-62493322,hs11:65384107-65384107;hs11:65430839-65430839,hs11:63533129-63533129;hs11:63533000-63533000,hs11:62493318-62493318;hs16:12002319-12002319,hs16:12002645-12002645;hs5:164888567-164888567,hs5:164995690-164995690;hs11:62493322-62493322,hs11:65384107-65384107;hs7:79979985-79979985,hs7:79979905-79979905;hs11:63533000-63533000,hs11:62493318-62493318;hs11:63533000-63533000,hs11:62493318-62493318;hs18:45333973-45333973,hs1:178469117-178469117;hs11:62572909-62572909,hs6:35436603-35436603;hs4:63432159-63432159,hs4:63432036-63432036;hs11:62572909-62572909,hs6:35436603-35436603;hs11:62493322-62493322,hs11:65384107-65384107;hs6:3457888-3457888,hs11:65430842-65430842	PCNXL3;HNRNPUL2;HNRNPUL2-BSCL2_C11orf95;C11orf95;HNRNPUL2_C11orf95;RPL10A;NXF1;HNRNPUL2-BSCL2	St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C1orf95,RELA;
CTDB0175	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	11	Ependymoma	Next Generation Sequencing	Homo sapiens	ST8	Illumina HighSeq	chr2:10001-81600:1;chr3:60201-187500:1;chr7:159106701-159128500:1;chr11:1282285-1283001:-1;chr11:44546631-44546759:-1;chr11:65226635-65226761:-1;chr11:65431401-65432927:-1;chr11:134893601-134946400:1;chr14:107216201-107289500:1;chr18:77999101-78017200:1	hs11:1282285-1282285,hs11:44546760-44546760;hs11:44546631-44546631,hs11:63532380-63532380;hs11:65226763-65226763,hs11:65432928-65432928;hs11:1481510-1481510,hs11:1482374-1482374;hs11:65226635-65226635,hs11:1283002-1283002;hs11:65431350-65431350,hs11:63532607-63532607	MUC5B;C11orf95;BRSK2	St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C1orf95,RELA;
CTDB0176	Research	24553141	Parker M, Mohankumar KM, Punchihewa C, Weinlich R, Dalton JD, Li Y, Lee R, Tatevossian RG, Phoenix TN, Thiruvenkatam R, White E, Tang B, Orisme W, Gupta K, Rusch M, Chen X, Li Y, Nagahawhatte P, Hedlund E, Finkelstein D, Wu G, Shurtleff S, Easton J, Boggs	C11orf95-RELA fusions drive oncogenic NF-kappaB signalling in ependymoma.	Nature	2014 Feb	4,11	Ependymoma	Next Generation Sequencing	Homo sapiens	ST16	Illumina HighSeq	chr1:81217101-81237400:-1;chr1:98589401-98654300:-1;chr2:59847801-59874500:-1;chr2:108558401-108583500:-1;chr2:139818501-139848900:-1;chr3:79636601-79660200:-1;chr3:168690401-168722700:-1;chr4:46101501-46124200:-1;chr4:117824865-117827924:-1;chr5:102843880-102847057:-1;chr6:22580203-22599200:-1;chr10:25623101-25665700:-1;chr10:57239213-57269300:-1;chr11:50539301-50543138:1;chr11:50547301-50566700:-1;chr11:50567567-56288679:-1;chr11:56288680-56289476:-1;chr11:57745112-57745285:-1;chr11:59235143-62303918:-1;chr11:91405151-91405481:-1;chr11:94930463-94931480:-1;chr11:104878828-104879567:-1;chr11:113887101-113887569:-1;chr11:116173026-116173734:-1;chr12:82104001-82131200:-1;chr12:88263601-88271326:-1;chr12:88271390-88290300:-1;chr14:19000101-20208100:-1;chr14:62772301-62808000:-1;chr18:58463901-58490800:-1;chrY:2649501-59033300:-1	hs11:124223124-124223124,hs11:124238938-124238938;hs4:117824865-117824865,hs4:117827925-117827925;hs4:117888344-117888344,hs4:117920171-117920171;hs11:120951839-120951839,hs11:94931481-94931481;hs5:103793701-103793701,hs5:104042547-104042547;hs11:113887570-113887570,hs11:57745286-57745286;hs11:59235143-59235143,hs11:91405482-91405482;hs11:101981768-101981768,hs11:63530974-63530974;hs11:56288680-56288680,hs11:57745112-57745112;hs11:91405151-91405151,hs11:121006568-121006568;hs11:116173026-116173026,hs11:121006909-121006909;hs4:170778649-170778649,hs4:170778917-170778917;hs2:97835742-97835742,hs2:96600330-96600330;hs5:102843880-102843880,hs5:102847058-102847058;hs11:113887041-113887041,hs11:76925957-76925957;hs11:116173735-116173735,hs11:62303919-62303919;hs11:76924222-76924222,hs11:94930463-94930463;hs11:117895034-117895034,hs11:56289477-56289477;hs11:104878828-104878828,hs11:104879568-104879568;hs4:182472980-182472980,hs11:112813940-112813940	SESN3_TBCEL;C11orf95_YAP1;OR8U8;TECTA;ANKRD36;AHNAK;MYO7A_SESN3;LOC100526771_OR8U8;CASP5_CASP5	St. Jude Children's Research Hospital - Washington University Pediatric Cancer Genome Project, Memphis, Tennessee 38105, USA	Members of the nuclear factor-kappaB (NF-kappaB) family of transcriptional regulators are central mediators of the cellular inflammatory response. Although constitutive NF-kappaB signalling is present in most human tumours, mutations in pathway members are rare, complicating efforts to understand and block aberrant NF-kappaB activity in cancer. Here we show that more than two-thirds of supratentorial ependymomas contain oncogenic fusions between RELA, the principal effector of canonical NF-kappaB signalling, and an uncharacterized gene, C11orf95. In each case, C11orf95-RELA fusions resulted from chromothripsis involving chromosome 11q13.1. C11orf95-RELA fusion proteins translocated spontaneously to the nucleus to activate NF-kappaB target genes, and rapidly transformed neural stem cells--the cell of origin of ependymoma--to form these tumours in mice. Our data identify a highly recurrent genetic alteration of RELA in human cancer, and the C11orf95-RELA fusion protein as a potential therapeutic target in supratentorial ependymoma.	GRCh37/hg19			EGAS00001000254	Yes	C11orf95,YAP1;MYO7A,SESN3
CTDB0177	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	15,21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD9020a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0178	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD9021a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0179	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD9022a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0180	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD9023a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0181	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD4117a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0182	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	15,21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD7170a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0183	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	15,21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD7171a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0184	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	15,21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD10008a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0185	Research	24670643	Li Y, Schwab C, Ryan SL, Papaemmanuil E, Robinson HM, Jacobs P, Moorman AV, Dyer S, Borrow J, Griffiths M, Heerema NA, Carroll AJ, Talley P, Bown N, Telford N, Ross FM, Gaunt L, McNally RJ, Young BD, Sinclair P, Rand V, Teixeira MR, Joseph O, Robinson B, 	Constitutional and somatic rearrangement of chromosome 21 in acute lymphoblastic leukaemia.	Nature	2014 Apr	15,21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD10009a	Illumina HiSeq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Changes in gene dosage are a major driver of cancer, known to be caused by a finite, but increasingly well annotated, repertoire of mutational mechanisms. This can potentially generate correlated copy-number alterations across hundreds of linked genes, as exemplified by the 2% of childhood acute lymphoblastic leukaemia (ALL) with recurrent amplification of megabase regions of chromosome 21 (iAMP21). We used genomic, cytogenetic and transcriptional analysis, coupled with novel bioinformatic approaches, to reconstruct the evolution of iAMP21 ALL. Here we show that individuals born with the rare constitutional Robertsonian translocation between chromosomes 15 and 21, rob(15;21)(q10;q10)c, have approximately 2,700-fold increased risk of developing iAMP21 ALL compared to the general population. In such cases, amplification is initiated by a chromothripsis event involving both sister chromatids of the Robertsonian chromosome, a novel mechanism for cancer predisposition. In sporadic iAMP21, breakage-fusion-bridge cycles are typically the initiating event, often followed by chromothripsis. In both sporadic and rob(15;21)c-associated iAMP21, the final stages frequently involve duplications of the entire abnormal chromosome. The end-product is a derivative of chromosome 21 or the rob(15;21)c chromosome with gene dosage optimized for leukaemic potential, showing constrained copy-number levels over multiple linked genes. Thus, dicentric chromosomes may be an important precipitant of chromothripsis, as we show rob(15;21)c to be constitutionally dicentric and breakage-fusion-bridge cycles generate dicentric chromosomes somatically. Furthermore, our data illustrate that several cancer-specific mutational processes, applied sequentially, can coordinate to fashion copy-number profiles over large genomic scales, incrementally refining the fitness benefits of aggregated gene dosage changes.	GRCh37/hg19			EGAD00001000658	Yes	NA
CTDB0186	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	13,20	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0384	Illumina HiSeq 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Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	MTUS2,UCKL1;MTUS2,STAC2;DIAPH3,BMP7;DOK5,MTUS2;DIDO1,BEST3
CTDB0187	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	17	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0833	Illumina HiSeq 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Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	TBC1D16,KANSL1
CTDB0188	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	X	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_1074	Illumina HiSeq 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Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	PPP1R3F,ATRX
CTDB0189	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	6	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_1430	Illumina HiSeq 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Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	TRIM26,MDC1
CTDB0190	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	9	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_1527	Illumina HiSeq 2000		hs1:14815932-14815932,hs1:15279324-15279324;hs1:84518094-84518094,hs2:72559973-72559973;hs1:94557656-94557656,hs1:95030924-95030924;hs1:148928328-148928328,hs2:91848054-91848054;hs2:11220260-11220260,hs12:70285490-70285490;hs2:36567772-36567772,hs2:144565145-144565145;hs2:36567781-36567781,hs2:36568063-36568063;hs2:55400986-55400986,hs2:188649956-188649956;hs2:133459272-133459272,hs2:133460396-133460396;hs2:134187405-134187405,hs2:134233446-134233446;hs2:154637041-154637041,hs12:27352539-27352539;hs2:154637226-154637226,hs12:26616002-26616002;hs2:160149189-160149189,hs17:32859605-32859605;hs2:181868467-181868467,hs2:181868548-181868548;hs2:185469657-185469657,hs2:185471526-185471526;hs3:19686994-19686994,hs3:45012058-45012058;hs3:44884661-44884661,hs3:132849902-132849902;hs3:60117508-60117508,hs3:60213309-60213309;hs3:60312792-60312792,hs3:60463221-60463221;hs3:60321022-60321022,hs3:60475090-60475090;hs3:60489902-60489902,hs3:60561145-60561145;hs3:78036982-78036982,hs12:30186017-30186017;hs3:131265559-131265559,hs3:131267973-131267973;hs3:132725456-132725456,hs3:19919903-19919903;hs4:121671864-121671864,hs21:43328371-43328371;hs4:137647748-137647748,hs6:13191274-13191274;hs5:20728063-20728063,hs5:20728246-20728246;hs5:28692759-28692759,hs5:28716107-28716107;hs5:81709331-81709331,hs5:81869806-81869806;hs6:909992-909992,hs6:909680-909680;hs6:13191179-13191179,hs6:19552312-19552312;hs6:79452855-79452855,hs6:79453181-79453181;hs6:111627656-111627656,hs9:27894135-27894135;hs6:111627906-111627906,hs9:27894850-27894850;hs6:147082917-147082917,hs6:13191277-13191277;hs6:162881053-162881053,hs6:163169356-163169356;hs7:14549342-14549342,hs7:14553234-14553234;hs7:43792510-43792510,hs7:43715048-43715048;hs7:55515221-55515221,hs7:55519802-55519802;hs7:102479154-102479154,hs7:102647535-102647535;hs8:21348247-21348247,hs8:38580230-38580230;hs8:30068001-30068001,hs8:30070627-30070627;hs8:36033789-36033789,hs8:90361210-90361210;hs8:36036067-36036067,hs8:36039121-36039121;hs8:38468414-38468414,hs13:25473722-25473722;hs8:127770177-127770177,hs8:129295656-129295656;hs8:127835272-127835272,hs8:129291463-129291463;hs8:127835343-127835343,hs10:122929007-122929007;hs8:127840493-127840493,hs8:129557677-129557677;hs8:127910603-127910603,hs10:122699911-122699911;hs8:127910999-127910999,hs10:122973397-122973397;hs8:128049168-128049168,hs8:128530580-128530580;hs8:128049290-128049290,hs8:129574034-129574034;hs8:128057423-128057423,hs8:128648393-128648393;hs8:128062704-128062704,hs8:128653093-128653093;hs8:128091386-128091386,hs8:128716554-128716554;hs8:128098720-128098720,hs8:129606301-129606301;hs8:128253770-128253770,hs8:129600700-129600700;hs8:128254407-128254407,hs8:128737967-128737967;hs8:128261067-128261067,hs8:129704272-129704272;hs8:128268748-128268748,hs8:129602962-129602962;hs8:128457328-128457328,hs8:128530784-128530784;hs8:128583356-128583356,hs8:128651307-128651307;hs8:128680357-128680357,hs8:128518778-128518778;hs8:128686157-128686157,hs8:128560607-128560607;hs8:128794903-128794903,hs10:122960199-122960199;hs8:129291464-129291464,hs10:122929008-122929008;hs8:129739860-129739860,hs8:127740855-127740855;hs9:5567421-5567421,hs9:4471045-4471045;hs9:5585307-5585307,hs9:4962651-4962651;hs9:6017773-6017773,hs9:22712995-22712995;hs9:6049094-6049094,hs9:107510295-107510295;hs9:6742311-6742311,hs9:129977689-129977689;hs9:7036512-7036512,hs9:125990253-125990253;hs9:7088434-7088434,hs9:78462736-78462736;hs9:7342899-7342899,hs9:89181699-89181699;hs9:7693355-7693355,hs9:103970580-103970580;hs9:9845711-9845711,hs9:76596915-76596915;hs9:10155874-10155874,hs9:73115250-73115250;hs9:11952993-11952993,hs9:12112100-12112100;hs9:11953396-11953396,hs9:105606604-105606604;hs9:12479163-12479163,hs9:97311724-97311724;hs9:12873108-12873108,hs9:112756911-112756911;hs9:13070763-13070763,hs9:112584448-112584448;hs9:15202384-15202384,hs9:135521271-135521271;hs9:15577294-15577294,hs9:94427114-94427114;hs9:17770514-17770514,hs9:24125486-24125486;hs9:18930469-18930469,hs9:111503009-111503009;hs9:19588487-19588487,hs9:88831696-88831696;hs9:20044444-20044444,hs9:21469247-21469247;hs9:21550386-21550386,hs9:19591824-19591824;hs9:22170983-22170983,hs9:105713839-105713839;hs9:24019025-24019025,hs9:97321657-97321657;hs9:24699197-24699197,hs9:94298177-94298177;hs9:25080520-25080520,hs9:25670817-25670817;hs9:25885035-25885035,hs9:121717914-121717914;hs9:25915996-25915996,hs9:134650973-134650973;hs9:27814176-27814176,hs9:94491647-94491647;hs9:28074052-28074052,hs9:91251679-91251679;hs9:29265771-29265771,hs9:36951369-36951369;hs9:29268327-29268327,hs15:98633601-98633601;hs9:32322003-32322003,hs9:21984033-21984033;hs9:33519538-33519538,hs9:17733694-17733694;hs9:33520209-33520209,hs9:94381287-94381287;hs9:33808517-33808517,hs9:101171163-101171163;hs9:35191191-35191191,hs9:89719222-89719222;hs9:37579961-37579961,hs9:38356863-38356863;hs9:44091403-44091403,hs9:76284795-76284795;hs9:44109974-44109974,hs9:94341584-94341584;hs9:44115736-44115736,hs9:75845150-75845150;h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DM5;ADGB;TMEM108;CENPP;PCSK5;BICD1;KAZN;ABCA4;ATE1;SLCO1A2;ABCC9;METTL20;PARPBP;CENPJ;KLHL28;FAM179B;AKAP8;ZNF492;EXOC6B;KIF15;ZDHHC3;COA1;PDCD1LG2;TTC39B;CCDC171;UNC13B;PAX5;FBXO10;TMEM2;RORB;RMI1;FBP2;C9orf3;EPB41L4B;PALM2;SUSD1;RALGPS1;SWI5;TTF1;DDX31	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	KDM4C,RALGPS1;KDM4C,STRBP;CCDC171,ROR2;EPB41L4B,PTPRD;SUSD1,CDK5RAP2
CTDB0191	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	7	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_1712	Illumina HiSeq 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Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	TTYH3,SPTB;DFNA5,EPDR1;ORC5,MUC19
CTDB0192	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	8	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_3213	Illumina HiSeq 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Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	KBTBD11,SUSD2;MSRA,DLGAP2;MSRA,ENPP2;GATA4,DLC1;ENPP2,WDR67
CTDB0193	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	18	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_3845	Illumina HiSeq 2000		hs1:69113072-69113072,hs1:69115367-69115367;hs1:73878392-73878392,hs22:29065566-29065566;hs1:75772648-75772648,hs12:41847723-41847723;hs1:79201648-79201648,hs1:79577132-79577132;hs1:184124974-184124974,hs1:184124797-184124797;hs1:216516019-216516019,hs1:216507900-216507900;hs1:235864000-235864000,hs1:235867946-235867946;hs1:246528229-246528229,hs1:246494790-246494790;hs2:43453622-43453622,hs2:43686088-43686088;hs2:91765062-91765062,hs2:91764992-91764992;hs2:139624940-139624940,hs6:157962378-157962378;hs2:145871813-145871813,hs2:146066383-146066383;hs2:171881079-171881079,hs12:14939656-14939656;hs2:209027352-209027352,hs6:108332298-108332298;hs3:60387844-60387844,hs3:60553593-60553593;hs3:60460501-60460501,hs3:60504662-60504662;hs3:60460501-60460501,hs3:60504662-60504662;hs3:71446126-71446126,hs8:22717711-22717711;hs3:167454947-167454947,hs3:167652922-167652922;hs3:175291231-175291231,hs3:175291356-175291356;hs4:95648337-95648337,hs4:95649750-95649750;hs5:30025549-30025549,hs5:30049532-30049532;hs5:59116252-59116252,hs5:59142420-59142420;hs5:102455060-102455060,hs5:102454816-102454816;hs5:163186102-163186102,hs11:46316545-46316545;hs6:23049976-23049976,hs22:29065880-29065880;hs6:42443406-42443406,hs7:91739514-91739514;hs6:71278966-71278966,hs6:155438242-155438242;hs6:113920867-113920867,hs6:121385577-121385577;hs6:120155454-120155454,hs6:122135650-122135650;hs6:120155624-120155624,hs6:133850889-133850889;hs6:120255362-120255362,hs6:113921033-113921033;hs6:133850604-133850604,hs6:165277581-165277581;hs6:147898453-147898453,hs6:147838086-147838086;hs6:157967739-157967739,hs6:157968471-157968471;hs6:157967739-157967739,hs6:157968471-157968471;hs6:157967914-157967914,hsX:33491045-33491045;hs6:165277482-165277482,hs6:122135732-122135732;hs7:30139059-30139059,hs7:30155476-30155476;hs7:44962408-44962408,hs7:44962719-44962719;hs7:52656804-52656804,hsY:9429664-9429664;hs7:77888211-77888211,hs14:71210733-71210733;hs7:110296970-110296970,hs7:110624926-110624926;hs7:110505190-110505190,hs7:110565576-110565576;hs7:110667526-110667526,hs7:110665784-110665784;hs7:117668504-117668504,hs7:117679569-117679569;hs7:117668868-117668868,hs9:119588371-119588371;hs7:128129991-128129991,hs11:32388070-32388070;hs8:57496946-57496946,hs4:56491227-56491227;hs8:87104824-87104824,hs14:31147626-31147626;hs8:124476615-124476615,hs8:124503115-124503115;hs8:141167084-141167084,hs8:141167425-141167425;hs10:54478955-54478955,hs14:31146030-31146030;hs10:59467201-59467201,hs10:59467326-59467326;hs10:62762266-62762266,hs13:103179993-103179993;hs10:68755092-68755092,hs10:68866332-68866332;hs10:113223222-113223222,hs14:59220674-59220674;hs10:118031089-118031089,hs10:118033744-118033744;hs11:66305148-66305148,hs11:66305467-66305467;hs11:74100610-74100610,hs11:74102831-74102831;hs11:88446035-88446035,hs11:88450626-88450626;hs12:17585082-17585082,hs12:17587927-17587927;hs12:24387412-24387412,hs12:26493371-26493371;hs12:24387737-24387737,hs12:25457096-25457096;hs12:24429229-24429229,hs12:24470525-24470525;hs12:24470049-24470049,hs12:28179225-28179225;hs12:24767220-24767220,hs12:24769270-24769270;hs12:24773553-24773553,hs12:26373765-26373765;hs12:25313198-25313198,hs12:26294294-26294294;hs12:25338655-25338655,hs12:25996541-25996541;hs12:25441706-25441706,hs12:25443502-25443502;hs12:25456694-25456694,hs12:25548073-25548073;hs12:25457258-25457258,hs12:25339221-25339221;hs12:25478701-25478701,hs12:26381999-26381999;hs12:25498649-25498649,hs12:28154287-28154287;hs12:25534701-25534701,hs12:25536326-25536326;hs12:25534881-25534881,hs12:26929291-26929291;hs12:25535897-25535897,hs12:25534721-25534721;hs12:25547201-25547201,hs12:26356494-26356494;hs12:25547686-25547686,hs12:25548196-25548196;hs12:25911509-25911509,hs12:28333090-28333090;hs12:25937804-25937804,hs12:25945118-25945118;hs12:25945660-25945660,hs12:28333288-28333288;hs12:26356649-26356649,hs12:26524788-26524788;hs12:26357435-26357435,hs12:24387409-24387409;hs12:26929480-26929480,hs12:25535892-25535892;hs12:28330336-28330336,hs12:25945117-25945117;hs12:28332768-28332768,hs12:28333081-28333081;hs12:29079890-29079890,hs12:29048414-29048414;hs12:29107111-29107111,hs12:29107265-29107265;hs12:29107119-29107119,hs12:29109488-29109488;hs12:83684206-83684206,hs12:83705809-83705809;hs12:99999903-99999903,hs12:100685315-100685315;hs13:89183158-89183158,hs14:31147883-31147883;hs13:89183164-89183164,hs14:31147565-31147565;hs14:31150728-31150728,hs14:86515632-86515632;hs14:71211086-71211086,hs7:77888197-77888197;hs15:100349144-100349144,hs15:100349234-100349234;hs16:10858717-10858717,hs16:10858555-10858555;hs16:73018393-73018393,hs16:73085774-73085774;hs16:78541610-78541610,hs16:78842929-78842929;hs16:78628492-78628492,hs16:78678496-78678496;hs16:78688258-78688258,hs16:78729961-78729961;hs16:78737379-78737379,hs16:78782211-78782211;hs18:626936-626936,hsX:150454645-150454645;hs18:1500899-1500899,hs18:10239106-10239106;hs18:8563290-8563290,hs18:42442098-42442098;hs18:9608759-9608759,hs18:9608843-9608843;hs18:10916543-10916543,hs18:42800744-42800744;hs18:13967775-13967775,hs18:44880221-44880221;hs18:14379781-14379781,hs18:28298422-28298422;hs18:18842407-18842407,hs18:53004169-53004169;hs18:22335340-22335340,hs18:43003627-43003627;hs18:22336064-22336064,hs18:42442244-42442244;hs18:24012368-24012368,hs18:53163074-53163074;hs18:34340072-34340072,hs18:18842123-18842123;hs18:44396866-44396866,hs18:18842194-18842194;hs18:53004345-53004345,hs18:53163072-53163072;hs18:53162699-53162699,hs18:53207622-53207622;hs18:53375819-53375819,hs18:43003626-43003626;hs18:53375821-53375821,hs18:22335232-22335232;hs20:52451641-52451641,hs20:52451124-52451124;hs21:22021973-22021973,hs14:59220583-59220583;hs21:36257690-36257690,hs21:36252702-36252702;hs21:36258998-36258998,hs21:36316326-36316326;hsX:79944913-79944913,hsX:79877371-79877371	WWOX;FHIT;SSPN;ZDHHC14;TCF4;IMMP2L;CCDC91;SCFD1;ITPR2;RUNX1;CASC1;GREB1L;SLC14A2;TTC28;SMYD3;NAALADL2;CTNNA3;PDE4D;THADA;MAP3K9;SAMD5;MAGI2;ZFHX3;TRAPPC9;PLEKHA8;LYST;USH2A;ZDHHC24;PGM2L1;GRM5;CTD-2054N24.2;NUBP1;PPP4R1;SETBP1;GIN1;EYA4;LRRTM3;ANKS1B;TIAM2;NMU;CREB3L1;PDZRN4;FHOD3;PIEZO2;ASTN2;FOXP1;SLC44A5;GFRA1;WBP11;SCYL2;CLUL1;PIAS2;ZFP36L2;TLK1;CRYGA;SERPINI1;C6orf57;AKAP9;METTL2B;PEBP4;ATP6V0D2;BRWD3	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	FHOD3,GREB1L
CTDB0194	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	10	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0023	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0195	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	8	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0031	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0196	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	10	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0052	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0197	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	11	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0053	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0198	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	1	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0008	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0199	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	9	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0010	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0200	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	8	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0015	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0201	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	5	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0021	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0202	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	6	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_40325	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0203	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	5	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_40328	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0204	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	8	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_40357	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0205	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	22	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_40336	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0206	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	16	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6003	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0207	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	10	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_40364	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0208	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	7	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_40365	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0209	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	18	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0001	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0210	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	8	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0056	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0211	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	3	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0061	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0212	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	9	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0063	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0213	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	10	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_0572	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0214	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	6	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_1642	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0215	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	9	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_2442	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0216	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	8	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_3519	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0217	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	9	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6005	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0218	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	14	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6036	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0219	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	12	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6039	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0220	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	18	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6040	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0221	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	1	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6052	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0222	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	5	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6081	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0223	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	1	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6082	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0224	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	2	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6087	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0225	Research	25351503	Nones K, Waddell N, Wayte N, Patch AM, Bailey P, Newell F, Holmes O, Fink JL, Quinn MC, Tang YH, Lampe G, Quek K, Loffler KA, Manning S, Idrisoglu S, Miller D, Xu Q, Waddell N, Wilson PJ, Bruxner TJ, Christ AN, Harliwong I, Nourse C, Nourbakhsh E, Anderso	Genomic catastrophes frequently arise in esophageal adenocarcinoma and drive tumorigenesis.	Nat Commun	2014 Oct	1	Esophageal adenocarcinoma	Next Generation Sequencing	Homo sapiens	OESO_6091	Illumina BeadChip				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Oesophageal adenocarcinoma (EAC) incidence is rapidly increasing in Western countries. A better understanding of EAC underpins efforts to improve early detection and treatment outcomes. While large EAC exome sequencing efforts to date have found recurrent loss-of-function mutations, oncogenic driving events have been underrepresented. Here we use a combination of whole-genome sequencing (WGS) and single-nucleotide polymorphism-array profiling to show that genomic catastrophes are frequent in EAC, with almost a third (32%, n=40/123) undergoing chromothriptic events. WGS of 22 EAC cases show that catastrophes may lead to oncogene amplification through chromothripsis-derived double-minute chromosome formation (MYC and MDM2) or breakage-fusion-bridge (KRAS, MDM2 and RFC3). Telomere shortening is more prominent in EACs bearing localized complex rearrangements. Mutational signature analysis also confirms that extreme genomic instability in EAC can be driven by somatic BRCA2 mutations. These findings suggest that genomic catastrophes have a significant role in the malignant transformation of EAC.	GRCh37/hg19			EGAS00001000750	Yes	NA
CTDB0226	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	1	Glioblastoma	Next Generation Sequencing	Homo sapiens	GBM_3_T	Illumina paired-end sequencing	chr1:1473900-1483900:-1;chr1:16337864-16347864:1;chr1:31188956-31198956:-1;chr1:31406425-31416425:1;chr1:43875362-43885362:-1;chr1:43910380-43920380:1;chr1:47724126-47734126:1;chr1:47833374-47843374:-1;chr1:68864547-68874547:-1;chr1:69203040-69213040:1;chr1:115424482-115434482:1;chr1:152583725-152593725:-1;chr1:202564758-202574758:1;chr1:209875072-209885072:1;chr1:222848998-222858998:-1;chr1:222869277-222879277:-1;chr2:124605911-124615911:1;chr2:239782842-239792842:-1;chr3:66288911-66298911:-1;chr4:49222803-49232803:1;chr4:59792957-59802957:-1;chr4:167586041-167596041:-1;chr5:469679-479679:1;chr5:143961445-143971445:1;chr6:17684703-17694703:1;chr6:63598668-63608668:-1;chr6:87836217-87846217:1;chr6:87903230-87913230:-1;chr6:119213764-119223764:-1;chr6:148704461-148714461:1;chr6:157709391-157719391:-1;chr7:20871764-20881764:-1;chr7:45342151-45352151:1;chr7:54442601-54452601:-1;chr7:55364942-55374942:1;chr7:64008939-64018939:1;chr7:74119690-74129690:-1;chr7:89691813-89701813:1;chr7:98889464-98899464:-1;chr7:99049088-99059088:1;chr7:155117625-155127625:-1;chr8:537803-547803:-1;chr8:124059516-124069516:-1;chr8:144031199-144041199:-1;chr9:33497840-33507840:1;chr9:33828151-33838151:-1;chr9:88059120-88069120:1;chr12:155502-165502:-1;chr12:58012428-58022428:1;chr12:58124857-58134857:-1;chr12:58165193-58175193:1;chr12:58293239-58303239:-1;chr12:59585626-59595626:1;chr12:60070221-60080221:-1;chr12:60240803-60250803:1;chr12:60312049-60322049:-1;chr12:60896441-60906441:1;chr12:61189444-61199444:-1;chr12:61528736-61538736:1;chr12:62372141-62382141:-1;chr12:62397311-62407311:1;chr12:62454499-62464499:-1;chr12:62540747-62550747:-1;chr12:62556039-62566039:1;chr12:62586105-62596105:1;chr12:62606297-62616297:1;chr12:63092161-63102161:-1;chr12:63193292-63203292:1;chr12:64501633-64511633:-1;chr12:64703554-64713554:1;chr12:65518347-65528347:-1;chr12:65548635-65558635:1;chr12:65593703-65603703:-1;chr12:65628803-65638803:1;chr12:66252334-66262334:-1;chr12:66282585-66292585:1;chr12:67222929-67232929:-1;chr12:67374611-67384611:1;chr12:68503822-68513822:-1;chr12:68538847-68548847:1;chr12:69109888-69119888:-1;chr12:69135193-69145193:-1;chr12:69262332-69272332:1;chr12:69629710-69639710:-1;chr12:69664804-69674804:1;chr12:69753079-69763079:-1;chr12:70038769-70048769:1;chr12:70571382-70581382:-1;chr12:70671527-70681527:1;chr12:71402327-71412327:-1;chr12:71608784-71618784:1;chr12:73090452-73100452:1;chr12:73591943-73601943:-1;chr12:74657443-74667443:1;chr12:74770975-74780975:-1;chr12:76372914-76382914:1;chr12:79055800-79065800:1;chr12:80167827-80177827:-1;chr12:80223100-80233100:1;chr12:80345783-80355783:-1;chr12:81462149-81472149:-1;chr12:82694720-82704720:1;chr12:83581735-83591735:1;chr12:83868047-83878047:-1;chr12:84779568-84789568:1;chr12:85123639-85133639:-1;chr12:122584226-122594226:-1;chr12:124445485-124455485:1;chr12:124536239-124546239:-1;chr13:58210070-58220070:-1;chr13:58422511-58432511:1;chr13:114448806-114458806:-1;chr14:19450369-19460369:-1;chr14:19479572-19489572:1;chr14:77379686-77389686:-1;chr14:77793984-77803984:1;chr14:87492583-87502583:1;chr14:106064937-106074937:1;chr16:628413-638413:-1;chr16:53450723-53460723:-1;chr17:20654872-20664872:-1;chr17:41101455-41111455:-1;chr17:41117231-41127231:-1;chr17:73137170-73147170:-1;chr17:73305559-73315559:1;chr17:73490192-73500192:1;chr19:15352967-15362967:-1;chr19:22633246-22643246:-1;chr19:22693818-22703818:1;chr19:39654171-39664171:1;chr19:42001729-42011729:1;chr19:44917853-44927853:-1;chr19:45563362-45573362:1;chr19:54090926-54100926:-1;chr20:29543855-29553855:-1;chr20:34954187-34964187:-1;chr20:60495841-60505841:1;chr21:10637520-10647520:-1;chr22:17229291-17239291:-1;chr22:20191610-20201610:-1;chr22:22729659-22739659:1;chr22:22761513-22771513:-1;chr22:23613231-23623231:1;chr22:24092290-24102290:1;chr22:24154290-24164290:-1;chr22:24522084-24532084:-1;chr22:26276205-26286205:1;chr22:50776853-50786853:-1;chrX:129043680-129053680:-1;chrX:129100675-129110675:1;chrY:9896479-9906479:-1	hs1:31195314-31195486,hs1:31409176-31409467;hs1:68848516-68848729,hs1:69012083-69012312;hs1:209878533-209878812,hs1:211252936-211253159;hs1:209879248-209879475,hs1:211279556-211279907;hs1:210967918-210968127,hs1:211278665-211278930;hs1:210968042-210968182,hs1:218774393-218774514;hs1:210968056-210968193,hs1:222857715-222857949;hs1:210968255-210968506,hs1:218778799-218779082;hs1:211253088-211253356,hs1:218778997-218779285;hs1:211253245-211253413,hs1:218779174-218779372;hs1:211277937-211278053,hs1:218774395-218774531;hs1:211279261-211279507,hs1:222862505-222862786;hs1:211279875-211279985,hs1:218779009-218779148;hs1:218774393-218774516,hs1:218779139-218779349;hs7:32396769-32397029,hs7:32406271-32406481;hs7:46160967-46161151,hs7:51162404-51162650;hs7:51080387-51080715,hs7:54949871-54950175;hs7:54510018-54510254,hs7:54524204-54524390;hs7:54671300-54671479,hs7:55352155-55352347;hs7:54896110-54896364,hs7:55775806-55776051;hs7:54910860-54911054,hs7:54919401-54919573;hs7:55110821-55110968,hs7:55111740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of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0227	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	1,6	Glioblastoma	Next Generation Sequencing	Homo sapiens	GBM_6_T	Illumina paired-end 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of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0228	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	3	Glioblastoma	Next Generation Sequencing	Homo sapiens	GBM_8_T	Illumina paired-end 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of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0229	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	9,12,21	Glioblastoma	Next Generation Sequencing	Homo sapiens	GBM_9_T	Illumina paired-end sequencing	chr1:147783685-147793685:1;chr1:180189188-180199188:1;chr1:180204188-180214188:-1;chr2:132978550-132988550:-1;chr2:143154687-143164687:1;chr2:146874558-146884558:-1;chr2:239782842-239792842:-1;chr2:240820510-240830510:-1;chr3:13753079-13763079:1;chr3:13774319-13784319:-1;chr3:38635682-38645682:-1;chr3:38690804-38700804:1;chr3:111865461-111875461:1;chr3:111956240-111966240:-1;chr3:113454964-113464964:1;chr3:113608707-113618707:-1;chr3:188256512-188266512:1;chr3:188387084-188397084:-1;chr3:193129316-193139316:1;chr3:193150909-193160909:-1;chr3:193845764-193855764:1;chr3:193866021-193876021:-1;chr4:3433221-3443221:1;chr4:20386821-20396821:1;chr4:20577907-20587907:-1;chr4:23821860-23831860:1;chr4:24022577-24032577:-1;chr4:24274237-24284237:1;chr4:24455515-24465515:-1;chr4:59792957-59802957:-1;chr4:78083375-78093375:-1;chr4:167586041-167596041:-1;chr5:663946-673946:1;chr5:97579286-97589286:-1;chr5:151344936-151354936:1;chr5:171340862-171350862:1;chr5:171367104-171377104:-1;chr6:266754-276754:-1;chr6:13848308-13858308:1;chr6:13879758-13889758:-1;chr6:119213764-119223764:-1;chr6:157709391-157719391:-1;chr6:167934630-167944630:-1;chr7:1334772-1344772:-1;chr7:1462411-1472411:1;chr7:1542934-1552934:-1;chr7:1563387-1573387:1;chr7:1598617-1608617:-1;chr7:1915807-1925807:-1;chr7:5232273-5242273:-1;chr7:5654010-5664010:-1;chr7:7043160-7053160:-1;chr7:44410109-44420109:-1;chr7:44440157-44450157:1;chr7:55964053-55974053:-1;chr7:66317948-66327948:-1;chr7:89691813-89701813:1;chr7:97823042-97833042:1;chr7:97858288-97868288:-1;chr7:104933970-104943970:1;chr7:127755670-127765670:1;chr7:127776296-127786296:-1;chr7:155117625-155127625:-1;chr8:144031199-144041199:-1;chr9:21267120-21277120:1;chr9:21288295-21298295:-1;chr9:21389078-21399078:1;chr9:21640555-21650555:1;chr9:22051826-22061826:-1;chr9:22225109-22235109:-1;chr9:22514593-22524593:1;chr9:22584037-22594037:-1;chr9:22609332-22619332:1;chr9:23294659-23304659:-1;chr9:23376222-23386222:1;chr9:23420485-23430485:-1;chr9:23653442-23663442:1;chr9:24229330-24239330:-1;chr9:25468995-25478995:1;chr9:25980154-25990154:-1;chr9:27294915-27304915:1;chr9:27341810-27351810:-1;chr9:108460003-108470003:1;chr9:139137092-139147092:1;chr9:139273468-139283468:-1;chr9:139385702-139395702:1;chr9:139426023-139436023:-1;chr11:3626990-3636990:-1;chr11:79741982-79751982:1;chr11:80564250-80574250:-1;chr11:89850991-89860991:-1;chr12:155502-165502:-1;chr12:20888039-20898039:1;chr12:67547097-67557097:-1;chr12:67807034-67817034:1;chr12:68159573-68169573:1;chr12:68473740-68483740:1;chr12:68745818-68755818:-1;chr12:68791645-68801645:1;chr12:69022852-69032852:-1;chr12:69079600-69089600:1;chr12:69181023-69191023:-1;chr12:69339318-69349318:1;chr12:69477463-69487463:-1;chr12:69599204-69609204:1;chr12:69669934-69679934:-1;chr12:69732547-69742547:1;chr12:114543222-114553222:-1;chr12:122584226-122594226:-1;chr13:114448806-114458806:-1;chr14:80505462-80515462:-1;chr14:84987295-84997295:-1;chr14:92483798-92493798:1;chr14:92510498-92520498:-1;chr14:105594882-105604882:1;chr15:73616132-73626132:-1;chr15:73651137-73661137:1;chr16:628413-638413:-1;chr16:1469260-1479260:1;chr16:1504869-1514869:-1;chr16:26402273-26412273:1;chr17:472976-482976:-1;chr17:483565-493565:1;chr17:80178649-80188649:1;chr17:80193818-80203818:-1;chr21:10637520-10647520:-1;chr22:44723940-44733940:-1;chr22:44743983-44753983:1;chr22:50175693-50185693:-1;chr22:50689936-50699936:1;chrY:9458259-9468259:1;chrY:9519351-9529351:-1;chrY:9644399-9654399:1	hs3:188257651-188257872,hs3:188393998-188394263;hs4:20389666-20389915,hs4:23824005-23824238;hs4:20582784-20583075,hs4:24459108-24459408;hs4:23528245-23528479,hs4:24279174-24279434;hs4:45340767-45340893,hs4:45567554-45567714;hs9:21275793-21275978,hs9:21644900-21645126;hs9:21292849-21293090,hs9:21494754-21495052;hs9:21393744-21393945,hs9:22057421-22057582;hs9:21485781-21486028,hs9:24314378-24314587;hs9:22230593-22230829,hs9:26105667-26105879;hs9:22460985-22461161,hs9:23423524-23423701;hs9:22462340-22462588,hs9:26954266-26954522;hs9:22516924-22517199,hs9:23383739-23384043;hs9:22611758-22611912,hs9:27301103-27301397;hs9:23572510-23572693,hs9:27411818-27412026;hs9:23572685-23572972,hs9:25550536-25550790;hs9:23658644-23658896,hs9:26118209-26118481;hs9:24232873-24233163,hs9:24656454-24656648;hs9:25471276-25471476,hs9:26057747-26057967;hs9:25549461-25549754,hs9:26735608-26735925;hs9:25983638-25983905,hs9:26119534-26119803;hs9:26058018-26058296,hs9:26546235-26546544;hs9:26106062-26106316,hs9:27348591-27348870;hs9:26549731-26550006,hs9:26742169-26742450;hs9:26704088-26704315,hs9:27413097-27413379;hs9:26705270-26705446,hs9:26959147-26959316;hs10:89526875-89527113,hs10:90662939-90663209;hs10:89628629-89628761,hs10:90697124-90697357;hs11:79747979-79748169,hs11:79769455-79769741;hs11:79772925-79773148,hs11:80570256-80570495;hs12:67550990-67551263,hs12:67877738-67877977;hs12:67586171-67586318,hs12:69189604-69189753;hs12:67601117-67601325,hs12:68408414-68408594;hs12:67601574-67601733,hs12:67790335-67790607;hs12:67620791-67621052,hs12:67782857-67783102;hs12:67630723-67630908,hs12:69513392-69513624;hs12:67633794-67634016,hs12:69218807-69218945;hs12:67680661-67680816,hs12:69588085-69588293;hs12:67690990-67691105,hs12:68774263-68774405;hs12:67691290-67691413,hs12:68781029-68781261;hs12:67705427-67705714,hs12:68076102-68076361;hs12:67730375-67730641,hs12:68771687-68771892;hs12:67739086-67739350,hs12:69267882-69268144;hs12:67764125-67764364,hs12:69291025-69291249;hs12:67782148-67782256,hs12:68750123-68750252;hs12:67787062-67787225,hs12:69779423-69779688;hs12:67788218-67788364,hs12:68394711-68394935;hs12:67956652-67956907,hs12:69778843-69779122;hs12:68074161-68074364,hs12:69293273-69293418;hs12:68114110-68114332,hs12:68125971-68126169;hs12:68364318-68364562,hs12:69737286-69737549;hs12:68397680-68397973,hs12:69518660-69518966;hs12:68400670-68400971,hs12:68468351-68468677;hs12:68400898-68401112,hs12:69247552-69247812;hs12:68405621-68405799,hs12:69274676-69274874;hs12:68411735-68411984,hs12:69588135-69588263;hs12:68414244-68414440,hs12:68786506-68786728;hs12:68414563-68414803,hs12:68431646-68431908;hs12:68414760-68414987,hs12:69589338-69589552;hs12:68419265-68419506,hs12:69284604-69284849;hs12:68446249-68446568,hs12:69294591-69294882;hs12:68447716-68448000,hs12:69293815-69294086;hs12:68452281-68452432,hs12:69574094-69574243;hs12:68787746-68788007,hs12:69557978-69558272;hs12:69034926-69035197,hs12:69557216-69557454;hs12:69077159-69077342,hs12:69242488-69242711;hs12:69186676-69187000,hs9:136844617-136844732;hs12:69189483-69189766,hs12:69562670-69562954;hs12:69310382-69310538,hs12:69325596-69325773;hs12:69532552-69532772,hs12:69694024-69694330;hs12:79278843-79279073,hs12:79279848-79280124;hs15:25355938-25356084,hs15:68741305-68741554;hs15:26166197-26166406,hs15:99358093-99358295;hs18:6746356-6746525,hs18:9355191-9355390;hs18:24963417-24963617,hs18:24964937-24965169;hs18:25735752-25736007,hs18:27396635-27396835		Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0230	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	7,20	Glioblastoma	Next Generation Sequencing	Homo sapiens	GBM_10_T	Illumina paired-end sequencing	chr1:15463796-15473796:-1;chr1:16087782-16097782:1;chr1:37565238-37575238:-1;chr1:37951289-37961289:1;chr1:38013271-38023271:-1;chr1:38144498-38154498:1;chr1:104088495-104098495:-1;chr1:115439999-115449999:1;chr1:120102462-120112462:1;chr2:5159707-5169707:-1;chr2:75420018-75430018:1;chr2:75494525-75504525:-1;chr2:89128108-89138108:-1;chr2:239782842-239792842:-1;chr2:240820510-240830510:-1;chr3:195752783-195762783:-1;chr4:28449053-28459053:1;chr4:28757412-28767412:-1;chr4:49634410-49644410:-1;chr4:59792957-59802957:-1;chr4:81922393-81932393:1;chr4:82180675-82190675:-1;chr4:105401709-105411709:1;chr4:106611187-106621187:-1;chr4:107480514-107490514:-1;chr4:107496455-107506455:1;chr4:113699460-113709460:1;chr4:114752477-114762477:-1;chr4:167586041-167596041:-1;chr4:179382464-179392464:1;chr4:180112836-180122836:-1;chr4:190184009-190194009:-1;chr4:190194203-190204203:1;chr5:71130528-71140528:-1;chr5:97579286-97589286:-1;chr5:104502308-104512308:1;chr5:104537169-104547169:-1;chr5:134250526-134260526:-1;chr5:134261166-134271166:1;chr5:164958018-164968018:1;chr5:164978148-164988148:-1;chr5:165018420-165028420:1;chr5:166494607-166504607:-1;chr5:166839906-166849906:1;chr5:174898085-174908085:1;chr5:174923556-174933556:-1;chr5:178920131-178930131:1;chr5:178955446-178965446:-1;chr6:119213764-119223764:-1;chr6:167934630-167944630:-1;chr7:54772075-54782075:-1;chr7:55308258-55318258:1;chr7:64057937-64067937:-1;chr7:151490490-151500490:-1;chr7:151596629-151606629:1;chr7:151713609-151723609:1;chr7:154749730-154759730:1;chr7:155117625-155127625:-1;chr7:155404970-155414970:-1;chr7:155470863-155480863:1;chr7:155579518-155589518:-1;chr8:144031199-144041199:-1;chr9:18353170-18363170:1;chr9:21122146-21132146:1;chr9:24488040-24498040:-1;chr9:27208016-27218016:-1;chr11:15601337-15611337:-1;chr11:16333209-16343209:1;chr11:48956302-48966302:1;chr12:155502-165502:-1;chr12:2812474-2822474:-1;chr12:12372496-12382496:1;chr12:12526446-12536446:-1;chr12:38173235-38183235:1;chr12:81462149-81472149:-1;chr12:108398305-108408305:1;chr12:122584226-122594226:-1;chr13:66913552-66923552:-1;chr13:114448806-114458806:-1;chr14:20541384-20551384:1;chr14:20553240-20563240:-1;chr16:28479802-28489802:-1;chr16:87948522-87958522:-1;chr19:2126613-2136613:-1;chr19:2579171-2589171:1;chr19:15433639-15443639:1;chr19:15443866-15453866:-1;chr20:7483369-7493369:1;chr20:7849854-7859854:-1;chr20:10000146-10010146:1;chr20:10020725-10030725:-1;chr20:10147968-10157968:1;chr20:10527557-10537557:-1;chr20:14430451-14440451:1;chr20:14450088-14460088:-1;chr20:34954187-34964187:-1;chr20:52816363-52826363:-1;chr21:10637520-10647520:-1;chr22:50776853-50786853:-1;chrX:118644507-118654507:-1;chrX:118654877-118664877:1;chrX:127369756-127379756:-1;chrY:15994871-16004871:1;chrY:16079200-16089200:-1;chrY:23647227-23657227:1;chrY:23748666-23758666:-1;chrY:28457355-28467355:-1;chrY:77458284-77468284:-1	hs1:15471020-15471135,hs20:52823000-52823146;hs1:45566619-45566844,hs6:87238326-87238396;hs1:56801753-56801811,hs16:85156219-85156265;hs1:120221247-120221318,hs2:130906766-130906987;hs4:17393815-17394078,hsX:53237945-53238014;hs4:28761499-28761685,hs4:28797388-28797553;hs4:82051015-82051178,hs4:82182814-82182916;hs4:82063773-82063874,hs4:105404940-105405052;hs4:82096701-82096790,hs4:105404954-105405056;hs4:113707566-113707748,hs4:114757573-114757813;hs4:180108938-180109021,hs4:180113837-180114112;hs5:164905564-164905677,hs5:165022361-165022460;hs5:174902726-174902991,hs5:174928546-174928773;hs6:68909698-68909748,hs9:101560727-101560796;hs7:41008361-41008558,hs7:41009008-41009259;hs7:54776605-54776814,hs7:55314446-55314690;hs7:54802834-54802958,hs7:55075327-55075473;hs7:54835064-54835185,hs7:54862014-54862229;hs7:54874826-54875049,hs7:54882410-54882525;hs7:54888182-54888360,hs7:55278805-55279035;hs7:54911240-54911344,hs7:54915760-54915933;hs7:54927349-54927607,hs7:55076010-55076285;hs7:54968445-54968692,hs7:55240950-55241203;hs7:54968766-54968943,hs7:55241304-55241534;hs7:54971109-54971231,hs7:55070613-55070733;hs7:55011430-55011535,hs7:55019742-55019868;hs7:55036491-55036712,hs7:55103207-55103452;hs7:55102899-55103026,hs7:55223218-55223379;hs7:55194031-55194157,hs7:55222048-55222265;hs7:55209570-55209838,hs7:55223464-55223748;hs7:150314480-150314640,hs7:151582417-151582645;hs7:150420079-150420204,hs7:151434716-151434963;hs7:151439895-151440011,hs7:151601368-151601505;hs7:151495821-151496048,hs7:151603027-151603232;hs7:151577493-151577733,hs7:151594688-151594941;hs7:151584022-151584253,hs7:151601720-151601819;hs7:154751221-154751402,hs7:155128712-155128948;hs7:154783139-154783323,hs7:154807210-154807463;hs7:154805745-154805877,hs7:155580617-155580776;hs7:154806472-154806663,hs7:155412342-155412456;hs7:155094402-155094626,hs7:155411165-155411394;hs7:155412336-155412406,hs7:155481146-155481221;hs8:77957237-77957297,hs8:78003437-78003497;hs9:18358406-18358592,hs9:27213453-27213608;hs9:21130169-21130357,hs9:24494259-24494429;hs9:24584121-24584290,hs9:24590638-24590843;hs12:25718373-25718423,hs12:25749632-25749867;hs16:20940071-20940122,hs6:29853122-29853216;hs18:14387933-14387999,hs2:86282474-86282699;hs18:74793571-74793644,hs6:142519220-142519279;hs19:2132304-2132497,hs19:2602419-2602665;hs19:19924778-19924833,hs19:20466062-20466165;hs20:7485256-7485480,hs7:151603232-151603409;hs20:7485294-7485483,hs20:7568756-7568831;hs20:7485307-7485519,hs20:7858926-7859088;hs20:7567604-7567816,hs7:151602268-151602441;hs20:7858552-7858801,hs7:151603149-151603394;hs20:7859740-7859930,hs7:151603494-151603632;hs20:10023614-10023851,hs20:10538626-10538877;hs20:10533315-10533448,hs7:151439697-151439817;hs20:10539191-10539393,hs7:151598544-151598720		Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0231	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	1	Glioblastoma	Next Generation Sequencing	Homo sapiens	GBM_13_T	Illumina paired-end sequencing	chr1:1473900-1483900:-1;chr1:1551635-1561635:1;chr1:3449021-3459021:-1;chr1:3550481-3560481:1;chr1:5100041-5110041:1;chr1:5119899-5129899:-1;chr1:6305284-6315284:-1;chr1:6392746-6402746:1;chr1:6643789-6653789:1;chr1:6684084-6694084:-1;chr1:7510842-7520842:1;chr1:7808228-7818228:1;chr1:7823416-7833416:-1;chr1:7940209-7950209:1;chr1:8404605-8414605:-1;chr1:8659571-8669571:1;chr1:8776326-8786326:-1;chr1:29104029-29114029:1;chr1:29164947-29174947:-1;chr1:29533361-29543361:1;chr1:31320068-31330068:-1;chr1:32889919-32899919:1;chr1:32913996-32923996:-1;chr1:35689182-35699182:1;chr1:35913488-35923488:-1;chr1:35964642-35974642:1;chr1:36015190-36025190:-1;chr1:36035190-36045190:1;chr1:36738433-36748433:-1;chr1:104078440-104088440:-1;chr1:104302999-104312999:-1;chr2:110251448-110261448:-1;chr2:133112726-133122726:1;chr2:239782842-239792842:-1;chr2:240820510-240830510:-1;chr3:26418714-26428714:1;chr3:26440642-26450642:-1;chr3:75633940-75643940:-1;chr4:32843693-32853693:-1;chr4:59792957-59802957:-1;chr4:167586041-167596041:-1;chr5:71130528-71140528:-1;chr5:97579286-97589286:-1;chr6:119208764-119218764:-1;chr6:121356779-121366779:1;chr6:121368492-121378492:-1;chr6:157709391-157719391:-1;chr6:167934630-167944630:-1;chr7:1462411-1472411:1;chr7:1598617-1608617:-1;chr7:5795557-5805557:1;chr7:17311561-17321561:-1;chr7:17381954-17391954:1;chr7:24632043-24642043:-1;chr7:24708535-24718535:1;chr7:37681722-37691722:1;chr7:37829380-37839380:-1;chr7:44101536-44111536:-1;chr7:44259616-44269616:1;chr7:44279616-44289616:-1;chr7:46277990-46287990:1;chr7:46538429-46548429:-1;chr7:46835589-46845589:1;chr7:46860185-46870185:-1;chr7:47338918-47348918:-1;chr7:48229521-48239521:-1;chr7:48240125-48250125:-1;chr7:54720253-54730253:-1;chr7:55470927-55480927:1;chr7:58026538-58036538:1;chr7:63420797-63430797:-1;chr7:82371999-82381999:-1;chr7:87480469-87490469:1;chr7:97676376-97686376:-1;chr7:105245683-105255683:-1;chr7:107104811-107114811:-1;chr7:107124869-107134869:1;chr7:108966633-108976633:-1;chr7:109154192-109164192:1;chr7:109716189-109726189:1;chr7:116966422-116976422:-1;chr7:117057200-117067200:1;chr7:117154148-117164148:-1;chr7:117279506-117289506:1;chr7:117979873-117989873:-1;chr7:120212430-120222430:1;chr7:124971074-124981074:-1;chr7:125563328-125573328:-1;chr7:125908056-125918056:1;chr7:134718723-134728723:-1;chr7:134744068-134754068:1;chr7:142181863-142191863:-1;chr7:148721779-148731779:1;chr7:148939448-148949448:-1;chr7:149462471-149472471:1;chr7:149522848-149532848:-1;chr7:155117625-155127625:-1;chr8:16279220-16289220:1;chr8:32686630-32696630:-1;chr8:118188271-118198271:1;chr8:118228745-118238745:-1;chr8:144031199-144041199:-1;chr9:5038685-5048685:1;chr9:5079758-5089758:-1;chr9:5924441-5934441:1;chr9:5962458-5972458:-1;chr9:8961291-8971291:1;chr9:12713364-12723364:-1;chr9:13137514-13147514:1;chr9:13242749-13252749:-1;chr9:14603432-14613432:1;chr9:14681933-14691933:-1;chr9:15615226-15625226:1;chr9:15975329-15985329:-1;chr9:19505692-19515692:1;chr9:22412620-22422620:1;chr9:23400330-23410330:-1;chr9:23531978-23541978:-1;chr9:24395430-24405430:1;chr9:25660339-25670339:-1;chr9:28445744-28455744:1;chr9:31454589-31464589:-1;chr9:136110676-136120676:-1;chr10:31573788-31583788:1;chr10:31790278-31800278:-1;chr10:32088852-32098852:1;chr10:32139068-32149068:-1;chr10:37410938-37420938:1;chr10:37528393-37538393:-1;chr10:37611471-37621471:1;chr10:37657405-37667405:-1;chr11:49521210-49531210:1;chr11:49712975-49722975:-1;chr12:155502-165502:-1;chr12:10553933-10563933:1;chr12:52911054-52921054:-1;chr12:52941275-52951275:1;chr12:122584226-122594226:-1;chr13:41967871-41977871:1;chr13:114448806-114458806:-1;chr15:102423383-102433383:1;chr16:52187648-52197648:-1;chr18:14776372-14786372:1;chr18:14899878-14909878:-1;chr18:40587348-40597348:-1;chr19:1292451-1302451:-1;chr19:11800006-11810006:1;chr19:22325082-22335082:1;chr20:29543855-29553855:-1;chr20:31265235-31275235:1;chr20:58413300-58423300:-1;chr20:58501073-58511073:1;chr20:60874673-60884673:1;chr21:9523596-9533596:-1;chr21:9998622-10008622:1;chr21:10637520-10647520:-1;chr21:11048456-11058456:-1;chr21:11135793-11145793:1;chr22:42018682-42028682:1;chrX:115145778-115155778:-1;chrY:7983379-7993379:-1;chrY:19369648-19379648:1;chrY:19400376-19410376:-1	hs1:3454237-3454412,hs1:8511349-8511599;hs1:6303332-6303446,hs1:8662465-8662702;hs1:6396205-6396311,hs1:8689355-8689488;hs1:7515413-7515532,hs1:8683090-8683238;hs1:7517175-7517317,hs1:8781980-8782132;hs1:7813832-7814013,hs1:8504093-8504366;hs1:8662134-8662267,hs1:8700311-8700464;hs1:8662450-8662595,hs1:8700382-8700601;hs1:8663190-8663299,hs1:8708867-8709022;hs1:8663761-8663882,hs1:35971087-35971297;hs1:8664123-8664237,hs1:29579822-29579944;hs1:8699913-8700065,hs1:35940156-35940291;hs1:29170571-29170685,hs1:35969711-35969815;hs1:29535725-29535945,hs1:36867509-36867730;hs1:31804836-31804997,hs1:36742016-36742126;hs1:31808516-31808702,hs1:35920291-35920469;hs1:31867117-31867365,hs1:36741388-36741637;hs3:47233651-47233938,hs3:47257174-47257381;hs7:375899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of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0232	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	2,3,9,10	Glioblastoma	Next Generation Sequencing	Homo sapiens	GBM_16_T	Illumina paired-end sequencing	chr1:2354953-2364953:1;chr1:2488566-2498566:-1;chr1:3373066-3383066:1;chr1:3525417-3535417:-1;chr1:8756113-8766113:-1;chr1:9155983-9165983:1;chr1:26060504-26070504:-1;chr1:26080609-26090609:1;chr1:37827296-37837296:1;chr1:37845289-37855289:-1;chr1:53128976-53138976:-1;chr1:53553994-53563994:1;chr1:104088495-104098495:-1;chr1:113372689-113382689:-1;chr1:191020292-191030292:1;chr1:191089707-191099707:-1;chr1:199315848-199325848:1;chr1:199424289-199434289:-1;chr1:204255393-204265393:-1;chr1:204564030-204574030:1;chr1:204971336-204981336:1;chr1:205067107-205077107:-1;chr1:205174084-205184084:-1;chr1:205447688-205457688:1;chr1:241741270-241751270:-1;chr2:97851959-97861959:-1;chr2:110251448-110261448:-1;chr2:212877226-212887226:1;chr2:239002055-239012055:1;chr2:239067730-239077730:-1;chr2:239782842-239792842:-1;chr2:240820510-240830510:-1;chr3:49149108-49159108:-1;chr3:49414617-49424617:1;chr3:183621218-183631218:1;chr3:183651744-183661744:-1;chr3:183693230-183703230:1;chr3:183713462-183723462:-1;chr3:183902649-183912649:1;chr3:183943657-183953657:-1;chr4:9232732-9242732:-1;chr4:59792957-59802957:-1;chr4:68128286-68138286:1;chr4:69541180-69551180:-1;chr4:132687808-132697808:1;chr4:167586041-167596041:-1;chr5:71130528-71140528:-1;chr5:97579286-97589286:-1;chr5:123968850-123978850:-1;chr5:124368193-124378193:1;chr5:135121725-135131725:-1;chr6:19032877-19042877:1;chr6:19047967-19057967:-1;chr6:47596472-47606472:1;chr6:47610244-47620244:-1;chr6:115272553-115282553:-1;chr6:119208764-119218764:-1;chr6:150256643-150266643:1;chr6:157709391-157719391:-1;chr6:167934630-167944630:-1;chr7:917429-927429:1;chr7:1462411-1472411:1;chr7:1542934-1552934:-1;chr7:1563387-1573387:1;chr7:1598617-1608617:-1;chr7:1993209-2003209:-1;chr7:2219477-2229477:-1;chr7:2506126-2516126:1;chr7:2663158-2673158:1;chr7:2737626-2747626:-1;chr7:4810785-4820785:1;chr7:4872109-4882109:-1;chr7:5222098-5232098:-1;chr7:5643860-5653860:-1;chr7:32808272-32818272:-1;chr7:33101282-33111282:1;chr7:35619459-35629459:-1;chr7:52833438-52843438:-1;chr7:53393785-53403785:-1;chr7:54477687-54487687:1;chr7:55281047-55291047:1;chr7:56913110-56923110:1;chr7:64514540-64524540:1;chr7:86862134-86872134:1;chr7:139493115-139503115:-1;chr7:139870422-139880422:1;chr7:149462471-149472471:1;chr7:149522848-149532848:-1;chr7:155117625-155127625:-1;chr8:9049806-9059806:1;chr8:9059885-9069885:-1;chr8:144031199-144041199:-1;chr8:145803185-145813185:-1;chr9:17880957-17890957:1;chr9:17953899-17963899:-1;chr9:18016176-18026176:1;chr9:18052794-18062794:-1;chr9:18133305-18143305:1;chr9:18183384-18193384:-1;chr9:18260405-18270405:1;chr9:18338170-18348170:-1;chr9:18353170-18363170:1;chr9:21878937-21888937:1;chr9:22067070-22077070:1;chr9:22681750-22691750:-1;chr9:34187903-34197903:-1;chr9:34241078-34251078:1;chr9:34942013-34952013:-1;chr9:36129248-36139248:1;chr9:138317356-138327356:1;chr9:139831461-139841461:1;chr9:140123170-140133170:-1;chr10:25088099-25098099:-1;chr10:25103376-25113376:1;chr10:26060380-26070380:-1;chr10:26131006-26141006:1;chr10:26172277-26182277:-1;chr10:26294884-26304884:1;chr10:26522187-26532187:-1;chr10:26791820-26801820:1;chr10:27183994-27193994:-1;chr10:27744376-27754376:1;chr10:27953921-27963921:-1;chr10:28673927-28683927:1;chr10:37485221-37495221:-1;chr11:388007-398007:1;chr11:414941-424941:-1;chr11:22512827-22522827:1;chr11:22598729-22608729:-1;chr11:67373802-67383802:1;chr12:155502-165502:-1;chr12:132305490-132315490:1;chr13:66913552-66923552:-1;chr13:100990944-101000944:-1;chr13:101436045-101446045:1;chr13:114448806-114458806:-1;chr14:39084534-39094534:-1;chr14:77177990-77187990:-1;chr14:77445776-77455776:1;chr14:104543384-104553384:1;chr14:104654090-104664090:-1;chr15:29824310-29834310:1;chr15:35415407-35425407:-1;chr15:35466166-35476166:1;chr15:50721384-50731384:-1;chr15:91186798-91196798:-1;chr15:91643788-91653788:1;chr16:304346-314346:1;chr16:349783-359783:-1;chr16:488491-498491:1;chr16:849127-859127:-1;chr16:1014450-1024450:1;chr16:51963859-51973859:1;chr16:52043194-52053194:-1;chr16:84524165-84534165:-1;chr16:84913925-84923925:1;chr16:88470192-88480192:1;chr16:88718417-88728417:-1;chr16:88758801-88768801:1;chr16:89136346-89146346:-1;chr16:89213215-89223215:1;chr16:89270988-89280988:-1;chr16:89685017-89695017:-1;chr17:21497908-21507908:-1;chr17:34050036-34060036:-1;chr17:34131752-34141752:1;chr17:41283112-41293112:1;chr17:41612981-41622981:-1;chr17:41846365-41856365:1;chr17:64041851-64051851:-1;chr17:64479464-64489464:1;chr17:66056863-66066863:1;chr17:66073850-66083850:-1;chr17:77071345-77081345:1;chr17:77151812-77161812:-1;chr17:77693713-77703713:-1;chr19:41669886-41679886:-1;chr19:42745266-42755266:1;chr19:42800952-42810952:-1;chr19:57997414-58007414:1;chr19:58025636-58035636:-1;chr21:10637520-10647520:-1;chr21:18416854-18426854:-1;chr21:45654111-45664111:1;chr21:45750759-45760759:-1;chr21:46881668-46891668:1;chr21:47036409-47046409:1;chr21:47058756-47068756:-1;chr21:47528556-47538556:1;chr21:47574070-47584070:-1;chr22:24590016-24600016:-1;chr22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110794		Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0233	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	2,17	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	LUAD_1_T	Illumina paired-end sequencing	chr1:148940228-148950228:-1;chr1:149936099-149946099:-1;chr1:152197617-152207617:1;chr1:152315064-152325064:-1;chr1:157316602-157326602:-1;chr1:197559930-197569930:1;chr1:207631620-207641620:1;chr1:207888651-207898651:-1;chr2:11400508-11410508:-1;chr2:11436066-11446066:1;chr2:38540683-38550683:1;chr2:39257158-39267158:-1;chr2:39282681-39292681:1;chr2:41531621-41541621:-1;chr2:41546798-41556798:1;chr2:86028254-86038254:-1;chr2:86078657-86088657:1;chr2:124605911-124615911:1;chr2:132978550-132988550:-1;chr3:193381476-193391476:-1;chr3:193396666-193406666:1;chr4:9813954-9823954:-1;chr4:179490192-179500192:-1;chr4:179510276-179520276:1;chr5:45905339-45915339:-1;chr5:56315967-56325967:-1;chr5:71945183-71955183:-1;chr5:72040614-72050614:1;chr5:99748808-99758808:1;chr5:122137209-122147209:-1;chr5:122167980-122177980:1;chr5:138855975-138865975:1;chr5:165180957-165190957:-1;chr5:165216420-165226420:1;chr5:180679560-180689560:1;chr6:57428986-57438986:-1;chr6:57480768-57490768:1;chr6:95624366-95634366:-1;chr6:95634641-95644641:1;chr7:32667085-32677085:1;chr7:32851742-32861742:1;chr7:106945234-106955234:-1;chr7:106992032-107002032:1;chr7:111616013-111626013:-1;chr8:111020753-111030753:-1;chr8:117778597-117788597:1;chr8:127048441-127058441:-1;chr10:2376201-2386201:-1;chr10:118762650-118772650:-1;chr10:118778064-118788064:1;chr10:128454292-128464292:-1;chr10:131768628-131778628:-1;chr11:85686911-85696911:-1;chr11:85697359-85707359:1;chr11:127200702-127210702:-1;chr12:34529334-34539334:-1;chr12:133804878-133814878:1;chr13:19481471-19491471:-1;chr13:21881835-21891835:-1;chr13:39607322-39617322:-1;chr13:51064467-51074467:1;chr14:70918701-70928701:1;chr14:71476489-71486489:1;chr15:85948730-85958730:-1;chr15:85964235-85974235:1;chr16:33901402-33911402:1;chr16:73673067-73683067:-1;chr16:73688402-73698402:1;chr17:21456957-21466957:1;chr19:24588662-24598662:-1;chr19:27727495-27737495:1;chr21:9822869-9832869:-1;chr22:28247796-28257796:-1;chrX:21287666-21297666:-1;chrX:21317929-21327929:1;chrX:41205597-41215597:1;chrY:21479752-21489752:-1	hs1:67662697-67662953,hs1:233747886-233748131;hs1:67703934-67704113,hs1:234390975-234391159;hs1:67780997-67781267,hs1:195983406-195983636;hs1:74792790-74792960,hs1:74796480-74796674;hs2:89302599-89302803,hs2:124335000-124335193;hs2:95329273-95329446,hs2:116874022-116874292;hs2:102517743-102517860,hs2:104620327-104620644;hs2:104629776-104629972,hs2:117429240-117429370;hs2:170655803-170655988,hs2:202125711-202125899;hs2:170786393-170786611,hs2:202131323-202131565;hs2:201341700-201341951,hs2:202135719-202136013;hs4:96044249-96044379,hs4:96046029-96046288;hs5:25187734-25187930,hs8:69393370-69393573;hs6:6742975-6743057,hs6:6746597-6746832;hs9:33356561-33356785,hs9:35409720-35409960;hs13:57758221-57758409,hs13:57789127-57789282;hs17:4960469-4960766,hs2:86085633-86085807;hs17:5173123-5173207,hs17:15192589-15192726;hs17:5234872-5235096,hs17:15224741-15224995;hs17:13380866-13381164,hs2:104610499-104610757;hs17:14148681-14148853,hs2:124328944-124329102;hs17:14355131-14355364,hs17:21248423-21248665;hs17:14676724-14676991,hs2:88931961-88932190;hs17:15272955-15273201,hs17:16587537-16587824;hs17:15274207-15274472,hs2:124330365-124330612;hs17:15372418-15372664,hs2:88930900-88931136;hs17:15737992-15738207,hs17:21251465-21251671;hs17:15867193-15867484,hs17:22127631-22127868;hs17:21251312-21251541,hs2:124331647-124331904;hs17:21402352-21402596,hs2:86034683-86034949;hs18:2666733-2666912,hs18:3029184-3029362;hs19:43038834-43039060,hs19:43809952-43810148		Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0234	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	8,20	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	LUAD_5_T	Illumina paired-end 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8-30563885,hs21:31306096-31306282;hs21:37186860-37187085,hs21:37190336-37190509;hs21:38559973-38560286,hs21:38827838-38828119;hs21:42056175-42056455,hs21:42058651-42058908;hsX:109171077-109171322,hsX:109217183-109217343;hsX:119555397-119555649,hsX:120450873-120451163		Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0235	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	3,7	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	LUSC_1_T	Illumina paired-end sequencing	chr1:110174616-110184616:1;chr1:117863955-117873955:-1;chr2:17237674-17247674:-1;chr2:39166903-39176903:-1;chr2:39343310-39353310:-1;chr2:68617207-68627207:1;chr2:74584625-74594625:-1;chr2:74604643-74614643:1;chr2:98886029-98896029:-1;chr2:100380369-100390369:1;chr2:172436011-172446011:-1;chr2:197830578-197840578:-1;chr2:197865973-197875973:1;chr2:206125567-206135567:-1;chr2:206175797-206185797:1;chr2:224188225-224198225:1;chr2:234631310-234641310:1;chr2:234654919-234664919:-1;chr3:54868490-54878490:-1;chr3:54913612-54923612:1;chr3:108076138-108086138:1;chr3:108091589-108101589:-1;chr3:111523330-111533330:-1;chr3:111667356-111677356:-1;chr3:112361611-112371611:1;chr3:115457198-115467198:1;chr3:121070932-121080932:-1;chr3:162438355-162448355:-1;chr3:183112735-183122735:1;chr3:183877649-183887649:-1;chr3:183907649-183917649:1;chr3:184410779-184420779:1;chr3:185581099-185591099:-1;chr3:185736433-185746433:1;chr3:193866021-193876021:-1;chr4:1993628-2003628:1;chr4:3951871-3961871:1;chr4:4105312-4115312:1;chr4:7299995-7309995:1;chr4:8856057-8866057:1;chr4:8871057-8881057:-1;chr4:12917739-12927739:1;chr4:39769663-39779663:-1;chr4:41313229-41323229:-1;chr4:41356370-41366370:-1;chr4:44004315-44014315:1;chr4:65181343-65191343:1;chr4:68128286-68138286:1;chr4:68146332-68156332:-1;chr5:49441885-49451885:-1;chr5:49642670-49652670:1;chr6:150256643-150266643:1;chr7:5822212-5832212:1;chr7:10777273-10787273:1;chr7:23155201-23165201:-1;chr7:23327435-23337435:1;chr7:50631902-50641902:1;chr7:128687355-128697355:-1;chr7:128717705-128727705:1;chr7:130404067-130414067:1;chr7:133229330-133239330:1;chr7:136626865-136636865:-1;chr7:137858406-137868406:-1;chr7:138876200-138886200:-1;chr7:138951156-138961156:1;chr7:140488357-140498357:-1;chr7:140768011-140778011:1;chr7:140952178-140962178:1;chr7:141033409-141043409:1;chr7:141565579-141575579:1;chr7:142445922-142455922:-1;chr7:142528023-142538023:1;chr7:143735665-143745665:-1;chr7:145311665-145321665:1;chr7:146728647-146738647:-1;chr7:146753896-146763896:1;chr7:146805095-146815095:-1;chr7:146901529-146911529:1;chr7:148277469-148287469:-1;chr7:148501062-148511062:1;chr7:149334899-149344899:-1;chr7:149542855-149552855:1;chr7:151166849-151176849:-1;chr7:151713609-151723609:1;chr7:152731740-152741740:1;chr8:34077130-34087130:-1;chr8:39725295-39735295:1;chr8:82429449-82439449:1;chr9:5516936-5526936:-1;chr9:5582768-5592768:1;chr9:44783996-44793996:-1;chr9:92987579-92997579:-1;chr9:141006140-141016140:1;chr10:81298027-81308027:-1;chr10:89467332-89477332:1;chr10:89728185-89738185:-1;chr10:105530013-105540013:-1;chr10:105620597-105630597:1;chr11:47243802-47253802:-1;chr11:47294425-47304425:-1;chr11:47849500-47859500:1;chr11:55473419-55483419:1;chr11:67742772-67752772:-1;chr13:25590516-25600516:-1;chr14:28414071-28424071:-1;chr15:22520531-22530531:1;chr15:45352830-45362830:-1;chr15:51853581-51863581:1;chr15:54094990-54104990:-1;chr16:24465970-24475970:-1;chr16:54413308-54423308:-1;chr16:85428893-85438893:1;chr16:85443732-85453732:-1;chr18:77861588-77871588:1;chr20:29937815-29947815:1;chr20:41927158-41937158:1;chr20:43211644-43221644:1;chr21:9822869-9832869:-1;chr22:19165006-19175006:-1;chr22:19251387-19261387:1;chr22:25454112-25464112:-1;chr22:39950402-39960402:-1;chr22:39960402-39970402:1;chr22:41112932-41122932:1;chrX:3121022-3131022:1;chrX:13087172-13097172:1	hs1:191412530-191412670,hs1:191414542-191414677;hs2:36403481-36403741,hs8:82432277-82432523;hs2:50183943-50184168,hs2:50185273-50185538;hs2:127879049-127879263,hs2:127880346-127880545;hs2:141065925-141066135,hs3:186373289-186373501;hs2:141066193-141066354,hs3:186373715-186373885;hs2:144639396-144639638,hs2:144647251-144647487;hs2:197835225-197835416,hs2:197870125-197870380;hs2:206131333-206131523,hs2:206179197-206179430;hs3:54870581-54870819,hs3:54918046-54918288;hs3:97003408-97003624,hs3:97005297-97005560;hs3:111674048-111674278,hs3:112366472-112366731;hs3:126081434-126081584,hs3:126082892-126083030;hs3:146177264-146177523,hs7:148285901-148286134;hs3:146199506-146199770,hs7:148281976-148282227;hs3:159322016-159322226,hs3:171513494-171513694;hs3:160359611-160359834,hs3:160360586-160360810;hs3:161855203-161855337,hs3:171513970-171514121;hs3:161944959-161945169,hs3:165907170-165907428;hs3:172783316-172783480,hs3:174420114-174420246;hs3:177119294-177119404,hs3:177135472-177135598;hs3:184276793-184276971,hs3:184403003-184403184;hs3:185586166-185586314,hs3:185744438-185744583;hs4:12923079-12923302,hs5:39795701-39795890;hs4:41310328-41310561,hs4:41342292-41342536;hs4:63742053-63742208,hs9:115559750-115559951;hs4:113403770-113403963,hs4:113499662-113499832;hs4:168462793-168462995,hs4:168476004-168476237;hs5:109479055-109479216,hs7:141025880-141026033;hs7:8060909-8061039,hsX:100267523-100267687;hs7:23159549-23159712,hs7:23330045-23330236;hs7:54136774-54136937,hs7:118968050-118968211;hs7:128700389-128700656,hs7:128701576-128701823;hs7:130412144-130412289,hs7:137856740-137856900;hs7:133237439-133237700,hs7:142442083-142442325;hs7:136630244-136630462,hs7:140775318-140775553;hs7:140492663-140492900,hs7:143740391-143740631;hs7:140492747-140492949,hs7:143740403-143740652;hs7:141030092-141030315,hs7:141572726-141572903;hs7:142530915-142531156,hs7:145315601-145315864;hs7:146731840-146732006,hs7:149985474-149985595;hs7:146759340-146759492,hs7:149547305-149547464;hs7:146809224-146809420,hs7:152635776-152635932;hs7:146903406-146903550,hs7:149800648-149800816;hs7:148283441-148283617,hs7:149969193-149969406;hs7:148285689-148285814,hs7:149969607-149969786;hs7:149340242-149340434,hs7:149442191-149442323;hs7:151173861-151174082,hs7:152631575-152631820;hs7:151716734-151716946,hs7:152725830-152725993;hs7:152721560-152721732,hs7:152737110-152737250;hs9:5524755-5524964,hs9:5589040-5589228;hs10:49926242-49926464,hs12:52908394-52908632;hs10:89472935-89473189,hs10:89735926-89736200;hs10:105532756-105532959,hs10:105626130-105626311;hs10:133531068-133531237,hs3:186374965-186375127;hs11:47301317-47301534,hs11:47854330-47854587;hs12:67361606-67361818,hs12:67363097-67363246;hs12:100800092-100800325,hs3:186374067-186374254;hs12:100800316-100800555,hs3:186373784-186374031;hs14:28273437-28273685,hs14:28422743-28422992;hs14:87299646-87299876,hs4:137213989-137214209;hs14:87299935-87300135,hs4:137213861-137214024;hs19:43467954-43468141,hs3:186378696-186378880;hs20:41933787-41934030,hs20:41958478-41958709;hs20:52256378-52256591,hs20:52257132-52257345;hs22:29065644-29065856,hs4:121140174-121140382;hsX:35881159-35881413,hsX:35883863-35884107		Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0236	Research	23410887	Malhotra A, Lindberg M, Faust GG, Leibowitz ML, Clark RA, Layer RM, Quinlan AR, Hall IM	Breakpoint profiling of 64 cancer genomes reveals numerous complex rearrangements spawned by homology-independent mechanisms	Genome Research	2013 May	4	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	LUSC_6_T	Illumina paired-end sequencing	chr1:2621456-2631456:1;chr1:12875195-12885195:1;chr2:53487784-53497784:-1;chr2:61757332-61767332:1;chr2:69621469-69631469:1;chr3:16681981-16691981:1;chr3:16692016-16702016:-1;chr3:123954097-123964097:-1;chr3:123994333-124004333:1;chr3:125894402-125904402:-1;chr3:126137175-126147175:-1;chr3:126238053-126248053:1;chr3:126826061-126836061:-1;chr3:127201582-127211582:1;chr3:160193597-160203597:-1;chr3:161781275-161791275:1;chr3:162070154-162080154:1;chr3:162213236-162223236:-1;chr3:162223432-162233432:-1;chr3:163651024-163661024:1;chr3:164710418-164720418:1;chr3:164805791-164815791:-1;chr3:166261326-166271326:-1;chr3:169184907-169194907:1;chr3:171676517-171686517:1;chr3:171758212-171768212:-1;chr3:172102009-172112009:-1;chr3:172418761-172428761:1;chr3:173302406-173312406:-1;chr3:174210577-174220577:1;chr3:174455890-174465890:1;chr3:174561287-174571287:-1;chr3:174643697-174653697:-1;chr3:174764522-174774522:1;chr3:177036375-177046375:-1;chr3:177736190-177746190:-1;chr3:177771312-177781312:1;chr3:178732630-178742630:1;chr3:181662670-181672670:-1;chr3:182006156-182016156:-1;chr3:182149281-182159281:-1;chr3:182810497-182820497:1;chr3:182877795-182887795:1;chr3:182954983-182964983:-1;chr3:184518058-184528058:-1;chr3:184864947-184874947:1;chr3:189358868-189368868:1;chr3:189368884-189378884:-1;chr4:65151104-65161104:1;chr4:65166112-65176112:-1;chr4:84488129-84498129:1;chr4:116644241-116654241:1;chr4:116837164-116847164:-1;chr4:156873692-156883692:1;chr4:185728917-185738917:1;chr5:7269171-7279171:1;chr5:19868916-19878916:1;chr5:49400855-49410855:1;chr6:57353526-57363526:-1;chr6:151154680-151164680:1;chr6:151191757-151201757:-1;chr7:105607885-105617885:-1;chr7:105668230-105678230:1;chr7:127545620-127555620:1;chr7:127570686-127580686:-1;chr7:145249542-145259542:1;chr7:145712487-145722487:-1;chr8:37595380-37605380:-1;chr8:39913897-39923897:1;chr8:42334194-42344194:-1;chr8:50651925-50661925:-1;chr8:53445822-53455822:1;chr8:56052281-56062281:-1;chr8:56173159-56183159:1;chr8:59017974-59027974:-1;chr8:59145377-59155377:1;chr8:71017020-71027020:-1;chr8:77593047-77603047:-1;chr8:125612834-125622834:-1;chr8:126437506-126447506:-1;chr8:128724200-128734200:1;chr8:141416204-141426204:1;chr8:141660459-141670459:-1;chr8:146116950-146126950:1;chr9:13046915-13056915:-1;chr10:2457205-2467205:-1;chr10:5849505-5859505:1;chr10:5976733-5986733:1;chr11:420288-430288:1;chr11:13765712-13775712:-1;chr11:13845835-13855835:1;chr11:14236525-14246525:-1;chr11:14266598-14276598:-1;chr11:14605355-14615355:1;chr11:14829917-14839917:1;chr11:15420516-15430516:1;chr11:15440576-15450576:-1;chr11:16077676-16087676:1;chr11:16133221-16143221:1;chr11:16408772-16418772:-1;chr11:17040485-17050485:1;chr11:18040184-18050184:-1;chr11:18112431-18122431:1;chr11:18719154-18729154:-1;chr11:22804550-22814550:1;chr11:24209969-24219969:-1;chr11:24604401-24614401:1;chr11:24746684-24756684:-1;chr11:25649497-25659497:1;chr11:26633694-26643694:-1;chr11:26834542-26844542:1;chr11:127282028-127292028:-1;chr11:129975024-129985024:-1;chr12:6203180-6213180:1;chr12:7785820-7795820:1;chr12:22938762-22948762:1;chr12:25109710-25119710:-1;chr12:31760400-31770400:1;chr12:44513336-44523336:-1;chr12:45192842-45202842:1;chr12:46059970-46069970:-1;chr12:46075128-46085128:1;chr12:56901951-56911951:-1;chr12:65142007-65152007:-1;chr12:71043747-71053747:1;chr12:71792898-71802898:-1;chr12:78581255-78591255:1;chr12:79482308-79492308:-1;chr12:80563330-80573330:1;chr12:87846949-87856949:1;chr12:89518904-89528904:1;chr14:29874443-29884443:1;chr14:29949669-29959669:-1;chr14:43834712-43844712:1;chr14:43850145-43860145:-1;chr14:100792509-100802509:-1;chr14:105449153-105459153:1;chr14:106799007-106809007:-1;chr14:106820839-106830839:1;chr16:4676715-4686715:-1;chr16:35015790-35025790:1;chr16:46457004-46467004:1;chr17:25979864-25989864:-1;chr19:16622827-16632827:-1;chr19:16733918-16743918:1;chr19:37282007-37292007:-1;chr20:47804721-47814721:1;chr21:15482341-15492341:-1;chr21:19557283-19567283:-1;chr21:35710063-35720063:1;chr22:18299203-18309203:-1;chr22:18452999-18462999:1;chr22:41484513-41494513:-1;chr22:41747848-41757848:1;chr22:50689936-50699936:1;chrX:56656485-56666485:1;chrX:125431028-125441028:-1;chrY:17411397-17421397:1;chrY:18015495-18025495:-1;chrY:18942830-18952830:-1;chrY:19286059-19296059:1;chrY:20018908-20028908:1	hs1:147116615-147116893,hs1:147120869-147121148;hs1:212322984-212323212,hs1:212324814-212325001;hs1:234564021-234564282,hs1:234587501-234587954;hs2:32906614-32906917,hs2:32921215-32921425;hs2:53495643-53495909,hs3:126131196-126131471;hs2:154819579-154819814,hs2:154953737-154953946;hs3:31398352-31398601,hs3:31402489-31402661;hs3:115901255-115901491,hs3:116286453-116286709;hs3:116567516-116567777,hs3:117530598-117530834;hs3:119795240-119795433,hs3:119806196-119806413;hs3:123958208-123958550,hs3:125897569-125897980;hs3:123997938-123998202,hs3:126832853-126833249;hs3:126240717-126241097,hs3:185241635-185241979;hs3:127181365-127181806,hs3:177743376-177743682;hs3:127188124-1271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of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, Virginia 22903, USA	Tumor genomes are generally thought to evolve through a gradual accumulation of mutations, but the observation that extraordinarily complex rearrangements can arise through single mutational events suggests that evolution may be accelerated by punctuated changes in genome architecture. To assess the prevalence and origins of complex genomic rearrangements (CGRs), we mapped 6179 somatic structural variation breakpoints in 64 cancer genomes from seven tumor types and screened for clusters of three or more interconnected breakpoints. We find that complex breakpoint clusters are extremely common: 154 clusters comprise 25% of all somatic breakpoints, and 75% of tumors exhibit at least one complex cluster. Based on copy number state profiling, 63% of breakpoint clusters are consistent with being CGRs that arose through a single mutational event. CGRs have diverse architectures including focal breakpoint clusters, large-scale rearrangements joining clusters from one or more chromosomes, and staggeringly complex chromothripsis events. Notably, chromothripsis has a significantly higher incidence in glioblastoma samples (39%) relative to other tumor types (9%). Chromothripsis breakpoints also show significantly elevated intra-tumor allele frequencies relative to simple SVs, which indicates that they arise early during tumorigenesis or confer selective advantage. Finally, assembly and analysis of 4002 somatic and 6982 germline breakpoint sequences reveal that somatic breakpoints show significantly less microhomology and fewer templated insertions than germline breakpoints, and this effect is stronger at CGRs than at simple variants. These results are inconsistent with replication-based models of CGR genesis and strongly argue that nonhomologous repair of concurrently arising DNA double-strand breaks is the predominant mechanism underlying complex cancer genome rearrangements.	GRCh37/hg19				Yes	NA
CTDB0237	Research	21349919	Kloosterman WP, Guryev V, van Roosmalen M, Duran KJ, de Bruijn E, Bakker SC, Letteboer T, van Nesselrooij B, Hochstenbach R, Poot M, Cuppen E	Chromothripsis as a mechanism driving complex de novo structural rearrangements in the germline	Human Molecular Genetics	2011 May	1,4,10	Congenital abnormality	Next Generation Sequencing	Homo sapiens	Child	AB SOLiD 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of Medical Genetics, University Medical Center Utrecht, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands	A variety of mutational mechanisms shape the dynamic architecture of human genomes and occasionally result in congenital defects and disease. Here, we used genome-wide long mate-pair sequencing to systematically screen for inherited and de novo structural variation in a trio including a child with severe congenital abnormalities. We identified 4321 inherited structural variants and 17 de novo rearrangements. We characterized the de novo structural changes to the base-pair level revealing a complex series of balanced inter- and intra-chromosomal rearrangements consisting of 12 breakpoints involving chromosomes 1, 4 and 10. Detailed inspection of breakpoint regions indicated that a series of simultaneous double-stranded DNA breaks caused local shattering of chromosomes. Fusion of the resulting chromosomal fragments involved non-homologous end joining, since junction points displayed limited or no homology and small insertions and deletions. The pattern of random joining of chromosomal fragments that we observe here strongly resembles the somatic rearrangement patterns--termed chromothripsis--that have recently been described in deranged cancer cells. We conclude that a similar mechanism may also drive the formation of de novo structural variation in the germline.	GRCh37/hg19					NA
CTDB0238	Research	22553170	Lapuk AV, Wu C, Wyatt AW, McPherson A, McConeghy BJ, Brahmbhatt S, Mo F, Zoubeidi A, Anderson S, Bell RH, Haegert A, Shukin R, Wang Y, Fazli L, Hurtado-Coll A, Jones EC, Hach F, Hormozdiari F, Hajirasouliha I, Boutros PC, Bristow RG, Zhao Y, Marra MA, Fanjul A, Maher CA, Chinnaiyan AM, Rubin MA, Beltran H, Sahinalp SC, Gleave ME, Volik SV, Collins CC	From sequence to molecular pathology, and a mechanism driving the neuroendocrine phenotype in prostate cancer	Journal of Pathology	2012 Jul	2,9	Prostate cancer	Next Generation Sequencing	Homo sapiens	890	Illumina GA-IIx			FUBP1;ETV1;DENND1A;ANXA4;ANXA4;TMEM67;ABL1;ANXA4;ABL1;ANXA4;RALGPS1;EXOC6B;GPR107;C2orf28;MAP3K5;TCF12;ZNF638;KCNS3;PPM1G;SLC35D2;LPPR1;MRPL50;DTNB;SPTLC1;TMEM55A;LCLAT1;ABL1;ANXA4	Vancouver Prostate Centre and Department of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada	The current paradigm of cancer care relies on predictive nomograms which integrate detailed histopathology with clinical data. However, when predictions fail, the consequences for patients are often catastrophic, especially in prostate cancer where nomograms influence the decision to therapeutically intervene. We hypothesized that the high dimensional data afforded by massively parallel sequencing (MPS) is not only capable of providing biological insights, but may aid molecular pathology of prostate tumours. We assembled a cohort of six patients with high-risk disease, and performed deep RNA and shallow DNA sequencing in primary tumours and matched metastases where available. Our analysis identified copy number abnormalities, accurately profiled gene expression levels, and detected both differential splicing and expressed fusion genes. We revealed occult and potentially dormant metastases, unambiguously supporting the patients' clinical history, and implicated the REST transcriptional complex in the development of neuroendocrine prostate cancer, validating this finding in a large independent cohort. We massively expand on the number of novel fusion genes described in prostate cancer; provide fresh evidence for the growing link between fusion gene aetiology and gene expression profiles; and show the utility of fusion genes for molecular pathology. Finally, we identified chromothripsis in a patient with chronic prostatitis. Our results provide a strong foundation for further development of MPS-based molecular pathology.	NCBI 36/hg18				Yes	ADAMTS12,PXDNL;CPLX2,UBXD8;EBF1,FBXL17;EBF1,FEM1C;EFNA5,PCDHB7;JMY,DMGDH;KCNN2,EBF1;LMAN2,AP3S1;NDUFAF2,MAST4;PDE4D,C5orf47;PDE4D,FAM172A;PDE4D,PPP2R2B;PDE8B,UIMC1;PPP2R2B,FAM172A;RASGRF2,RNF145;TRIM40,FBXO38;YTHDC2,PPP2R2B;ZFP62,RGNEF
CTDB0239	Research	23930239	Jianming Pei, Suresh C. Jhanwar, Joseph R. Testa	Chromothripsis in a case of TP53-deficient chronic lymphocytic leukemia	Leukemia Research Reports	2012 Nov	2,5,6,7	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	23930239_1	Affymetrix CytoScan HD array			TP53;IGH	Cancer Biology Program and Clinical Cytogenomics Laboratory, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA	We describe genomic findings in a case of CLL with del(17p13.1) by FISH, in which SNP array analysis revealed chromothripsis, a phenomenon by which regions of the cancer genome are shattered and recombined to generate frequent oscillations between two DNA copy number states.The findings illustrate the value of SNP arrays for precise whole genome profiling in CLL and for the detection of alterations that would be overlooked with a standard FISH panel. This second report of chromothripsis in CLL indicates that this phenomenon is a recurrent change in this disease.					Yes	NA
CTDB0240	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N492TL	Complete Genomics		hs5:505880-505880,hs5:141253644-141253644;hs5:2421826-2421826,hs5:146308075-146308075;hs5:4760501-4760501,hs5:39019225-39019225;hs5:6137111-6137111,hs5:90083731-90083731;hs5:9324431-9324431,hs5:41655885-41655885;hs5:9348873-9348873,hs5:114934028-114934028;hs5:11760417-11760417,hs5:27977696-27977696;hs5:13740640-13740640,hs5:59051499-59051499;hs5:15207741-15207741,hs5:41831767-41831767;hs5:15339020-15339020,hs5:41383777-41383777;hs5:19602595-19602595,hs5:28426332-28426332;hs5:20521548-20521548,hs5:169638752-169638752;hs5:24418024-24418024,hs5:109984353-109984353;hs5:26262890-26262890,hs5:50161614-50161614;hs5:27389679-27389679,hs5:132703955-132703955;hs5:27535183-27535183,hs5:33692907-33692907;hs5:28873420-28873420,hs5:178557781-178557781;hs5:28924692-28924692,hs5:122291307-122291307;hs5:30589928-30589928,hs5:178667344-178667344;hs5:30770897-30770897,hs5:53518132-53518132;hs5:33011850-33011850,hs5:139625724-139625724;hs5:36788007-36788007,hs5:149500684-149500684;hs5:36797381-36797381,hs5:109207907-109207907;hs5:37140742-37140742,hs5:60973020-60973020;hs5:38571443-38571443,hs5:68203915-68203915;hs5:41418732-41418732,hs5:148933418-148933418;hs5:41541102-41541102,hs5:125328732-125328732;hs5:43639564-43639564,hs5:158490933-158490933;hs5:44373067-44373067,hs5:71098824-71098824;hs5:45055480-45055480,hs5:177848295-177848295;hs5:45057254-45057254,hs5:112392319-112392319;hs5:50407386-50407386,hs5:78154960-78154960;hs5:53863615-53863615,hs5:76256564-76256564;hs5:57512095-57512095,hs5:148720678-148720678;hs5:61516365-61516365,hs5:138483460-138483460;hs5:70843575-70843575,hs5:109781889-109781889;hs5:78635147-78635147,hs5:169531256-169531256;hs5:90575199-90575199,hs5:142383814-142383814;hs5:91243045-91243045,hs5:93940836-93940836;hs5:91441785-91441785,hs5:110077083-110077083;hs5:95075493-95075493,hs5:126417393-126417393;hs5:95261550-95261550,hs5:141060222-141060222;hs5:98600449-98600449,hs5:177811525-177811525;hs5:99956677-99956677,hs5:135239174-135239174;hs5:101858877-101858877,hs5:160932164-160932164;hs5:103192066-103192066,hs5:177979903-177979903;hs5:113236269-113236269,hs5:178642678-178642678;hs5:116457059-116457059,hs5:171255958-171255958;hs5:119534979-119534979,hs5:131370638-131370638;hs5:125289905-125289905,hs5:150102063-150102063;hs5:130324660-130324660,hs5:167149479-167149479;hs5:132176217-132176217,hs5:158096347-158096347;hs5:132196513-132196513,hs5:167151738-167151738;hs5:132251922-132251922,hs5:140616096-140616096;hs5:132493349-132493349,hs5:132591487-132591487;hs5:134154919-134154919,hs5:173159070-173159070;hs5:140463799-140463799,hs5:142297549-142297549;hs5:144833647-144833647,hs5:150825682-150825682;hs5:146526208-146526208,hs5:167029541-167029541;hs5:164298340-164298340,hs5:167285101-167285101;hs5:164573095-164573095,hs5:167787947-167787947;hs5:165603857-165603857,hs5:171465871-171465871;hs5:170958662-170958662,hs5:171713363-171713363;hs5:177851040-177851040,hs5:180195641-180195641;hs3:178233865-178233865,hs3:178332685-178332685;hs5:11541345-11541345,hs5:11755381-11755381;hs6:5445744-5445744,hs6:5671590-5671590;hs14:44715816-44715816,hs14:44734659-44734659;hs16:3753627-3753627,hs16:3762464-3762464;hs17:54050349-54050349,hs17:54057465-54057465;hs4:129405538-129405538,hs4:129422086-129422086;hs6:13176292-13176292,hs6:13397191-13397191;hs1:48974695-48974695,hs1:49515675-49515675;hs5:49506125-49506125,hs5:50224586-50224586;hs5:70902060-70902060,hs5:71433225-71433225;hs6:135771909-135771909,hs6:136018407-136018407;hs5:11473966-11473966,hs5:41777864-41777864;hs5:11542809-11542809,hs5:35839131-35839131;hs5:33894406-33894406,hs5:93855734-93855734;hs5:34878110-34878110,hs5:156313530-156313530;hs5:38579619-38579619,hs5:126735475-126735475;hs5:39168312-39168312,hs5:94103833-94103833;hs5:41005814-41005814,hs5:159577401-159577401;hs5:41853139-41853139,hs5:146102139-146102139;hs5:53251364-53251364,hs5:156451003-156451003;hs5:59086727-59086727,hs5:156307553-156307553;hs5:71683647-71683647,hs5:132253793-132253793;hs5:72382145-72382145,hs5:167028264-167028264;hs5:83558368-83558368,hs5:121731381-121731381;hs5:90267221-90267221,hs5:178551397-178551397;hs5:90267793-90267793,hs5:178511862-178511862;hs5:96144197-96144197,hs5:141473898-141473898;hs5:108753408-108753408,hs5:143519149-143519149;hs5:108755217-108755217,hs5:178235334-178235334;hs5:109210284-109210284,hs5:170600741-170600741;hs5:112340955-112340955,hs5:132923989-132923989;hs5:120006212-120006212,hs5:159577091-159577091;hs5:121735139-121735139,hs5:130964530-130964530;hs5:124102723-124102723,hs5:145361285-145361285;hs5:128885117-128885117,hs5:175902268-175902268;hs5:132909120-132909120,hs5:171459992-171459992;hs5:140170777-140170777,hs5:167788756-167788756;hs5:142409706-142409706,hs5:178669991-178669991;hs8:4692429-4692429,hs8:24356666-24356666	ARHGAP26;CTNNBL1;FOXF1;KCNH4;NAALADL1;PLAC8L1;SETD4;STAT1;ZNF8	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	ADAMTS12,C5orf36;ADAMTS19,CDHR2;ARHGAP26,ADAMTS2;ARL15,HAVCR2;C7,FABP6;CTNND2,OXCT1;CTNND2,SPEF2;DCP2,FSTL4;EDIL3,SNCAIP;ERAP1,NDFIP1;FCHO2,ODZ2;FSTL4,STK10;FYB,MCTP1;GPR98,ADAMTS2;LIFR,MEGF10;MAN2A1,RANBP17;MIR548C,RANBP17;OXCT1,PPP2R2B;PCDHA1,WWC1;PCDHA2,WWC1;PCDHA3,WWC1;PCDHA4,WWC1;PDE4D,TIMD4;PJA2,YIPF5;PJA2,ZNF354B;PRR16,FABP6;PTCD2,AFF4;SNCAIP,RAPGEF6;TTC23L,TIMD4;ZNF608,SH3RF2
CTDB0241	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N538TL	Complete Genomics		hs2:1629495-1629495,hs2:4971716-4971716;hs2:19125378-19125378,hs2:215040847-215040847;hs2:20655605-20655605,hs2:44666705-44666705;hs2:25439850-25439850,hs2:199935988-199935988;hs2:30619023-30619023,hs2:31660629-31660629;hs2:40222494-40222494,hs2:202705596-202705596;hs2:41367311-41367311,hs2:212743852-212743852;hs2:42011658-42011658,hs2:216844557-216844557;hs2:188967801-188967801,hs2:194767753-194767753;hs2:202353096-202353096,hs2:204977981-204977981;hs5:1578270-1578270,hs5:39064700-39064700;hs2:212480998-212480998,hs2:212952292-212952292;hs2:15898276-15898276,hs2:16271009-16271009;hs2:15930080-15930080,hs2:16269291-16269291;hs2:15948577-15948577,hs2:16234802-16234802;hs5:38883315-38883315,hs5:39066367-39066367;hs2:1105044-1105044,hs2:31199750-31199750;hs2:31322993-31322993,hs2:33324081-33324081;hs2:39780932-39780932,hs2:215671609-215671609;hs2:44821923-44821923,hs13:42812212-42812212;hs2:47489141-47489141,hs2:198007444-198007444;hs2:49227921-49227921,hs2:190028718-190028718;hs2:203104371-203104371,hs2:212078773-212078773	CRIM1;OR4P4;POGLUT1;TMC3	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	BMPR2,ERBB4;C2orf34,ENOX1;EHD3,LTBP1;FSHR,WDR75;MSH2,SF3B1;SNTG2,GALNT14;TMEM178,ABCA12
CTDB0242	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	6	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N407TL	Complete Genomics		hs6:38539704-38539704,hs6:108711967-108711967;hs6:41708159-41708159,hs6:45087656-45087656;hs6:127711927-127711927,hs6:131526385-131526385;hs2:196497954-196497954,hs2:196505613-196505613;hs6:39449778-39449778,hs6:39485401-39485401;hs6:131528411-131528411,hs6:131546204-131546204;hs22:30280946-30280946,hs22:30286044-30286044;hsX:122562539-122562539,hsX:122574195-122574195;hs6:18213646-18213646,hs6:18565726-18565726;hs6:43115746-43115746,hs6:43509863-43509863;hs13:101516808-101516808,hs17:28722554-28722554;hs13:101523938-101523938,hs17:28722549-28722549	FCGR2A;MIIP;MUC16;OR10Q1;ZFAT	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	NA
CTDB0243	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N753TL	Complete Genomics		hs1:43550391-43550391,hs1:161137536-161137536;hs5:14255630-14255630,hs5:17856351-17856351;hs5:60039862-60039862,hs5:141362204-141362204;hs5:126099096-126099096,hs5:134753058-134753058;hs5:136472159-136472159,hs5:137940753-137940753;hs5:145341640-145341640,hs5:145361236-145361236;hs10:70729772-70729772,hs10:70737811-70737811;hs11:44895990-44895990,hs11:44896817-44896817;hs12:40841359-40841359,hs12:40841865-40841865;hs9:27421249-27421249,hs9:27972515-27972515;hs5:14256356-14256356,hs5:132193461-132193461;hs9:27421249-27421249,hs9:27972515-27972515;hs11:70865620-70865620,hs17:35675500-35675500	ADAM30;BOD1L;KIF26A;KRTAP3-1;NOTCH4;PLUNC	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	TRIO,SHROOM1
CTDB0244	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	7	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N576TL	Complete Genomics		hs7:131301886-131301886,hs7:137807517-137807517;hs7:138568124-138568124,hs7:144486452-144486452;hs4:140860021-140860021,hs4:140867894-140867894;hs7:158389517-158389517,hs7:158393750-158393750;hs20:29501539-29501539,hs20:29516663-29516663;hs7:130203199-130203199,hs7:130273577-130273577;hs19:47272759-47272759,hs19:47387875-47387875;hs2:1078827-1078827,hs7:141014176-141014176;hs7:120491640-120491640,hs7:122005096-122005096;hs7:134395002-134395002,hs7:153549143-153549143	FAN1;OR10P1;PLD2;RASL11B	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	AGBL3,DPP6;C7orf58,CADPS2
CTDB0245	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N752TL	Complete Genomics		hs5:1302619-1302619,hs5:60127804-60127804;hs5:1349452-1349452,hs5:59877248-59877248;hs5:1365627-1365627,hs5:1474540-1474540;hs5:1378862-1378862,hs5:60032833-60032833;hs5:1491572-1491572,hs5:59886460-59886460;hs5:1524079-1524079,hs5:61340494-61340494;hs5:59538740-59538740,hs5:61369479-61369479;hs5:59801960-59801960,hs5:61323633-61323633	BRD7;CCDC108;CGNL1;DICER1;DOPEY2;MS4A4A;ORAI2;RGS5;SORCS3;TRAPPC6A;UBE4A;ZNF133	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	NA
CTDB0246	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N608TL	Complete Genomics		hs2:2550381-2550381,hs2:3431067-3431067;hs2:2639213-2639213,hs2:10383039-10383039;hs2:6542796-6542796,hs2:10257701-10257701;hs2:6947668-6947668,hs2:67119025-67119025;hs2:3176129-3176129,hs2:3179801-3179801;hs18:22361089-22361089,hs18:22384304-22384304;hs1:2449506-2449506,hs1:2450345-2450345;hs2:5730602-5730602,hs2:5892139-5892139;hs2:15872213-15872213,hs2:16299993-16299993;hs2:15945514-15945514,hs2:16227645-16227645;hs2:15980651-15980651,hs2:16167752-16167752;hs2:9954405-9954405,hs2:10361304-10361304;hs16:49140173-49140173,hs16:55776951-55776951	ACCN2;ACTR8;ADAMTS14;AKAP9;ALG13;ATP5J2;PTCD1;BUD31;PTCD1;C11ORF57;CACNB3;CEP350;CMAS;CSNK1G3;DARC;DDX55;DKK2;EHF;FAM102B;GPATCH4;IGSF22;LPIN1;MARK2;NAA25;NCKAP5;NQO1;OR51D1;PHC2;PIKFYVE;RIN2;RORC;RPS4X;Sep-09;SH3D19;SIX6;SRCRB4D;STK17A;TNPO2	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	TAF1B,HPCAL1
CTDB0247	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	8	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N481TL	Complete Genomics		hs8:19394927-19394927,hs8:128581556-128581556;hs8:128673342-128673342,hs8:128828072-128828072;hs6:31705218-31705218,hs6:169722886-169722886;hs11:77714161-77714161,hs17:25450547-25450547;hs11:77731716-77731716,hs17:25420373-25420373	ANO8;CWC22;FSIP2;GCDH;OIT3;SPTBN2;SVEP1;ZNF717	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	NA
CTDB0248	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N089TL	Complete Genomics		hs2:15259690-15259690,hs2:17211150-17211150;hs2:15437344-15437344,hs2:18841374-18841374;hs2:16002229-16002229,hs2:17494713-17494713;hs2:15276162-15276162,hs2:15594793-15594793;hs2:15284228-15284228,hs2:15435375-15435375;hsX:31276736-31276736,hsX:31626677-31626677;hs2:15143406-15143406,hs2:15564750-15564750;hs2:15217378-15217378,hs2:15597428-15597428;hs2:15488389-15488389,hs2:15648338-15648338;hs2:15614719-15614719,hs2:15634535-15634535;hs2:15648481-15648481,hs2:15950632-15950632;hs2:16079331-16079331,hs2:16932295-16932295;hs2:16221504-16221504,hs2:17046405-17046405;hs2:17894520-17894520,hs2:18522189-18522189;hs2:17926477-17926477,hs2:18518516-18518516;hs2:17931561-17931561,hs2:18241363-18241363;hs2:15140067-15140067,hs2:15743648-15743648;hs2:15219810-15219810,hs2:15723914-15723914;hs2:15232487-15232487,hs2:15904695-15904695;hs2:15380005-15380005,hs2:15836765-15836765;hs2:15482088-15482088,hs2:15708736-15708736;hs2:15482253-15482253,hs2:15938098-15938098;hs2:15896932-15896932,hs2:16149877-16149877;hs2:15955364-15955364,hs2:16004421-16004421;hs2:18040639-18040639,hs2:18789042-18789042;hs2:18084508-18084508,hs2:18842282-18842282;hs2:18238406-18238406,hs2:19028097-19028097;hs2:15651391-15651391,hs2:16045907-16045907;hs2:15035945-15035945,hs2:16009656-16009656;hs2:15614877-15614877,hs2:16057654-16057654;hs2:15616160-15616160,hs2:15650353-15650353	C7ORF31;PPFIA4;PROKR2;SCRIB;USP7	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	NBAS,DDX1
CTDB0249	Research	22367537	Jan J. Molenaar, JanKoster, Danny A. Zwijnenburg, Peter van Sluis, Linda J. Valentijn, Ida van der Ploeg, Mohamed Hamdi, Johan van Nes, Bart A. Westerman, Jennemiek van Arkel, Marli E. Ebus, Franciska Haneveld, Arjan Lakeman, Linda Schild, Piet Molenaar, Peter Stroeken, Max M. van Noesel, Ingrid Øra,, Evan E. Santo, Huib N. Caron, Ellen M. Westerhout, Rogier Versteeg 	Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes	Nature	2012 Mar	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N637TL	Complete Genomics		hs2:10458133-10458133,hs2:17135483-17135483;hs2:11805167-11805167,hs2:16140340-16140340;hs2:16025716-16025716,hs2:17563029-17563029;hs19:1215676-1215676,hs19:7820235-7820235;hs11:95222567-95222567,hs11:95223463-95223463;hs2:10321927-10321927,hs2:10362208-10362208;hs2:10321996-10321996,hs2:10367260-10367260;hs2:10348048-10348048,hs2:10367736-10367736;hs2:11658726-11658726,hs2:11867762-11867762;hs2:11658726-11658726,hs2:11867762-11867762;hs2:10359771-10359771,hs2:10545424-10545424;hs2:10426590-10426590,hs2:10524071-10524071;hs2:10265983-10265983,hs2:10530762-10530762;hs2:10266189-10266189,hs2:11720410-11720410;hs2:10367713-10367713,hs2:11216962-11216962;hs2:11821650-11821650,hs2:17823178-17823178;hs19:19496274-19496274,hs19:56017091-56017091	BNIPL;CIC;KRIT1;NPHP1;SLC17A7;ST6GAL2;TAS2R30	Department of Oncogenomics, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands	Neuroblastoma is a childhood tumour of the peripheral sympathetic nervous system. The pathogenesis has for a long time been quite enigmatic, as only very few gene defects were identified in this often lethal tumour. Frequently detected gene alterations are limited to MYCN amplification (20%) and ALK activations (7%). Here we present a whole-genome sequence analysis of 87 neuroblastoma of all stages. Few recurrent amino-acid-changing mutations were found. In contrast, analysis of structural defects identified a local shredding of chromosomes, known as chromothripsis, in 18% of high-stage neuroblastoma. These tumours are associated with a poor outcome. Structural alterations recurrently affected ODZ3, PTPRD and CSMD1, which are involved in neuronal growth cone stabilization. In addition, ATRX, TIAM1 and a series of regulators of the Rac/Rho pathway were mutated, further implicating defects in neuritogenesis in neuroblastoma. Most tumours with defects in these genes were aggressive high-stage neuroblastomas, but did not carry MYCN amplifications. The genomic landscape of neuroblastoma therefore reveals two novel molecular defects, chromothripsis and neuritogenesis gene alterations, which frequently occur in high-risk tumours.	NCBI 36/hg18			EGAS00001000222	Yes	C2orf48,NTSR2;GREB1,LPIN1;HPCAL1,PQLC3;LPIN1,GEN1
CTDB0250	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-182	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0251	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-506	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0252	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-591	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0253	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-586	Illumina HiSeq 2000			PVT1;NDRG1	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,NDRG1
CTDB0254	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-524	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0255	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-1003	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0256	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-1377	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0257	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-1240	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0258	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-1338	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0259	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB-548	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0260	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	D458	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0261	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	D425	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0262	Research	22832581	Northcott PA, Shih DJ, Peacock J, Garzia L, Morrissy AS, Zichner T, Stutz AM, Korshunov A, Reimand J, Schumacher SE, Beroukhim R, Ellison DW, Marshall CR, Lionel AC, Mack S, Dubuc A, Yao Y, Ramaswamy V, Luu B, Rolider A, Cavalli FM, Wang X, Remke M, Wu X, Chiu RY, Chu A, Chuah E, Corbett RD, Hoad GR, Jackman SD, Li Y, Lo A, Mungall KL, Nip KM, Qian JQ, Raymond AG, Thiessen NT, Varhol RJ, Birol I, Moore RA, Mungall AJ, Holt R, Kawauchi D, Roussel MF, Kool M, Jones DT, Witt H, Fernandez-L A, Kenney AM, Wechsler-Reya RJ, Dirks P, Aviv T, Grajkowska WA, Perek-Polnik M, Haberler CC, Delattre O, Reynaud SS, Doz FF, Pernet-Fattet SS, Cho BK, Kim SK, Wang KC, Scheurlen W, Eberhart CG, Fevre-Montange M, Jouvet A, Pollack IF, Fan X, Muraszko KM, Gillespie GY, Di Rocco C, Massimi L, Michiels EM, Kloosterhof NK, French PJ, Kros JM, Olson JM, Ellenbogen RG, Zitterbart K, Kren L, Thompson RC, Cooper MK, Lach B, McLendon RE, Bigner DD, Fontebasso A, Albrecht S, Jabado N, Lindsey JC, Bailey S, Gupta N, Weiss WA, Bognar L, Klekner A, Van Meter TE, Kumabe T, Tominaga T, Elbabaa SK, Leonard JR, Rubin JB, Liau LM, Van Meir EG, Fouladi M, Nakamura H, Cinalli G, Garami M, Hauser P, Saad AG, Iolascon A, Jung S, Carlotti CG, Vibhakar R, Ra YS, Robinson S, Zollo M, Faria CC, Chan JA, Levy ML, Sorensen PH, Meyerson M, Pomeroy SL, Cho YJ, Bader GD, Tabori U, Hawkins CE, Bouffet E, Scherer SW, Rutka JT, Malkin D, Clifford SC, Jones SJ, Korbel JO, Pfister SM, Marra MA, Taylor MD	Subgroup-specific structural variation across 1,000 medulloblastoma genomes	Nature	2012 Aug	8	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MED8A	Illumina HiSeq 2000			PVT1;MYC	Developmental & Stem Cell Biology Program, The Hospital for Sick Children,101 College Street, TMDT-11-401M, Toronto, Ontario M5G 1L7, Canada.	Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4a. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-beta signalling in Group 3, and NF-kB signalling in Group 4, suggest future avenues for rational, targeted therapy. Subgroup-specific structural variation across 1,000 medulloblastoma genomes.	NCBI 36/hg18	GSE37385		EGAD00001000158	Yes	PVT1,MYC
CTDB0263	Research	22927308	Wu C, Wyatt AW, McPherson A, Lin D, McConeghy BJ, Mo F, Shukin R, Lapuk AV, Jones SJ, Zhao Y, Marra MA, Gleave ME, Volik SV, Wang Y, Sahinalp SC, Collins CC	Poly-gene fusion transcripts and chromothripsis in prostate cancer.	Genes Chromosomes Cancer	2012 Dec	1,8,12	Prostate cancer	Next Generation Sequencing	Homo sapiens	LTL-313H	Illumina Genome Analyzer II			GRIN3B;MARCH10;ITGAE;CMYA5;SULT1C3;VN1R2;SLC2A9;AL160314.1;STARD8;SMC1B;DNAH6;KIF1A;KLHDC7A;SLC18A1;NOD2;TMX4;SPAG17;F13A1;STK31;RTTN;CXorf22;SYT6;FRAS1;CYB561;DNAH9;ATAD1;NR5A2;DACT1;STRA6;ZNF804B;NOTCH4;ACCN2;RAG1;PPPDE1;GPR98;CAPN14;FERMT1;TTN;DUOX1;KRT75;LRP4;FAT1;C12orf63;STARD13;ZNF192;DLGAP5;TRPV4;OAS1;SLC27A6;FAM55B;C14orf39;ERCC6;FRK;DMXL2;SYNPO2;ZMIZ1;TECTA;NAT8;TGFBR3;BTNL2;SCNN1B;UGT2B15;KIAA1109;ZBBX;NPBWR1;ODF3;AKR7L;RNF212;PDILT;C6orf170;EFHB;PAPLN;AC145676.2;SLC9A10;ARHGAP42;GNRHR2;YSK4;MMP26;FAM179A;SYDE2;OR5H2;SLC6A17;DNAH17;LCN8;C10orf131;SLC14A2;PTX4;C20orf201;SCD5;GSDMC;CRNKL1;CD6;VWDE;MYO7A;INPP5B;GSG2;IYD;OR2C1;PCDHA4;OR2W3;LMLN;DISC1;ZNF407;BCMO1;ADAMTSL1;SLCO1B3;HGF;FBXW12;C6orf97;CRYGB;AL353597.1;ALG8;TBC1D22A;SLC28A1;CX3CR1;ENG;AK7;ZFAT;GLI3;ZNF474;UNC13D;CELA2B;SUSD3;MUC5AC;ADNP2;GPR19;C7orf57;C11orf72;AMPH;BTN3A2;SPATA7;DNAH3;FAM57A;ANKS1B;TEP1;SCAND3;FAM196A;MBD5;HRNR;MARCH8;ZRANB3;SIVA1;FRMPD2;C9orf96;ATR;WDR27;DNAH14;THBS1;E2F7;ZNF681;KIAA1009;KALRN;PCLO;A2ML1;MATN2;GABRR2;FLG;ANKRD18B;SLC12A7;MSX1;GAB1;CIT;ATAD5;PDE4DIP;AC007601.1;DNAH7;MBOAT2;C19orf45;FNIP2;RPS27;CCDC141;KDM4D;SCFD2;ALPK1;MED12L;TRANK1;ALS2CR8;WDR78;C9orf171;FLG2;NLRP8;ARMC2;IFIH1;KIF21B;SLC7A8;NEU3;ZNF772;FAM161A;DNAH11;TCHH;NAV2;OTUD4;SCIN;PAQR5;MBLAC2;KIAA1211;SLC26A8;FTCD;SLC4A7;ANKRD44;LTN1;UTP20;ZNF519;KIAA0319;SV2C;PSMB8;DSC3;PTCH1;SEMG2;MLXIPL;SPZ1;ACAA2;LTK;DFFB;FAM186B;SETBP1;CLOCK;GLYATL3;BCAS1;LARP1;TOPBP1;TMPRSS3;EDAR;DNAH1;SLC5A4;TLN2;CECR2;EXPH5;URB2;C5orf42;MATN3;CAST;SPRY1;SRD5A1;ZNF184;TPO;THAP6;KDM1B;DECR2;CCDC48;AC083883.1;BIRC6;LRTOMT;IL28RA;OMA1;BRCA1;PDIA3;ZNF671;PLAC8L1;MYOF;CELSR2;PPARGC1B;TES;C9orf68;MFSD6;MRAP;ZNF484;GRIN3A;TARBP1;SPRED2;GLB1;MAN2B2;UBA6;SCAMP3;ZNF382;KIAA0556;VEZT;MLF1IP;TNKS1BP1;SP2;PARD3B;MAGI1;SON;EFHC1;TAF1D;WDR60;ZNF226;CLCN2;KIAA1324;MCM3AP;DNAJC2;SH3BP1;TSEN2;CHTF18;ST3GAL6;RASA1;COBLL1;DAGLB;NSD1;DOT1L;PPOX;SLC4A3;USPL1;SLC5A6;SCNN1D;UBN1;ODF3B;TOP3B;NMRAL1;DCP1B;EIF2AK1;CHID1;NAT10;SEC14L2;NUMB;ALDH3B2;RET;KIAA1543;SMARCA2;ZNF662;XXbac-B461K10.4;ZNF737;TRDMT1;POLN;ZNF584;MAPT;SMPDL3B;SCYL3;CAPN13;THADA;ACOT6;PKP2;C21orf59;DHX58;CCDC36;DNAJB7;ATM;C14orf145;CEP55;SLC38A9;CASP2;TOR1AIP1;RIN2;ZSWIM6;ZNF202;SGSM3;ERV3;TUBGCP5;NEIL3;ETAA1;MARCH3;ALG14;SEC16A;ESF1;C7orf63;CALML4;PPIF;CCDC66;CLCC1;DDX51;ANKRD12;ZDHHC6;MYNN;STAT2;NRSN2;SUPT16H;FAM184B;WNK2;CCDC85C;DMAP1;COMMD5;GALNT11;C14orf79;DERL3;WDR41;NCAPH2;PAAF1;ANKRD16;ITIH4;ZNF773;ACTR8;C1orf112;CHD7;SLC25A45;ANKK1;THEG;PLCH2;CTDSPL;PRDM15;CPT1A;STH;SLC23A1;ANKRD5;BLM;ADI1;SYNRG;AGMAT;MKI67;POP1;R3HDM1;RAD17;CWC22;PUS1;KRI1;DOM3Z;ZDHHC5;ZRANB2;CCT7;KIF15;TACC2;KIF13A;AC006547.14;LRRC63;CAPN12;CLMN;ARHGAP11A;OBSCN;MCF2L;NUPL2;CYP1A1;ARHGEF12;PREPL;SGOL2;HMMR;GTF3C3;GCC2;CCDC14;UIMC1;RSPH3;ZNF808;LIFR;CBS;LIMCH1;VSIG2;ARID5B;LTBP4;CCDC116;ZNF530;ZNF93;FEZ2;C10orf18;C9orf102;NOC3L;KIAA0802;RAB3GAP1;SYNE1;ZXDC;SMARCAL1;COX17;TCF20;ZNF830;ZNF708;USP8;LAMP1;PITRM1;ALG3;NKTR;MRPS15;DNAJC28;SDCCAG8;STON2;RPAP1;TRIOBP;CSMD3;CCDC138;PISD;ZNF440;GTPBP5;IQSEC1;SFI1;GEMIN5;PIK3R3;HYAL2;VKORC1L1;GTPBP10;PCDHB8;WDR76;NIT1;MOV10L1;TRAK2;DICER1;ABCC4;EMID2;SMC2;CASP9;GEN1;USP19;ZNF571;ABHD14B;IL4R;SLC22A18;NCDN;MUC20;OSCP1;NEK11;HES2;FBXO17;AC008074.1;ACTR1B;GFER;MYO6;DGKQ;HLA-DMA;SLC35C1;MARCH7;EFCAB10;TTC21B;PDZD2;PACRGL;C1orf50;CLK1;RP11-382J12.1;TCIRG1;PLEKHG2;GPATCH8;HNRNPF;IDUA;KTN1;ANKRD31;FBP2;C12orf43;ALMS1;F12;DOK7;IDO2;RHBDF2;FAM178B;C10orf62;FBF1;POFUT1;AKAP1;RGAG4;NUP210;PRKDC;YLPM1;AC127496.3;FAM186A;CYP2A7;SCN1B;TG;PI3;EXOC3;PM20D1;RP11-50B3.2;ZMAT4;SLC7A9;CXorf30;C2orf73;C10orf68;BSN;AC022415.1;SYNGR1;BCR;VTN;EPHA8;TP53;PCDHA1;C16orf46;RIBC2;CDKL5;UGGT2;CYP2D7P1;OCRL;RP4-695O20;SAC3D1	Vancouver Prostate Centre and Department of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada	Complex genome rearrangements are frequently observed in cancer but their impact on tumor molecular biology is largely unknown. Recent studies have identified a new phenomenon involving the simultaneous generation of tens to hundreds of genomic rearrangements, called chromothripsis. To understand the molecular consequences of these events, we sequenced the genomes and transcriptomes of two prostate tumors exhibiting evidence of chromothripsis. We identified several complex fusion transcripts, each containing sequence from three different genes, originating from different parts of the genome. One such poly-gene fusion transcript appeared to be expressed from a chain of small genomic fragments. Furthermore, we detected poly-gene fusion transcripts in the prostate cancer cell line LNCaP, suggesting they may represent a common phenomenon. Finally in one tumor with chromothripsis, we identified multiple mutations in the p53 signaling pathway, expanding on recent work associating aberrant DNA damage response mechanisms with chromothripsis. Overall, our data show that chromothripsis can manifest as massively rearranged transcriptomes. The implication that multigenic changes can give rise to poly-gene fusion transcripts is potentially of great significance to cancer genetics.	NCBI 36/hg18				Yes	ARF3,RUNX1T1;ATP6V1C1,TSTA3;BAALC,TRAPPC9;BCAT1,ATF7IP;BCAT1,LOH12CR1;BCAT1,TMTC2;C12orf59,TTLL9;C12orf59,UBE2V2;C6orf145,FARS2;C6orf145,PRPF4B;C6orf145,RNF165;CA2,C4BPA;CA2,RUNX1T1;CELSR1,PTDSS1;EEF1D,SDC4;KIAA1467,C12orf59;PACS1,PTEN;PDRG1,ARF3;PDRG1,RUNX1T1;PDRG1,ZNF623;PTDSS1,LOH12CR1;PTDSS1,SOX5;PTDSS1,SPRYD3;PTDSS1,UBE2V2;RNF165,SSR1;RUNX1T1,ARF3;RUNX1T1,C12orf35;RUNX1T1,HHAT;RUNX1T1,SDC4;RUNX1T1,SOX5;SDC4,PTDSS1;SLC25A21,C14ORF25;SLC35B1,PEMT;SLC35B11,PEMT;SLC6A17,CA2;SNX16,CA2;SPRYD3,PTDSS1;SSR1,RNF165;ST8SIA1,PDRG1;TENC1,TTLL9;TMPRSS2,ERG;TRAPPC9,SPRYD3;TRAPPC9,ZNF623;TTLL9,C12ORF57;TTLL9,C21orf59;TTLL9,KIAA1467;UCRC,C1orf194;USP34,AHSA2;USP34,C2orf74;ZNF623,TRAPPC9
CTDB0264	Research	22927308	Wu C, Wyatt AW, McPherson A, Lin D, McConeghy BJ, Mo F, Shukin R, Lapuk AV, Jones SJ, Zhao Y, Marra MA, Gleave ME, Volik SV, Wang Y, Sahinalp SC, Collins CC	Poly-gene fusion transcripts and chromothripsis in prostate cancer.	Genes Chromosomes Cancer	2012 Dec	6,10	Prostate cancer	Next Generation Sequencing	Homo sapiens	LNCaP	Illumina Genome Analyzer II				Vancouver Prostate Centre and Department of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada	Complex genome rearrangements are frequently observed in cancer but their impact on tumor molecular biology is largely unknown. Recent studies have identified a new phenomenon involving the simultaneous generation of tens to hundreds of genomic rearrangements, called chromothripsis. To understand the molecular consequences of these events, we sequenced the genomes and transcriptomes of two prostate tumors exhibiting evidence of chromothripsis. We identified several complex fusion transcripts, each containing sequence from three different genes, originating from different parts of the genome. One such poly-gene fusion transcript appeared to be expressed from a chain of small genomic fragments. Furthermore, we detected poly-gene fusion transcripts in the prostate cancer cell line LNCaP, suggesting they may represent a common phenomenon. Finally in one tumor with chromothripsis, we identified multiple mutations in the p53 signaling pathway, expanding on recent work associating aberrant DNA damage response mechanisms with chromothripsis. Overall, our data show that chromothripsis can manifest as massively rearranged transcriptomes. The implication that multigenic changes can give rise to poly-gene fusion transcripts is potentially of great significance to cancer genetics.	NCBI 36/hg18				Yes	CYP2C19,PDE6C;CYP2C19,FAM190B;CYP2C18,SOD2;SNX9,CYP2C19
CTDB0265	Research	22927308	Wu C, Wyatt AW, McPherson A, Lin D, McConeghy BJ, Mo F, Shukin R, Lapuk AV, Jones SJ, Zhao Y, Marra MA, Gleave ME, Volik SV, Wang Y, Sahinalp SC, Collins CC	Poly-gene fusion transcripts and chromothripsis in prostate cancer.	Genes Chromosomes Cancer	2012 Dec	2,9	Prostate cancer	Next Generation Sequencing	Homo sapiens	890	Illumina Genome Analyzer II				Vancouver Prostate Centre and Department of Urologic Sciences, University of British Columbia, Vancouver, BC, Canada	Complex genome rearrangements are frequently observed in cancer but their impact on tumor molecular biology is largely unknown. Recent studies have identified a new phenomenon involving the simultaneous generation of tens to hundreds of genomic rearrangements, called chromothripsis. To understand the molecular consequences of these events, we sequenced the genomes and transcriptomes of two prostate tumors exhibiting evidence of chromothripsis. We identified several complex fusion transcripts, each containing sequence from three different genes, originating from different parts of the genome. One such poly-gene fusion transcript appeared to be expressed from a chain of small genomic fragments. Furthermore, we detected poly-gene fusion transcripts in the prostate cancer cell line LNCaP, suggesting they may represent a common phenomenon. Finally in one tumor with chromothripsis, we identified multiple mutations in the p53 signaling pathway, expanding on recent work associating aberrant DNA damage response mechanisms with chromothripsis. Overall, our data show that chromothripsis can manifest as massively rearranged transcriptomes. The implication that multigenic changes can give rise to poly-gene fusion transcripts is potentially of great significance to cancer genetics.	NCBI 36/hg18				Yes	FUBP1,ETV1;KCNS3,PPM1G;SLC35D2,LPPR1;SLC35D2,MRPL50;ZNF638,KCNS3
CTDB0266	Research	23334667	Brastianos PK, Horowitz PM, Santagata S, Jones RT, McKenna A, Getz G, Ligon KL, Palescandolo E, Van Hummelen P, Ducar MD, Raza A, Sunkavalli A, Macconaill LE, Stemmer-Rachamimov AO, Louis DN, Hahn WC, Dunn IF, Beroukhim R	Genomic sequencing of meningiomas identifies oncogenic SMO and AKT1 mutations.	Nat Genet	2013 Mar	1	Meningioma	Next Generation Sequencing	Homo sapiens	MEN0017	Illumina HiSeq 2000		hs1:80589104-80589104,hs1:90870420-90870420;hs1:68000835-68000835,hs1:95538220-95538220;hs1:48880153-48880153,hs1:171741093-171741093;hs1:48881168-48881168,hs1:77612749-77612749;hs1:158828097-158828097,hs1:187549966-187549966;hs1:109163626-109163626,hs1:187277742-187277742;hs1:58421895-58421895,hs1:118155121-118155121;hs1:80323486-80323486,hs1:100225718-100225718;hs1:95875799-95875799,hs1:171930057-171930057;hs1:77604362-77604362,hs1:171918762-171918762;hs1:100228338-100228338,hs1:179526744-179526744;hs1:80320704-80320704,hs1:171918676-171918676;hs1:171933392-171933392,hs1:179641879-179641879;hs1:80320463-80320463,hs1:158825374-158825374;hs1:80319755-80319755,hs1:179527604-179527604;hs1:80323468-80323468,hs1:158825237-158825237;hs1:68000518-68000518,hs1:171929471-171929471;hs1:100228246-100228246,hs1:171917627-171917627;hs1:80325391-80325391,hs1:171922625-171922625;hs1:158828219-158828219,hs1:159614118-159614118;hs1:171749005-171749005,hs1:171938423-171938423;hs1:68020725-68020725,hs1:179524736-179524736;hs1:101963877-101963877,hs1:189981533-189981533;hs1:32007608-32007608,hs1:51630376-51630376;hs1:105077445-105077445,hs1:105098493-105098493;hs1:50367901-50367901,hs1:62435264-62435264;hs1:51793777-51793777,hs1:77595973-77595973;hs1:88831228-88831228,hs1:95948591-95948591;hs1:171921987-171921987,hs1:171951323-171951323;hs1:4200762-4200762,hs1:101186002-101186002;hs1:39578703-39578703,hs1:101398110-101398110;hs1:63343134-63343134,hs1:82455808-82455808;hs1:100224749-100224749,hs1:171930170-171930170;hs1:58439620-58439620,hs1:108360324-108360324;hs1:72006848-72006848,hs1:105092212-105092212;hs1:100224110-100224110,hs1:171938268-171938268;hs1:48879478-48879478,hs1:80328473-80328473;hs1:38050332-38050332,hs1:39576150-39576150;hs1:179524915-179524915,hs1:189943790-189943790;hs1:68005693-68005693,hs1:100225462-100225462;hs1:102483233-102483233,hs1:105090171-105090171;hs1:68030155-68030155,hs1:149394091-149394091;hs12:113888190-113888190,hs12:113889327-113889327;hs6:125047720-125047720,hsX:140770594-140770594	NEGR1	Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA	Meningiomas are the most common primary nervous system tumor. The tumor suppressor NF2 is disrupted in approximately half of all meningiomas, but the complete spectrum of genetic changes remains undefined. We performed whole-genome or whole-exome sequencing on 17 meningiomas and focused sequencing on an additional 48 tumors to identify and validate somatic genetic alterations. Most meningiomas had simple genomes, with fewer mutations, rearrangements and copy-number alterations than reported in other tumors in adults. However, several meningiomas harbored more complex patterns of copy-number changes and rearrangements, including one tumor with chromothripsis. We confirmed focal NF2 inactivation in 43% of tumors and found alterations in epigenetic modifiers in an additional 8% of tumors. A subset of meningiomas lacking NF2 alterations harbored recurrent oncogenic mutations in AKT1 (p.Glu17Lys) and SMO (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways. These mutations were present in therapeutically challenging tumors of the skull base and higher grade. These results begin to define the spectrum of genetic alterations in meningiomas and identify potential therapeutic targets.	GRCh37/hg19		phs000552		Yes	AGBL4,INADL;DAB1,FAM46C;DAB1,VAV3;DNM3,TDRD5;FRRS1,DNM3;FRRS1,NPHS2;GNL2,MACF1;MACF1,SLC30A7;METTL13,DNM3;PIGK,DNM3;SPATA6,PIGK;TTC39A,PIGK
CTDB0267	Research	22388000	Chiang C, Jacobsen JC, Ernst C, Hanscom C, Heilbut A, Blumenthal I, Mills RE, Kirby A, Lindgren AM, Rudiger SR, McLaughlan CJ, Bawden CS, Reid SJ, Faull RL, Snell RG, Hall IM, Shen Y, Ohsumi TK, Borowsky ML, Daly MJ, Lee C, Morton CC, MacDonald ME, Gusella JF, Talkowski ME	Complex reorganization and predominant non-homologous repair following chromosomal breakage in karyotypically balanced germline rearrangements and transgenic integration.	Nat Genet	2012 Mar	5,X	Germline	Next Generation Sequencing	Homo sapiens	BSID42	Illumina HiSeq 2000		hsX:110368673-110368673,hs5:90466028-90466028;hs5:90502468-90502468,hsX:130567294-130567294;hs5:90711091-90711091,hs5:90892029-90892029;hs5:90892144-90892144,hsX:131442883-131442883;hsX:110368663-110368663,hs5:90719199-90719199;hsX:131438029-131438029,hs5:92483810-92483810;hs5:90494025-90494025,hs5:90892027-90892027;hs5:90494024-90494024,hs5:90502468-90502468;hs5:90691787-90691787,hs5:90886192-90886192;hs5:92932823-92932823,hs5:90693163-90693163;hs5:92483805-92483805,hs5:90719148-90719148;hs5:90892142-90892142,hs5:90466010-90466010;hs5:90886193-90886193,hs5:92932823-92932823;hsX:130567294-130567294,hs5:90711016-90711016		Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts, USA	We defined the genetic landscape of balanced chromosomal rearrangements at nucleotide resolution by sequencing 141 breakpoints from cytogenetically interpreted translocations and inversions. We confirm that the recently described phenomenon of 'chromothripsis' (massive chromosomal shattering and reorganization) is not unique to cancer cells but also occurs in the germline, where it can resolve to a relatively balanced state with frequent inversions. We detected a high incidence of complex rearrangements (19.2%) and substantially less reliance on microhomology (31%) than previously observed in benign copy-number variants (CNVs). We compared these results to experimentally generated DNA breakage-repair by sequencing seven transgenic animals, revealing extensive rearrangement of the transgene and host genome with similar complexity to human germline alterations. Inversion was the most common rearrangement, suggesting that a combined mechanism involving template switching and non-homologous repair mediates the formation of balanced complex rearrangements that are viable, stably replicated and transmitted unaltered to subsequent generations.	GRCh37/hg19				No	NA
CTDB0268	Research	22388000	Chiang C, Jacobsen JC, Ernst C, Hanscom C, Heilbut A, Blumenthal I, Mills RE, Kirby A, Lindgren AM, Rudiger SR, McLaughlan CJ, Bawden CS, Reid SJ, Faull RL, Snell RG, Hall IM, Shen Y, Ohsumi TK, Borowsky ML, Daly MJ, Lee C, Morton CC, MacDonald ME, Gusella JF, Talkowski ME	Complex reorganization and predominant non-homologous repair following chromosomal breakage in karyotypically balanced germline rearrangements and transgenic integration.	Nat Genet	2012 Mar	3,5,7	Germline	Next Generation Sequencing	Homo sapiens	BSID43	Illumina HiSeq 2000		hs3:155627600-155627600,hs7:120004011-120004011;hs7:119889673-119889673,hs3:155627601-155627601;hs3:152159406-152159406,hs7:119999922-119999922;hs7:120765008-120765008,hs3:152159406-152159406;hs7:119646830-119646830,hs7:120254239-120254239;hs7:119889690-119889690,hs7:119646829-119646829;hs7:119995774-119995774,hs7:119999919-119999919;hs7:122606556-122606556,hs7:120254240-120254240;hs5:87073891-87073891,hs7:119995778-119995778;hs7:122606486-122606486,hs5:87073908-87073908;hs7:120004010-120004010,hs7:120766450-120766450		Center for Human Genetic Research, Massachusetts General Hospital, Boston, Massachusetts, USA	We defined the genetic landscape of balanced chromosomal rearrangements at nucleotide resolution by sequencing 141 breakpoints from cytogenetically interpreted translocations and inversions. We confirm that the recently described phenomenon of 'chromothripsis' (massive chromosomal shattering and reorganization) is not unique to cancer cells but also occurs in the germline, where it can resolve to a relatively balanced state with frequent inversions. We detected a high incidence of complex rearrangements (19.2%) and substantially less reliance on microhomology (31%) than previously observed in benign copy-number variants (CNVs). We compared these results to experimentally generated DNA breakage-repair by sequencing seven transgenic animals, revealing extensive rearrangement of the transgene and host genome with similar complexity to human germline alterations. Inversion was the most common rearrangement, suggesting that a combined mechanism involving template switching and non-homologous repair mediates the formation of balanced complex rearrangements that are viable, stably replicated and transmitted unaltered to subsequent generations.	GRCh37/hg19				No	NA
CTDB0269	Research	22608083	Nik-Zainal S, Van Loo P, Wedge DC, Alexandrov LB, Greenman CD, Lau KW, Raine K, Jones D, Marshall J, Ramakrishna M, Shlien A, Cooke SL, Hinton J, Menzies A, Stebbings LA, Leroy C, Jia M, Rance R, Mudie LJ, Gamble SJ, Stephens PJ, McLaren S, Tarpey PS, Papaemmanuil E, Davies HR, Varela I, McBride DJ, Bignell GR, Leung K, Butler AP, Teague JW, Martin S, Jonsson G, Mariani O, Boyault S, Miron P, Fatima A, Langerod A, Aparicio SA, Tutt A, Sieuwerts AM, Borg A, Thomas G, Salomon AV, Richardson AL, Borresen-Dale AL, Futreal PA, Stratton MR, Campbell PJ; Breast Cancer Working Group of the International Cancer Genome Consortium	The life history of 21 breast cancers	Cell	2012 May	2,4,18,21	Breast cancer	Next Generation Sequencing	Homo sapiens	PD4120a	Illumina GAIIx or Hiseq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	Cancer evolves dynamically as clonal expansions supersede one another driven by shifting selective pressures, mutational processes, and disrupted cancer genes. These processes mark the genome, such that a cancer's life history is encrypted in the somatic mutations present. We developed algorithms to decipher this narrative and applied them to 21 breast cancers. Mutational processes evolve across a cancer's lifespan, with many emerging late but contributing extensive genetic variation. Subclonal diversification is prominent, and most mutations are found in just a fraction of tumor cells. Every tumor has a dominant subclonal lineage, representing more than 50% of tumor cells. Minimal expansion of these subclones occurs until many hundreds to thousands of mutations have accumulated, implying the existence of long-lived, quiescent cell lineages capable of substantial proliferation upon acquisition of enabling genomic changes. Expansion of the dominant subclone to an appreciable mass may therefore represent the final rate-limiting step in a breast cancer's development, triggering diagnosis.	GRCh37/hg19				Yes	NA
CTDB0270	Research	22608084	Nik-Zainal S, Alexandrov LB, Wedge DC, Van Loo P, Greenman CD, Raine K, Jones D, Hinton J, Marshall J, Stebbings LA, Menzies A, Martin S, Leung K, Chen L, Leroy C, Ramakrishna M, Rance R, Lau KW, Mudie LJ, Varela I, McBride DJ, Bignell GR, Cooke SL, Shlien A, Gamble J, Whitmore I, Maddison M, Tarpey PS, Davies HR, Papaemmanuil E, Stephens PJ, McLaren S, Butler AP, Teague JW, Jonsson G, Garber JE, Silver D, Miron P, Fatima A, Boyault S, Langerod A, Tutt A, Martens JW, Aparicio SA, Borg A, Salomon AV, Thomas G, Borresen-Dale AL, Richardson AL, Neuberger MS, Futreal PA, Campbell PJ, Stratton MR; Breast Cancer Working Group of the International Cancer Genome Consortium	Mutational processes molding the genomes of 21 breast cancers	Cell	2012 May	6	Breast cancer	Next Generation Sequencing	Homo sapiens	PD4107a	Illumina GAIIx or Hiseq 2000				Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK	All cancers carry somatic mutations. The patterns of mutation in cancer genomes reflect the DNA damage and repair processes to which cancer cells and their precursors have been exposed. To explore these mechanisms further, we generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes. Multiple distinct single- and double-nucleotide substitution signatures were discernible. Cancers with BRCA1 or BRCA2 mutations exhibited a characteristic combination of substitution mutation signatures and a distinctive profile of deletions. Complex relationships between somatic mutation prevalence and transcription were detected. A remarkable phenomenon of localized hypermutation, termed kataegis, was observed. Regions of kataegis differed between cancers but usually colocalized with somatic rearrangements. Base substitutions in these regions were almost exclusively of cytosine at TpC dinucleotides. The mechanisms underlying most of these mutational signatures are unknown. However, a role for the APOBEC family of cytidine deaminases is proposed.	GRCh37/hg19				Yes	NA
CTDB0271	Research	22980976	Govindan R, Ding L, Griffith M, Subramanian J, Dees ND, Kanchi KL, Maher CA, Fulton R, Fulton L, Wallis J, Chen K, Walker J, McDonald S, Bose R, Ornitz D, Xiong D, You M, Dooling DJ, Watson M, Mardis ER, Wilson RK	Genomic landscape of non-small cell lung cancer in smokers and never-smokers	Cell	2012 Sep	5,10,12,17,20	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	LUC7	Illumina	chr10:0-42644756:0;chr10:42644757-42644997:1;chr10:42644998-42680939:0;chr10:42680940-42681264:1;chr10:42681265-42832236:0;chr10:42832237-42833689:1;chr10:42833690-42903614:0;chr10:42903615-42970797:1;chr10:42970798-42970989:0;chr10:42970990-42990784:1;chr10:42990785-43008961:0;chr10:43008962-43048280:1;chr10:43048281-43062123:0;chr10:43062124-43062931:1;chr10:43062932-43156174:0;chr10:43156175-43157224:1;chr10:43157225-43169643:0;chr10:43169644-43187171:1;chr10:43187172-43189817:0;chr10:43189818-43210023:1;chr10:43191482-43201901:1;chr10:43210024-43221303:0;chr10:43221304-43232607:1;chr10:43232608-43277952:0;chr10:43277953-43330385:1;chr10:43330386-43366967:0;chr10:43366968-43369508:1;chr10:43369509-43474463:0;chr10:43474464-43476955:1;chr10:43476956-43572473:0;chr10:43572474-43625799:1;chr10:43625800-43633932:0;chr10:43633933-43680756:1;chr10:43680757-43689981:0;chr10:43689982-43762367:1;chr10:43762368-44124263:0;chr10:44124264-44170151:1;chr10:44126329-44127012:1;chr10:44126394-44126830:1;chr10:44170152-44236883:0;chr10:44236884-44237798:1;chr10:44237799-44273008:0;chr10:44273009-44274273:1;chr10:44274274-44340752:0;chr10:44340753-44346070:1;chr10:44346071-44407890:0;chr10:44407891-44409684:1;chr10:44409346-44409954:1;chr10:44409955-44434449:0;chr10:44434450-44439914:1;chr10:44439915-44755048:0;chr10:44755049-44757261:1;chr10:44757262-44787704:0;chr10:44787705-44789157:1;chr10:44789158-44793036:0;chr10:44793037-44881941:1;chr10:44881942-44910095:0;chr10:44910096-44910601:1;chr10:44910602-45086654:0;chr10:45086655-45097552:1;chr10:45097553-46111037:0;chr10:46111038-46168261:1;chr10:46168262-46951470:0;chr10:46951471-46966835:1;chr10:46952761-46971400:1;chr10:46971401-46993544:0;chr10:46993545-47005643:1;chr10:47005644-47011751:0;chr10:47011752-47174018:1;chr10:47083533-47088320:1;chr10:47096453-47099716:1;chr10:47133337-47133898:1;chr10:47174019-47556163:0;chr10:47556164-47566804:1;chr10:47566805-47594377:0;chr10:47594378-47595651:1;chr10:47595652-47620143:0;chr10:47620144-47644793:1;chr10:47644794-47658232:0;chr10:47658233-47701446:1;chr10:47701447-48324786:0;chr10:48324787-48332197:1;chr10:48332198-48355022:0;chr10:48355023-48373866:1;chr10:48357925-48358600:1;chr10:48373867-48381485:0;chr10:48381486-48390991:1;chr10:48390992-48413090:0;chr10:48413091-48416853:1;chr10:48416854-48425783:0;chr10:48425784-48439166:1;chr10:48439167-49360854:0;chr10:49360855-49482941:1;chr10:49407710-49409697:1;chr10:49482942-49500740:0;chr10:49500741-49501460:1;chr10:49501461-49514688:0;chr10:49514689-49647403:1;chr10:49647404-49654075:0;chr10:49654076-49864310:1;chr10:49718567-49719632:1;chr10:49754516-49754758:1;chr10:49832048-49833138:1;chr10:49864311-49872242:0;chr10:49872243-49880469:1;chr10:49880470-50184595:0;chr10:50184596-50186927:1;chr10:50186928-50192607:0;chr10:50192608-50226942:1;chr10:50222332-50323559:1;chr10:50323560-50329882:0;chr10:50329883-50359592:1;chr10:50339198-50342065:1;chr10:50359593-50362771:0;chr10:50362772-50396630:1;chr10:50396631-50504155:0;chr10:50504156-50507063:1;chr10:50507064-50507185:0;chr10:50507186-50535537:1;chr10:50535538-50572235:0;chr10:50572236-50603986:1;chr10:50603987-50627321:0;chr10:50627322-50680949:1;chr10:50663413-50747584:1;chr10:50723150-50747584:1;chr10:50747585-50817139:0;chr10:50817140-50901939:1;chr10:50818346-50820766:1;chr10:50887683-50918307:1;chr10:50911034-50911419:1;chr10:50918308-50942685:0;chr10:50942686-50970425:1;chr10:50970426-50979885:0;chr10:50979886-50981345:1;chr10:50981346-51023140:0;chr10:51023141-51023608:1;chr10:51023609-51532100:0;chr10:51532101-51532572:1;chr10:51532573-51535124:0;chr10:51535125-51535474:1;chr10:51535475-51549496:0;chr10:51549497-51562590:1;chr10:51562591-51565106:0;chr10:51565107-51590734:1;chr10:51590735-52024736:0;chr10:52024737-52026575:1;chr10:52026576-52065343:0;chr10:52065344-52384923:1;chr10:52232573-52234006:1;chr10:52384924-135374737:0;chr11:0-134452384:0;chr12:0-55224301:0;chr12:55224302-55252177:1;chr12:55252178-55341800:0;chr12:55341801-55378530:1;chr12:55378531-55413727:0;chr12:55413728-55423801:1;chr12:55423802-55587664:0;chr12:55587665-55588570:1;chr12:55588571-55640980:0;chr12:55640981-55642086:1;chr12:55642087-55656321:0;chr12:55656322-55657215:1;chr12:55657216-55705617:0;chr12:55705618-55706541:1;chr12:55706542-55714343:0;chr12:55714344-55715408:1;chr12:55715409-55770580:0;chr12:55770581-55771520:1;chr12:55771521-55782227:0;chr12:55782228-55783158:1;chr12:55783159-55794212:0;chr12:55794213-55795289:1;chr12:55795290-55845996:0;chr12:55845997-55846936:1;chr12:55846937-55862982:0;chr12:55862983-55863922:1;chr12:55863923-57316936:0;chr12:57316937-57328189:1;chr12:57328190-57345214:0;chr12:57345215-57353158:1;chr12:57348915-57400297:1;chr12:57388229-57390469:1;chr12:57400298-57403779:0;chr12:57403780-57422667:1;chr12:57422300-57444982:1;chr12:57444983-57449424:0;chr12:57449425-57481846:1;chr12:57481847-57489185:0;chr12:57489186-57525922:1;chr12:57522275-57607134:1;chr12:57588286-57588359:1;chr12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of Internal Medicine, Division of Oncology, Washington University School of Medicine, St. Louis, MO 63110, USA	We report the results of whole-genome and transcriptome sequencing of tumor and adjacent normal tissue samples from 17 patients with non-small cell lung carcinoma (NSCLC). We identified 3,726 point mutations and more than 90 indels in the coding sequence, with an average mutation frequency more than 10-fold higher in smokers than in never-smokers. Novel alterations in genes involved in chromatin modification and DNA repair pathways were identified, along with DACH1, CFTR, RELN, ABCB5, and HGF. Deep digital sequencing revealed diverse clonality patterns in both never-smokers and smokers. All validated EFGR and KRAS mutations were present in the founder clones, suggesting possible roles in cancer initiation. Analysis revealed 14 fusions, including ROS1 and ALK, as well as novel metabolic enzymes. Cell-cycle and JAK-STAT pathways are significantly altered in lung cancer, along with perturbations in 54 genes that are potentially targetable with currently available drugs.	NCBI 36/hg18				Yes	CDH12,C17orf28;COL23A1,PPM1H;FAM19A2,ANKFN1;FRS2,KCNMB4;RASSF3,TTYH2;SGMS1,STK10;TNIP1,GRIP1
CTDB0272	Research	23622249	Baca SC, Prandi D, Lawrence MS, Mosquera JM, Romanel A, Drier Y, Park K, Kitabayashi N, MacDonald TY, Ghandi M, Van Allen E, Kryukov GV, Sboner A, Theurillat JP, Soong TD, Nickerson E, Auclair D, Tewari A, Beltran H, Onofrio RC, Boysen G, Guiducci C, Barbieri CE, Cibulskis K, Sivachenko A, Carter SL, Saksena G, Voet D, Ramos AH, Winckler W, Cipicchio M, Ardlie K, Kantoff PW, Berger MF, Gabriel SB, Golub TR, Meyerson M, Lander ES, Elemento O, Getz G, Demichelis F, Rubin MA, Garraway LA	Punctuated evolution of prostate cancer genomes	Cell	2013 Apr	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR-4240	Illumina 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s17:28234791-28234791,hs17:28504265-28504265;hs1:53934406-53934406,hs10:121839093-121839093;hs2:3028194-3028194,hs2:5405183-5405183;hs3:95603862-95603862,hs20:43877450-43877450;hs4:38707775-38707775,hs6:16451138-16451138;hs4:72349157-72349157,hs9:68458031-68458031;hs5:174735682-174735682,hs17:37706997-37706997;hs17:35875710-35875710,hs17:39725909-39725909;hs1:65265150-65265150,hs3:169164605-169164605;hs1:65270801-65270801,hs3:169739027-169739027;hs2:25064638-25064638,hs17:45460714-45460714;hs3:79123742-79123742,hs5:98699524-98699524;hs3:79123778-79123778,hs5:98699838-98699838;hs3:68750411-68750411,hs11:102260307-102260307;hs6:57321666-57321666,hs6:75597990-75597990;hs17:35875727-35875727,hs17:39726419-39726419;hs17:43283417-43283417,hs17:45438048-45438048;hs1:117114140-117114140,hs10:126563867-126563867;hs3:67814589-67814589,hs3:74269927-74269927;hs3:188344787-188344787,hs7:106905327-106905327;hs3:70854854-70854854,hs13:29208573-29208573;hs16:23860010-23860010,hsX:53648872-53648872	AATF;ACADL;ACLY;ACSS2;ADAM23;ADAMTS3;ADAMTS6;ADCY3;AGBL4;AGT;AKAP6;AMFR;ANKRD18A;ANKRD46;AP2B1;APOF;ARCN1;ATAD2;ATF6;ATXN1;ATXN10;AUTS2;BAZ1A;BBS9;BCKDHA;BCL2;BLMH;BRAF;C12orf42;C17orf57;C1QBP;C20orf194;C21orf34;C3P1;C9orf171;C9orf47;CABC1;CCDC55;CCDC73;CD58;CHD1L;CHD4;CLN3;CLTA;COG5;CPD;CRTC3;CTNNA3;CWC27;DISC1;DNAH14;DNAH3;EDARADD;EEA1;EFCAB5;EHBP1L1;ENOX1;EPB41L4B;EXTL3;FAM164A;FAM178A;FAM179B;FAM188B;FBXW2;FGGY;FLJ22536;FN1;FOXA1;FREM2;FRMD6;FSTL4;GALNT10;GMPPB;GNB2L1;GRIA4;GRK5;GRXCR1;GUCY1B3;HGSNAT;HMGCLL1;HPCAL1;HUWE1;ICK;IFT80;IL1RAPL1;KBTBD2;KCNAB1;KCTD20;KDM4C;KIAA0247;KIAA0586;KIAA1549;KLHL11;KRT9;KRTAP4;LHPP;LIG3;LOC100289019;LPP;LRCH3;LYPLAL1;MARK1;MBP;ME3;MECOM;MICAL2;MKLN1;MOBKL1A;MTHFD1L;MYH7B;MYLPF;NAA25;NBPF10;NBR1;NBR2;NCKAP5;NCOA3;NCRNA00265;NDRG1;NDST3;NEO1;NME7;NOP2;NPAS3;NRF1;NRK;NTM;NUP88;NVL;OPHN1;PAK1;PCDH15;PDE11A;PDE4DIP;PEX12;PHACTR1;PHLDB1;PPM1D;PRIM2;PRKCB;PTEN;PTPRD;PTPRJ;RAB3IP;RAD51L3;RAI1;RASAL2;RASIP1;RASL10B;RAVER2;RGS10;RNF157;ROBO1;ROD1;RSRC1;RXFP1;S1PR3;SEMA3E;SEMA4G;SERGEF;SGMS2;SH3PXD2B;SIRPD;SLC17A3;SLC25A16;SLC25A25;SLC39A8;SLC39A9;SLC4A11;SLC4A4;SLC6A14;SLC7A2;SMTN;SMURF2;SNX29;SOBP;SORCS3;SPDEF;SPPL2B;SSH2;STARD9;STAT2;SYNPO;TAOK1;TBC1D10B;TET1;THRB;TMCC1;TMED3;TMEM135;TMPRSS15;TRAFD1;TUBG2;USP24;USP28;UTRN;VKORC1L1;VPS13A;WAC;WHSC1L1;WIPF2;ZCCHC6;ZNF350;ZNF516;ZNF627;ZNF704;	Harvard Medical School, Boston, MA 02115, USA	The analysis of exonic DNA from prostate cancers has identified recurrently mutated genes, but the spectrum of genome-wide alterations has not been profiled extensively in this disease. We sequenced the genomes of 57 prostate tumors and matched normal tissues to characterize somatic alterations and to study how they accumulate during oncogenesis and progression. By modeling the genesis of genomic rearrangements, we identified abundant DNA translocations and deletions that arise in a highly interdependent manner. This phenomenon, which we term chromoplexy, frequently accounts for the dysregulation of prostate cancer genes and appears to disrupt multiple cancer genes coordinately. Our modeling suggests that chromoplexy may induce considerable genomic derangement over relatively few events in prostate cancer and other neoplasms, supporting a model of punctuated cancer evolution. By characterizing the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events along which chromoplexy may drive prostate carcinogenesis.	GRCh37/hg19		phs000447		Yes	AATF,NBR2;ACADL,UTRN;ACSS2,MYH7B;ADCY3,C17orf57;ADCY3,ENOX1;AGBL4,CD58;AGBL4,GRK5;AGBL4,LHPP;AGBL4,RGS10;AKAP6,NPAS3;ANKRD46,NDRG1;ARCN1,PHLDB1;BLMH,AP2B1;BLMH,LIG3;BLMH,RAD51L3;C9orf47,S1PR3;CCDC73,BCKDHA;CHD1L,CABC1;CPD,AP2B1;EFCAB5,PEX12;FAM178A,SEMA4G;FGGY,MKLN1;FN1,ACLY;FN1,KLHL11;GNB2L1,EEA1;ICK,TMPRSS15;LPP,COG5;NAA25,TRAFD1;NOP2,CHD4;NPAS3,WIPF2;NRF1,BRAF;NUP88,C1QBP;PHACTR1,SEMA3E;PRKCB,HUWE1;RASL10B,WIPF2;RAVER2,MECOM;SGMS2,SPDEF;SLC25A16,TET1;SLC25A25,LOC100289019;SLC4A11,C20orf194;SMURF2,LOC146880;SSH2,CCDC55;STAT2,APOF;SYNRG,KRT9;TBC1D10B,MYLPF;THRB,SH3PXD2B;TMED3,AATF;VKORC1L1,KIAA0586;ZNF516,MBP
CTDB0273	Research	23622249	Baca SC, Prandi D, Lawrence MS, Mosquera JM, Romanel A, Drier Y, Park K, Kitabayashi N, MacDonald TY, Ghandi M, Van Allen E, Kryukov GV, Sboner A, Theurillat JP, Soong TD, Nickerson E, Auclair D, Tewari A, Beltran H, Onofrio RC, Boysen G, Guiducci C, Barbieri CE, Cibulskis K, Sivachenko A, Carter SL, Saksena G, Voet D, Ramos AH, Winckler W, Cipicchio M, Ardlie K, Kantoff PW, Berger MF, Gabriel SB, Golub TR, Meyerson M, Lander ES, Elemento O, Getz G, Demichelis F, Rubin MA, Garraway LA	Punctuated evolution of prostate cancer genomes	Cell	2013 Apr	1,2,3,4,5,6,7,8,9,11,13,14,15,X	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR-02-1431	Illumina GAIIx	chr10:0-67545254:0;chr10:129455829-129459318:-1;chr10:129459319-135534747:0;chr10:67545255-67549814:-1;chr10:67549815-129455828:0;chr11:0-49250219:0;chr11:132575105-132615767:-1;chr11:132615768-135006516:0;chr11:49250220-49287712:-1;chr11:49287713-132575104:0;chr12:0-133851895:0;chr13:0-85392661:0;chr13:108217365-108250572:-1;chr13:108250573-115169878:0;chr13:85392662-86207104:-1;chr13:86207105-108217364:0;chr14:0-107349540:0;chr15:0-52861486:0;chr15:52861487-53659730:1;chr15:53659731-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-241965993:0;chr1:241965994-241995938:-1;chr1:241995939-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-52498618:0;chr2:104789047-104797265:-1;chr2:104797266-126969343:0;chr2:126969344-127756885:-1;chr2:127756886-142833158:0;chr2:142833159-142847882:-1;chr2:142847883-155270304:0;chr2:155270305-155281646:-1;chr2:155281647-197657982:0;chr2:197657983-197683092:-1;chr2:197683093-198242393:0;chr2:198242394-198244545:-1;chr2:198244546-243199373:0;chr2:52498619-52501611:-1;chr2:52501612-59078160:0;chr2:59078161-59149061:-1;chr2:59149062-77766624:0;chr2:77766625-77798281:-1;chr2:77798282-80644092:0;chr2:80644093-80646143:-1;chr2:80646144-104789046:0;chr3:0-85952199:0;chr3:117935414-117954225:-1;chr3:117954226-160555652:0;chr3:160555653-160558994:-1;chr3:160558995-198022430:0;chr3:85952200-86114743:-1;chr3:86114744-90208845:0;chr3:90208846-90235690:-1;chr3:90235691-117935413:0;chr4:0-94349975:0;chr4:134550464-135258385:-1;chr4:135258386-191154276:0;chr4:94349976-94351912:-1;chr4:94351913-94539030:0;chr4:94539031-95167855:-1;chr4:95167856-134550463:0;chr5:0-18641232:0;chr5:18641233-19329676:-1;chr5:19012943-19343598:1;chr5:19343599-94041031:0;chr5:94041032-94498258:1;chr5:94498259-180915260:0;chr6:0-5070180:0;chr6:101260703-101263866:-1;chr6:101263867-103241132:0;chr6:103241133-103275724:-1;chr6:103275725-103302116:0;chr6:103302117-103333320:-1;chr6:103333321-122554530:0;chr6:122554531-122608457:-1;chr6:122608458-134438039:0;chr6:134438040-134459816:-1;chr6:134459817-171115067:0;chr6:5070181-5132765:-1;chr6:5132766-101260702:0;chr7:0-20433373:0;chr7:118809514-118883331:-1;chr7:118883332-119263653:0;chr7:119263654-119291227:-1;chr7:119291228-147385287:0;chr7:147385288-148101813:-1;chr7:148101814-152087761:0;chr7:152087762-152103550:-1;chr7:152103551-159138663:0;chr7:20433374-20441518:-1;chr7:20441519-41025413:0;chr7:41025414-41824223:-1;chr7:41824224-45995688:0;chr7:45995689-46071005:-1;chr7:46071006-46317388:0;chr7:46317389-46321362:-1;chr7:46321363-77772933:0;chr7:77772934-77776018:-1;chr7:77776019-83111113:0;chr7:83111114-83115293:-1;chr7:83115294-118809513:0;chr8:0-32129017:0;chr8:131671600-131697049:-1;chr8:131697050-132276884:0;chr8:132276885-132287641:-1;chr8:132287642-132746769:0;chr8:132746770-132750237:-1;chr8:132750238-136751739:0;chr8:136751740-137028417:-1;chr8:136927139-137293743:1;chr8:137293744-139077960:0;chr8:139077961-139641656:1;chr8:139641657-146364022:0;chr8:32129018-32135301:-1;chr8:32135302-50214898:0;chr8:50214899-51040240:1;chr8:50981269-51041041:-1;chr8:51041042-51508856:0;chr8:51508857-51531230:-1;chr8:51531231-55322070:0;chr8:55322071-55352467:-1;chr8:55352468-80858815:0;chr8:80858816-80860719:-1;chr8:80860720-85861245:0;chr8:85861246-85890883:-1;chr8:85890884-86912501:0;chr8:86912502-87003330:-1;chr8:87003331-87665849:0;chr8:87665850-87669585:-1;chr8:87669586-91825338:0;chr8:91825339-91830532:-1;chr8:91830533-131671599:0;chr9:0-4900731:0;chr9:30793045-30794774:-1;chr9:30794775-141213431:0;chr9:4900732-4995618:-1;chr9:4995619-6155342:0;chr9:6155343-6192058:-1;chr9:6192059-30793044:0;chrX:0-7414957:0;chrX:31395775-32195892:-1;chrX:32195893-78186096:0;chrX:7414958-8154831:1;chrX:78186097-78201384:-1;chrX:78201385-155270560:0;chrX:8154832-31395774:0;chrY:0-59373566:0	hs8:88444790-88444790,hs8:90229035-90229035;hs7:152103766-152103766,hs7:156644296-156644296;hs3:115157725-115157725,hsX:4019043-4019043;hs7:14785798-14785798,hs7:52411078-52411078;hs1:169439367-169439367,hs1:171045440-171045440;hs8:116041630-116041630,hs8:116171546-116171546;hs8:87873356-87873356,hs8:112670050-112670050;hs8:136557816-136557816,hs8:139692286-139692286;hs8:90238545-90238545,hs8:116061928-116061928;hs3:86105633-86105633,hs15:54383778-54383778;hsX:2449849-2449849,hsX:3137358-3137358;hs8:90092628-90092628,hs8:116850971-116850971;hs8:114040910-114040910,hs8:116175660-116175660;hs8:136592574-136592574,hs8:139572037-139572037;hs8:138882260-138882260,hs8:140974471-140974471;hs1:171045319-171045319,hs8:52284010-52284010;hs2:77610181-77610181,hs2:78170622-78170622;hs2:164326644-164326644,hs2:167606878-167606878;hs8:4025875-4025875,hs8:36625542-36625542;hs8:35993705-35993705,hs8:43527623-43527623;hs8:112754737-112754737,hs8:115726913-115726913;hs13:64460372-64460372,hs13:66472279-66472279;hs2:76145178-76145178,hs5:18457753-18457753;hs4:44915946-44915946,hs4:113127435-113127435;hs8:50216472-50216472,hs8:130558868-130558868;hs8:114013420-114013420,hs8:115721893-115721893;hs14:39923296-39923296,hs14:43107410-43107410;hsX:4930607-4930607,hsX:4938138-4938138;hs5:98256742-98256742,hs5:99280047-99280047;hs8:90133287-90133287,hs8:112671823-112671823;hs2:77674188-77674188,hs4:46290749-46290749;hs4:27979076-27979076,hs4:136740936-136740936;hs8:52264078-52264078,hs8:130582837-130582837;hs8:136877146-136877146,hs8:142113675-142113675;hs9:1670923-1670923,hs9:1695367-1695367;hs9:2632778-2632778,hs9:26963127-26963127;hs9:23582504-23582504,hs9:26955470-26955470;hs9:24777078-24777078,hs9:26371655-26371655;hs9:27729871-27729871,hs9:28470220-28470220;hs13:31061124-31061124,hs13:64135871-64135871;hs13:56750309-56750309,hs13:57607302-57607302;hs13:57669915-57669915,hs13:85630331-85630331;hs13:65778580-65778580,hs13:92113698-92113698;hsX:4976938-4976938,hsX:5391903-5391903;hs3:88081022-88081022,hs15:52791571-52791571;hs4:27745169-27745169,hs4:133627272-133627272;hs4:95127227-95127227,hs4:135195589-135195589;hs5:19361340-19361340,hs5:21625809-21625809;hs6:90869553-90869553,hs6:123731636-123731636;hs8:52539714-52539714,hs8:137790265-137790265;hs8:49137367-49137367,hs8:49431946-49431946;hs9:6690452-6690452,hs9:26943913-26943913;hs9:2052279-2052279,hs9:6746237-6746237;hs13:65786323-65786323,hs13:93273413-93273413;hs15:53829618-53829618,hs15:54258984-54258984;hsX:4945988-4945988,hsX:4979967-4979967;hs1:159921266-159921266,hs8:52631893-52631893;hs2:167589155-167589155,hs2:167694612-167694612;hs3:88050525-88050525,hs15:54295228-54295228;hs4:29546066-29546066,hs4:134418999-134418999;hs6:125444471-125444471,hs6:154207139-154207139;hs6:125896195-125896195,hs6:154255959-154255959;hs8:137859944-137859944,hs8:140069949-140069949;hs9:5914588-5914588,hs9:23433893-23433893;hs9:23455553-23455553,hs9:23980728-23980728;hs9:22020223-22020223,hs9:23970229-23970229;hs11:39325780-39325780,hs11:50618346-50618346;hs11:92475524-92475524,hs11:93298097-93298097;hs11:104221487-104221487,hs11:123210014-123210014;hs12:8403983-8403983,hs12:21911486-21911486;hs13:58385698-58385698,hs13:86444491-86444491;hsX:4936961-4936961,hsX:6215749-6215749;hsX:5110346-5110346,hsX:31416137-31416137;hs2:76166833-76166833,hs5:18551499-18551499;hs4:23169502-23169502,hs4:113629528-113629528;hs4:28910346-28910346,hs4:136631126-136631126;hs4:28986703-28986703,hs4:136641655-136641655;hs4:94545124-94545124,hs4:137852151-137852151;hs5:90731114-90731114,hs5:122080976-122080976;hs5:44910022-44910022,hs7:125256605-125256605;hs7:118850336-118850336,hs7:119110809-119110809;hs7:118883044-118883044,hs7:119107948-119107948;hs8:50217368-50217368,hs8:131711241-131711241;hs8:66501200-66501200,hs8:86999483-86999483;hs8:73988138-73988138,hs8:81321279-81321279;hs8:88431572-88431572,hs8:116853723-116853723;hs8:136978703-136978703,hs8:140080123-140080123;hs9:4770018-4770018,hs9:22331713-22331713;hs9:27753057-27753057,hs9:28490220-28490220;hs11:48339472-48339472,hs11:50619336-50619336;hs13:57920871-57920871,hs13:87070764-87070764;hs13:58599274-58599274,hs13:85644630-85644630;hs13:59098792-59098792,hs13:63893584-63893584;hs2:49765606-49765606,hs2:77167507-77167507;hs2:49998655-49998655,hs2:77574881-77574881;hs2:51225797-51225797,hs2:77181096-77181096;hs2:78282194-78282194,hs2:79844405-79844405;hs2:77667040-77667040,hs4:46286087-46286087;hs3:84440292-84440292,hs3:90204656-90204656;hs4:22870514-22870514,hs4:45779267-45779267;hs4:28092640-28092640,hs4:28355153-28355153;hs4:29570572-29570572,hs4:137160938-137160938;hs4:44913815-44913815,hs4:113136675-113136675;hs5:98257938-98257938,hs5:99283729-99283729;hs7:14795256-14795256,hs7:52401524-52401524;hs8:50205937-50205937,hs8:137867696-137867696;hs8:50454725-50454725,hs8:137076795-137076795;hs8:67409910-67409910,hs8:86926799-86926799;hs8:136924749-136924749,hs8:139588787-139588787;hs9:1624743-1624743,hs9:1682033-1682033;hs9:3147234-3147234,hs9:5906789-5906789;hs9:22071852-22071852,hs9:26502846-26502846;hs11:39340722-39340722,hs11:48486777-48486777;hs11:106096264-106096264,hs11:124118376-124118376;hs14:42193229-42193229,hs14:43044808-43044808;hs15:52507787-52507787,hs15:53761708-53761708;hs16:51546616-51546616,hs16:64121812-64121812;hs1:74792478-74792478,hs1:76065256-76065256;hs2:57943555-57943555,hs2:122681951-122681951;hs2:164552575-164552575,hs2:168378700-168378700;hs2:178306107-178306107,hs2:190532495-190532495;hs3:86003798-86003798,hs15:52544930-52544930;hs3:87703641-87703641,hs15:54675076-54675076;hs3:115155729-115155729,hsX:3183174-3183174;hs4:27844711-27844711,hs4:95167071-95167071;hs4:135943420-135943420,hs4:137123865-137123865;hs4:27842120-27842120,hs6:76524106-76524106;hs5:90545223-90545223,hs5:120237484-120237484;hs6:125843913-125843913,hs6:126053498-126053498;hs8:32559232-32559232,hs8:43552072-43552072;hs8:50001571-50001571,hs8:52570515-52570515;hs8:73948540-73948540,hs8:79794511-79794511;hs8:79774499-79774499,hs8:80846934-80846934;hs8:128871825-128871825,hs8:128879145-128879145;hs8:32025920-32025920,hs8:43557518-43557518;hs9:3151660-3151660,hs9:3622838-3622838;hs9:4815577-4815577,hs9:25322806-25322806;hs9:6709112-6709112,hs9:24597564-24597564;hs11:49287620-49287620,hs11:50617978-50617978;hs11:92474484-92474484,hs11:93296046-93296046;hs13:61065813-61065813,hs13:90634375-90634375;hs14:39887340-39887340,hs14:42242719-42242719;hsX:2455194-2455194,hsX:4066756-4066756;hs2:49773472-49773472,hs2:51208489-51208489;hs3:84456694-84456694,hs3:90199717-90199717;hs3:85003733-85003733,hs15:54705099-54705099;hs4:95136910-95136910,hs4:136908830-136908830;hs4:135673338-135673338,hs4:136684728-136684728;hs5:19321201-19321201,hs5:21121226-21121226;hs8:49939587-49939587,hs8:50025000-50025000;hs8:51038773-51038773,hs8:52290090-52290090;hs8:80856946-80856946,hs8:128880521-128880521;hs8:128872898-128872898,hs8:128883878-128883878;hs8:130545199-130545199,hs8:137865060-137865060;hs9:23518088-23518088,hs9:26125080-26125080;hs13:60738822-60738822,hs13:92231190-92231190;hs13:64143269-64143269,hs13:85395863-85395863;hs1:15418738-15418738,hs1:16754968-16754968;hs2:80027309-80027309,hs2:80933382-80933382;hs2:125499785-125499785,hs7:48541441-48541441;hs3:86077291-86077291,hs15:53024265-53024265;hs3:86112420-86112420,hs15:54426448-54426448;hs4:28089372-28089372,hs4:28354821-28354821;hs4:133974315-133974315,hs4:136909899-136909899;hs4:136887824-136887824,hs4:136928611-136928611;hs4:134557930-134557930,hs4:136908865-136908865;hs4:137876905-137876905,hs6:76522771-76522771;hs5:20920680-20920680,hs5:21595298-21595298;hs5:90567606-90567606,hs5:120072268-120072268;hs6:81652151-81652151,hs8:137154041-137154041;hs8:32559354-32559354,hs8:43595433-43595433;hs8:49638191-49638191,hs8:137871849-137871849;hs9:5215504-5215504,hs9:25640788-25640788;hs11:47814735-47814735,hs11:50621976-50621976;hs14:39792179-39792179,hs14:40042512-40042512;hs11:48338375-48338375,hs11:49286883-49286883	ABCA13;AGPS;ARPP19;ASCC3;ASNSD1;BACH2;C8orf46;C8orf84;CADM2;CDKN2B-AS1;CHD1;CNGB3;CNTNAP2;CNTNAP5;COL22A1;CSMD1;CSMD3;CTAGE5;CTNNA2;DGKB;DIAPH3;DMD;EFCAB1;FAM155A;FAT3;FBXO33;FIGN;GABRA2;GALNT13;GPC5;GRID2;GTF3C3;IFT74;ITGB8;JAK2;KAZ;KDM4C;KHDRBS3;LINGO2;LMBR1;LRFN5;LRP1B;LRRTM4;LYRM4;MAGI2;MCTP1;MLANA;MLL3;MRPS28;MYO5A;MYO5C;MYO6;NECAB1;NRG1;NRXN1;NUP160;OPCML;OR8G1;P2RY10;PLAA;PPM1L;PVT1;PXDNL;RCL1;SEMA3E;SLC19A2;SLC44A5;SMARCA2;SMARCAD1;SNTG1;SPATA21;TDRD3;TERF1;TNNI3K;TRAPPC9;TRDN;UNC13C;VLDLR;WDR72;	Harvard Medical School, Boston, MA 02115, USA	The analysis of exonic DNA from prostate cancers has identified recurrently mutated genes, but the spectrum of genome-wide alterations has not been profiled extensively in this disease. We sequenced the genomes of 57 prostate tumors and matched normal tissues to characterize somatic alterations and to study how they accumulate during oncogenesis and progression. By modeling the genesis of genomic rearrangements, we identified abundant DNA translocations and deletions that arise in a highly interdependent manner. This phenomenon, which we term chromoplexy, frequently accounts for the dysregulation of prostate cancer genes and appears to disrupt multiple cancer genes coordinately. Our modeling suggests that chromoplexy may induce considerable genomic derangement over relatively few events in prostate cancer and other neoplasms, supporting a model of punctuated cancer evolution. By characterizing the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events along which chromoplexy may drive prostate carcinogenesis.	GRCh37/hg19		phs000447		Yes	AGPS,ASNSD1;BACH2,TRDN;CADM2,MYO5C;CADM2,UNC13C;CNTNAP5,ABCA13;DIAPH3,GPC5;FBXO33,LRFN5;GRID2,SMARCAD1;KAZ,SPATA21;KHDRBS3,COL22A1;LRRTM4,GABRA2;MLL3,LMBR1;MRPS28,PVT1;NRXN1,LRRTM4;SMARCA2,KDM4C;SNTG1,PXDNL;TNNI3K,SLC44A5;VLDLR,IFT74
CTDB0274	Research	23622249	Baca SC, Prandi D, Lawrence MS, Mosquera JM, Romanel A, Drier Y, Park K, Kitabayashi N, MacDonald TY, Ghandi M, Van Allen E, Kryukov GV, Sboner A, Theurillat JP, Soong TD, Nickerson E, Auclair D, Tewari A, Beltran H, Onofrio RC, Boysen G, Guiducci C, Barbieri CE, Cibulskis K, Sivachenko A, Carter SL, Saksena G, Voet D, Ramos AH, Winckler W, Cipicchio M, Ardlie K, Kantoff PW, Berger MF, Gabriel SB, Golub TR, Meyerson M, Lander ES, Elemento O, Getz G, Demichelis F, Rubin MA, Garraway LA	Punctuated evolution of prostate cancer genomes	Cell	2013 Apr	1,2,4,5,6,7,8,10,12,13,15,X	Prostate cancer	Next Generation Sequencing	Homo sapiens	P05-620	Illumina 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Medical School, Boston, MA 02115, USA	The analysis of exonic DNA from prostate cancers has identified recurrently mutated genes, but the spectrum of genome-wide alterations has not been profiled extensively in this disease. We sequenced the genomes of 57 prostate tumors and matched normal tissues to characterize somatic alterations and to study how they accumulate during oncogenesis and progression. By modeling the genesis of genomic rearrangements, we identified abundant DNA translocations and deletions that arise in a highly interdependent manner. This phenomenon, which we term chromoplexy, frequently accounts for the dysregulation of prostate cancer genes and appears to disrupt multiple cancer genes coordinately. Our modeling suggests that chromoplexy may induce considerable genomic derangement over relatively few events in prostate cancer and other neoplasms, supporting a model of punctuated cancer evolution. By characterizing the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events along which chromoplexy may drive prostate carcinogenesis.	GRCh37/hg19		phs000447		Yes	AGL,S1PR1;BEND5,TTC28;C10orf18,NMT2;CD38,LDB2;CLVS1,NKAIN3;CNBD1,GABRG3;CNTNAP5,LRP1B;CNTNAP5,ZEB2;CUBN,MLLT10;GPR39,NCKAP5;IRAK3,GRIP1;IWS1,LRP1B;JAKMIP1,KCNIP4;LHCGR,FLJ40330;LNPEP,SLCO6A1;LYN,CYP7B1;NKAIN2,SLC2A12;NKAIN2,TBPL1;ODZ3,STOX2;PARK2,PACRG;RTCD1,CD247;SERAC1,PACRG;SLCO4C1,FNIP1;SYNJ2,LPAL2;TMBIM4,GRIP1;USP15,GRIP1;ZEB1,C10orf68
CTDB0275	Research	23622249	Baca SC, Prandi D, Lawrence MS, Mosquera JM, Romanel A, Drier Y, Park K, Kitabayashi N, MacDonald TY, Ghandi M, Van Allen E, Kryukov GV, Sboner A, Theurillat JP, Soong TD, Nickerson E, Auclair D, Tewari A, Beltran H, Onofrio RC, Boysen G, Guiducci C, Barbieri CE, Cibulskis K, Sivachenko A, Carter SL, Saksena G, Voet D, Ramos AH, Winckler W, Cipicchio M, Ardlie K, Kantoff PW, Berger MF, Gabriel SB, Golub TR, Meyerson M, Lander ES, Elemento O, Getz G, Demichelis F, Rubin MA, Garraway LA	Punctuated evolution of prostate cancer genomes	Cell	2013 Apr	1,2,3,4,5,6,7,8,9,10,11.12,13,14,16,18	Prostate cancer	Next Generation Sequencing	Homo sapiens	P07-837	Illumina GAIIx	chr10:0-48306147:0;chr10:48306148-48308685:-1;chr10:48308686-56887177:0;chr10:56887178-57278579:-1;chr10:57278580-58351326:0;chr10:58351327-58353667:-1;chr10:58353668-91455960:0;chr10:91455961-91457753:-1;chr10:91457754-135534747:0;chr11:0-100455595:0;chr11:100455596-100458880:-1;chr11:100458881-101032307:0;chr11:101032308-101046549:-1;chr11:101046550-101227741:0;chr11:101227742-101229298:-1;chr11:101229299-122554109:0;chr11:122554110-122592020:-1;chr11:122592021-135006516:0;chr12:0-18093018:0;chr12:130470361-130475618:-1;chr12:130475619-133851895:0;chr12:18093019-18132905:-1;chr12:18132906-82083659:0;chr12:82083660-82086191:-1;chr12:82086192-83914810:0;chr12:83914811-83940823:-1;chr12:83940824-83946194:0;chr12:83946195-83951946:-1;chr12:83951947-130470360:0;chr13:0-49466741:0;chr13:49466742-49470127:-1;chr13:49470128-66306134:0;chr13:66306135-66345555:-1;chr13:66345556-67361323:0;chr13:67361324-67378876:-1;chr13:67378877-71313228:0;chr13:71313229-71314931:-1;chr13:71314932-85275132:0;chr13:85275133-85406868:-1;chr13:85406869-115169878:0;chr14:0-29254698:0;chr14:29254699-29256010:-1;chr14:29256011-107349540:0;chr15:0-102531392:0;chr16:0-46786125:0;chr16:46786126-46792736:-1;chr16:46792737-60099927:0;chr16:60099928-60107713:-1;chr16:60107714-65191699:0;chr16:65191700-65193852:-1;chr16:65193853-90354753:0;chr17:0-81195210:0;chr18:0-58870645:0;chr18:58870646-58888958:-1;chr18:58888959-78077248:0;chr19:0-59128983:0;chr1:0-74275561:0;chr1:157437672-157483853:-1;chr1:157483854-157529865:0;chr1:157529866-157991572:-1;chr1:157991573-191100804:0;chr1:191100805-191764780:-1;chr1:191764781-195158205:0;chr1:195158206-195162275:-1;chr1:195162276-195687563:0;chr1:195687564-196331431:1;chr1:196331432-213936324:0;chr1:213936325-213978828:-1;chr1:213978829-213985252:0;chr1:213985253-214291488:-1;chr1:214291489-249250621:0;chr1:74275562-74543357:-1;chr1:74543358-74717562:0;chr1:74717563-74734684:-1;chr1:74734685-98868286:0;chr1:98868287-98879108:-1;chr1:98879109-157437671:0;chr20:0-63025520:0;chr21:0-33244273:0;chr21:33244274-33257808:1;chr21:33257809-48129895:0;chr22:0-51304566:0;chr2:0-36783130:0;chr2:108600786-108603058:-1;chr2:108603059-115587112:0;chr2:115587113-116104622:-1;chr2:116104623-126683099:0;chr2:126683100-126690201:-1;chr2:126690202-200198016:0;chr2:200198017-200202450:-1;chr2:200202451-243199373:0;chr2:36783131-36792425:-1;chr2:36792426-41506590:0;chr2:41506591-41510095:-1;chr2:41510096-108600785:0;chr3:0-13560059:0;chr3:13560060-13975783:-1;chr3:13975784-97478252:0;chr3:160498400-160509709:-1;chr3:160509710-198022430:0;chr3:97478253-97490714:1;chr3:97490715-160498399:0;chr4:0-63461618:0;chr4:101851372-101860883:-1;chr4:101860884-118459739:0;chr4:118459740-118496684:-1;chr4:118496685-131078247:0;chr4:131078248-131341209:-1;chr4:131341210-136847779:0;chr4:136847780-137719893:-1;chr4:137719894-158636194:0;chr4:158636195-158659698:-1;chr4:158659699-165480854:0;chr4:165480855-165482531:-1;chr4:165482532-180509325:0;chr4:180509326-181369943:-1;chr4:181369944-191154276:0;chr4:63461619-63749508:-1;chr4:63749509-101851371:0;chr5:0-25746136:0;chr5:101426460-101616895:1;chr5:101616896-102031693:0;chr5:102031694-102685835:-1;chr5:102174970-102344661:-1;chr5:102685836-180915260:0;chr5:25746137-25849725:-1;chr5:25849726-28668691:0;chr5:28668692-28671091:-1;chr5:28671092-91996106:0;chr5:91996107-92031510:-1;chr5:92031511-92465034:0;chr5:92465035-92471311:-1;chr5:92471312-97046165:0;chr5:97046166-97359160:1;chr5:97359161-97819013:0;chr5:97819014-97910310:-1;chr5:97910311-98601120:0;chr5:98601121-98848867:1;chr5:98667029-99104792:1;chr5:99104793-99659596:0;chr5:99659597-99738763:-1;chr5:99738764-101426459:0;chr6:0-48899576:0;chr6:48899577-48902556:-1;chr6:48902557-56208185:0;chr6:56208186-56209956:-1;chr6:56209957-84846953:0;chr6:84846954-84907408:-1;chr6:84907409-97023511:0;chr6:97023512-97071598:-1;chr6:97071599-171115067:0;chr7:0-32521336:0;chr7:149299057-150055949:1;chr7:150055950-159138663:0;chr7:32521337-32639855:-1;chr7:32639856-52944488:0;chr7:52944489-52945925:-1;chr7:52945926-61065859:0;chr7:61065860-61850256:-1;chr7:61850257-83867078:0;chr7:83867079-83890714:-1;chr7:83890715-84554812:0;chr7:84554813-84941346:-1;chr7:84941347-149299056:0;chr8:0-35009330:0;chr8:35009331-35037790:-1;chr8:35037791-47609563:0;chr8:47609564-48138941:-1;chr8:48138942-64626657:0;chr8:64626658-64644053:-1;chr8:64644054-146364022:0;chr9:0-8117074:0;chr9:8117075-8813716:1;chr9:8746203-8847456:-1;chr9:8847457-141213431:0;chrX:0-44726064:0;chrX:44726065-44736052:-1;chrX:44736053-155270560:0;chrY:0-59373566:0	hs8:33588296-33588296,hs8:33843616-33843616;hs7:84933870-84933870,hs7:114253520-114253520;hs7:84033328-84033328,hs7:113043568-113043568;hs8:33614817-33614817,hs8:33874889-33874889;hs2:200250719-200250719,hs2:201160988-201160988;hs8:14746503-14746503,hs8:111260220-111260220;hs10:53905507-53905507,hs10:87951131-87951131;hs10:58095842-58095842,hs10:88478649-88478649;hs10:57678808-57678808,hs10:59705957-59705957;hs10:54007781-54007781,h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Medical School, Boston, MA 02115, USA	The analysis of exonic DNA from prostate cancers has identified recurrently mutated genes, but the spectrum of genome-wide alterations has not been profiled extensively in this disease. We sequenced the genomes of 57 prostate tumors and matched normal tissues to characterize somatic alterations and to study how they accumulate during oncogenesis and progression. By modeling the genesis of genomic rearrangements, we identified abundant DNA translocations and deletions that arise in a highly interdependent manner. This phenomenon, which we term chromoplexy, frequently accounts for the dysregulation of prostate cancer genes and appears to disrupt multiple cancer genes coordinately. Our modeling suggests that chromoplexy may induce considerable genomic derangement over relatively few events in prostate cancer and other neoplasms, supporting a model of punctuated cancer evolution. By characterizing the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events along which chromoplexy may drive prostate carcinogenesis.	GRCh37/hg19		phs000447		Yes	CISD1,ATAD1;DPP10,TPTE;EYS,RIMS1;FAM5C,KCNT2;GAD2,RAB18;HEBP1,GUCY2C;KIF21A,SLC2A13;LRP6,GRIN2B;NTNG1,WDR47;PAM,CAMK4;PCDH15,PAPSS2;PJA2,CAMK4;PRKG1,GRID1;SLCO6A1,PAM;SPOCK3,GALNTL6
CTDB0276	Research	23622249	Baca SC, Prandi D, Lawrence MS, Mosquera JM, Romanel A, Drier Y, Park K, Kitabayashi N, MacDonald TY, Ghandi M, Van Allen E, Kryukov GV, Sboner A, Theurillat JP, Soong TD, Nickerson E, Auclair D, Tewari A, Beltran H, Onofrio RC, Boysen G, Guiducci C, Barbieri CE, Cibulskis K, Sivachenko A, Carter SL, Saksena G, Voet D, Ramos AH, Winckler W, Cipicchio M, Ardlie K, Kantoff PW, Berger MF, Gabriel SB, Golub TR, Meyerson M, Lander ES, Elemento O, Getz G, Demichelis F, Rubin MA, Garraway LA	Punctuated evolution of prostate cancer genomes	Cell	2013 Apr	1,2,3,4,5,6,8,9,11,13,15,17,18,21,22	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR-06-1749	Illumina 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Medical School, Boston, MA 02115, USA	The analysis of exonic DNA from prostate cancers has identified recurrently mutated genes, but the spectrum of genome-wide alterations has not been profiled extensively in this disease. We sequenced the genomes of 57 prostate tumors and matched normal tissues to characterize somatic alterations and to study how they accumulate during oncogenesis and progression. By modeling the genesis of genomic rearrangements, we identified abundant DNA translocations and deletions that arise in a highly interdependent manner. This phenomenon, which we term chromoplexy, frequently accounts for the dysregulation of prostate cancer genes and appears to disrupt multiple cancer genes coordinately. Our modeling suggests that chromoplexy may induce considerable genomic derangement over relatively few events in prostate cancer and other neoplasms, supporting a model of punctuated cancer evolution. By characterizing the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events along which chromoplexy may drive prostate carcinogenesis.	GRCh37/hg19		phs000447		Yes	ANK1,MYST3;C13orf16,DSCR4;C18orf55,ZNF407;C3orf31,STT3B;C3orf66,PLCXD2;CDH12,EDIL3;CNTN4,VGLL4;CNTN5,ARHGAP42;CNTN5,MMP12;CNTN6,SLC6A1;COL9A1,NCOA7;CTH,CASC3;DOK6,CD226;DOPEY1,NKAIN2;DOPEY1,SNAP91;DPP10,GALNT13;EDEM1,HRH1;ELOVL4,NKAIN2;GAB4,EFCAB6;ITPR1,EDEM1;LINGO2,DDX58;LOC100128164,SEC62;LOC285375,LOC646498;LOC646498,CCDC36;RELT,ELFN2;STT3B,CCDC36;TMEM123,ARHGAP32;TRIM59,ZBBX;UBR1,DLL3;UBR1,LRRC37B2;VGLL4,CCDC36;VGLL4,ZNF407;WWOX,GAN
CTDB0277	Research	23622249	Baca SC, Prandi D, Lawrence MS, Mosquera JM, Romanel A, Drier Y, Park K, Kitabayashi N, MacDonald TY, Ghandi M, Van Allen E, Kryukov GV, Sboner A, Theurillat JP, Soong TD, Nickerson E, Auclair D, Tewari A, Beltran H, Onofrio RC, Boysen G, Guiducci C, Barbieri CE, Cibulskis K, Sivachenko A, Carter SL, Saksena G, Voet D, Ramos AH, Winckler W, Cipicchio M, Ardlie K, Kantoff PW, Berger MF, Gabriel SB, Golub TR, Meyerson M, Lander ES, Elemento O, Getz G, Demichelis F, Rubin MA, Garraway LA	Punctuated evolution of prostate cancer genomes	Cell	2013 Apr	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,18,20,21,X,Y	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR-08-556	Illumina 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Medical School, Boston, MA 02115, USA	The analysis of exonic DNA from prostate cancers has identified recurrently mutated genes, but the spectrum of genome-wide alterations has not been profiled extensively in this disease. We sequenced the genomes of 57 prostate tumors and matched normal tissues to characterize somatic alterations and to study how they accumulate during oncogenesis and progression. By modeling the genesis of genomic rearrangements, we identified abundant DNA translocations and deletions that arise in a highly interdependent manner. This phenomenon, which we term chromoplexy, frequently accounts for the dysregulation of prostate cancer genes and appears to disrupt multiple cancer genes coordinately. Our modeling suggests that chromoplexy may induce considerable genomic derangement over relatively few events in prostate cancer and other neoplasms, supporting a model of punctuated cancer evolution. By characterizing the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events along which chromoplexy may drive prostate carcinogenesis.	GRCh37/hg19		phs000447		Yes	ABCA13,FIGNL1;ABLIM1,CASC2;AMPH,VPS41;AQR,INO80;ARID1B,ZDHHC14;BRD8,HARS;C9orf150,C9orf93;C9orf46,MLANA;C9orf46,PTPRD;CCDC18,GCLM;CDH2,TTC28;CDS1,ARHGAP24;CELF4,PIK3C3;CHL1,CNTN6;CNBD1,MMP16;CYB5R4,TBX18;DDX10,SKA3;DOK6,NETO1;DOPEY2,DYRK1A;DPY19L1,POU6F2;EEPD1,ELMO1;EEPD1,POU6F2;ELMO1,C7orf10;EXOC3,CEP72;EYS,ARID1B;EYS,SYNE1;FNBP1L,BCAR3;GHR,PRKD1;GLRA3,WDR17;GRIN2B,PIK3C2G;HECW1,ABCA13;HERPUD2,POU6F2;KCND2,SPTLC3;KCNJ6,DSCR4;KDM4C,PTPRD;KIAA0895,AMPH;KIAA0895,POU6F2;KIAA1328,RIT2;KIAA1712,GLRA3;MLANA,KDM4C;MYL1,CPS1;NCAM1,USP28;NHSL2,NCRNA00182;PLXNC1,NTN4;POU6F2,C7orf10;PRIM2,EYS;PRSS3,UBE2R2;PTPRD,NFIB;RFTN1,CADM2;RFX3,IL33;RFX3,INSL6;RIC3,TRIM66;RIT2,ZNF407;SLC23A2,SPTLC3;TBC1D5,CADM2;WDFY3,ARHGAP24
CTDB0278	Research	23622249	Baca SC, Prandi D, Lawrence MS, Mosquera JM, Romanel A, Drier Y, Park K, Kitabayashi N, MacDonald TY, Ghandi M, Van Allen E, Kryukov GV, Sboner A, Theurillat JP, Soong TD, Nickerson E, Auclair D, Tewari A, Beltran H, Onofrio RC, Boysen G, Guiducci C, Barbieri CE, Cibulskis K, Sivachenko A, Carter SL, Saksena G, Voet D, Ramos AH, Winckler W, Cipicchio M, Ardlie K, Kantoff PW, Berger MF, Gabriel SB, Golub TR, Meyerson M, Lander ES, Elemento O, Getz G, Demichelis F, Rubin MA, Garraway LA	Punctuated evolution of prostate cancer genomes	Cell	2013 Apr	1,2,3,4,5,6,7,8,10,11,12,13,18,X	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR-3042	Illumina 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19;LOC646982;LRP1B;LRRC58;LSAMP;MCC;MECOM;MEGF10;MEI1;MIR548A3;MIR548G;MMP16;MRPS28;NAALAD2;NCRNA00259;NEK1;NKAIN2;NKAIN3;NSMAF;ODF2L;ODZ2;ODZ3;OPCML;OR52I1;PCDH7;PCYT1B;PDE7A;PDZD2;PEMT;PHF3;PIKFYVE;PKIA;PKIB;PLCL1;PLS3;PPM1L;PRDM6;PRKCA;PTPRJ;RAB38;ROBO1;ROBO2;RRH;SCHIP1;SCLT1;SDR16C5;SELT;SERPINB2;SERPINB8;SERPINI2;SGCZ;SI;SLC22A3;SLC25A15;SLCO1A2;SMC4;SMC6;SNCAIP;SOX5;SPIN4;SSBP2;STXBP5L;TAF1A;TCERG1L;THNSL1;THSD7B;TMEM132D;TOMM70A;TOX;TRAPPC9;TRDN;TRIM55;U2AF1;UGGT2;VPS54;VWC2;WDR41;WDR49;WWTR1;XKR4;ZNF717;ZNF804A;	Harvard Medical School, Boston, MA 02115, USA	The analysis of exonic DNA from prostate cancers has identified recurrently mutated genes, but the spectrum of genome-wide alterations has not been profiled extensively in this disease. We sequenced the genomes of 57 prostate tumors and matched normal tissues to characterize somatic alterations and to study how they accumulate during oncogenesis and progression. By modeling the genesis of genomic rearrangements, we identified abundant DNA translocations and deletions that arise in a highly interdependent manner. This phenomenon, which we term chromoplexy, frequently accounts for the dysregulation of prostate cancer genes and appears to disrupt multiple cancer genes coordinately. Our modeling suggests that chromoplexy may induce considerable genomic derangement over relatively few events in prostate cancer and other neoplasms, supporting a model of punctuated cancer evolution. By characterizing the clonal hierarchy of genomic lesions in prostate tumors, we charted a path of oncogenic events along which chromoplexy may drive prostate carcinogenesis.	GRCh37/hg19		phs000447		Yes	TAF1A,FAM117B;C2orf27A,IFIH1;THSD7B,LRP1B;VPS54,TRAPPC9;LSAMP,GSK3B;ROBO1,PKIB;CHL1,ODZ3;MIR548G,TOMM70A;ROBO1,NKAIN2;FSTL1,NCRNA00259;SELT,NKAIN2;MIR548A3,STXBP5L;DDX60L,GALNTL6;ANK2,CAMK2D;COL25A1,ENPEP;SCLT1,CDH12;EGF,CDH12;NEK1,CSTF1;WDR41,ARSB;FBXL17,TCERG1L;SNCAIP,PRDM6;IQGAP2,KIAA0355;NKAIN2,LAMA2;TRDN,PTPRK;SLC22A3,FGD4;AVL9,GRB10;XKR4,CLVS1;XKR4,CLVS1;XKR4,CYP7B1;XKR4,NKAIN3;SGCZ,PKIA;HEY1,KIRREL3;RAB38,NAALAD2;COG6,SLC25A15;DZIP1,U2AF1;SERPINB2,SERPINB8;AMMECR1,AMOT
CTDB0279	Methodology	23940299	Sanborn JZ, Salama SR, Grifford M, Brennan CW, Mikkelsen T, Jhanwar S, Katzman S, Chin L, Haussler D	Double minute chromosomes in glioblastoma multiforme are revealed by precise reconstruction of oncogenic amplicons	Cancer Research	2013 Oct 	9,12	Glioblastoma	Next Generation Sequencing	Homo sapiens	TCGA-06-0648		chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-65837944:0;chr12:65837945-66055069:1;chr12:66055070-66055380:0;chr12:66055381-66072676:1;chr12:66072677-66075067:0;chr12:66075068-66100528:1;chr12:66100529-66344990:0;chr12:66344991-66358803:1;chr12:66358804-66359378:0;chr12:66359379-66448933:1;chr12:66448934-66681859:0;chr12:66681860-66764263:1;chr12:66764264-67035467:0;chr12:67035468-67050196:1;chr12:67050197-67051074:0;chr12:67051075-67085451:1;chr12:67085452-67316332:0;chr12:67316333-67368167:1;chr12:67368168-67451017:0;chr12:67451018-67459422:1;chr12:67459423-67472942:0;chr12:67472943-67530895:1;chr12:67530896-67531675:0;chr12:67531676-67537257:1;chr12:67537177-67628514:1;chr12:67628515-67770598:0;chr12:67770599-67890243:1;chr12:67890244-67960817:0;chr12:67960818-68022264:1;chr12:68022265-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-135834391:0;chr9:135834392-135834618:1;chr9:135834619-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs12:66358555-66358803,hs12:66763926-66764263;hs12:67810680-67810853,hsX:54320719-54320744;hs12:66350731-66350875,hsX:101299719-101299730;hs12:66650577-66650728,hs12:68023553-68023715;hs12:67053755-67053878,hs3:185454999-185455012;hs12:66054835-66055069,hs9:135834530-135834618;hs12:67363426-67363508,hs12:67528856-67528980;hs12:66687266-66687380,hs12:67533819-67533978;hs12:66398631-66398792,hs13:99673601-99673672;hs12:66074586-66074631,hs12:66681079-66681202;hs12:65957502-65957622,hs22:48775252-48775370;hs12:66055381-66055730,hs12:67537177-67537541;hs12:66344991-66345249,hs12:68021986-68022264;hs12:66054950-66055111,hs12:67472904-67473224;hs12:66733983-66734166,hs12:67580167-67580368;hs12:67051075-67051320,hs12:67451018-67451391;hs12:65837945-65838144,hs12:66448613-66448929;hs12:67815282-67815471,hs5:136666111-136666114;hs12:67527252-67527522,hs8:97167579-97167625;hs12:66748792-66748921,hs22:48937381-48937494;hs12:66100207-66100528,hs12:66681860-66682114;hs12:66420984-66421144,hs22:48835485-48835755;hs12:65929775-65929897,hs16:72726677-72726693;hs12:66073329-66073520,hs12:68065659-68065870;hs12:65896905-65897114,hs22:48637321-48637414;hs12:67073429-67073694,hs2:210642752-210642758;hs12:65839551-65839775,hs12:67825318-67825523;hs12:66075068-66075262,hs12:66359379-66359603;hs12:66700571-66700720,hs12:67072869-67072995;hs12:67530575-67530895,hs12:67770599-67770946;hs12:66072398-66072676,hs12:67889923-67890243;hs12:67085146-67085451,hs12:67536855-67537257;hs12:66050493-66050661,hs12:67577290-67577451;hs12:67531676-67531994,hs12:67628278-67628514;hs12:65887474-65887619,hs12:66694681-66694764;hs12:67818920-67819049,hs12:67980392-67980597;hs12:66732589-66732838,hs12:67580851-67581048;hs12:65837358-65837535,hs12:66164005-66164163;hs12:67367906-67368167,hs12:67960818-67961176;hs12:66687038-66687251,hs12:66754719-66754944;hs12:66683943-66684150,hs12:67805028-67805235;hs12:66755375-66755599,hs22:48635052-48635262;hs12:66025353-66025516,hs12:67554147-67554310;hs12:66016636-66016807,hs12:67058039-67058166;hs12:77803075-77803262,hs12:77803962-77804154;hs12:66243020-66243174,hs12:68065211-68065389;hs12:67049932-67050196,hs12:67316333-67316622;hs12:67515167-67515368,hs22:48690695-48690822;hs12:67321187-67321363,hs12:67843584-67843723;hs12:66400478-66400626,hs12:66412238-66412335;hs12:67035468-67035754,hs12:67459177-67459422;hs12:67074005-67074173,hs12:67844346-67844539;hs12:67472943-67473166,hs9:135834392-135834455;hs12:66401802-66401926,hs22:48848404-48848491;hs11:79450674-79450830,hs11:80247904-80248042;hs11:79425728-79425819,hs11:79447098-79447288;hs10:41728216-41728245,hs12:34745551-34745589;hs10:89516908-89517093,hs10:90653020-90653202;hs17:38912647-38912708,hs18:22227376-22227382;hs17:53013168-53013311,hs9:133612391-133612402;hs16:33857992-33859041,hsY:10627235-10628113;hs16:44958667-44959283,hs16:44960910-44961126;hs18:23217516-23217616,hs18:23218933-23219067;hs18:9228780-9228918,hs18:28596414-28596522;hs18:6736317-6736424,hs18:9345292-9345390;hs18:23989851-23990016,hs18:25650633-25650732;hs22:43109344-43109475,hs22:47708183-47708278;hs22:16885769-16885970,hs22:27523748-27523905;hs22:32763567-32763679,hs22:34393075-34393220;hs22:48678833-48678909,hs22:48852675-48852853;hs22:22015300-22015539,hs22:47777107-47777218;hs22:48673340-48673445,hs22:48722186-48722353;hs22:24929222-24929428,hs22:40784068-40784160;hs21:9720926-9720996,hs22:31454215-31454364;hs4:19998865-19999046,hs4:23433162-23433339;hs4:20191878-20192072,hs4:24068204-24068405;hs4:132809659-132809830,hs9:46294195-46294249;hs4:23137392-23137577,hs4:23888373-23888532;hs3:189740345-189740559,hs3:189876644-189876856;hs3:189738944-189739176,hs3:189742505-189742694;hs2:34557918-34557933,hs8:1416822-1416965;hs2:90966487-90967031,hs2:90977116-90978255;hs2:132762009-132762204,hs4:49210357-49210657;hs9:26048012-26048215,hs9:26536336-26536547;hs9:26539731-26539905,hs9:26732158-26732349;hs9:21475882-21476028,hs9:24304363-24304486;hs9:22220584-22220728,hs9:26095687-26095879;hs9:22507025-22507200,hs9:23373840-23374045;hs9:22452340-22452487,hs9:26944351-26944522;hs9:26694112-26694315,hs9:27403094-27403295;hs9:26695268-26695371,hs9:26949108-26949215;hs9:21383845-21383945,hs9:22047421-22047481;hs9:23562681-23562871,hs9:25540621-25540790;hs9:25539461-25539653,hs9:26725709-26725925;hs9:25461325-25461478,hs9:26047803-26047970;hs9:23648745-23648896,hs9:26108310-26108481;hs9:22601786-22601913,hs9:27291204-27291405	AK127888;ALG10;ALG10B;ANKRD20A2;BC022082;C4orf33;C8orf37;C9orf11;C9orf82;CAND1;CDKN2B;CPM;CPSF6;DMRTA1;DQ575272;DYRK2;ELAVL2;FAM75A7;GRIP1;IFNA2;IFNA8;IFNE;IFNG;IFT74;LYZ;MDM1;MDM2;MED27;MGC50273;MOBKL2B;MTAP;NAV3;NUP107;PLAA;RAP1B;RAPGEF1;SLC35E3;SYT1;tmp_locus_39;TUSC1;VAV2;YEATS4;	Five3 Genomics, LLC, Santa Cruz, CA, 9506	DNA sequencing offers a powerful tool in oncology based on the precise definition of structural rearrangements and copy number in tumor genomes. Here, we describe the development of methods to compute copy number and detect structural variants to locally reconstruct highly rearranged regions of the tumor genome with high precision from standard, short-read, paired-end sequencing datasets. We find that circular assemblies are the most parsimonious explanation for a set of highly amplified tumor regions in a subset of glioblastoma multiforme samples sequenced by The Cancer Genome Atlas (TCGA) consortium, revealing evidence for double minute chromosomes in these tumors. Further, we find that some samples harbor multiple circular amplicons and, in some cases, further rearrangements occurred after the initial amplicon-generating event. Fluorescence in situ hybridization analysis offered an initial confirmation of the presence of double minute chromosomes. Gene content in these assemblies helps identify likely driver oncogenes for these amplicons. RNA-seq data available for one double minute chromosome offered additional support for our local tumor genome assemblies, and identified the birth of a novel exon made possible through rearranged sequences present in the double minute chromosomes. Our method was also useful for analysis of a larger set of glioblastoma multiforme tumors for which exome sequencing data are available, finding evidence for oncogenic double minute chromosomes in more than 20% of clinical specimens examined, a frequency consistent with previous estimates.					Yes	NA
CTDB0280	Research	22926521	Schepeler T, Lamy P, Hvidberg V, Laurberg JR, Fristrup N, Reinert T, Bartkova J, Tropia L, Bartek J, Halazonetis TD, Pan CC, Borre M, Dyrskjot L, Orntoft TF	A high resolution genomic portrait of bladder cancer: correlation between genomic aberrations and the DNA damage response	Oncogene	2013 Aug 	8	Bladder cancer	SNP Array	Homo sapiens	B1735	Affymetrix SNP 6.0	chr10:0-62759:0;chr10:135356696-135374737:0;chr10:28819363-135356695:-1;chr10:55106654-82886849:1;chr10:62760-42919144:1;chr10:84041293-84120682:1;chr11:0-188509:0;chr11:134449983-134452384:0;chr11:188510-134449982:-1;chr11:55844245-57208782:1;chr12:0-132349534:0;chr13:0-47869578:0;chr13:47869579-51359596:-1;chr13:51359597-56965032:0;chr13:56965033-64574504:-1;chr13:64574505-114142980:0;chr14:0-18072124:0;chr14:105952894-105989097:0;chr14:105989098-106356482:-1;chr14:106356483-106368585:0;chr14:18072125-105952893:-1;chr14:20981847-22390230:1;chr15:0-18846948:0;chr15:100286565-100338915:0;chr15:18846949-72101389:-1;chr15:62433956-100286564:1;chr15:89058903-100286564:-1;chr16:0-777:0;chr16:29769296-47443493:1;chr16:30536196-69429180:-1;chr16:69429181-69761496:0;chr16:69761497-88815037:-1;chr16:778-29917385:-1;chr16:88815038-88827254:0;chr17:0-526:0;chr17:22359448-78774742:0;chr17:527-22359447:-1;chr18:0-76117153:0;chr19:0-41910:0;chr19:41911-63789667:1;chr19:63789668-63811651:0;chr1:0-247249719:0;chr20:0-9305:0;chr20:62426599-62435964:0;chr20:9306-62426598:1;chr21:0-9965425:0;chr21:42848164-46921386:-1;chr21:46921387-46944323:0;chr21:9965426-46921386:1;chr22:0-14432528:0;chr22:14432529-15566422:-1;chr22:15566423-19174824:0;chr22:19174825-49581322:-1;chr22:49581323-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-6246866:0;chr5:180722928-180857866:0;chr5:49473152-180722927:-1;chr5:6246867-6629631:-1;chr5:6629632-9415932:0;chr5:9415933-9666220:-1;chr5:9666221-49473151:0;chr6:0-94661:0;chr6:13024644-13042233:-1;chr6:170892932-170899992:0;chr6:32173957-32294274:-1;chr6:32732822-46986613:-1;chr6:36760762-44020003:1;chr6:46986614-56641250:0;chr6:533262-1077236:-1;chr6:56641251-57419168:1;chr6:56900795-60414872:-1;chr6:58249221-61966190:1;chr6:61966190-170892931:-1;chr6:64720033-65084155:1;chr6:94662-36415922:1;chr7:0-52911:0;chr7:158819767-158821424:0;chr7:52912-158819766:1;chr8:0-21254:0;chr8:146268961-146274826:0;chr8:21255-43924583:-1;chr8:37244074-37709713:1;chr8:39600479-39633022:1;chr8:39988202-146268960:1;chr9:0-36430:0;chr9:13340082-16838616:1;chr9:140211217-140273252:0;chr9:26901712-37913961:1;chr9:36431-140211216:-1;chr9:36431-8471745:1;chr9:70136750-70160650:1;chrX:0-154913754:0;chrY:0-57772954:0		LRP1B	Department of Molecular Medicine, Aarhus University Hospital, Skejby, Aarhus N, Denmark	One major challenge in cancer research is to understand the complex interplay between the DNA damage response (DDR), genomic integrity, and tumor development. To address these issues, we analyzed 43 bladder tumor genomes from 22 patients using single nucleotide polymorphism (SNP) arrays, and tissue expression of multiple DDR proteins, including Timeless and its interaction partner Tipin. The SNP profiles confirmed and extended known copy number alterations (CNAs) at high resolution, showed clustering of CNAs at nine common fragile sites, and revealed that most metachronous tumors were clonally related. The occurrence of many novel uniparental disomy regions (UPDs) was of potential functional importance in some tumors because UPDs spanned mutated FGFR3 and PIK3CA alleles, and also homozygous deletion of the CDKN2A tumor suppressor locus. The DDR signaling as evaluated by phospho-epitope-specific antibodies against Ser139-phosphorylated H2A histone family member X (gama-H2AX), ataxia telangiectasia mutated (ATM), and ATM- and Rad3-related (ATR) was commonly activated in tumors with both moderate and high extent of accumulated genomic aberrations, the latter tumors showing a more frequent loss of ATM expression. Strikingly, the tumor genomes exhibiting the most complex alterations were associated with a high Ki67-proliferation index, abundant Timeless but not Tipin expression, aberrant p53 expression, and homozygous CDKN2A deletions. Of clinical relevance, evaluation of a tissue microarray (TMA; n=319) showed that abundant Timeless expression was associated with risk of progression to muscle-invasive disease (P<0.0005; hazard ratio, 2.4; 95% confidence interval, 1.6-3.8) and higher T stage (P<0.05). Univariate analysis confirmed this association (P=0.006) in an independent cohort (n=241) but statistical significance was not reached in a multivariate model. Overall, our results are consistent with DDR activation preceding the accumulation of genomic aberrations. Tumors with extensive genomic rearrangements were associated with inactivation of CDKN2A, excessive proliferation, and robust Timeless expression, the latter also correlating with the risk of disease progression. Moreover, we provide evidence to suggest that UPDs likely contribute to bladder tumorigenesis. 	NCBI 36/hg18				Yes	NA
CTDB0281	Research	22926521	Schepeler T, Lamy P, Hvidberg V, Laurberg JR, Fristrup N, Reinert T, Bartkova J, Tropia L, Bartek J, Halazonetis TD, Pan CC, Borre M, Dyrskjot L, Orntoft TF	A high resolution genomic portrait of bladder cancer: correlation between genomic aberrations and the DNA damage response	Oncogene	2013 Aug 	15	Bladder cancer	SNP Array	Homo sapiens	B2120	Affymetrix SNP 6.0	chr10:0-62759:0;chr10:135356696-135374737:0;chr10:28819363-135356695:-1;chr10:42942834-52884342:1;chr10:62760-42919144:1;chr11:0-188509:0;chr11:134449983-134452384:0;chr11:188510-134449982:-1;chr12:0-20703:0;chr12:132288264-132349534:0;chr12:20704-80221556:1;chr12:80221557-89016946:0;chr12:89016947-132288263:1;chr13:0-17924949:0;chr13:103350604-104079457:-1;chr13:104998316-105367736:-1;chr13:114076551-114126500:-1;chr13:114126501-114142980:0;chr13:17924950-114126500:1;chr13:39619501-40139362:-1;chr13:47869579-51359596:-1;chr13:56965033-64574504:-1;chr13:73176342-75200116:-1;chr13:77127934-81311465:-1;chr14:0-18072124:0;chr14:101148001-106356482:1;chr14:106356483-106368585:0;chr14:18072125-105952893:-1;chr14:20981847-22390230:1;chr14:22549488-22646058:1;chr14:32914815-32950451:1;chr14:44643030-44743518:1;chr14:44836032-46201834:1;chr14:55134198-64178550:1;chr14:65958113-67624680:1;chr14:67759880-67992179:1;chr14:70435216-77591627:1;chr15:0-18276341:0;chr15:100286565-100338915:0;chr15:18276342-18839951:-1;chr15:18276342-25501400:1;chr15:18846949-72101389:-1;chr15:26256457-26741881:1;chr15:45744994-51572163:1;chr15:59331351-62058525:1;chr15:62433956-100286564:1;chr15:72391771-78476143:-1;chr15:87323116-87996311:-1;chr15:89058903-100286564:-1;chr16:0-777:0;chr16:10239513-10553903:1;chr16:12926490-16537186:1;chr16:29917386-30536195:0;chr16:30536196-69429180:-1;chr16:69429181-69761496:0;chr16:69761497-88815037:-1;chr16:778-29917385:-1;chr16:88815038-88827254:0;chr16:9717766-9722139:1;chr17:0-21973579:0;chr17:21973580-78643088:1;chr17:27910816-33759421:-1;chr17:41101479-41501468:-1;chr17:45290083-45355051:-1;chr17:74341747-74431623:-1;chr17:76450575-77638327:-1;chr17:78153535-78643088:-1;chr17:78643089-78774742:0;chr18:0-1542:0;chr18:1543-218211:1;chr18:1543-76116029:-1;chr18:67812516-67815816:1;chr18:67943708-68000326:1;chr18:68867536-69174534:1;chr18:69222596-69369586:1;chr18:76116030-76117153:0;chr19:0-41910:0;chr19:41911-28414212:-1;chr19:41911-63789667:1;chr19:63789668-63811651:0;chr1:0-554559:0;chr1:110591317-247191012:1;chr1:247191013-247249719:0;chr1:554560-141577170:-1;chr20:0-9305:0;chr20:62426599-62435964:0;chr20:9306-62426598:1;chr21:0-9965425:0;chr21:42848164-46921386:-1;chr21:46921387-46944323:0;chr21:9965426-20877324:-1;chr21:9965426-46921386:1;chr22:0-15658264:0;chr22:15658265-15734134:-1;chr22:15734135-19174824:0;chr22:19174825-49581322:-1;chr22:31723725-37054519:1;chr22:49581323-49691432:0;chr2:0-2784:0;chr2:242738131-242951149:0;chr2:2785-141043480:1;chr2:2785-242738130:-1;chr3:0-35345:0;chr3:18965512-47731811:1;chr3:35346-18650563:1;chr3:35346-95002438:-1;chr3:95002439-199501827:0;chr4:0-2281:0;chr4:191261906-191273063:0;chr4:2282-191261905:-1;chr5:0-68532:0;chr5:180722928-180857866:0;chr5:49473152-180722927:-1;chr5:68533-49586994:1;chr6:0-94661:0;chr6:170892932-170899992:0;chr6:36415923-36760761:0;chr6:36760762-44020003:1;chr6:44020004-49037968:0;chr6:49037969-49108396:1;chr6:49108397-51068545:0;chr6:51068546-55876400:1;chr6:55876401-56641250:0;chr6:56641251-57419168:1;chr6:57419169-58249220:0;chr6:58249221-61966190:1;chr6:61966190-170892931:-1;chr6:62178982-62299803:1;chr6:64720033-65084155:1;chr6:94662-36415922:1;chr7:0-52911:0;chr7:11158045-11853724:-1;chr7:158819767-158821424:0;chr7:52912-158819766:1;chr7:9047113-10279718:-1;chr8:0-21254:0;chr8:146268961-146274826:0;chr8:21255-43924583:-1;chr8:2129727-2169873:1;chr8:39988202-146268960:1;chr9:0-36430:0;chr9:140211217-140273252:0;chr9:36431-140211216:-1;chrX:0-154913754:0;chrY:0-57772954:0			Department of Molecular Medicine, Aarhus University Hospital, Skejby, Aarhus N, Denmark	One major challenge in cancer research is to understand the complex interplay between the DNA damage response (DDR), genomic integrity, and tumor development. To address these issues, we analyzed 43 bladder tumor genomes from 22 patients using single nucleotide polymorphism (SNP) arrays, and tissue expression of multiple DDR proteins, including Timeless and its interaction partner Tipin. The SNP profiles confirmed and extended known copy number alterations (CNAs) at high resolution, showed clustering of CNAs at nine common fragile sites, and revealed that most metachronous tumors were clonally related. The occurrence of many novel uniparental disomy regions (UPDs) was of potential functional importance in some tumors because UPDs spanned mutated FGFR3 and PIK3CA alleles, and also homozygous deletion of the CDKN2A tumor suppressor locus. The DDR signaling as evaluated by phospho-epitope-specific antibodies against Ser139-phosphorylated H2A histone family member X (gama-H2AX), ataxia telangiectasia mutated (ATM), and ATM- and Rad3-related (ATR) was commonly activated in tumors with both moderate and high extent of accumulated genomic aberrations, the latter tumors showing a more frequent loss of ATM expression. Strikingly, the tumor genomes exhibiting the most complex alterations were associated with a high Ki67-proliferation index, abundant Timeless but not Tipin expression, aberrant p53 expression, and homozygous CDKN2A deletions. Of clinical relevance, evaluation of a tissue microarray (TMA; n=319) showed that abundant Timeless expression was associated with risk of progression to muscle-invasive disease (P<0.0005; hazard ratio, 2.4; 95% confidence interval, 1.6-3.8) and higher T stage (P<0.05). Univariate analysis confirmed this association (P=0.006) in an independent cohort (n=241) but statistical significance was not reached in a multivariate model. Overall, our results are consistent with DDR activation preceding the accumulation of genomic aberrations. Tumors with extensive genomic rearrangements were associated with inactivation of CDKN2A, excessive proliferation, and robust Timeless expression, the latter also correlating with the risk of disease progression. Moreover, we provide evidence to suggest that UPDs likely contribute to bladder tumorigenesis. 	NCBI 36/hg18				Yes	NA
CTDB0282	Methodology	23972288	Chen K, Navin NE, Wang Y, Schmidt HK, Wallis JW, Niu B, Fan X, Zhao H, McLellan MD, Hoadley KA, Mardis ER, Ley TJ, Perou CM, Wilson RK, Ding L	BreakTrans: uncovering the genomic architecture of gene fusions	Genome Biology	2013 Aug	2	Breast cancer	Next Generation Sequencing	Homo sapiens	A0YG				PPP3R1;USP34;LTBP1;TTC27;	Department of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, Texas 77030, USA	Producing gene fusions through genomic structural rearrangements is a major mechanism for tumor evolution. Therefore, accurately detecting gene fusions and the originating rearrangements is of great importance for personalized cancer diagnosis and targeted therapy. We present a tool, BreakTrans, that systematically maps predicted gene fusions to structural rearrangements. Thus, BreakTrans not only validates both types of predictions, but also provides mechanistic interpretations. BreakTrans effectively validates known fusions and discovers novel events in a breast cancer cell line. Applying BreakTrans to 43 breast cancer samples in The Cancer Genome Atlas identifies 90 genomically validated gene fusions. BreakTrans is available at http://bioinformatics.mdanderson.org/main/BreakTrans. 	NCBI 36/hg18		phs000178		Yes	PPP3R1,TTC27
CTDB0284	Research	24055055	Li S, Shen D, Shao J, Crowder R, Liu W, Prat A, He X, Liu S, Hoog J, Lu C, Ding L, Griffith OL, Miller C, Larson D, Fulton RS, Harrison M, Mooney T, McMichael JF, Luo J, Tao Y, Goncalves R, Schlosberg C, Hiken JF, Saied L, Sanchez C, Giuntoli T, Bumb C, Cooper C, Kitchens RT, Lin A, Phommaly C, Davies SR, Zhang J, Kavuri MS, McEachern D, Dong YY, Ma C, Pluard T, Naughton M, Bose R, Suresh R, McDowell R, Michel L, Aft R, Gillanders W, DeSchryver K, Wilson RK, Wang S, Mills GB, Gonzalez-Angulo A, Edwards JR, Maher C, Perou CM, Mardis ER, Ellis MJ	Endocrine-therapy-resistant ESR1 variants revealed by genomic characterization of breast-cancer-derived xenografts	Cell Reports	2013 Sep	1,2,3,4,6,7,9,10,11,12,13,14,15,16,17,18,19,20,21,X	Breast cancer	Next Generation Sequencing	Homo sapiens	WHIM8	Illumina	chr10:0-76919999:0;chr10:101490001-111219999:0;chr10:111220000-112660000:-1;chr10:112660001-135374737:0;chr10:76920000-80910000:1;chr10:76920000-80950000:1;chr10:80950001-80969999:0;chr10:80970000-81220000:1;chr10:81220001-81259999:0;chr10:81260000-81540000:1;chr10:81540001-81559999:0;chr10:81560000-82430000:1;chr10:82430001-82759999:0;chr10:82760000-83840000:-1;chr10:83840001-83849999:0;chr10:83850000-84890000:1;chr10:83860000-84890000:1;chr10:84890001-85149999:0;chr10:85150000-86220000:1;chr10:86220001-86239999:0;chr10:86240000-91130000:-1;chr10:91130001-91139999:0;chr10:91140000-93900000:1;chr10:91150000-94310000:1;chr10:94310001-94329999:0;chr10:94330000-101490000:-1;chr11:0-69999:0;chr11:14810000-16990000:-1;chr11:16990001-24279999:0;chr11:24280000-31320000:-1;chr11:270000-2010000:-1;chr11:31320001-36759999:0;chr11:3220001-3329999:0;chr11:3330000-4200000:-1;chr11:36760000-37290000:-1;chr11:37290001-37549999:0;chr11:37550000-42910000:-1;chr11:4200001-4299999:0;chr11:42910001-45329999:0;chr11:4300000-9660000:-1;chr11:45330000-47190000:-1;chr11:47190001-55219999:0;chr11:55220000-55550000:1;chr11:55550001-55569999:0;chr11:55570000-61310000:-1;chr11:61310001-134452384:0;chr11:70000-3220000:-1;chr11:9660001-14809999:0;chr12:0-64969999:0;chr12:120360000-121510000:-1;chr12:130830000-131990000:-1;chr12:132260001-132349534:0;chr12:64970000-74360000:-1;chr12:74360001-74369999:0;chr12:74370000-78630000:-1;chr12:74380000-78630000:-1;chr12:78630001-78649999:0;chr12:78650000-132260000:-1;chr13:0-17929999:0;chr13:17930000-55570000:-1;chr13:55570001-60399999:0;chr13:60400000-67060000:1;chr13:67060001-114142980:0;chr14:0-19499999:0;chr14:101400001-101799999:0;chr14:101800000-102780000:1;chr14:102780001-105609999:0;chr14:105610000-106340000:1;chr14:105640000-106340000:1;chr14:106340001-106368585:0;chr14:19500000-26220000:-1;chr14:26220001-26229999:0;chr14:26230000-32930000:1;chr14:26240000-32930000:1;chr14:32930001-32949999:0;chr14:32950000-36740000:-1;chr14:36740001-36749999:0;chr14:36750000-38780000:1;chr14:36760000-38790000:1;chr14:38790001-38809999:0;chr14:38810000-42880000:-1;chr14:42880001-42899999:0;chr14:42900000-43310000:-1;chr14:43310001-43329999:0;chr14:43330000-69720000:-1;chr14:69720001-70579999:0;chr14:70580000-78330000:-1;chr14:78330001-94499999:0;chr14:94500000-95010000:-1;chr14:95010001-97739999:0;chr14:97740000-101230000:1;chr14:97740000-101400000:1;chr15:0-18279999:0;chr15:100250001-100338915:0;chr15:18280000-18640000:-1;chr15:18640001-20219999:0;chr15:20220000-21060000:-1;chr15:21060001-21199999:0;chr15:21200000-26230000:-1;chr15:26230001-26619999:0;chr15:26620000-32470000:-1;chr15:32470001-32639999:0;chr15:32640000-41630000:-1;chr15:41630001-41779999:0;chr15:41780000-57200000:-1;chr15:57200001-57829999:0;chr15:57830000-62470000:-1;chr15:62470001-65219999:0;chr15:65220000-67050000:-1;chr15:67050001-74479999:0;chr15:74480000-80360000:-1;chr15:80360001-81019999:0;chr15:81020000-84910000:-1;chr15:84910001-84989999:0;chr15:84990000-86580000:-1;chr15:86580001-86729999:0;chr15:86730000-88020000:-1;chr15:88020001-88029999:0;chr15:88030000-88920000:1;chr15:88040000-88920000:1;chr15:88920001-90249999:0;chr15:90250000-91680000:1;chr15:90250000-91700000:1;chr15:91700001-92579999:0;chr15:92580000-94710000:1;chr15:94710001-95529999:0;chr15:95530000-97040000:1;chr15:97040001-98279999:0;chr15:98280000-100250000:1;chr15:98290000-100250000:1;chr16:0-3249999:0;chr16:3250000-3800000:-1;chr16:3800001-49069999:0;chr16:49070000-51800000:1;chr16:49080000-51700000:1;chr16:51800001-51819999:0;chr16:51820000-69390000:-1;chr16:69390001-69769999:0;chr16:69770000-72940000:-1;chr16:72940001-73029999:0;chr16:73030000-88800000:-1;chr16:86930000-88560000:-1;chr16:88800001-88827254:0;chr17:0-59999:0;chr17:16590001-16689999:0;chr17:16690000-18280000:-1;chr17:18280001-18419999:0;chr17:18420000-18860000:-1;chr17:18860001-19079999:0;chr17:19080000-21120000:-1;chr17:21120001-21139999:0;chr17:21140000-21290000:-1;chr17:21290001-21709999:0;chr17:2150000-2700000:-1;chr17:21710000-22150000:-1;chr17:21720000-22150000:-1;chr17:22150001-24659999:0;chr17:24660000-25940000:1;chr17:25940001-26079999:0;chr17:26080000-29200000:-1;chr17:29200001-29209999:0;chr17:29210000-30680000:1;chr17:29220000-30700000:1;chr17:30700001-30719999:0;chr17:30720000-31500000:-1;chr17:31500001-31899999:0;chr17:31900000-33350000:-1;chr17:33350001-33919999:0;chr17:33920000-35830000:1;chr17:34750000-35450000:1;chr17:35830001-35849999:0;chr17:35850000-36340000:-1;chr17:36340001-36549999:0;chr17:36550000-38590000:-1;chr17:38590001-38779999:0;chr17:38780000-40490000:-1;chr17:40490001-40499999:0;chr17:40500000-41150000:1;chr17:40510000-41150000:1;chr17:41150001-41169999:0;chr17:41170000-41510000:-1;chr17:41510001-41529999:0;chr17:41530000-41710000:-1;chr17:41710001-42149999:0;chr17:4190000-4920000:-1;chr17:42150000-44610000:-1;chr17:44610001-44719999:0;chr17:44720000-45050000:-1;chr17:45050001-45069999:0;chr17:45070000-46360000:1;chr17:46360001-48339999:0;chr17:48340000-48630000:1;chr17:48630001-49829999:0;chr17:49830000-50140000:1;chr17:50140001-52279999:0;chr17:52280000-57180000:1;chr17:52490000-56180000:1;chr17:57180001-57449999:0;chr17:57450000-58390000:-1;chr17:58390001-59199999:0;chr17:59200000-63420000:-1;chr17:60000-16590000:-1;chr17:63420001-64019999:0;chr17:640000-1900000:-1;chr17:64020000-64570000:-1;chr17:64030000-64570000:-1;chr17:64570001-64649999:0;chr17:64650000-65910000:-1;chr17:65910001-65929999:0;chr17:65930000-66390000:-1;chr17:66390001-66409999:0;chr17:66410000-68280000:-1;chr17:66420000-68280000:-1;chr17:68280001-69379999:0;chr17:69380000-74960000:-1;chr17:7000000-7690000:-1;chr17:70550000-71640000:-1;chr17:74960001-75239999:0;chr17:75240000-77300000:-1;chr17:76550000-77300000:-1;chr17:77300001-77539999:0;chr17:77540000-78620000:-1;chr17:78620001-78774742:0;chr18:0-18229999:0;chr18:18230000-24500000:-1;chr18:24500001-24519999:0;chr18:24520000-27170000:1;chr18:24540000-27170000:1;chr18:27170001-27189999:0;chr18:27190000-37320000:-1;chr18:37320001-37329999:0;chr18:37330000-38000000:1;chr18:37340000-38000000:1;chr18:38000001-38019999:0;chr18:38020000-38460000:-1;chr18:38460001-38479999:0;chr18:38480000-41890000:1;chr18:38480000-41960000:1;chr18:41960001-42279999:0;chr18:42280000-45170000:1;chr18:45170001-45189999:0;chr18:45190000-48610000:-1;chr18:48610001-48689999:0;chr18:48690000-51560000:-1;chr18:51560001-51569999:0;chr18:51570000-54220000:1;chr18:51580000-56330000:1;chr18:55310000-56330000:1;chr18:56330001-56839999:0;chr18:56840000-70260000:-1;chr18:70260001-72919999:0;chr18:72920000-76090000:1;chr18:72930000-75600000:1;chr18:75670000-76090000:1;chr18:76090001-76117153:0;chr19:0-439999:0;chr19:1230001-37639999:0;chr19:37640000-43850000:1;chr19:43850001-43869999:0;chr19:43870000-53090000:-1;chr19:43890000-44500000:-1;chr19:440000-1230000:-1;chr19:45340000-46000000:-1;chr19:49860000-51210000:-1;chr19:51490000-53090000:-1;chr19:53090001-53109999:0;chr19:53110000-53150000:-1;chr19:53150001-53169999:0;chr19:53170000-55980000:-1;chr19:53170000-63780000:-1;chr19:58730000-59410000:-1;chr19:59920000-60910000:-1;chr19:63780001-63811651:0;chr1:0-609999:0;chr1:1240001-1449999:0;chr1:144110000-144530000:1;chr1:144530001-144669999:0;chr1:144670000-145880000:1;chr1:144810000-145870000:1;chr1:1450000-3690000:-1;chr1:145880001-145969999:0;chr1:145970000-146290000:1;chr1:146290001-147309999:0;chr1:147310000-147460000:1;chr1:147460001-148029999:0;chr1:148030000-150100000:1;chr1:148030000-159710000:1;chr1:156470000-158100000:1;chr1:159710001-159769999:0;chr1:159770000-194900000:1;chr1:194900001-195089999:0;chr1:195090000-197900000:1;chr1:197900001-198039999:0;chr1:198040000-214280000:1;chr1:214280001-232309999:0;chr1:232310000-247170000:1;chr1:247170001-247249719:0;chr1:3690001-144109999:0;chr1:610000-1240000:-1;chr20:0-49009999:0;chr20:49010000-62410000:1;chr20:50280000-51500000:1;chr20:51910000-54340000:1;chr20:54970000-59500000:1;chr20:62410001-62435964:0;chr21:0-13379999:0;chr21:13380000-23200000:-1;chr21:23200001-34959999:0;chr21:34960000-46920000:1;chr21:34970000-36280000:1;chr21:37670000-39540000:1;chr21:39810000-41750000:1;chr21:42270000-42870000:1;chr21:46920001-46944323:0;chr22:0-49691432:0;chr2:0-121949999:0;chr2:121950000-130930000:-1;chr2:130930001-131029999:0;chr2:131030000-132470000:-1;chr2:132470001-132849999:0;chr2:132850000-231060000:-1;chr2:231060001-232129999:0;chr2:232130000-242160000:-1;chr2:242160001-242369999:0;chr2:242370000-242730000:-1;chr2:242730001-242951149:0;chr3:0-49999:0;chr3:101630001-102079999:0;chr3:102080000-102700000:-1;chr3:102700001-111079999:0;chr3:10300000-12550000:1;chr3:111080000-112730000:-1;chr3:112730001-117459999:0;chr3:117460000-121750000:-1;chr3:121750001-121909999:0;chr3:121910000-143150000:-1;chr3:12930000-17430000:1;chr3:143150001-143959999:0;chr3:143960000-147530000:-1;chr3:147530001-149039999:0;chr3:149040000-157470000:-1;chr3:157470001-160649999:0;chr3:160650000-163980000:-1;chr3:163980001-164119999:0;chr3:164120000-169700000:-1;chr3:169700001-169709999:0;chr3:169710000-170850000:1;chr3:169720000-171210000:1;chr3:171210001-171229999:0;chr3:171230000-180530000:-1;chr3:17430001-17449999:0;chr3:17450000-46320000:-1;chr3:180530001-180659999:0;chr3:180660000-196830000:-1;chr3:196830001-196889999:0;chr3:196890000-196950000:-1;chr3:196950001-196969999:0;chr3:196970000-199420000:-1;chr3:199420001-199501827:0;chr3:46320001-46479999:0;chr3:46480000-68000000:-1;chr3:48640000-49490000:-1;chr3:50000-17430000:1;chr3:50000-9510000:1;chr3:68000001-68159999:0;chr3:68160000-75750000:-1;chr3:75750001-75959999:0;chr3:75960000-76300000:-1;chr3:76300001-76489999:0;chr3:76490000-85260000:-1;chr3:85260001-85409999:0;chr3:85410000-90580000:-1;chr3:90580001-96099999:0;chr3:96100000-101630000:-1;chr4:0-639999:0;chr4:17180001-18929999:0;chr4:18930000-48770000:-1;chr4:190760001-191273063:0;chr4:3530001-3549999:0;chr4:3550000-3600000:-1;chr4:3600001-3619999:0;chr4:3620000-17180000:-1;chr4:48770001-52379999:0;chr4:52380000-6890000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of Breast Oncology, Division of Oncology, Department of Internal Medicine, Washington University in St. Louis, St. Louis, MO 63110, USA	To characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained with high fidelity. However, at the single-nucleotide level, variable numbers of PDX-specific somatic events were documented, although they were only rarely functionally significant. Variant allele frequencies were often preserved in the PDXs, demonstrating that clonal representation can be transplantable. Estrogen-receptor-positive PDXs were associated with ESR1 ligand-binding-domain mutations, gene amplification, or an ESR1/YAP1 translocation. These events produced different endocrine-therapy-response phenotypes in human, cell line, and PDX endocrine-response studies. Hence, deeply sequenced PDX models are an important resource for the search for genome-forward treatment options and capture endocrine-drug-resistance etiologies that are not observed in standard cell lines. The originating tumor genome provides a benchmark for assessing genetic drift and clonal representation after transplantation. 	NCBI 36/hg18		phs000611		Yes	NA
CTDB0285	Research	24055055	Li S, Shen D, Shao J, Crowder R, Liu W, Prat A, He X, Liu S, Hoog J, Lu C, Ding L, Griffith OL, Miller C, Larson D, Fulton RS, Harrison M, Mooney T, McMichael JF, Luo J, Tao Y, Goncalves R, Schlosberg C, Hiken JF, Saied L, Sanchez C, Giuntoli T, Bumb C, Cooper C, Kitchens RT, Lin A, Phommaly C, Davies SR, Zhang J, Kavuri MS, McEachern D, Dong YY, Ma C, Pluard T, Naughton M, Bose R, Suresh R, McDowell R, Michel L, Aft R, Gillanders W, DeSchryver K, Wilson RK, Wang S, Mills GB, Gonzalez-Angulo A, Edwards JR, Maher C, Perou CM, Mardis ER, Ellis MJ	Endocrine-therapy-resistant ESR1 variants revealed by genomic characterization of breast-cancer-derived xenografts	Cell Reports	2013 Sep	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	Next Generation Sequencing	Homo 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rX:25240000-30960000:-1;chrX:270000-810000:-1;chrX:27440000-30960000:-1;chrX:30960001-31869999:0;chrX:31870000-32430000:1;chrX:32430001-32599999:0;chrX:32600000-38510000:-1;chrX:32610000-38510000:-1;chrX:3680001-3969999:0;chrX:38510001-40189999:0;chrX:3970000-6500000:-1;chrX:40190000-42790000:-1;chrX:40570000-42790000:-1;chrX:42790001-43479999:0;chrX:43480000-45230000:1;chrX:43590000-44170000:1;chrX:44640000-45230000:1;chrX:45230001-51699999:0;chrX:51700000-52110000:-1;chrX:52110001-53119999:0;chrX:53120000-54090000:1;chrX:54090001-54519999:0;chrX:54520000-57320000:-1;chrX:57320001-67859999:0;chrX:6500001-25239999:0;chrX:67860000-76140000:-1;chrX:69960000-71000000:-1;chrX:76140001-77339999:0;chrX:77340000-82140000:1;chrX:810001-829999:0;chrX:82140001-83239999:0;chrX:830000-940000:-1;chrX:83240000-85170000:1;chrX:83320000-85170000:1;chrX:85170001-86689999:0;chrX:86690000-93490000:1;chrX:93490001-93509999:0;chrX:93510000-97890000:-1;chrX:940001-1289999:0;chrX:97890001-100129999:0;chrY:0-57772954:0			Section of Breast Oncology, Division of Oncology, Department of Internal Medicine, Washington University in St. Louis, St. Louis, MO 63110, USA	To characterize patient-derived xenografts (PDXs) for functional studies, we made whole-genome comparisons with originating breast cancers representative of the major intrinsic subtypes. Structural and copy number aberrations were found to be retained with high fidelity. However, at the single-nucleotide level, variable numbers of PDX-specific somatic events were documented, although they were only rarely functionally significant. Variant allele frequencies were often preserved in the PDXs, demonstrating that clonal representation can be transplantable. Estrogen-receptor-positive PDXs were associated with ESR1 ligand-binding-domain mutations, gene amplification, or an ESR1/YAP1 translocation. These events produced different endocrine-therapy-response phenotypes in human, cell line, and PDX endocrine-response studies. Hence, deeply sequenced PDX models are an important resource for the search for genome-forward treatment options and capture endocrine-drug-resistance etiologies that are not observed in standard cell lines. The originating tumor genome provides a benchmark for assessing genetic drift and clonal representation after transplantation. 	NCBI 36/hg18		phs000611		Yes	C1orf182,MLL3;ESR1,YAP1
CTDB0286	Research	22123490	Kitada K, Aida S, Aikawa S	Coamplification of multiple regions of chromosome 2, including MYCN, in a single patchwork amplicon in cancer cell lines	Cytogenetic and Genome Research	2011 Nov 	2	Neuroblastoma	Array CGH	Homo sapiens	IMR-32	Agilent SurePrint G3 human CGH arrays	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-14657088:0;chr2:14657089-16041259:1;chr2:16041260-17219745:0;chr2:17219746-17233242:1;chr2:17233243-29549878:0;chr2:29549879-29777721:1;chr2:29777722-53254629:0;chr2:53254630-53454473:1;chr2:53454474-66346579:0;chr2:66346580-66576580:1;chr2:66576581-68025605:0;chr2:68025606-69255606:1;chr2:69255607-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0	hs2:69255606-69255606,hs2:17233242-17233242;hs2:17219746-17219746,hs2:14657089-14657089;hs2:16041259-16041259,hs2:53454473-53454473;hs2:53254630-53254630,hs2:29777721-29777721;hs2:29549879-29549879,hs2:66346580-66346580	MYCN;ANTXR1;NNG1;MEIS1	Kamakura Research Laboratories, Chugai Pharmaceutical Co. Ltd., Kamakura, Japan	Coamplification of multiple segments of chromosome 2, including an MYCN-bearing segment, was examined in 2 cancer cell lines, NCI-H69 (lung cancer) and IMR-32 (neuroblastoma). High-resolution array-CGH analysis revealed 13 and 6 highly amplified segments located at different sites in chromosome 2 in NCI-H69 and IMR-32, respectively. FISH analysis demonstrated that these segments were co-localized in double minutes in NCI-H69 and in homogeneously staining regions in IMR-32. Connectivity of the segments was determined by a PCR assay using designed primer sets. It was found that all the segments were connected to each other irrespective of their order and orientation against the genome sequence, and a single chain-like cluster was configured in both cell lines. Such patchwork structures of the amplicons suggest the possibility that massive genomic rearrangements, explained by the single catastrophic event model, are involved in the formation of the amplicons, enabling the coamplification of different chromosomal regions including the MYCN locus. The model comprises massive fragmentation of chromosomes and random rejoining of the fragments.	NCBI 36/hg18				Yes	ANTXR1,NNG1
CTDB0287	Research	22123490	Kitada K, Aida S, Aikawa S	Coamplification of multiple regions of chromosome 2, including MYCN, in a single patchwork amplicon in cancer cell lines	Cytogenetic and Genome Research	2011 Nov 	2	Small cell lung cancer	Array CGH	Homo sapiens	NCI-H69	Agilent SurePrint G3 human CGH arrays	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-15968981:0;chr2:134993920-135131902:1;chr2:135131903-137295959:0;chr2:137295960-137307960:1;chr2:137307961-140224587:0;chr2:140224588-140612621:1;chr2:140612622-145554322:0;chr2:145554323-145604323:1;chr2:145604324-242951149:0;chr2:15968982-16082369:1;chr2:16082370-16091320:0;chr2:16091321-16106321:1;chr2:16106322-53013053:0;chr2:53013054-53044885:1;chr2:53044886-53058402:0;chr2:53058403-53115124:1;chr2:53115125-53132779:0;chr2:53132780-53387222:1;chr2:53387223-53401052:0;chr2:53401053-53770309:1;chr2:53682561-53768531:1;chr2:53770310-53784166:0;chr2:53784167-53813298:1;chr2:53813299-77065691:0;chr2:77065692-77074080:1;chr2:77074081-86584943:0;chr2:86584944-86587727:1;chr2:86587728-134993919:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0	hs2:16106321-16106321,hs2:145554323-145554323;hs2:145604323-145604323,hs2:77065692-77065692;hs2:77074080-77074080,hs2:86584944-86584944;hs2:86587727-86587727,hs2:53813298-53813298;hs2:53784167-53784167,hs2:15968982-15968982;hs2:16082369-16082369,hs2:53682561-53682561;hs2:53768531-53768531,hs2:53770309-53770309;hs2:53401053-53401053,hs2:53387222-53387222;hs2:53132780-53132780,hs2:53115124-53115124;hs2:53058403-53058403,hs2:140224588-140224588;hs2:140612621-140612621,hs2:134993920-134993920;hs2:135131902-135131902,hs2:53013054-53013054;hs2:53044885-53044885,hs2:137295960-137295960	MYCN	Kamakura Research Laboratories, Chugai Pharmaceutical Co. Ltd., Kamakura, Japan	Coamplification of multiple segments of chromosome 2, including an MYCN-bearing segment, was examined in 2 cancer cell lines, NCI-H69 (lung cancer) and IMR-32 (neuroblastoma). High-resolution array-CGH analysis revealed 13 and 6 highly amplified segments located at different sites in chromosome 2 in NCI-H69 and IMR-32, respectively. FISH analysis demonstrated that these segments were co-localized in double minutes in NCI-H69 and in homogeneously staining regions in IMR-32. Connectivity of the segments was determined by a PCR assay using designed primer sets. It was found that all the segments were connected to each other irrespective of their order and orientation against the genome sequence, and a single chain-like cluster was configured in both cell lines. Such patchwork structures of the amplicons suggest the possibility that massive genomic rearrangements, explained by the single catastrophic event model, are involved in the formation of the amplicons, enabling the coamplification of different chromosomal regions including the MYCN locus. The model comprises massive fragmentation of chromosomes and random rejoining of the fragments.	NCBI 36/hg18				Yes	NA
CTDB0288	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	7,12	Glioblastoma	Next Generation Sequencing	Homo sapiens	06-0152-01A				EGFR;CDK4;MDM2	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0289	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	1,2	Glioblastoma	Next Generation Sequencing	Homo sapiens	06-0210-01A				MDM4	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0290	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	4,7	Glioblastoma	Next Generation Sequencing	Homo sapiens	06-0211-01A				EGFR;PDGFRA	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0291	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	4,7	Glioblastoma	Next Generation Sequencing	Homo sapiens	06-0211-02A				EGFR;PDGFRA	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0292	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	12	Glioblastoma	Next Generation Sequencing	Homo sapiens	06-0648-01A				CAND1;MDM2;CPM	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0293	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	7	Glioblastoma	Next Generation Sequencing	Homo sapiens	14-1402-01A				EGFR	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0294	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	7	Glioblastoma	Next Generation Sequencing	Homo sapiens	14-1402-02A				EGFR	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0295	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	4,12	Glioblastoma	Next Generation Sequencing	Homo sapiens	19-5960-01A				CDK4	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0296	Methodology	25938371	Chen X, Gupta P, Wang J, Nakitandwe J, Roberts K, Dalton JD, Parker M, Patel S, Holmfeldt L, Payne D, Easton J, Ma J, Rusch M, Wu G, Patel A, Baker SJ, Dyer MA, Shurtleff S, Espy S, Pounds S, Downing JR, Ellison DW, Mullighan CG, Zhang J	CONSERTING: integrating copy-number analysis with structural-variation detection	Nature methods	2015 Jun	7	Glioblastoma	Next Generation Sequencing	Homo sapiens	27-1831-01A				EGFR	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	We developed Copy Number Segmentation by Regression Tree in Next Generation Sequencing (CONSERTING), an algorithm for detecting somatic copy-number alteration (CNA) using whole-genome sequencing (WGS) data. CONSERTING performs iterative analysis of segmentation on the basis of changes in read depth and the detection of localized structural variations, with high accuracy and sensitivity. Analysis of 43 cancer genomes from both pediatric and adult patients revealed novel oncogenic CNAs, complex rearrangements and subclonal CNAs missed by alternative approaches. 	GRCh37/hg19		phs000340;phs000352;phs000218;phs000178		Yes	NA
CTDB0297	Research	24613276	Laurie CC, Laurie CA, Smoley SA, Carlson EE, Flinn I, Fridley BL, Greisman HA, Gribben JG, Jelinek DF, Nelson SC, Paietta E, Schaid D, Sun Z, Tallman MS, Weinshilboum R, Kay NE, Shanafelt TD	Acquired chromosomal anomalies in chronic lymphocytic leukemia patients compared with more than 50,000 quasi-normal participants	Cancer Genetics	2014 Jan	11	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	10	Illumina HumanOmni-Quad v1.0_B SNP microarray	chr10:0-88086:0;chr10:1333199-135374737:0;chr10:88087-1333198:-1;chr11:0-15590802:0;chr11:115677786-118336936:0;chr11:118336937-126720615:-1;chr11:126720616-128026677:0;chr11:128026678-134367886:-1;chr11:134367887-134452384:0;chr11:15590803-16626283:-1;chr11:16626284-34146998:0;chr11:34146999-34894477:-1;chr11:34894478-35227176:0;chr11:35227177-43341509:-1;chr11:43341510-48614745:0;chr11:48614746-51417246:-1;chr11:51417247-54508765:0;chr11:54508766-59693555:-1;chr11:59693556-77902555:0;chr11:77902556-83268891:-1;chr11:83268892-83735129:0;chr11:83735130-84917636:-1;chr11:84917637-86301560:0;chr11:86301561-88846159:-1;chr11:88846160-88994233:0;chr11:88994234-91701474:-1;chr11:91701475-95876561:0;chr11:95876562-115677785:-1;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-35281164:0;chr2:35281165-39625508:-1;chr2:39625509-53383060:0;chr2:53383061-54247074:-1;chr2:54247075-55473113:0;chr2:55473114-55837433:-1;chr2:55837434-56709282:0;chr2:56709283-59433830:-1;chr2:59433831-242951149:0;chr3:0-199501827:0;chr4:0-70092923:0;chr4:121277543-123877604:-1;chr4:123877605-191273063:0;chr4:70092924-73761895:-1;chr4:73761896-77315141:0;chr4:77315142-90447261:-1;chr4:90447262-121277542:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Biostatistics Department, University of Washington, Seattle, WA, USA	Pretherapy patients with chronic lymphocytic leukemia (CLL) from US Intergroup trial E2997 were analyzed with single nucleotide polymorphism microarrays to detect acquired chromosomal anomalies. The four CLL-typical anomalies (11q-, +12, 13q-, and 17p-) were found at expected frequencies. Acquired anomalies in other regions account for 70% of the total detected anomalies, and their number per participant has a significant effect on progression-free survival after adjusting for the effects of 17p- (and other covariates). These results were compared with those from a previous study of more than 50,000 participants from the GENEVA consortium of genome-wide association studies, which analyzed individuals with a variety of medical conditions and healthy controls. The percentage of individuals with acquired anomalies is vastly different between the two studies (GENEVA 0.8%; E2997 80%). The composition of the anomalies also differs, with GENEVA having a higher percentage of acquired uniparental disomies and a lower percentage of deletions. The four common CLL anomalies are among the most frequent in GENEVA participants, some of whom may have CLL-precursor conditions or early stages of CLL. However, the patients from E2997 (and other studies of symptomatic CLL) have recurrent acquired anomalies that were not found in GENEVA participants, thus identifying genomic changes that may be unique to symptomatic stages of CLL. 	NCBI 36/hg18		phs000621		Yes	NA
CTDB0298	Research	24613276	Laurie CC, Laurie CA, Smoley SA, Carlson EE, Flinn I, Fridley BL, Greisman HA, Gribben JG, Jelinek DF, Nelson SC, Paietta E, Schaid D, Sun Z, Tallman MS, Weinshilboum R, Kay NE, Shanafelt TD	Acquired chromosomal anomalies in chronic lymphocytic leukemia patients compared with more than 50,000 quasi-normal participants	Cancer Genetics	2014 Jan	9	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	86	Illumina HumanOmni-Quad v1.0_B SNP microarray	chr10:0-135374737:0;chr11:0-129814088:0;chr11:129814089-134443680:-1;chr11:134443681-134452384:0;chr12:0-132349534:0;chr13:0-18086615:0;chr13:18086616-26402964:-1;chr13:26402965-114142980:0;chr14:0-67341733:0;chr14:67341734-92271752:-1;chr14:92271753-106368585:0;chr15:0-18421385:0;chr15:18421386-39191343:-1;chr15:39191344-39197996:0;chr15:39197997-41345866:-1;chr15:41345867-100338915:0;chr16:0-88827254:0;chr17:0-7213:0;chr17:19280415-78774742:0;chr17:7214-19280414:-1;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-13591801:0;chr21:13591802-23456930:-1;chr21:23456931-46944323:0;chr22:0-49691432:0;chr2:0-40813:0;chr2:208997028-231626311:-1;chr2:231626312-242951149:0;chr2:40814-88909336:1;chr2:88909337-208997027:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-9769250:0;chr6:45857783-57482074:-1;chr6:57482075-61949076:0;chr6:61949077-66859614:-1;chr6:66859615-66865882:0;chr6:66865883-67814410:-1;chr6:67814411-67827225:0;chr6:67827226-74890125:-1;chr6:74890126-74907772:0;chr6:74907773-75471929:-1;chr6:75471930-170899992:0;chr6:9769251-45857783:-1;chr7:0-158821424:0;chr8:0-185253:0;chr8:185254-38182392:-1;chr8:38182393-146274826:0;chr9:0-36586:0;chr9:105644055-109189988:0;chr9:109189989-110587420:-1;chr9:110587421-117495647:0;chr9:117495648-140186312:-1;chr9:140186313-140273252:0;chr9:14484389-16800346:0;chr9:16800347-22040873:-1;chr9:22040874-25320809:0;chr9:25320810-33808257:-1;chr9:33808258-67656949:0;chr9:36587-6530540:1;chr9:6530541-9876402:0;chr9:67656950-84950566:-1;chr9:84950567-91964998:0;chr9:91964999-92295939:-1;chr9:92295940-92675795:0;chr9:92675796-94618312:-1;chr9:94618313-96040218:0;chr9:96040219-96470652:-1;chr9:96470653-99476878:0;chr9:9876403-14484388:-1;chr9:99476879-105644054:-1;chrX:0-154913754:0;chrY:0-57772954:0			Biostatistics Department, University of Washington, Seattle, WA, USA	Pretherapy patients with chronic lymphocytic leukemia (CLL) from US Intergroup trial E2997 were analyzed with single nucleotide polymorphism microarrays to detect acquired chromosomal anomalies. The four CLL-typical anomalies (11q-, +12, 13q-, and 17p-) were found at expected frequencies. Acquired anomalies in other regions account for 70% of the total detected anomalies, and their number per participant has a significant effect on progression-free survival after adjusting for the effects of 17p- (and other covariates). These results were compared with those from a previous study of more than 50,000 participants from the GENEVA consortium of genome-wide association studies, which analyzed individuals with a variety of medical conditions and healthy controls. The percentage of individuals with acquired anomalies is vastly different between the two studies (GENEVA 0.8%; E2997 80%). The composition of the anomalies also differs, with GENEVA having a higher percentage of acquired uniparental disomies and a lower percentage of deletions. The four common CLL anomalies are among the most frequent in GENEVA participants, some of whom may have CLL-precursor conditions or early stages of CLL. However, the patients from E2997 (and other studies of symptomatic CLL) have recurrent acquired anomalies that were not found in GENEVA participants, thus identifying genomic changes that may be unique to symptomatic stages of CLL. 	NCBI 36/hg18		phs000621		Yes	NA
CTDB0299	Research	24613276	Laurie CC, Laurie CA, Smoley SA, Carlson EE, Flinn I, Fridley BL, Greisman HA, Gribben JG, Jelinek DF, Nelson SC, Paietta E, Schaid D, Sun Z, Tallman MS, Weinshilboum R, Kay NE, Shanafelt TD	Acquired chromosomal anomalies in chronic lymphocytic leukemia patients compared with more than 50,000 quasi-normal participants	Cancer Genetics	2014 Jan	9	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	203	Illumina HumanOmni-Quad v1.0_B SNP microarray	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-38410:0;chr3:17985707-38126735:-1;chr3:38126736-52498444:0;chr3:38411-9799651:-1;chr3:52498445-57909692:-1;chr3:57909693-71780450:0;chr3:71780451-90525615:-1;chr3:90525616-199501827:0;chr3:9799652-17985706:0;chr4:0-175186278:0;chr4:175186279-183245566:-1;chr4:183245567-184392508:0;chr4:184392509-191176659:-1;chr4:191176660-191273063:0;chr5:0-150543494:0;chr5:150543495-155946409:-1;chr5:155946410-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-21067715:0;chr9:113585700-114548976:0;chr9:114548977-115764223:-1;chr9:115764224-116210061:0;chr9:116210062-116488534:-1;chr9:116488535-118543174:0;chr9:118543175-121780706:-1;chr9:121780707-127831310:0;chr9:127831311-131697340:-1;chr9:131697341-140273252:0;chr9:21067716-21772164:-1;chr9:21772165-25430149:0;chr9:25430150-29024430:-1;chr9:29024431-29066690:0;chr9:29066691-29253492:-1;chr9:29253493-66579043:0;chr9:66579044-77281262:-1;chr9:77281263-77788424:0;chr9:77788425-93549966:-1;chr9:93549967-93557535:0;chr9:93557536-93911541:-1;chr9:93911542-99260626:0;chr9:99260627-113585699:-1;chrX:0-154913754:0;chrY:0-57772954:0			Biostatistics Department, University of Washington, Seattle, WA, USA	Pretherapy patients with chronic lymphocytic leukemia (CLL) from US Intergroup trial E2997 were analyzed with single nucleotide polymorphism microarrays to detect acquired chromosomal anomalies. The four CLL-typical anomalies (11q-, +12, 13q-, and 17p-) were found at expected frequencies. Acquired anomalies in other regions account for 70% of the total detected anomalies, and their number per participant has a significant effect on progression-free survival after adjusting for the effects of 17p- (and other covariates). These results were compared with those from a previous study of more than 50,000 participants from the GENEVA consortium of genome-wide association studies, which analyzed individuals with a variety of medical conditions and healthy controls. The percentage of individuals with acquired anomalies is vastly different between the two studies (GENEVA 0.8%; E2997 80%). The composition of the anomalies also differs, with GENEVA having a higher percentage of acquired uniparental disomies and a lower percentage of deletions. The four common CLL anomalies are among the most frequent in GENEVA participants, some of whom may have CLL-precursor conditions or early stages of CLL. However, the patients from E2997 (and other studies of symptomatic CLL) have recurrent acquired anomalies that were not found in GENEVA participants, thus identifying genomic changes that may be unique to symptomatic stages of CLL. 	NCBI 36/hg18		phs000621		Yes	NA
CTDB0300	Research	22267523	Jiang Z, Jhunjhunwala S, Liu J, Haverty PM, Kennemer MI, Guan Y, Lee W, Carnevali P, Stinson J, Johnson S, Diao J, Yeung S, Jubb A, Ye W, Wu TD, Kapadia SB, de Sauvage FJ, Gentleman RC, Stern HM, Seshagiri S, Pant KP, Modrusan Z, Ballinger DG, Zhang Z	The effects of hepatitis B virus integration into the genomes of hepatocellular carcinoma patients	Genome Research	2012 Apr	11	Hepatocellular carcinoma	Next Generation Sequencing	Homo sapiens	H384			hs1:237459374-237459731,hs11:69326266-69326793;hs1:237803220-237803554,hs11:69030220-69030519;hs11:68174928-68175207,hs11:111576997-111577265;hs11:68263776-68263934,hs11:111568063-111568201;hs11:68834611-68835103,hs11:69063232-69063535;hs11:69455238-69455748,hs11:99220072-99220607;hs11:69462705-69463095,hs11:99264863-99265121;hs11:69463061-69463415,hs11:69520345-69520543;hs11:69463944-69464292,hs13:111314565-111314959;hs11:69488929-69489325,hs11:99528987-99529335;hs11:99100510-99100897,hsX:1907040-1907618;hs12:7177879-7178352,hs12:7299289-7299792;hs13:107169509-107169692,hs13:108423879-108424078;hs13:107183258-107183591,hs13:107213137-107213501;hs13:108210800-108211323,hs13:109282898-109283336	CCND1;CNTN5;FGF19;LRP5;MYEOV;ORAOV1;PPP6R3;SIK2;TPCN2;	Department of Bioinformatics and Computational Biology, Genentech Inc, South San Francisco, California 94080, USA	Hepatitis B virus (HBV) infection is a leading risk factor for hepatocellular carcinoma (HCC). HBV integration into the host genome has been reported, but its scale, impact and contribution to HCC development is not clear. Here, we sequenced the tumor and nontumor genomes (>80X coverage) and transcriptomes of four HCC patients and identified 255 HBV integration sites. Increased sequencing to 240X coverage revealed a proportionally higher number of integration sites. Clonal expansion of HBV-integrated hepatocytes was found specifically in tumor samples. We observe a diverse collection of genomic perturbations near viral integration sites, including direct gene disruption, viral promoter-driven human transcription, viral-human transcript fusion, and DNA copy number alteration. Thus, we report the most comprehensive characterization of HBV integration in hepatocellular carcinoma patients. Such widespread random viral integration will likely increase carcinogenic opportunities in HBV-infected individuals.	GRCh37/hg19		phs000384		Yes	CCND1,CARS2;CCND1,CNTN5;CCND1,FGF19;LRP5,SIK2;ORAOV1,CNTN5;PPP6R3,SIK2;TPCN2,MYEOV
CTDB0301	Research	23496902	Jiao X, Hooper SD, Djureinovic T, Larsson C, Warnberg F, Tellgren-Roth C, Botling J, Sjoblom T	Gene rearrangements in hormone receptor negative breast cancers revealed by mate pair sequencing	BMC Genomics	2013 Mar	1,2,3,7,8,11,15,16,17,20,21,X,Y	Breast cancer	Next Generation Sequencing	Homo sapiens	118T	SOLiD3	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-55004818:0;chr15:55004819-58879386:-1;chr15:58879387-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-63476667:0;chr1:195690043-195690469:1;chr1:195690470-230523907:0;chr1:230523908-230528509:-1;chr1:230528510-247249719:0;chr1:63476668-63482030:-1;chr1:63482031-195690042:0;chr20:0-36255835:0;chr20:36255836-36257151:1;chr20:36257152-62435964:0;chr21:0-25220500:0;chr21:25220501-31517907:-1;chr21:31517908-46944323:0;chr22:0-49691432:0;chr2:0-70513576:0;chr2:70513577-70517836:-1;chr2:70517837-242951149:0;chr3:0-108519519:0;chr3:108519520-108524650:-1;chr3:108524651-134804179:0;chr3:134804180-134808444:-1;chr3:134808445-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-92600482:0;chr8:131918874-131923624:-1;chr8:131923625-141235875:0;chr8:141235876-141237150:1;chr8:141237151-143351438:0;chr8:143351439-143352831:1;chr8:143352832-146274826:0;chr8:92600483-92611590:-1;chr8:92611591-131918873:0;chr9:0-140273252:0;chrX:0-135125055:0;chrX:135125056-135131089:-1;chrX:135131090-154913754:0;chrY:0-57772954:0	hs2:172601516-172601516,hs2:175539159-175539159;hs15:57988348-57988348,hs15:58249409-58249409;hs15:59317692-59317692,hs15:67919721-67919721;hs21:27096176-27096176,hs21:40613558-40613558;hs21:27644155-27644155,hs21:30032969-30032969;hs21:30027728-30027728,hs21:45978888-45978888;hs11:55961514-55961514,hs11:70335355-70335355;hs21:26319139-26319139,hs21:34978397-34978397;hs11:55962145-55962145,hs11:70334660-70334660;hs15:58018756-58018756,hs21:45973422-45973422;hs15:58619373-58619373,hs21:34837891-34837891;hs15:59163813-59163813,hs21:26902586-26902586;hs15:69536585-69536585,hs21:16947278-16947278;hs7:89920909-89920909,hs17:22927514-22927514;hs15:58070776-58070776,hs21:40545794-40545794;hs15:71192826-71192826,hs21:18664764-18664764;hs15:67813088-67813088,hs21:17096313-17096313;hs1:203406073-203406073,hs17:67941744-67941744;hs15:56785572-56785572,hs21:35493037-35493037;hs15:56819851-56819851,hs21:26290149-26290149;hs15:56825407-56825407,hs21:35138237-35138237;hs15:57924318-57924318,hs21:36836122-36836122;hs15:58970133-58970133,hs21:28088365-28088365;hs15:58983956-58983956,hs21:46011615-46011615;hs15:59145037-59145037,hs21:40791222-40791222;hs15:63964813-63964813,hs21:30497263-30497263;hs15:64142747-64142747,hs21:34848420-34848420;hs15:69312660-69312660,hs21:28871349-28871349;hs15:70901061-70901061,hs21:38513266-38513266;hs16:33846095-33846095,hs24:10617572-10617572	ADAM10;ADCY8;APP;C15orf50;CHN1;CLDN14;CLIC6;CRB1;DSCAM;DSTYK;GRIK1;KSR1;LOC344595;MAP1D;NEO1;PRSS7;RAB11A;RCAN1;RORA;RUNX1;SHANK2;TCF12;THSD4;TIAM1;TOPBP1;TRAPPC9;TSNARE1;	Department of Immunology, Genetics, and Pathology, Uppsala University, Uppsala, SE 751 85, Sweden	BACKGROUND: Chromosomal rearrangements in the form of deletions, insertions, inversions and translocations are frequently observed in breast cancer genomes, and a subset of these rearrangements may play a crucial role in tumorigenesis. To identify novel somatic chromosomal rearrangements, we determined the genome structures of 15 hormone-receptor negative breast tumors by long-insert mate pair massively parallel sequencing. RESULTS: We identified and validated 40 somatic structural alterations, including the recurring fusion between genes DDX10 and SKA3 and translocations involving the EPHA5 gene. Other rearrangements were found to affect genes in pathways involved in epigenetic regulation, mitosis and signal transduction, underscoring their potential role in breast tumorigenesis. RNA interference-mediated suppression of five candidate genes (DDX10, SKA3, EPHA5, CLTC and TNIK) led to inhibition of breast cancer cell growth. Moreover, downregulation of DDX10 in breast cancer cells lead to an increased frequency of apoptotic nuclear morphology. CONCLUSIONS: Using whole genome mate pair sequencing and RNA interference assays, we have discovered a number of novel gene rearrangements in breast cancer genomes and identified DDX10, SKA3, EPHA5, CLTC and TNIK as potential cancer genes with impact on the growth and proliferation of breast cancer cells. 	NCBI 36/hg18				Yes	ADAM10,APP;ADAM10,RUNX1;MEGF11,RCAN1;RORA,DSCAM
CTDB0302	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	11	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL060	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-60135986:0;chr11:102484994-105626485:-1;chr11:105626486-107429518:0;chr11:107429519-108827021:-1;chr11:108827022-109142986:0;chr11:109142987-114315496:-1;chr11:114315497-115772845:0;chr11:115772846-116519019:-1;chr11:116519020-119593663:0;chr11:119593664-120699800:-1;chr11:120699801-121840815:0;chr11:121840816-123275276:-1;chr11:123275277-134452384:0;chr11:60135987-60796999:-1;chr11:60797000-102484993:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0303	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	3	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL175up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-106658335:0;chr3:106658336-108421254:-1;chr3:108421255-117982410:0;chr3:117982411-123699590:-1;chr3:123699591-132094098:0;chr3:132094099-132464500:-1;chr3:132464501-132664121:0;chr3:132664122-146476071:-1;chr3:146476072-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0304	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	9,15	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL259up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-18276341:0;chr15:100286565-100338915:0;chr15:18276342-30905963:-1;chr15:30905964-32887157:0;chr15:32887158-46449080:-1;chr15:46449081-51938390:0;chr15:51938391-55169874:-1;chr15:55169875-98156853:0;chr15:98156854-100286564:-1;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-2172289:0;chr9:101714048-101724151:0;chr9:101724152-111739097:-1;chr9:111739098-140273252:0;chr9:14572421-20553798:0;chr9:20553799-32860406:-1;chr9:2172290-4329207:-1;chr9:32860407-32860854:0;chr9:32860855-36874813:1;chr9:36874814-70130415:0;chr9:4329208-5119013:0;chr9:5119014-14572420:-1;chr9:70130416-81358290:-1;chr9:81358291-81358421:0;chr9:81358422-101714047:1;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0305	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	2,8	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL269up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-59565606:0;chr2:111149065-112828328:-1;chr2:112828329-165284219:0;chr2:165284220-166919690:-1;chr2:166919691-171468527:0;chr2:171468528-172046546:-1;chr2:172046547-176248648:0;chr2:176248649-176824870:-1;chr2:176824871-178272553:0;chr2:178272554-180127517:-1;chr2:180127518-182667909:0;chr2:182667910-183995267:-1;chr2:183995268-185551104:0;chr2:185551105-189536072:-1;chr2:189536073-200288762:0;chr2:200288763-201948900:-1;chr2:201948901-204367611:0;chr2:204367612-209066946:-1;chr2:209066947-209802628:0;chr2:209802629-210858261:-1;chr2:210858262-223396325:0;chr2:223396326-226389803:-1;chr2:226389804-242951149:0;chr2:59565607-63157944:1;chr2:63157945-63163576:0;chr2:63163577-75819642:1;chr2:75819643-111149064:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-38162914:0;chr8:38162915-40264829:-1;chr8:40264830-48463332:0;chr8:48463333-48752079:-1;chr8:48752080-58390943:0;chr8:58390944-64602899:-1;chr8:64602900-70645031:0;chr8:70645032-72011812:-1;chr8:72011813-77954414:0;chr8:77954415-80170682:-1;chr8:80170683-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0306	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	2	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL287up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-2771:0;chr2:18968900-34493565:0;chr2:2772-18968899:-1;chr2:34493566-52456236:-1;chr2:52456237-55689565:0;chr2:55689566-58397402:-1;chr2:58397403-66744891:0;chr2:66744892-86807366:-1;chr2:86807367-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0307	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	1	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL293up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-6181716:0;chr1:108545037-110478611:-1;chr1:110478612-115474186:0;chr1:115474187-117860862:-1;chr1:117860863-247249719:0;chr1:41776339-42476711:-1;chr1:42476712-76587476:0;chr1:6181717-9105521:-1;chr1:76587477-77290475:-1;chr1:77290476-77790158:0;chr1:77790159-78745998:-1;chr1:78745999-81170853:0;chr1:81170854-85012152:-1;chr1:85012153-89058530:0;chr1:89058531-95482527:-1;chr1:9105522-41776338:0;chr1:95482528-108545036:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0308	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	6	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL300up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-13130713:0;chr6:13130714-30368961:-1;chr6:141550230-142146472:-1;chr6:142146473-170899992:0;chr6:30368962-38572563:0;chr6:38572564-74660435:-1;chr6:74660436-141550229:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0309	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	6	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL066	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-94648:0;chr6:104456117-131403627:0;chr6:131403628-135722572:-1;chr6:135722573-158212103:0;chr6:1485308-21598311:0;chr6:158212104-158256190:-1;chr6:158256191-170899992:0;chr6:21598312-30559883:-1;chr6:30559884-43419066:0;chr6:43419067-74537921:-1;chr6:74537922-96392731:0;chr6:94649-1485307:1;chr6:96392732-104456116:-1;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0310	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	9	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL067	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-6229927:0;chr9:134464983-135623426:0;chr9:135623427-140211203:1;chr9:140211204-140273252:0;chr9:16649260-70133637:0;chr9:6229928-6291157:-1;chr9:6291158-6534765:0;chr9:6534766-16649259:-1;chr9:70133638-70788159:-1;chr9:70788160-71007979:0;chr9:71007980-79558276:-1;chr9:79558277-92605773:0;chr9:92605774-134464982:-1;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0311	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	17	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL077	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-513:0;chr17:2180649-3765470:0;chr17:23747045-78774742:0;chr17:3765471-5803018:-1;chr17:514-2180648:-1;chr17:5803019-7006097:0;chr17:7006098-7946630:-1;chr17:7946631-8703256:0;chr17:8703257-23747044:-1;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0312	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	13	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL104	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-40350248:0;chr13:40350249-40807123:-1;chr13:40807124-45814699:0;chr13:45814700-46261011:-1;chr13:46261012-47441703:0;chr13:47441704-48167674:-1;chr13:48167675-48401438:0;chr13:48401439-50271572:-1;chr13:50271573-50350855:0;chr13:50350856-50394321:-1;chr13:50394322-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0313	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	15	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL173up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-32451386:0;chr15:32451387-39315978:-1;chr15:39315979-50042146:0;chr15:50042147-54732740:-1;chr15:54732741-83956290:0;chr15:83956291-87312981:-1;chr15:87312982-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0314	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	14	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL182up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-62916329:0;chr14:62916330-64451324:-1;chr14:64451325-66924574:0;chr14:66924575-67349109:-1;chr14:67349110-68774305:0;chr14:68774306-70635712:-1;chr14:70635713-71420608:0;chr14:71420609-73782090:-1;chr14:73782091-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0315	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	11	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL210up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-60213474:0;chr11:117469701-120284568:0;chr11:120284569-122491536:-1;chr11:122491537-122545917:0;chr11:122545918-122900680:-1;chr11:122900681-134452384:0;chr11:60213475-63748377:-1;chr11:63748378-76186932:0;chr11:76186933-117469700:-1;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0316	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	2	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL236up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-42506337:0;chr2:100948167-111159725:0;chr2:111159726-112194596:-1;chr2:112194597-113366646:0;chr2:113366647-115093496:-1;chr2:115093497-135157627:0;chr2:135157628-136837001:-1;chr2:136837002-171514115:0;chr2:171514116-172077646:-1;chr2:172077647-201421698:0;chr2:201421699-204439764:-1;chr2:204439765-242951149:0;chr2:42506338-48582437:-1;chr2:48582438-96099906:0;chr2:96099907-100948166:-1;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0317	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	9,13	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL263up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-43576588:0;chr13:106878224-114126500:-1;chr13:114126501-114142980:0;chr13:43576589-44695858:-1;chr13:44695859-47237563:0;chr13:47237564-48828370:-1;chr13:48828371-48828643:0;chr13:48828644-50691845:-1;chr13:50691846-51974706:0;chr13:51974707-55476935:-1;chr13:55476936-80419771:0;chr13:80419772-85048205:-1;chr13:85048206-85638599:0;chr13:85638600-90543572:-1;chr13:90543573-106878223:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0318	Research	23047824	Edelmann J, Holzmann K, Miller F, Winkler D, Buhler A, Zenz T, Bullinger L, Kuhn MW, Gerhardinger A, Bloehdorn J, Radtke I, Su X, Ma J, Pounds S, Hallek M, Lichter P, Korbel J, Busch R, Mertens D, Downing JR, Stilgenbauer S, Dohner H	High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations	Blood	2012 Dec	2,5	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	CLL267up	Affymetrix Human SNPArray 6.0	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-167124683:0;chr2:167124684-170891195:-1;chr2:170891196-178272540:0;chr2:178272541-180648285:-1;chr2:180648286-182257504:0;chr2:182257505-183959860:-1;chr2:183959861-208884588:0;chr2:208884589-210984140:-1;chr2:210984141-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-5448825:0;chr5:113020008-113424277:-1;chr5:113424278-113699666:0;chr5:113699667-113743974:-1;chr5:113743975-114158359:0;chr5:114158360-116586372:-1;chr5:116586373-120729373:0;chr5:120729374-127600968:-1;chr5:127600969-180857866:0;chr5:5448826-6695426:-1;chr5:6695427-113020007:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Internal Medicine III, Ulm University, Ulm, Germany	To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphism-array analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n = 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-of-heterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.21 (5% of patients) to a segment 486 kb proximal to the MYC locus. 13q deletions exhibited proximal and distal breakpoint cluster regions. Among the most common novel lesions were deletions at 15q15.1 (4% of patients), with the smallest deletion (70.48 kb) found in the MGA locus. Sequence analysis of MGA in 59 samples revealed a truncating mutation in one CLL patient lacking a 15q deletion. MNT at 17p13.3, which in addition to MGA and MYC encodes for the network of MAX-interacting proteins, was also deleted recurrently.	NCBI 36/hg18	GSE36908			Yes	NA
CTDB0319	Research	23796897	Zheng S, Fu J, Vegesna R, Mao Y, Heathcock LE, Torres-Garcia W, Ezhilarasan R, Wang S, McKenna A, Chin L, Brennan CW, Yung WK, Weinstein JN, Aldape KD, Sulman EP, Chen K, Koul D, Verhaak RG	A survey of intragenic breakpoints in glioblastoma identifies a distinct subset associated with poor survival	Genes & Development	2013 Jul 	12	Glioblastoma	Next Generation Sequencing	Homo sapiens	TCGA-06-0129			hs12:32552893-32552893,hs12:40619357-40619357;hs12:6954966-6954966,hs12:95869847-95869847;hs12:51386593-hs12:48501148-48516550;hs6:3410422-3410422,hs6:47221257-47221257;hs12:69864310-69885431,hs12:57957222-57957222;hs12:56663345-56664102,hs12:6964565-6964565;hs12:53861077-53861077,hs12:100482873-100482873;hs12:27156169-27156169,hs12:103670988-103670988;hs6:33393680-33393680,hs6:44220782-44220782;hs12:81929201-82147752,hs12:63954442-63954442;hs12:40345059-40345059,hs12:110834257-110834257;hs6:34791125-34791125,hs12:91358103-91358103;hs12:105538650-105538650,hs12:71928895-71928895;hs12:132630210-132629150,hs12:113837515-113837515;hs6:37623476-37626021,hs6:43126555-43126555;hs4:140222985-140222985,hs9:113638002-113638002;hs12:69756687-69756687,hs12:132522227-132527849	ANAPC7;C12orf42;COQ10A;DPY19L2;EP400;EPYC;FGD4;FRS2;Gene_B;GNB3;KIAA1033;KIF5A;LGR5;LRRK2;METAP2;NOC4L;PCBP2;PFKM;PPFIA2;SDS;SLC11A2;SLC2A13;TM7SF3;UHRF1BP1L;USP5;YEATS4;	Department of Bioinformatics and Computational Biology	With the advent of high-throughput sequencing technologies, much progress has been made in the identification of somatic structural rearrangements in cancer genomes. However, characterization of the complex alterations and their associated mechanisms remains inadequate. Here, we report a comprehensive analysis of whole-genome sequencing and DNA copy number data sets from The Cancer Genome Atlas to relate chromosomal alterations to imbalances in DNA dosage and describe the landscape of intragenic breakpoints in glioblastoma multiforme (GBM). Gene length, guanine-cytosine (GC) content, and local presence of a copy number alteration were closely associated with breakpoint susceptibility. A dense pattern of repeated focal amplifications involving the murine double minute 2 (MDM2)/cyclin-dependent kinase 4 (CDK4) oncogenes and associated with poor survival was identified in 5% of GBMs. Gene fusions and rearrangements were detected concomitant within the breakpoint-enriched region. At the gene level, we noted recurrent breakpoints in genes such as apoptosis regulator FAF1. Structural alterations of the FAF1 gene disrupted expression and led to protein depletion. Restoration of the FAF1 protein in glioma cell lines significantly increased the FAS-mediated apoptosis response. Our study uncovered a previously underappreciated genomic mechanism of gene deregulation that can confer growth advantages on tumor cells and may generate cancer-specific vulnerabilities in subsets of GBM. 	NCBI 36/hg18				Yes	COQ10A,USP5;FGD4,LRRK2;FRS2,KIF5A;GNB3,METAP2;KIAA1033,LGR5;NOC4L,SDS;PCBP2,UHRF1BP1L;PPFIA2,DPY19L2;SLC11A2,PFKM;SLC2A13,ANAPC7;TM7SF3,C12orf42;UHRF1BP1,EPYC;YEATS4,EP400
CTDB0320	Research	25178926	Conconi D, Panzeri E, Redaelli S, Bovo G, Vigano P, Strada G, Dalpra L, Bentivegna A	Chromosomal imbalances in human bladder urothelial carcinoma: similarities and differences between biopsy samples and cancer stem-like cells	BMC Cancer	2014 Sep 	6	Bladder cancer	Array CGH	Homo sapiens	36	Agilent SurePrint G3 Human CGH Microarray 8X60K	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-1135232:0;chr6:107207520-108013375:1;chr6:108013376-112208261:0;chr6:112208262-112512304:1;chr6:112512305-120033768:0;chr6:1135233-1135233:-1;chr6:1135234-3051601:0;chr6:11627813-14525354:1;chr6:120033769-122974823:1;chr6:122974824-123422158:0;chr6:123422159-124568813:1;chr6:124568814-125346033:0;chr6:125346034-132823273:1;chr6:132823274-146392494:0;chr6:14525355-16403510:0;chr6:146392495-170732174:-1;chr6:16403511-22397156:1;chr6:170732175-170899992:0;chr6:21107860-22397156:1;chr6:22397157-25428028:0;chr6:25428029-26797455:1;chr6:26797456-27107707:0;chr6:27107708-27263190:-1;chr6:27263191-27579787:0;chr6:27579788-30302271:-1;chr6:30302272-36788265:0;chr6:3051602-3600958:1;chr6:3600959-11627812:0;chr6:36788266-37917098:1;chr6:37917099-37957570:0;chr6:37957571-41426791:-1;chr6:41426792-41474744:0;chr6:41474745-48648336:1;chr6:41716419-43012857:1;chr6:45987212-47657919:1;chr6:48648337-49627984:0;chr6:49627985-52912395:-1;chr6:52912396-53384802:0;chr6:53384803-57298946:1;chr6:57298947-82896725:0;chr6:82896726-83392667:1;chr6:83392668-84856797:0;chr6:84856798-86137353:1;chr6:86137354-107207519:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Surgery and Translational Medicine, University of Milan-Bicocca, via Cadore 48, 20052 Monza, Italy	BACKGROUND: The existence of two distinct groups of tumors with different clinical characteristic is a remarkable feature of transitional cell carcinomas (TCCs) of the bladder. More than 70% are low-grade (LG) non-infiltrating (NI) cancers at diagnosis, but 60-80% of them recur at least one time and 10-20% progress in stage and grade. On the other hand, about 20% of tumors show muscle invasion (IN) and have a poor prognosis with <50% survival after 5 years. This study focuses on the complexity of the bladder cancer genome, and for the first time to our knowledge, on the possibility to compare genomic alterations of in vitro selected cancer stem-like cells (CSCs), and their original biopsy in order to identify different genomic signature already present in the early stages of tumorigenesis of LG and HG tumors. METHODS: We initially used conventional chromosome analysis on TCC biopsies with different histotypes (LG vs HG) in order to detect rough differences between them. Then, we performed array comparative genomic hybridization (aCGH) on 10 HG and 10 LG tumors providing an overview of copy number alterations (CNAs). Finally, we made a comparison of the overall CNAs in 16 biopsies and their respective CSCs isolated from them. RESULTS: Our findings indicate that LG and HG bladder cancer differ with regard to their genomic profile even in the early stage of tumorigenesis; moreover, we identified a subgroup of LG samples with a higher tendency to lose genomic regions which could represent a more aggressive phenotype. CONCLUSIONS: The outcomes not only provide valuable information to deeper studying TCC carcinogenesis, but also could help in the clinic for diagnosis and prognosis of patients who will benefit from a more aggressive therapy. 	NCBI 36/hg18				Yes	NA
CTDB0321	Research	25178926	Conconi D, Panzeri E, Redaelli S, Bovo G, Vigano P, Strada G, Dalpra L, Bentivegna A	Chromosomal imbalances in human bladder urothelial carcinoma: similarities and differences between biopsy samples and cancer stem-like cells	BMC Cancer	2014 Sep 	6	Bladder cancer	Array CGH	Homo sapiens	37	Agilent SurePrint G3 Human CGH Microarray 8X60K	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-295011:0;chr6:11110371-17397320:1;chr6:170734369-170899992:0;chr6:17397321-18704208:0;chr6:18704209-30343121:1;chr6:295012-9584745:-1;chr6:30343122-39615526:0;chr6:39615527-41420057:1;chr6:41420058-42438437:0;chr6:42438438-46607938:1;chr6:46607939-48489132:0;chr6:48489133-55026820:-1;chr6:55026821-55152486:0;chr6:55152487-57298946:1;chr6:57298947-62815576:0;chr6:62815577-170734368:-1;chr6:9584746-11110370:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0			Department of Surgery and Translational Medicine, University of Milan-Bicocca, via Cadore 48, 20052 Monza, Italy	BACKGROUND: The existence of two distinct groups of tumors with different clinical characteristic is a remarkable feature of transitional cell carcinomas (TCCs) of the bladder. More than 70% are low-grade (LG) non-infiltrating (NI) cancers at diagnosis, but 60-80% of them recur at least one time and 10-20% progress in stage and grade. On the other hand, about 20% of tumors show muscle invasion (IN) and have a poor prognosis with <50% survival after 5 years. This study focuses on the complexity of the bladder cancer genome, and for the first time to our knowledge, on the possibility to compare genomic alterations of in vitro selected cancer stem-like cells (CSCs), and their original biopsy in order to identify different genomic signature already present in the early stages of tumorigenesis of LG and HG tumors. METHODS: We initially used conventional chromosome analysis on TCC biopsies with different histotypes (LG vs HG) in order to detect rough differences between them. Then, we performed array comparative genomic hybridization (aCGH) on 10 HG and 10 LG tumors providing an overview of copy number alterations (CNAs). Finally, we made a comparison of the overall CNAs in 16 biopsies and their respective CSCs isolated from them. RESULTS: Our findings indicate that LG and HG bladder cancer differ with regard to their genomic profile even in the early stage of tumorigenesis; moreover, we identified a subgroup of LG samples with a higher tendency to lose genomic regions which could represent a more aggressive phenotype. CONCLUSIONS: The outcomes not only provide valuable information to deeper studying TCC carcinogenesis, but also could help in the clinic for diagnosis and prognosis of patients who will benefit from a more aggressive therapy. 	NCBI 36/hg18				Yes	NA
CTDB0322	Research	25079552	Collisson EA, Campbell JD, Brooks AN, Berger AH, Lee W, Chmielecki J, Beer DG, Cope L, Creighton CJ, Danilova L, Ding L, Getz G, Hammerman PS, Hayes DN, Hernandez B, Herman JG, Heymach JV, Jurisica I, Kucherlapati R, Kwiatkowski D, Ladanyi M, Robertson G, Schultz N, Shen R, Sinha R, Sougnez C, Tsao MS, Travis WD, Weinstein JN, Wigle DA, Wilkerson MD, Chu A, Cherniack AD, Hadjipanayis A, Rosenberg M, Weisenberger DJ, Laird PW, Radenbaugh A, Ma S, Stuart JM, Averett Byers L, Baylin SB, Govindan R, Meyerson M, Rosenberg M, Gabriel SB, Cibulskis K, Sougnez C, Kim J, Stewart C, Lichtenstein L, Lander ES, Lawrence MS, Getz, Kandoth C, Fulton R, Fulton LL, McLellan MD, Wilson RK, Ye K, Fronick CC, Maher CA, Miller CA, Wendl MC, Cabanski C, Ding L, Mardis E, Govindan R, Creighton CJ, Wheeler D, Balasundaram M, Butterfield YS, Carlsen R, Chu A, Chuah E, Dhalla N, Guin R, Hirst C, Lee D, Li HI, Mayo M, Moore RA, Mungall AJ, Schein JE, Sipahimalani P, Tam A, Varhol R, Robertson A, Wye N, Thiessen N, Holt RA, Jones SJ, Marra MA, Campbell JD, Brooks AN, Chmielecki J, Imielinski M, Onofrio RC, Hodis E, Zack T, Sougnez C, Helman E, Sekhar Pedamallu C, Mesirov J, Cherniack AD, Saksena G, Schumacher SE, Carter SL, Hernandez B, Garraway L, Beroukhim R, Gabriel SB, Getz G, Meyerson M, Hadjipanayis A, Lee S, Mahadeshwar HS, Pantazi A, Protopopov A, Ren X, Seth S, Song X, Tang J, Yang L, Zhang J, Chen PC, Parfenov M, Wei Xu A, Santoso N, Chin L, Park PJ, Kucherlapati R, Hoadley KA, Auman JT, Meng S, Shi Y, Buda E, Waring S, Veluvolu U, Tan D, Mieczkowski PA, Jones CD, Simons JV, Soloway MG, Bodenheimer T, Jefferys SR, Roach J, Hoyle AP, Wu J, Balu S, Singh D, Prins JF, Marron JS, Parker JS, Hayes DN, Perou CM, Liu J, Cope L, Danilova L, Weisenberger DJ, Maglinte DT, Lai PH, Bootwalla MS, Van Den Berg DJ, Triche T Jr, Baylin SB, Laird PW, Rosenberg M, Chin L, Zhang J, Cho J, DiCara D, Heiman D, Lin P, Mallard W, Voet D, Zhang H, Zou L, Noble MS, Lawrence MS, Saksena G, Gehlenborg N, Thorvaldsdottir H, Mesirov J, Nazaire MD, Robinson J, Getz G, Lee W, Aksoy BA, Ciriello G, Taylor BS, Dresdner G, Gao J, Gross B, Seshan VE, Ladanyi M, Reva B, Sinha R, Sumer SO, Weinhold N, Schultz N, Shen R, Sander C, Ng S, Ma S, Zhu J, Radenbaugh A, Stuart JM, Benz CC, Yau C, Haussler D, Spellman PT, Wilkerson MD, Parker JS, Hoadley KA, Kimes PK, Hayes DN, Perou CM, Broom BM, Wang J, Lu Y, Kwok Shing Ng P, Diao L, Averett Byers L, Liu W, Heymach JV, Amos CI, Weinstein JN, Akbani R, Mills GB, Curley E, Paulauskis J, Lau K, Morris S, Shelton T, Mallery D, Gardner J, Penny R, Saller C, Tarvin K, Richards WG, Cerfolio R, Bryant A, Raymond DP, Pennell NA, Farver C, Czerwinski C, Huelsenbeck-Dill L, Iacocca M, Petrelli N, Rabeno B, Brown J, Bauer T, Dolzhanskiy O, Potapova O, Rotin D, Voronina O, Nemirovich-Danchenko E, Fedosenko KV, Gal A, Behera M, Ramalingam SS, Sica G, Flieder D, Boyd J, Weaver J, Kohl B, Huy Quoc Thinh D, Sandusky G, Juhl H, Duhig E, Illei P, Gabrielson E, Shin J, Lee B, Rodgers K, Trusty D, Brock MV, Williamson C, Burks E, Rieger-Christ K, Holway A, Sullivan T, Wigle DA, Asiedu MK, Kosari F, Travis WD, Rekhtman N, Zakowski M, Rusch VW, Zippile P, Suh J, Pass H, Goparaju C, Owusu-Sarpong Y, Bartlett JM, Kodeeswaran S, Parfitt J, Sekhon H, Albert M, Eckman J, Myers JB, Cheney R, Morrison C, Gaudioso C, Borgia JA, Bonomi P, Pool M, Liptay MJ, Moiseenko F, Zaytseva I, Dienemann H, Meister M, Schnabel PA, Muley TR, Peifer M, Gomez-Fernandez C, Herbert L, Egea S, Huang M, Thorne LB, Boice L, Hill Salazar A, Funkhouser WK, Rathmell WK, Dhir R, Yousem SA, Dacic S, Schneider F, Siegfried JM, Hajek R, Watson MA, McDonald S, Meyers B, Clarke B, Yang IA, Fong KM, Hunter L, Windsor M, Bowman RV, Peters S, Letovanec I, Khan KZ, Jensen MA, Snyder EE, Srinivasan D, Kahn AB, Baboud J, Pot DA, Mills Shaw KR, Sheth M, Davidsen T, Demchok JA, Yang L, Wang Z, Tarnuzzer R, Zenklusen JC, Ozenberger BA, Sofia HJ, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS	Comprehensive molecular profiling of lung adenocarcinoma	Nature	2014 Jul 	1	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	TCGA-05-5715	Illumina HiSeq2000		hs1:154938559-154938559,hs1:174656755-174656755;hs9:22038088-22038088,hs9:32410826-32410826;hs20:32851674-32851674,hs20:34367049-34367049;hs1:110884862-110884862,hs1:111688869-111688869;hs1:160175959-160175959,hs1:201254023-201254023	CEPT1;PEA15;PKP1;RABGAP1L;RBM15;SHC1;	University of CaliforniaSan Francisco, San Francisco,California94158,USA	Adenocarcinoma of the lung is the leading cause of cancer death worldwide. Here we report molecular profiling of 230 resected lung adenocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses. High rates of somatic mutation were seen (mean 8.9 mutations per megabase). Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. EGFR mutations were more frequent in female patients, whereas mutations in RBM10 were more common in males. Aberrations in NF1, MET, ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. DNA and mRNA sequence from the same tumour highlighted splicing alterations driven by somatic genomic changes, including exon 14 skipping in MET mRNA in 4% of cases. MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. These data establish a foundation for classification and further investigations of lung adenocarcinoma molecular pathogenesis. 	GRCh37/hg19				Yes	PEA15,PKP1;RBM15,CEPT1;SHC1,RABGAP1L
CTDB0323	Research	25079552	Collisson EA, Campbell JD, Brooks AN, Berger AH, Lee W, Chmielecki J, Beer DG, Cope L, Creighton CJ, Danilova L, Ding L, Getz G, Hammerman PS, Hayes DN, Hernandez B, Herman JG, Heymach JV, Jurisica I, Kucherlapati R, Kwiatkowski D, Ladanyi M, Robertson G, Schultz N, Shen R, Sinha R, Sougnez C, Tsao MS, Travis WD, Weinstein JN, Wigle DA, Wilkerson MD, Chu A, Cherniack AD, Hadjipanayis A, Rosenberg M, Weisenberger DJ, Laird PW, Radenbaugh A, Ma S, Stuart JM, Averett Byers L, Baylin SB, Govindan R, Meyerson M, Rosenberg M, Gabriel SB, Cibulskis K, Sougnez C, Kim J, Stewart C, Lichtenstein L, Lander ES, Lawrence MS, Getz, Kandoth C, Fulton R, Fulton LL, McLellan MD, Wilson RK, Ye K, Fronick CC, Maher CA, Miller CA, Wendl MC, Cabanski C, Ding L, Mardis E, Govindan R, Creighton CJ, Wheeler D, Balasundaram M, Butterfield YS, Carlsen R, Chu A, Chuah E, Dhalla N, Guin R, Hirst C, Lee D, Li HI, Mayo M, Moore RA, Mungall AJ, Schein JE, Sipahimalani P, Tam A, Varhol R, Robertson A, Wye N, Thiessen N, Holt RA, Jones SJ, Marra MA, Campbell JD, Brooks AN, Chmielecki J, Imielinski M, Onofrio RC, Hodis E, Zack T, Sougnez C, Helman E, Sekhar Pedamallu C, Mesirov J, Cherniack AD, Saksena G, Schumacher SE, Carter SL, Hernandez B, Garraway L, Beroukhim R, Gabriel SB, Getz G, Meyerson M, Hadjipanayis A, Lee S, Mahadeshwar HS, Pantazi A, Protopopov A, Ren X, Seth S, Song X, Tang J, Yang L, Zhang J, Chen PC, Parfenov M, Wei Xu A, Santoso N, Chin L, Park PJ, Kucherlapati R, Hoadley KA, Auman JT, Meng S, Shi Y, Buda E, Waring S, Veluvolu U, Tan D, Mieczkowski PA, Jones CD, Simons JV, Soloway MG, Bodenheimer T, Jefferys SR, Roach J, Hoyle AP, Wu J, Balu S, Singh D, Prins JF, Marron JS, Parker JS, Hayes DN, Perou CM, Liu J, Cope L, Danilova L, Weisenberger DJ, Maglinte DT, Lai PH, Bootwalla MS, Van Den Berg DJ, Triche T Jr, Baylin SB, Laird PW, Rosenberg M, Chin L, Zhang J, Cho J, DiCara D, Heiman D, Lin P, Mallard W, Voet D, Zhang H, Zou L, Noble MS, Lawrence MS, Saksena G, Gehlenborg N, Thorvaldsdottir H, Mesirov J, Nazaire MD, Robinson J, Getz G, Lee W, Aksoy BA, Ciriello G, Taylor BS, Dresdner G, Gao J, Gross B, Seshan VE, Ladanyi M, Reva B, Sinha R, Sumer SO, Weinhold N, Schultz N, Shen R, Sander C, Ng S, Ma S, Zhu J, Radenbaugh A, Stuart JM, Benz CC, Yau C, Haussler D, Spellman PT, Wilkerson MD, Parker JS, Hoadley KA, Kimes PK, Hayes DN, Perou CM, Broom BM, Wang J, Lu Y, Kwok Shing Ng P, Diao L, Averett Byers L, Liu W, Heymach JV, Amos CI, Weinstein JN, Akbani R, Mills GB, Curley E, Paulauskis J, Lau K, Morris S, Shelton T, Mallery D, Gardner J, Penny R, Saller C, Tarvin K, Richards WG, Cerfolio R, Bryant A, Raymond DP, Pennell NA, Farver C, Czerwinski C, Huelsenbeck-Dill L, Iacocca M, Petrelli N, Rabeno B, Brown J, Bauer T, Dolzhanskiy O, Potapova O, Rotin D, Voronina O, Nemirovich-Danchenko E, Fedosenko KV, Gal A, Behera M, Ramalingam SS, Sica G, Flieder D, Boyd J, Weaver J, Kohl B, Huy Quoc Thinh D, Sandusky G, Juhl H, Duhig E, Illei P, Gabrielson E, Shin J, Lee B, Rodgers K, Trusty D, Brock MV, Williamson C, Burks E, Rieger-Christ K, Holway A, Sullivan T, Wigle DA, Asiedu MK, Kosari F, Travis WD, Rekhtman N, Zakowski M, Rusch VW, Zippile P, Suh J, Pass H, Goparaju C, Owusu-Sarpong Y, Bartlett JM, Kodeeswaran S, Parfitt J, Sekhon H, Albert M, Eckman J, Myers JB, Cheney R, Morrison C, Gaudioso C, Borgia JA, Bonomi P, Pool M, Liptay MJ, Moiseenko F, Zaytseva I, Dienemann H, Meister M, Schnabel PA, Muley TR, Peifer M, Gomez-Fernandez C, Herbert L, Egea S, Huang M, Thorne LB, Boice L, Hill Salazar A, Funkhouser WK, Rathmell WK, Dhir R, Yousem SA, Dacic S, Schneider F, Siegfried JM, Hajek R, Watson MA, McDonald S, Meyers B, Clarke B, Yang IA, Fong KM, Hunter L, Windsor M, Bowman RV, Peters S, Letovanec I, Khan KZ, Jensen MA, Snyder EE, Srinivasan D, Kahn AB, Baboud J, Pot DA, Mills Shaw KR, Sheth M, Davidsen T, Demchok JA, Yang L, Wang Z, Tarnuzzer R, Zenklusen JC, Ozenberger BA, Sofia HJ, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS	Comprehensive molecular profiling of lung adenocarcinoma	Nature	2014 Jul 	1	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	TCGA-50-5932	Illumina HiSeq2000		hs1:147129126-147129126,hs1:157775887-157775887;hs12:26133210-26133210,hs12:29769974-29769974;hs2:73751972-73751972,hs19:43017249-43017249;hs12:49216189-49216189,hs12:49334831-49334831	ACP6;FCRL1;	University of CaliforniaSan Francisco, San Francisco,California94158,USA	Adenocarcinoma of the lung is the leading cause of cancer death worldwide. Here we report molecular profiling of 230 resected lung adenocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses. High rates of somatic mutation were seen (mean 8.9 mutations per megabase). Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. EGFR mutations were more frequent in female patients, whereas mutations in RBM10 were more common in males. Aberrations in NF1, MET, ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. DNA and mRNA sequence from the same tumour highlighted splicing alterations driven by somatic genomic changes, including exon 14 skipping in MET mRNA in 4% of cases. MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. These data establish a foundation for classification and further investigations of lung adenocarcinoma molecular pathogenesis. 	GRCh37/hg19				Yes	ACP6,FCRL1
CTDB0324	Research	25079552	Collisson EA, Campbell JD, Brooks AN, Berger AH, Lee W, Chmielecki J, Beer DG, Cope L, Creighton CJ, Danilova L, Ding L, Getz G, Hammerman PS, Hayes DN, Hernandez B, Herman JG, Heymach JV, Jurisica I, Kucherlapati R, Kwiatkowski D, Ladanyi M, Robertson G, Schultz N, Shen R, Sinha R, Sougnez C, Tsao MS, Travis WD, Weinstein JN, Wigle DA, Wilkerson MD, Chu A, Cherniack AD, Hadjipanayis A, Rosenberg M, Weisenberger DJ, Laird PW, Radenbaugh A, Ma S, Stuart JM, Averett Byers L, Baylin SB, Govindan R, Meyerson M, Rosenberg M, Gabriel SB, Cibulskis K, Sougnez C, Kim J, Stewart C, Lichtenstein L, Lander ES, Lawrence MS, Getz, Kandoth C, Fulton R, Fulton LL, McLellan MD, Wilson RK, Ye K, Fronick CC, Maher CA, Miller CA, Wendl MC, Cabanski C, Ding L, Mardis E, Govindan R, Creighton CJ, Wheeler D, Balasundaram M, Butterfield YS, Carlsen R, Chu A, Chuah E, Dhalla N, Guin R, Hirst C, Lee D, Li HI, Mayo M, Moore RA, Mungall AJ, Schein JE, Sipahimalani P, Tam A, Varhol R, Robertson A, Wye N, Thiessen N, Holt RA, Jones SJ, Marra MA, Campbell JD, Brooks AN, Chmielecki J, Imielinski M, Onofrio RC, Hodis E, Zack T, Sougnez C, Helman E, Sekhar Pedamallu C, Mesirov J, Cherniack AD, Saksena G, Schumacher SE, Carter SL, Hernandez B, Garraway L, Beroukhim R, Gabriel SB, Getz G, Meyerson M, Hadjipanayis A, Lee S, Mahadeshwar HS, Pantazi A, Protopopov A, Ren X, Seth S, Song X, Tang J, Yang L, Zhang J, Chen PC, Parfenov M, Wei Xu A, Santoso N, Chin L, Park PJ, Kucherlapati R, Hoadley KA, Auman JT, Meng S, Shi Y, Buda E, Waring S, Veluvolu U, Tan D, Mieczkowski PA, Jones CD, Simons JV, Soloway MG, Bodenheimer T, Jefferys SR, Roach J, Hoyle AP, Wu J, Balu S, Singh D, Prins JF, Marron JS, Parker JS, Hayes DN, Perou CM, Liu J, Cope L, Danilova L, Weisenberger DJ, Maglinte DT, Lai PH, Bootwalla MS, Van Den Berg DJ, Triche T Jr, Baylin SB, Laird PW, Rosenberg M, Chin L, Zhang J, Cho J, DiCara D, Heiman D, Lin P, Mallard W, Voet D, Zhang H, Zou L, Noble MS, Lawrence MS, Saksena G, Gehlenborg N, Thorvaldsdottir H, Mesirov J, Nazaire MD, Robinson J, Getz G, Lee W, Aksoy BA, Ciriello G, Taylor BS, Dresdner G, Gao J, Gross B, Seshan VE, Ladanyi M, Reva B, Sinha R, Sumer SO, Weinhold N, Schultz N, Shen R, Sander C, Ng S, Ma S, Zhu J, Radenbaugh A, Stuart JM, Benz CC, Yau C, Haussler D, Spellman PT, Wilkerson MD, Parker JS, Hoadley KA, Kimes PK, Hayes DN, Perou CM, Broom BM, Wang J, Lu Y, Kwok Shing Ng P, Diao L, Averett Byers L, Liu W, Heymach JV, Amos CI, Weinstein JN, Akbani R, Mills GB, Curley E, Paulauskis J, Lau K, Morris S, Shelton T, Mallery D, Gardner J, Penny R, Saller C, Tarvin K, Richards WG, Cerfolio R, Bryant A, Raymond DP, Pennell NA, Farver C, Czerwinski C, Huelsenbeck-Dill L, Iacocca M, Petrelli N, Rabeno B, Brown J, Bauer T, Dolzhanskiy O, Potapova O, Rotin D, Voronina O, Nemirovich-Danchenko E, Fedosenko KV, Gal A, Behera M, Ramalingam SS, Sica G, Flieder D, Boyd J, Weaver J, Kohl B, Huy Quoc Thinh D, Sandusky G, Juhl H, Duhig E, Illei P, Gabrielson E, Shin J, Lee B, Rodgers K, Trusty D, Brock MV, Williamson C, Burks E, Rieger-Christ K, Holway A, Sullivan T, Wigle DA, Asiedu MK, Kosari F, Travis WD, Rekhtman N, Zakowski M, Rusch VW, Zippile P, Suh J, Pass H, Goparaju C, Owusu-Sarpong Y, Bartlett JM, Kodeeswaran S, Parfitt J, Sekhon H, Albert M, Eckman J, Myers JB, Cheney R, Morrison C, Gaudioso C, Borgia JA, Bonomi P, Pool M, Liptay MJ, Moiseenko F, Zaytseva I, Dienemann H, Meister M, Schnabel PA, Muley TR, Peifer M, Gomez-Fernandez C, Herbert L, Egea S, Huang M, Thorne LB, Boice L, Hill Salazar A, Funkhouser WK, Rathmell WK, Dhir R, Yousem SA, Dacic S, Schneider F, Siegfried JM, Hajek R, Watson MA, McDonald S, Meyers B, Clarke B, Yang IA, Fong KM, Hunter L, Windsor M, Bowman RV, Peters S, Letovanec I, Khan KZ, Jensen MA, Snyder EE, Srinivasan D, Kahn AB, Baboud J, Pot DA, Mills Shaw KR, Sheth M, Davidsen T, Demchok JA, Yang L, Wang Z, Tarnuzzer R, Zenklusen JC, Ozenberger BA, Sofia HJ, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS	Comprehensive molecular profiling of lung adenocarcinoma	Nature	2014 Jul 	3	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	TCGA-67-3771	Illumina HiSeq2000				University of CaliforniaSan Francisco, San Francisco,California94158,USA	Adenocarcinoma of the lung is the leading cause of cancer death worldwide. Here we report molecular profiling of 230 resected lung adenocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses. High rates of somatic mutation were seen (mean 8.9 mutations per megabase). Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. EGFR mutations were more frequent in female patients, whereas mutations in RBM10 were more common in males. Aberrations in NF1, MET, ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. DNA and mRNA sequence from the same tumour highlighted splicing alterations driven by somatic genomic changes, including exon 14 skipping in MET mRNA in 4% of cases. MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. These data establish a foundation for classification and further investigations of lung adenocarcinoma molecular pathogenesis. 	GRCh37/hg19				Yes	NA
CTDB0325	Research	25079552	Collisson EA, Campbell JD, Brooks AN, Berger AH, Lee W, Chmielecki J, Beer DG, Cope L, Creighton CJ, Danilova L, Ding L, Getz G, Hammerman PS, Hayes DN, Hernandez B, Herman JG, Heymach JV, Jurisica I, Kucherlapati R, Kwiatkowski D, Ladanyi M, Robertson G, Schultz N, Shen R, Sinha R, Sougnez C, Tsao MS, Travis WD, Weinstein JN, Wigle DA, Wilkerson MD, Chu A, Cherniack AD, Hadjipanayis A, Rosenberg M, Weisenberger DJ, Laird PW, Radenbaugh A, Ma S, Stuart JM, Averett Byers L, Baylin SB, Govindan R, Meyerson M, Rosenberg M, Gabriel SB, Cibulskis K, Sougnez C, Kim J, Stewart C, Lichtenstein L, Lander ES, Lawrence MS, Getz, Kandoth C, Fulton R, Fulton LL, McLellan MD, Wilson RK, Ye K, Fronick CC, Maher CA, Miller CA, Wendl MC, Cabanski C, Ding L, Mardis E, Govindan R, Creighton CJ, Wheeler D, Balasundaram M, Butterfield YS, Carlsen R, Chu A, Chuah E, Dhalla N, Guin R, Hirst C, Lee D, Li HI, Mayo M, Moore RA, Mungall AJ, Schein JE, Sipahimalani P, Tam A, Varhol R, Robertson A, Wye N, Thiessen N, Holt RA, Jones SJ, Marra MA, Campbell JD, Brooks AN, Chmielecki J, Imielinski M, Onofrio RC, Hodis E, Zack T, Sougnez C, Helman E, Sekhar Pedamallu C, Mesirov J, Cherniack AD, Saksena G, Schumacher SE, Carter SL, Hernandez B, Garraway L, Beroukhim R, Gabriel SB, Getz G, Meyerson M, Hadjipanayis A, Lee S, Mahadeshwar HS, Pantazi A, Protopopov A, Ren X, Seth S, Song X, Tang J, Yang L, Zhang J, Chen PC, Parfenov M, Wei Xu A, Santoso N, Chin L, Park PJ, Kucherlapati R, Hoadley KA, Auman JT, Meng S, Shi Y, Buda E, Waring S, Veluvolu U, Tan D, Mieczkowski PA, Jones CD, Simons JV, Soloway MG, Bodenheimer T, Jefferys SR, Roach J, Hoyle AP, Wu J, Balu S, Singh D, Prins JF, Marron JS, Parker JS, Hayes DN, Perou CM, Liu J, Cope L, Danilova L, Weisenberger DJ, Maglinte DT, Lai PH, Bootwalla MS, Van Den Berg DJ, Triche T Jr, Baylin SB, Laird PW, Rosenberg M, Chin L, Zhang J, Cho J, DiCara D, Heiman D, Lin P, Mallard W, Voet D, Zhang H, Zou L, Noble MS, Lawrence MS, Saksena G, Gehlenborg N, Thorvaldsdottir H, Mesirov J, Nazaire MD, Robinson J, Getz G, Lee W, Aksoy BA, Ciriello G, Taylor BS, Dresdner G, Gao J, Gross B, Seshan VE, Ladanyi M, Reva B, Sinha R, Sumer SO, Weinhold N, Schultz N, Shen R, Sander C, Ng S, Ma S, Zhu J, Radenbaugh A, Stuart JM, Benz CC, Yau C, Haussler D, Spellman PT, Wilkerson MD, Parker JS, Hoadley KA, Kimes PK, Hayes DN, Perou CM, Broom BM, Wang J, Lu Y, Kwok Shing Ng P, Diao L, Averett Byers L, Liu W, Heymach JV, Amos CI, Weinstein JN, Akbani R, Mills GB, Curley E, Paulauskis J, Lau K, Morris S, Shelton T, Mallery D, Gardner J, Penny R, Saller C, Tarvin K, Richards WG, Cerfolio R, Bryant A, Raymond DP, Pennell NA, Farver C, Czerwinski C, Huelsenbeck-Dill L, Iacocca M, Petrelli N, Rabeno B, Brown J, Bauer T, Dolzhanskiy O, Potapova O, Rotin D, Voronina O, Nemirovich-Danchenko E, Fedosenko KV, Gal A, Behera M, Ramalingam SS, Sica G, Flieder D, Boyd J, Weaver J, Kohl B, Huy Quoc Thinh D, Sandusky G, Juhl H, Duhig E, Illei P, Gabrielson E, Shin J, Lee B, Rodgers K, Trusty D, Brock MV, Williamson C, Burks E, Rieger-Christ K, Holway A, Sullivan T, Wigle DA, Asiedu MK, Kosari F, Travis WD, Rekhtman N, Zakowski M, Rusch VW, Zippile P, Suh J, Pass H, Goparaju C, Owusu-Sarpong Y, Bartlett JM, Kodeeswaran S, Parfitt J, Sekhon H, Albert M, Eckman J, Myers JB, Cheney R, Morrison C, Gaudioso C, Borgia JA, Bonomi P, Pool M, Liptay MJ, Moiseenko F, Zaytseva I, Dienemann H, Meister M, Schnabel PA, Muley TR, Peifer M, Gomez-Fernandez C, Herbert L, Egea S, Huang M, Thorne LB, Boice L, Hill Salazar A, Funkhouser WK, Rathmell WK, Dhir R, Yousem SA, Dacic S, Schneider F, Siegfried JM, Hajek R, Watson MA, McDonald S, Meyers B, Clarke B, Yang IA, Fong KM, Hunter L, Windsor M, Bowman RV, Peters S, Letovanec I, Khan KZ, Jensen MA, Snyder EE, Srinivasan D, Kahn AB, Baboud J, Pot DA, Mills Shaw KR, Sheth M, Davidsen T, Demchok JA, Yang L, Wang Z, Tarnuzzer R, Zenklusen JC, Ozenberger BA, Sofia HJ, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS	Comprehensive molecular profiling of lung adenocarcinoma	Nature	2014 Jul 	19	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	TCGA-49-4488	Illumina HiSeq2000		hs19:34171134-34171134,hs19:54941891-54941891;hs3:183967046-183967046,hs3:183967499-183967499;hs16:337134-337134,hs16:337641-337641;hs17:79281429-79281429,hs17:79496259-79496259;hs22:18958602-18958602,hs22:20254952-20254952;hs5:176057323-176057323,hs5:176057832-176057832;hs15:27471932-27471932,hs19:54971210-54971210;hs1:40633928-40633928,hsX:73229417-73229417	CHST8;	University of CaliforniaSan Francisco, San Francisco,California94158,USA	Adenocarcinoma of the lung is the leading cause of cancer death worldwide. Here we report molecular profiling of 230 resected lung adenocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses. High rates of somatic mutation were seen (mean 8.9 mutations per megabase). Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. EGFR mutations were more frequent in female patients, whereas mutations in RBM10 were more common in males. Aberrations in NF1, MET, ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. DNA and mRNA sequence from the same tumour highlighted splicing alterations driven by somatic genomic changes, including exon 14 skipping in MET mRNA in 4% of cases. MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. These data establish a foundation for classification and further investigations of lung adenocarcinoma molecular pathogenesis. 	GRCh37/hg19				Yes	CHST8,TTYH1
CTDB0326	Research	25079552	Collisson EA, Campbell JD, Brooks AN, Berger AH, Lee W, Chmielecki J, Beer DG, Cope L, Creighton CJ, Danilova L, Ding L, Getz G, Hammerman PS, Hayes DN, Hernandez B, Herman JG, Heymach JV, Jurisica I, Kucherlapati R, Kwiatkowski D, Ladanyi M, Robertson G, Schultz N, Shen R, Sinha R, Sougnez C, Tsao MS, Travis WD, Weinstein JN, Wigle DA, Wilkerson MD, Chu A, Cherniack AD, Hadjipanayis A, Rosenberg M, Weisenberger DJ, Laird PW, Radenbaugh A, Ma S, Stuart JM, Averett Byers L, Baylin SB, Govindan R, Meyerson M, Rosenberg M, Gabriel SB, Cibulskis K, Sougnez C, Kim J, Stewart C, Lichtenstein L, Lander ES, Lawrence MS, Getz, Kandoth C, Fulton R, Fulton LL, McLellan MD, Wilson RK, Ye K, Fronick CC, Maher CA, Miller CA, Wendl MC, Cabanski C, Ding L, Mardis E, Govindan R, Creighton CJ, Wheeler D, Balasundaram M, Butterfield YS, Carlsen R, Chu A, Chuah E, Dhalla N, Guin R, Hirst C, Lee D, Li HI, Mayo M, Moore RA, Mungall AJ, Schein JE, Sipahimalani P, Tam A, Varhol R, Robertson A, Wye N, Thiessen N, Holt RA, Jones SJ, Marra MA, Campbell JD, Brooks AN, Chmielecki J, Imielinski M, Onofrio RC, Hodis E, Zack T, Sougnez C, Helman E, Sekhar Pedamallu C, Mesirov J, Cherniack AD, Saksena G, Schumacher SE, Carter SL, Hernandez B, Garraway L, Beroukhim R, Gabriel SB, Getz G, Meyerson M, Hadjipanayis A, Lee S, Mahadeshwar HS, Pantazi A, Protopopov A, Ren X, Seth S, Song X, Tang J, Yang L, Zhang J, Chen PC, Parfenov M, Wei Xu A, Santoso N, Chin L, Park PJ, Kucherlapati R, Hoadley KA, Auman JT, Meng S, Shi Y, Buda E, Waring S, Veluvolu U, Tan D, Mieczkowski PA, Jones CD, Simons JV, Soloway MG, Bodenheimer T, Jefferys SR, Roach J, Hoyle AP, Wu J, Balu S, Singh D, Prins JF, Marron JS, Parker JS, Hayes DN, Perou CM, Liu J, Cope L, Danilova L, Weisenberger DJ, Maglinte DT, Lai PH, Bootwalla MS, Van Den Berg DJ, Triche T Jr, Baylin SB, Laird PW, Rosenberg M, Chin L, Zhang J, Cho J, DiCara D, Heiman D, Lin P, Mallard W, Voet D, Zhang H, Zou L, Noble MS, Lawrence MS, Saksena G, Gehlenborg N, Thorvaldsdottir H, Mesirov J, Nazaire MD, Robinson J, Getz G, Lee W, Aksoy BA, Ciriello G, Taylor BS, Dresdner G, Gao J, Gross B, Seshan VE, Ladanyi M, Reva B, Sinha R, Sumer SO, Weinhold N, Schultz N, Shen R, Sander C, Ng S, Ma S, Zhu J, Radenbaugh A, Stuart JM, Benz CC, Yau C, Haussler D, Spellman PT, Wilkerson MD, Parker JS, Hoadley KA, Kimes PK, Hayes DN, Perou CM, Broom BM, Wang J, Lu Y, Kwok Shing Ng P, Diao L, Averett Byers L, Liu W, Heymach JV, Amos CI, Weinstein JN, Akbani R, Mills GB, Curley E, Paulauskis J, Lau K, Morris S, Shelton T, Mallery D, Gardner J, Penny R, Saller C, Tarvin K, Richards WG, Cerfolio R, Bryant A, Raymond DP, Pennell NA, Farver C, Czerwinski C, Huelsenbeck-Dill L, Iacocca M, Petrelli N, Rabeno B, Brown J, Bauer T, Dolzhanskiy O, Potapova O, Rotin D, Voronina O, Nemirovich-Danchenko E, Fedosenko KV, Gal A, Behera M, Ramalingam SS, Sica G, Flieder D, Boyd J, Weaver J, Kohl B, Huy Quoc Thinh D, Sandusky G, Juhl H, Duhig E, Illei P, Gabrielson E, Shin J, Lee B, Rodgers K, Trusty D, Brock MV, Williamson C, Burks E, Rieger-Christ K, Holway A, Sullivan T, Wigle DA, Asiedu MK, Kosari F, Travis WD, Rekhtman N, Zakowski M, Rusch VW, Zippile P, Suh J, Pass H, Goparaju C, Owusu-Sarpong Y, Bartlett JM, Kodeeswaran S, Parfitt J, Sekhon H, Albert M, Eckman J, Myers JB, Cheney R, Morrison C, Gaudioso C, Borgia JA, Bonomi P, Pool M, Liptay MJ, Moiseenko F, Zaytseva I, Dienemann H, Meister M, Schnabel PA, Muley TR, Peifer M, Gomez-Fernandez C, Herbert L, Egea S, Huang M, Thorne LB, Boice L, Hill Salazar A, Funkhouser WK, Rathmell WK, Dhir R, Yousem SA, Dacic S, Schneider F, Siegfried JM, Hajek R, Watson MA, McDonald S, Meyers B, Clarke B, Yang IA, Fong KM, Hunter L, Windsor M, Bowman RV, Peters S, Letovanec I, Khan KZ, Jensen MA, Snyder EE, Srinivasan D, Kahn AB, Baboud J, Pot DA, Mills Shaw KR, Sheth M, Davidsen T, Demchok JA, Yang L, Wang Z, Tarnuzzer R, Zenklusen JC, Ozenberger BA, Sofia HJ, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS	Comprehensive molecular profiling of lung adenocarcinoma	Nature	2014 Jul 	20	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	TCGA-75-5146	Illumina HiSeq2000		hs20:37003684-37003684,hs20:37606817-37606817;hs20:42193179-42193179,hs20:46220158-46220158	LBP;SGK2;DHX35;NCOA3;	University of CaliforniaSan Francisco, San Francisco,California94158,USA	Adenocarcinoma of the lung is the leading cause of cancer death worldwide. Here we report molecular profiling of 230 resected lung adenocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses. High rates of somatic mutation were seen (mean 8.9 mutations per megabase). Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. EGFR mutations were more frequent in female patients, whereas mutations in RBM10 were more common in males. Aberrations in NF1, MET, ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. DNA and mRNA sequence from the same tumour highlighted splicing alterations driven by somatic genomic changes, including exon 14 skipping in MET mRNA in 4% of cases. MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. These data establish a foundation for classification and further investigations of lung adenocarcinoma molecular pathogenesis. 	GRCh37/hg19				Yes	LBP,DHX35;SGK2,NCOA3
CTDB0327	Research	25079552	Collisson EA, Campbell JD, Brooks AN, Berger AH, Lee W, Chmielecki J, Beer DG, Cope L, Creighton CJ, Danilova L, Ding L, Getz G, Hammerman PS, Hayes DN, Hernandez B, Herman JG, Heymach JV, Jurisica I, Kucherlapati R, Kwiatkowski D, Ladanyi M, Robertson G, Schultz N, Shen R, Sinha R, Sougnez C, Tsao MS, Travis WD, Weinstein JN, Wigle DA, Wilkerson MD, Chu A, Cherniack AD, Hadjipanayis A, Rosenberg M, Weisenberger DJ, Laird PW, Radenbaugh A, Ma S, Stuart JM, Averett Byers L, Baylin SB, Govindan R, Meyerson M, Rosenberg M, Gabriel SB, Cibulskis K, Sougnez C, Kim J, Stewart C, Lichtenstein L, Lander ES, Lawrence MS, Getz, Kandoth C, Fulton R, Fulton LL, McLellan MD, Wilson RK, Ye K, Fronick CC, Maher CA, Miller CA, Wendl MC, Cabanski C, Ding L, Mardis E, Govindan R, Creighton CJ, Wheeler D, Balasundaram M, Butterfield YS, Carlsen R, Chu A, Chuah E, Dhalla N, Guin R, Hirst C, Lee D, Li HI, Mayo M, Moore RA, Mungall AJ, Schein JE, Sipahimalani P, Tam A, Varhol R, Robertson A, Wye N, Thiessen N, Holt RA, Jones SJ, Marra MA, Campbell JD, Brooks AN, Chmielecki J, Imielinski M, Onofrio RC, Hodis E, Zack T, Sougnez C, Helman E, Sekhar Pedamallu C, Mesirov J, Cherniack AD, Saksena G, Schumacher SE, Carter SL, Hernandez B, Garraway L, Beroukhim R, Gabriel SB, Getz G, Meyerson M, Hadjipanayis A, Lee S, Mahadeshwar HS, Pantazi A, Protopopov A, Ren X, Seth S, Song X, Tang J, Yang L, Zhang J, Chen PC, Parfenov M, Wei Xu A, Santoso N, Chin L, Park PJ, Kucherlapati R, Hoadley KA, Auman JT, Meng S, Shi Y, Buda E, Waring S, Veluvolu U, Tan D, Mieczkowski PA, Jones CD, Simons JV, Soloway MG, Bodenheimer T, Jefferys SR, Roach J, Hoyle AP, Wu J, Balu S, Singh D, Prins JF, Marron JS, Parker JS, Hayes DN, Perou CM, Liu J, Cope L, Danilova L, Weisenberger DJ, Maglinte DT, Lai PH, Bootwalla MS, Van Den Berg DJ, Triche T Jr, Baylin SB, Laird PW, Rosenberg M, Chin L, Zhang J, Cho J, DiCara D, Heiman D, Lin P, Mallard W, Voet D, Zhang H, Zou L, Noble MS, Lawrence MS, Saksena G, Gehlenborg N, Thorvaldsdottir H, Mesirov J, Nazaire MD, Robinson J, Getz G, Lee W, Aksoy BA, Ciriello G, Taylor BS, Dresdner G, Gao J, Gross B, Seshan VE, Ladanyi M, Reva B, Sinha R, Sumer SO, Weinhold N, Schultz N, Shen R, Sander C, Ng S, Ma S, Zhu J, Radenbaugh A, Stuart JM, Benz CC, Yau C, Haussler D, Spellman PT, Wilkerson MD, Parker JS, Hoadley KA, Kimes PK, Hayes DN, Perou CM, Broom BM, Wang J, Lu Y, Kwok Shing Ng P, Diao L, Averett Byers L, Liu W, Heymach JV, Amos CI, Weinstein JN, Akbani R, Mills GB, Curley E, Paulauskis J, Lau K, Morris S, Shelton T, Mallery D, Gardner J, Penny R, Saller C, Tarvin K, Richards WG, Cerfolio R, Bryant A, Raymond DP, Pennell NA, Farver C, Czerwinski C, Huelsenbeck-Dill L, Iacocca M, Petrelli N, Rabeno B, Brown J, Bauer T, Dolzhanskiy O, Potapova O, Rotin D, Voronina O, Nemirovich-Danchenko E, Fedosenko KV, Gal A, Behera M, Ramalingam SS, Sica G, Flieder D, Boyd J, Weaver J, Kohl B, Huy Quoc Thinh D, Sandusky G, Juhl H, Duhig E, Illei P, Gabrielson E, Shin J, Lee B, Rodgers K, Trusty D, Brock MV, Williamson C, Burks E, Rieger-Christ K, Holway A, Sullivan T, Wigle DA, Asiedu MK, Kosari F, Travis WD, Rekhtman N, Zakowski M, Rusch VW, Zippile P, Suh J, Pass H, Goparaju C, Owusu-Sarpong Y, Bartlett JM, Kodeeswaran S, Parfitt J, Sekhon H, Albert M, Eckman J, Myers JB, Cheney R, Morrison C, Gaudioso C, Borgia JA, Bonomi P, Pool M, Liptay MJ, Moiseenko F, Zaytseva I, Dienemann H, Meister M, Schnabel PA, Muley TR, Peifer M, Gomez-Fernandez C, Herbert L, Egea S, Huang M, Thorne LB, Boice L, Hill Salazar A, Funkhouser WK, Rathmell WK, Dhir R, Yousem SA, Dacic S, Schneider F, Siegfried JM, Hajek R, Watson MA, McDonald S, Meyers B, Clarke B, Yang IA, Fong KM, Hunter L, Windsor M, Bowman RV, Peters S, Letovanec I, Khan KZ, Jensen MA, Snyder EE, Srinivasan D, Kahn AB, Baboud J, Pot DA, Mills Shaw KR, Sheth M, Davidsen T, Demchok JA, Yang L, Wang Z, Tarnuzzer R, Zenklusen JC, Ozenberger BA, Sofia HJ, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS, Travis WD, Cheney R, Clarke B, Dacic S, Duhig E, Funkhouser WK, Illei P, Farver C, Rekhtman N, Sica G, Suh J, Tsao MS	Comprehensive molecular profiling of lung adenocarcinoma	Nature	2014 Jul 	1,2,3,4,5,6,7,8,9,10,11,12,14,16,17,20,22	Non Small-cell lung cancer	Next Generation Sequencing	Homo sapiens	TCGA-05-4422	Illumina HiSeq2000		hs1:161007168-161007168,hs1:161009255-161009255;hs1:156049319-156049319,hs1:156052448-156052448;hs1:154990699-154990699,hs1:154991513-154991513;hs1:154965365-154965365,hs1:154966421-154966421;hs2:103353077-103353077,hs2:103353554-103353554;hs2:201753339-201753339,hs2:201754297-201754297;hs2:88368320-88368320,hs10:1391209-1391209;hs3:51989997-51989997,hs3:51992691-51992691;hs3:127391515-127391515,hs3:127392399-127392399;hs3:52719331-52719331,hs3:52720165-52720165;hs3:9438808-9438808,hs3:9439548-9439548;hs3:45829795-45829795,hs3:135878615-135878615;hs3:142456234-142456234,hs8:126352258-126352258;hs3:48301781-48301781,hs8:97835494-97835494;hs4:159592226-159592226,hs4:159593516-159593516;hs4:38086202-38086202,hs9:114659622-114659622;hs5:17216875-17216875,hs5:17219098-17219098;hs5:43191913-43191913,hs5:43192395-43192395;hs6:30614332-30614332,hs6:30615447-30615447;hs6:170151151-170151151,hs6:170151981-170151981;hs6:41747251-41747251,hs6:41749859-41749859;hs6:160210358-160210358,hs6:160211341-160211341;hs6:90961006-90961006,hs8:99794696-99794696;hs7:93527147-93527147,hs7:147670389-147670389;hs7:102104835-102104835,hs7:102105579-102105579;hs8:89312455-89312455,hs8:124351930-124351930;hs8:70742683-70742683,hs8:124427162-124427162;hs8:133052468-133052468,hs8:136487430-136487430;hs8:119311455-119311455,hs8:133052468-133052468;hs8:131078448-131078448,hs14:102603255-102603255;hs10:38465547-38465547,hs10:129739835-129739835;hs10:88717373-88717373,hs10:88718937-88718937;hs11:63764678-63764678,hs11:63766671-63766671;hs12:124117996-124117996,hs12:124118881-124118881;hs12:58165400-58165400,hs12:58166447-58166447;hs16:90038817-90038817,hs16:90039486-90039486;hs16:67700346-67700346,hs16:67701307-67701307;hs16:84178105-84178105,hs16:84179473-84179473;hs17:74722148-74722148,hs17:74723192-74723192;hs17:17942214-17942214,hs17:17943112-17943112;hs20:62329265-62329265,hs20:62330803-62330803;hs20:62375143-62375143,hs20:62375980-62375980;hs22:24951444-24951444,hs22:24952108-24952108;hs22:29655456-29655456,hs22:29656535-29656535	ABTB1;ADARB2;AFG3L1;ALKBH4;ARFRP1;ASAP1;ATAD2;ATPAF2;BACH2;BASP1;C16orf48;C16orf86;C17orf39;C17orf95;C22orf13;C4orf46;C6orf136;CENPBD1;CNTNAP2;DCST2;EIF2B1;EMID1;ETFDH;F11R;FAM119B;FLAD1;FRS3;GNGT1;GNL3;GPR62;GTF2H3;HSDL1;HSP90AA1;JMJD6;KHDRBS3;LENEP;LMNA;LOC440944;LRRC50;LRWD1;MACROD1;METTL1;MEX3A;MFSD9;MGC42105;MMP16;MMRN2;MRPL18;MSL2;NIF3L1;NSMCE2;OC90;OTUB1;PBRM1;PCBP4;PGCP;PODXL2;PPIL3;PRICKLE4;PTPRE;RHBDD3;RTEL1;TNFRSF6B;SAMD12;SETD5;SLC2A4RG;SLC6A20;SLCO5A1;SMYD1;SNCG;SNRPD3;STK3;TBC1D1;TCP1;TMEM182;TRPC1;UGCG;USF1;ZBTB46;ZBTB7B;ZNF131;ZNF589;	University of CaliforniaSan Francisco, San Francisco,California94158,USA	Adenocarcinoma of the lung is the leading cause of cancer death worldwide. Here we report molecular profiling of 230 resected lung adenocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses. High rates of somatic mutation were seen (mean 8.9 mutations per megabase). Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. EGFR mutations were more frequent in female patients, whereas mutations in RBM10 were more common in males. Aberrations in NF1, MET, ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. DNA and mRNA sequence from the same tumour highlighted splicing alterations driven by somatic genomic changes, including exon 14 skipping in MET mRNA in 4% of cases. MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. These data establish a foundation for classification and further investigations of lung adenocarcinoma molecular pathogenesis. 	GRCh37/hg19				Yes	ALKBH4,LRWD1;ASAP1,HSP90AA1;ATPAF2,C17orf39;BACH2,STK3;C16orf48,C16orf86;C22orf13,SNRPD3;C4orf46,ETFDH;C6orf134,C6orf136;CENPBD1,AFG3L1;EIF2B1,GTF2H3;EMID1,RHBDD3;F11R,USF1;FLAD1,LENEP;FRS3,PRICKLE4;GNGT1,CNTNAP2;GPR62,PCBP4;HSDL1,LRRC50;JMJD6,C17orf95;LOC100129055,PTPRE;LOC285696,BASP1;LOC440944,SETD5;METTL1,FAM119B;MEX3A,LMNA;MFSD9,TMEM182;MMP16,ATAD2;MMRN2,SNCG;OC90,KHDRBS3;OTUB1,MACROD1;PBRM1,GNL3;PODXL2,ABTB1;PPIL3,NIF3L1;RTEL1;TNFRSF6B,ARFRP1;SAMD12,OC90;SLC2A4RG,ZBTB46;SLC6A20,MSL2;SLCO5A1,ATAD2;SMYD1,ADARB2;TBC1D1,UGCG;TCP1,MRPL18;TCTE3,C6orf70;TRPC1,NSMCE2;ZBTB7B,DCST2;ZNF131,MGC42105;ZNF589,PGCP
CTDB0328	Research	25903014	Karrman K, Castor A, Behrendtz M, Forestier E, Olsson L, Ehinger M, Biloglav A, Fioretos T, Paulsson K, Johansson B	Deep sequencing and SNP array analyses of pediatric T-cell acute lymphoblastic leukemia reveal NOTCH1 mutations in minor subclones and a high incidence of uniparental isodisomies affecting CDKN2A	Journal of Hematology & Oncology	2015 Apr 	6	Acute lymphoblastic leukemia	SNP Array	Homo sapiens	U1	Illumina Humancnv370-Duo BeadChip	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-21884494:0;chr6:113895050-115470638:0;chr6:115470639-115965140:-1;chr6:115965141-117079874:0;chr6:117079875-119696844:-1;chr6:119696845-124344876:0;chr6:124344877-125649002:-1;chr6:125649003-128702993:0;chr6:128702994-129171964:-1;chr6:129171965-131033847:0;chr6:131033848-134133659:-1;chr6:134133660-137059441:0;chr6:137059442-140181508:-1;chr6:140181509-142439352:0;chr6:142439353-143807471:-1;chr6:143807472-143977499:0;chr6:143977500-151238363:-1;chr6:151238364-151523056:0;chr6:151523057-151988351:-1;chr6:151988352-152813956:0;chr6:152813957-156481213:-1;chr6:156481214-157274780:0;chr6:157274781-160952471:-1;chr6:160952472-161512963:0;chr6:161512964-167752761:-1;chr6:167752762-169723044:0;chr6:169723045-170507358:-1;chr6:170507359-171115067:0;chr6:21884495-21951866:-1;chr6:21951867-21964217:0;chr6:21964218-21974661:-1;chr6:21974662-70201286:0;chr6:70201287-70512716:1;chr6:70512717-79477494:0;chr6:79477495-113895049:-1;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0		CASP8AP2;	Department of Clinical Genetics, University and Regional Laboratories, Region Skane, SE-221 85, Lund, Sweden	BACKGROUND: Pediatric T-cell acute lymphoblastic leukemia (T-ALL) is a genetically heterogeneous disease that arises in a multistep fashion through acquisition of several genetic aberrations, subsequently giving rise to a malignant, clonal expansion of T-lymphoblasts. The aim of the present study was to identify additional as well as cooperative genetic events in T-ALL. METHODS: A population-based pediatric T-ALL series comprising 47 cases was investigated by SNP array and deep sequencing analyses of 75 genes, in order to ascertain pathogenetically pertinent aberrations and to identify cooperative events. RESULTS: The majority (92%) of cases harbored copy number aberrations/uniparental isodisomies (UPIDs), with a median of three changes (range 0-11) per case. The genes recurrently deleted comprised CDKN2A, CDKN2B, LEF1, PTEN, RBI, and STIL. No case had a whole chromosome UPID; in fact, literature data show that this is a rare phenomenon in T-ALL. However, segmental UPIDs (sUPIDs) were seen in 42% of our cases, with most being sUPID9p that always were associated with homozygous CDKN2A deletions, with a heterozygous deletion occurring prior to the sUPID9p in all instances. Among the 75 genes sequenced, 14 (19%) were mutated in 28 (72%) of 39 analyzed cases. The genes targeted are involved in signaling transduction, epigenetic regulation, and transcription. In some cases, NOTCH1 mutations were seen in minor subclones and lost at relapse; thus, such mutations can be secondary events. CONCLUSIONS: Deep sequencing and SNP array analyses of T-ALL revealed lack of wUPIDs, a high proportion of sUPID9p targeting CDKN2A, NOTCH1 mutations in subclones, and recurrent mutations of genes involved in signaling transduction, epigenetic regulation, and transcription.	GRCh37/hg19				Yes	NA
CTDB0329	Research	24670920	Fernandez-Cuesta L, Peifer M, Lu X, Sun R, Ozretic L, Seidel D, Zander T, Leenders F, George J, Muller C, Dahmen I, Pinther B, Bosco G, Konrad K, Altmuller J, Nurnberg P, Achter V, Lang U, Schneider PM, Bogus M, Soltermann A, Brustugun OT, Helland A, Solberg S, Lund-Iversen M, Ansen S, Stoelben E, Wright GM, Russell P, Wainer Z, Solomon B, Field JK, Hyde R, Davies MP, Heukamp LC, Petersen I, Perner S, Lovly CM, Cappuzzo F, Travis WD, Wolf J, Vingron M, Brambilla E, Haas SA, Buettner R, Thomas RK	Frequent mutations in chromatin-remodelling genes in pulmonary carcinoids	Nature Communications	2014 Mar 	3,12,13	Pulmonary carcinoid	Next Generation Sequencing	Homo sapiens	S00076	Illumina HiSeq2000		hs13:39540810-39541129,hs13:98628918-98634837;hs3:158072644-158262115,hs3:71630699-71630803;hs12:109490434-109495913,hs3:14239528-14239844;hs12:300116-304493,hs3:44490051-44492076;hs3:96706171-96706835,hs12:122243069-122244011;hs12:50571665-50575822,hs12:96679820-96683000;hs12:46123831-46125097,hs3:87299023-87302616;hs3:136581127-136647070,hs3:52156413-52159199;hs12:2906302-2913091,hs3:123550392-123550519;hs3:50471768-50513632,hs3:191047373-191047513;hs13:101707771-101712320,hs3:41268694-41268843;hs12:102517663-102517819,hs3:196678758-196678907;hs12:111057640-111066662,hs12:110002923-110011184;hs3:184684462-184711853,hs13:99908581-99908773;hs3:73651503-73673326,hs3:45707139-45714272;hs13:98086751-98087039,hs12:97303528-97306595;hs13:39917770-40175529,hs3:4725988-4726891;hs12:51818672-51818821,hs13:109817246-109817341;hs12:2102428-2113491,hs3:17447909-17448018;hs3:151597637-151598493,hs3:121544895-121547378;hs3:160783186-160783320,hs3:47956305-47956395;hs3:136471036-136471179,hs3:130744346-130744440	STOML3;1IPO5;RSRC1;1FOXP1;USP30;1LSM3;SLC6A12;1ZNF445;SETD1B;IEPHA6;CDK17;1LIMA1;ARID2;ICHMP2B;POC1A;1NCK1;FKBP4;1MYLK;CACNA2D2;1CCDC50;CTNNB1;1NALCN;C12orf48;1PIGZ;TCTN1;1MMAB;GPR18;1VPS8;PDZRN3;1LIMD1;NEDD1;1RAP2A;LHFP;1ITPR1;LOC100288040;1MYO16;TBC1D5;1DCP1B;SUCNR1;1IQCB1;PPM1L;1MAP4;STAG1;IASTE1;	Department of Translational Genomics, Center of Integrated Oncology Cologne-Bonn, Medical Faculty, University of Cologne, 50924 Cologne, Germany	Pulmonary carcinoids are rare neuroendocrine tumours of the lung. The molecular alterations underlying the pathogenesis of these tumours have not been systematically studied so far. Here we perform gene copy number analysis (n=54), genome/exome (n=44) and transcriptome (n=69) sequencing of pulmonary carcinoids and observe frequent mutations in chromatin-remodelling genes. Covalent histone modifiers and subunits of the SWI/SNF complex are mutated in 40 and 22.2% of the cases, respectively, with MEN1, PSIP1 and ARID1A being recurrently affected. In contrast to small-cell lung cancer and large-cell neuroendocrine lung tumours, TP53 and RB1 mutations are rare events, suggesting that pulmonary carcinoids are not early progenitor lesions of the highly aggressive lung neuroendocrine tumours but arise through independent cellular mechanisms. These data also suggest that inactivation of chromatin-remodelling genes is sufficient to drive transformation in pulmonary carcinoids. 	GRCh37/hg19				Yes	ARID2,ICHMP2B;C12orf48,1PIGZ;CACNA2D2,1CCDC50;CDK17,1LIMA1;CTNNB1,1NALCN;FKBP4,1MYLK;GPR18,1VPS8;LHFP,1ITPR1;LOC100288040,1MYO16;NEDD1,1RAP2A;PDZRN3,1LIMD1;POC1A,1NCK1;PPM1L,1MAP4;RSRC1,1FOXP1;SETD1B,IEPHA6;SLC6A12,1ZNF445;STAG1,IASTE1;STOML3,1IPO5;SUCNR1,1IQCB1;TBC1D5,1DCP1B;TCTN1,1MMAB;USP30,1LSM3
CTDB0330	Research	24550227	Messina M, Del Giudice I, Khiabanian H, Rossi D, Chiaretti S, Rasi S, Spina V, Holmes AB, Marinelli M, Fabbri G, Piciocchi A, Mauro FR, Guarini A, Gaidano G, Dalla-Favera R, Pasqualucci L, Rabadan R, Foa R	Genetic lesions associated with chronic lymphocytic leukemia chemo-refractoriness	Blood	2014 Apr 	6,8,9,13	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	7228	Affymetrix Human SNP Array 6.0				Hematology, Department of Cellular Biotechnologies and Hematology, Sapienza University, Rome, Italy	Fludarabine refractoriness (FR) represents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management. Although next-generation sequencing studies have led to the identification of a number of genes frequently mutated in FR-CLL, a comprehensive evaluation of the FR-CLL genome has not been reported. Toward this end, we studied 10 FR-CLLs by combining whole-exome sequencing and copy number aberration (CNA) analysis, which showed an average of 16.3 somatic mutations and 4 CNAs per sample. Screening of recurrently mutated genes in 48 additional FR-CLLs revealed that ~70% of FR-CLLs carry >=1 mutation in genes previously associated with CLL clinical course, including TP53 (27.5%), NOTCH1 (24.1%), SF3B1 (18.9%), and BIRC3 (15.5%). In addition, this analysis showed that 10.3% of FR-CLL cases display mutations of the FAT1 gene, which encodes for a cadherin-like protein that negatively regulates Wnt signaling, consistent with a tumor suppressor role. The frequency of FAT1-mutated cases was significantly higher in FR-CLL than in unselected CLLs at diagnosis (10.3% vs 1.1%, P = .004), suggesting a role in the development of a high-risk phenotype. These findings have general implications for the mechanisms leading to FR and point to Wnt signaling as a potential therapeutic target in FR-CLL.	NCBI 36/hg18	GSE51711			Yes	NA
CTDB0331	Research	24550227	Messina M, Del Giudice I, Khiabanian H, Rossi D, Chiaretti S, Rasi S, Spina V, Holmes AB, Marinelli M, Fabbri G, Piciocchi A, Mauro FR, Guarini A, Gaidano G, Dalla-Favera R, Pasqualucci L, Rabadan R, Foa R	Genetic lesions associated with chronic lymphocytic leukemia chemo-refractoriness	Blood	2014 Apr 	8,9,13	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	4845	Affymetrix Human SNP Array 6.0				Hematology, Department of Cellular Biotechnologies and Hematology, Sapienza University, Rome, Italy	Fludarabine refractoriness (FR) represents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management. Although next-generation sequencing studies have led to the identification of a number of genes frequently mutated in FR-CLL, a comprehensive evaluation of the FR-CLL genome has not been reported. Toward this end, we studied 10 FR-CLLs by combining whole-exome sequencing and copy number aberration (CNA) analysis, which showed an average of 16.3 somatic mutations and 4 CNAs per sample. Screening of recurrently mutated genes in 48 additional FR-CLLs revealed that ~70% of FR-CLLs carry >=1 mutation in genes previously associated with CLL clinical course, including TP53 (27.5%), NOTCH1 (24.1%), SF3B1 (18.9%), and BIRC3 (15.5%). In addition, this analysis showed that 10.3% of FR-CLL cases display mutations of the FAT1 gene, which encodes for a cadherin-like protein that negatively regulates Wnt signaling, consistent with a tumor suppressor role. The frequency of FAT1-mutated cases was significantly higher in FR-CLL than in unselected CLLs at diagnosis (10.3% vs 1.1%, P = .004), suggesting a role in the development of a high-risk phenotype. These findings have general implications for the mechanisms leading to FR and point to Wnt signaling as a potential therapeutic target in FR-CLL.	NCBI 36/hg18	GSE51711			Yes	NA
CTDB0332	Research	24550227	Messina M, Del Giudice I, Khiabanian H, Rossi D, Chiaretti S, Rasi S, Spina V, Holmes AB, Marinelli M, Fabbri G, Piciocchi A, Mauro FR, Guarini A, Gaidano G, Dalla-Favera R, Pasqualucci L, Rabadan R, Foa R	Genetic lesions associated with chronic lymphocytic leukemia chemo-refractoriness	Blood	2014 Apr 	8,9,13	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	6012	Affymetrix Human SNP Array 6.0				Hematology, Department of Cellular Biotechnologies and Hematology, Sapienza University, Rome, Italy	Fludarabine refractoriness (FR) represents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management. Although next-generation sequencing studies have led to the identification of a number of genes frequently mutated in FR-CLL, a comprehensive evaluation of the FR-CLL genome has not been reported. Toward this end, we studied 10 FR-CLLs by combining whole-exome sequencing and copy number aberration (CNA) analysis, which showed an average of 16.3 somatic mutations and 4 CNAs per sample. Screening of recurrently mutated genes in 48 additional FR-CLLs revealed that ~70% of FR-CLLs carry >=1 mutation in genes previously associated with CLL clinical course, including TP53 (27.5%), NOTCH1 (24.1%), SF3B1 (18.9%), and BIRC3 (15.5%). In addition, this analysis showed that 10.3% of FR-CLL cases display mutations of the FAT1 gene, which encodes for a cadherin-like protein that negatively regulates Wnt signaling, consistent with a tumor suppressor role. The frequency of FAT1-mutated cases was significantly higher in FR-CLL than in unselected CLLs at diagnosis (10.3% vs 1.1%, P = .004), suggesting a role in the development of a high-risk phenotype. These findings have general implications for the mechanisms leading to FR and point to Wnt signaling as a potential therapeutic target in FR-CLL.	NCBI 36/hg18	GSE51711			Yes	NA
CTDB0333	Research	24550227	Messina M, Del Giudice I, Khiabanian H, Rossi D, Chiaretti S, Rasi S, Spina V, Holmes AB, Marinelli M, Fabbri G, Piciocchi A, Mauro FR, Guarini A, Gaidano G, Dalla-Favera R, Pasqualucci L, Rabadan R, Foa R	Genetic lesions associated with chronic lymphocytic leukemia chemo-refractoriness	Blood	2014 Apr 	3,12	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	4380	Affymetrix Human SNP Array 6.0				Hematology, Department of Cellular Biotechnologies and Hematology, Sapienza University, Rome, Italy	Fludarabine refractoriness (FR) represents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management. Although next-generation sequencing studies have led to the identification of a number of genes frequently mutated in FR-CLL, a comprehensive evaluation of the FR-CLL genome has not been reported. Toward this end, we studied 10 FR-CLLs by combining whole-exome sequencing and copy number aberration (CNA) analysis, which showed an average of 16.3 somatic mutations and 4 CNAs per sample. Screening of recurrently mutated genes in 48 additional FR-CLLs revealed that ~70% of FR-CLLs carry >=1 mutation in genes previously associated with CLL clinical course, including TP53 (27.5%), NOTCH1 (24.1%), SF3B1 (18.9%), and BIRC3 (15.5%). In addition, this analysis showed that 10.3% of FR-CLL cases display mutations of the FAT1 gene, which encodes for a cadherin-like protein that negatively regulates Wnt signaling, consistent with a tumor suppressor role. The frequency of FAT1-mutated cases was significantly higher in FR-CLL than in unselected CLLs at diagnosis (10.3% vs 1.1%, P = .004), suggesting a role in the development of a high-risk phenotype. These findings have general implications for the mechanisms leading to FR and point to Wnt signaling as a potential therapeutic target in FR-CLL.	NCBI 36/hg18	GSE51711			Yes	NA
CTDB0334	Research	24550227	Messina M, Del Giudice I, Khiabanian H, Rossi D, Chiaretti S, Rasi S, Spina V, Holmes AB, Marinelli M, Fabbri G, Piciocchi A, Mauro FR, Guarini A, Gaidano G, Dalla-Favera R, Pasqualucci L, Rabadan R, Foa R	Genetic lesions associated with chronic lymphocytic leukemia chemo-refractoriness	Blood	2014 Apr 	14	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	9311	Affymetrix Human SNP Array 6.0				Hematology, Department of Cellular Biotechnologies and Hematology, Sapienza University, Rome, Italy	Fludarabine refractoriness (FR) represents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management. Although next-generation sequencing studies have led to the identification of a number of genes frequently mutated in FR-CLL, a comprehensive evaluation of the FR-CLL genome has not been reported. Toward this end, we studied 10 FR-CLLs by combining whole-exome sequencing and copy number aberration (CNA) analysis, which showed an average of 16.3 somatic mutations and 4 CNAs per sample. Screening of recurrently mutated genes in 48 additional FR-CLLs revealed that ~70% of FR-CLLs carry >=1 mutation in genes previously associated with CLL clinical course, including TP53 (27.5%), NOTCH1 (24.1%), SF3B1 (18.9%), and BIRC3 (15.5%). In addition, this analysis showed that 10.3% of FR-CLL cases display mutations of the FAT1 gene, which encodes for a cadherin-like protein that negatively regulates Wnt signaling, consistent with a tumor suppressor role. The frequency of FAT1-mutated cases was significantly higher in FR-CLL than in unselected CLLs at diagnosis (10.3% vs 1.1%, P = .004), suggesting a role in the development of a high-risk phenotype. These findings have general implications for the mechanisms leading to FR and point to Wnt signaling as a potential therapeutic target in FR-CLL.	NCBI 36/hg18	GSE51711			Yes	NA
CTDB0335	Research	24550227	Messina M, Del Giudice I, Khiabanian H, Rossi D, Chiaretti S, Rasi S, Spina V, Holmes AB, Marinelli M, Fabbri G, Piciocchi A, Mauro FR, Guarini A, Gaidano G, Dalla-Favera R, Pasqualucci L, Rabadan R, Foa R	Genetic lesions associated with chronic lymphocytic leukemia chemo-refractoriness	Blood	2014 Apr 	3,12	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	9244	Affymetrix Human SNP Array 6.0				Hematology, Department of Cellular Biotechnologies and Hematology, Sapienza University, Rome, Italy	Fludarabine refractoriness (FR) represents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management. Although next-generation sequencing studies have led to the identification of a number of genes frequently mutated in FR-CLL, a comprehensive evaluation of the FR-CLL genome has not been reported. Toward this end, we studied 10 FR-CLLs by combining whole-exome sequencing and copy number aberration (CNA) analysis, which showed an average of 16.3 somatic mutations and 4 CNAs per sample. Screening of recurrently mutated genes in 48 additional FR-CLLs revealed that ~70% of FR-CLLs carry >=1 mutation in genes previously associated with CLL clinical course, including TP53 (27.5%), NOTCH1 (24.1%), SF3B1 (18.9%), and BIRC3 (15.5%). In addition, this analysis showed that 10.3% of FR-CLL cases display mutations of the FAT1 gene, which encodes for a cadherin-like protein that negatively regulates Wnt signaling, consistent with a tumor suppressor role. The frequency of FAT1-mutated cases was significantly higher in FR-CLL than in unselected CLLs at diagnosis (10.3% vs 1.1%, P = .004), suggesting a role in the development of a high-risk phenotype. These findings have general implications for the mechanisms leading to FR and point to Wnt signaling as a potential therapeutic target in FR-CLL.	NCBI 36/hg18	GSE51711			Yes	NA
CTDB0336	Research	25497101	van Heesch S, Simonis M, van Roosmalen MJ, Pillalamarri V, Brand H, Kuijk EW, de Luca KL, Lansu N, Braat AK, Menelaou A, Hao W, Korving J, Snijder S, van der Veken LT, Hochstenbach R, Knegt AC, Duran K, Renkens I, Alekozai N, Jager M, Vergult S, Menten B, de Bruijn E, Boymans S, Ippel E, van Binsbergen E, Talkowski ME, Lichtenbelt K, Cuppen E, Kloosterman WP	Genomic and functional overlap between somatic and germline chromosomal rearrangements	Cell Reports	2014 Dec 	1,3,7,12	Congenital abnormality	Next Generation Sequencing	Homo sapiens	patient 1	SOLiD V4			DPYD;FOXP1;ETV1;SNX13;TMEM106B;AHR;ARL4A;	Hubrecht Institute-KNAW and University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, the Netherlands	Genomic rearrangements are a common cause of human congenital abnormalities. However, their origin and consequences are poorly understood. We performed molecular analysis of two patients with congenital disease who carried de novo genomic rearrangements. We found that the rearrangements in both patients hit genes that are recurrently rearranged in cancer (ETV1, FOXP1, and microRNA cluster C19MC) and drive formation of fusion genes similar to those described in cancer. Subsequent analysis of a large set of 552 de novo germline genomic rearrangements underlying congenital disorders revealed enrichment for genes rearranged in cancer and overlap with somatic cancer breakpoints. Breakpoints of common (inherited) germline structural variations also overlap with cancer breakpoints but are depleted for cancer genes. We propose that the same genomic positions are prone to genomic rearrangements in germline and soma but that timing and context of breakage determines whether developmental defects or cancer are promoted. 	GRCh37/hg19			PRJEB5063;PRJEB3030	No	DPYD,ETV1
CTDB0337	Research	24401281	Stevens-Kroef MJ, van den Berg E, Olde Weghuis D, Geurts van Kessel A, Pfundt R, Linssen-Wiersma M, Benjamins M, Dijkhuizen T, Groenen PJ, Simons A	Identification of prognostic relevant chromosomal abnormalities in chronic lymphocytic leukemia using microarray-based genomic profiling	Molecular Cytogenetics	2014 Jan 	11	Chronic lymphocytic leukemia	SNP Array	Homo sapiens	case 11	CytoSan HD array and HumanOmniExpress12v1.0 array				Department of Human Genetics, Radboud university medical center, P,O, Box 9101, Nijmegen 6500 HB, The Netherlands. Marian	BACKGROUND: Characteristic genomic abnormalities in patients with B cell chronic lymphocytic leukemia (CLL) have been shown to provide important prognostic information. Fluorescence in situ hybridization (FISH) and multiplex ligation-dependent probe amplification (MLPA), currently used in clinical diagnostics of CLL, are targeted tests aimed at specific genomic loci. Microarray-based genomic profiling is a new high-resolution tool that enables genome-wide analyses. The aim of this study was to compare two recently launched genomic microarray platforms, i.e., the CytoScan HD Array (Affymetrix) and the HumanOmniExpress Array (Illumina), with FISH and MLPA to ascertain whether these latter tests can be replaced by either one of the microarray platforms in a clinical diagnostic setting. RESULT: Microarray-based genomic profiling and FISH were performed in all 28 CLL patients. For an unbiased comparison of the performance of both microarray platforms 9 patients were evaluated on both platforms, resulting in the identification of exactly identical genomic aberrations. To evaluate the detection limit of the microarray platforms we included 7 patients in which the genomic abnormalities were present in a relatively low percentage of the cells (range 5-28%) as previously determined by FISH. We found that both microarray platforms allowed the detection of copy number abnormalities present in as few as 16% of the cells. In addition, we found that microarray-based genomic profiling allowed the identification of genomic abnormalities that could not be detected by FISH and/or MLPA, including a focal TP53 loss and copy neutral losses of heterozygosity of chromosome 17p. CONCLUSION: From our results we conclude that although the microarray platforms exhibit a somewhat lower limit of detection compared to FISH, they still allow the detection of copy number abnormalities present in as few as 16% of the cells. By applying similar interpretation criteria, the results obtained from both platforms were comparable. In addition, we conclude that both microarray platforms allow the identification of additional potential prognostic relevant abnormalities such as focal TP53 deletions and copy neutral losses of heterozygosity of chromosome 17p, which would have remained undetected by FISH or MLPA. The prognostic relevance of these novel genomic alterations requires further evaluation in prospective clinical trials. 	GRCh37/hg19				Yes	NA
CTDB0338	Research	24613930	Kelly LM, Barila G, Liu P, Evdokimova VN, Trivedi S, Panebianco F, Gandhi M, Carty SE, Hodak SP, Luo J, Dacic S, Yu YP, Nikiforova MN, Ferris RL, Altschuler DL, Nikiforov YE	Identification of the transforming STRN-ALK fusion as a potential therapeutic target in the aggressive forms of thyroid cancer	Proceedings of the National Academy of Sciences of the United States of America	2014 Mar 	2	Thyroid cancer	Next Generation Sequencing	Homo sapiens	11-14T	Illumina HiSeq2000			STRN;ALK;KLHL29;MRPL33;BRE;BIRC6;LTDP1;LINC00486;	Department of Pathology and Laboratory Medicine, Department of Pharmacology and Chemical Biology, Department of Otolaryngology, Department of Surgery, Division of Endocrine Surgery, and Department of Medicine, Division of Endocrinology and Metabolism, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213	Thyroid cancer is a common endocrine malignancy that encompasses well-differentiated as well as dedifferentiated cancer types. The latter tumors have high mortality and lack effective therapies. Using a paired-end RNA-sequencing approach, we report the discovery of rearrangements involving the anaplastic lymphoma kinase (ALK) gene in thyroid cancer. The most common of these involves a fusion between ALK and the striatin (STRN) gene, which is the result of a complex rearrangement involving the short arm of chromosome 2. STRN-ALK leads to constitutive activation of ALK kinase via dimerization mediated by the coiled-coil domain of STRN and to a kinase-dependent, thyroid-stimulating hormone-independent proliferation of thyroid cells. Moreover, expression of STRN-ALK transforms cells in vitro and induces tumor formation in nude mice. The kinase activity of STRN-ALK and the ALK-induced cell growth can be blocked by the ALK inhibitors crizotinib and TAE684. In addition to well-differentiated papillary cancer, STRN-ALK was found with a higher prevalence in poorly differentiated and anaplastic thyroid cancers, and it did not overlap with other known driver mutations in these tumors. Our data demonstrate that STRN-ALK fusion occurs in a subset of patients with highly aggressive types of thyroid cancer and provide initial evidence suggesting that it may represent a therapeutic target for these patients.	GRCh37/hg19				Yes	ALK,SRTN
CTDB0339	Research	24613930	Kelly LM, Barila G, Liu P, Evdokimova VN, Trivedi S, Panebianco F, Gandhi M, Carty SE, Hodak SP, Luo J, Dacic S, Yu YP, Nikiforova MN, Ferris RL, Altschuler DL, Nikiforov YE	Identification of the transforming STRN-ALK fusion as a potential therapeutic target in the aggressive forms of thyroid cancer	Proceedings of the National Academy of Sciences of the United States of America	2014 Mar 	2	Thyroid cancer	Next Generation Sequencing	Homo sapiens	233323T	Illumina HiSeq2000			STRN;ALK;KLHL29;MRPL33;BRE;BIRC6;LTDP1;LINC00486;	Department of Pathology and Laboratory Medicine, Department of Pharmacology and Chemical Biology, Department of Otolaryngology, Department of Surgery, Division of Endocrine Surgery, and Department of Medicine, Division of Endocrinology and Metabolism, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213	Thyroid cancer is a common endocrine malignancy that encompasses well-differentiated as well as dedifferentiated cancer types. The latter tumors have high mortality and lack effective therapies. Using a paired-end RNA-sequencing approach, we report the discovery of rearrangements involving the anaplastic lymphoma kinase (ALK) gene in thyroid cancer. The most common of these involves a fusion between ALK and the striatin (STRN) gene, which is the result of a complex rearrangement involving the short arm of chromosome 2. STRN-ALK leads to constitutive activation of ALK kinase via dimerization mediated by the coiled-coil domain of STRN and to a kinase-dependent, thyroid-stimulating hormone-independent proliferation of thyroid cells. Moreover, expression of STRN-ALK transforms cells in vitro and induces tumor formation in nude mice. The kinase activity of STRN-ALK and the ALK-induced cell growth can be blocked by the ALK inhibitors crizotinib and TAE684. In addition to well-differentiated papillary cancer, STRN-ALK was found with a higher prevalence in poorly differentiated and anaplastic thyroid cancers, and it did not overlap with other known driver mutations in these tumors. Our data demonstrate that STRN-ALK fusion occurs in a subset of patients with highly aggressive types of thyroid cancer and provide initial evidence suggesting that it may represent a therapeutic target for these patients.	GRCh37/hg19				Yes	ALK,SRTN
CTDB0340	Research	22622578	Berger MF, Hodis E, Heffernan TP, Deribe YL, Lawrence MS, Protopopov A, Ivanova E, Watson IR, Nickerson E, Ghosh P, Zhang H, Zeid R, Ren X, Cibulskis K, Sivachenko AY, Wagle N, Sucker A, Sougnez C, Onofrio R, Ambrogio L, Auclair D, Fennell T, Carter SL, Drier Y, Stojanov P, Singer MA, Voet D, Jing R, Saksena G, Barretina J, Ramos AH, Pugh TJ, Stransky N, Parkin M, Winckler W, Mahan S, Ardlie K, Baldwin J, Wargo J, Schadendorf D, Meyerson M, Gabriel SB, Golub TR, Wagner SN, Lander ES, Getz G, Chin L, Garraway LA	Melanoma genome sequencing reveals frequent PREX2 mutations	Nature	2012 May 	6,18	Melanoma	Next Generation Sequencing	Homo sapiens	ME020	Illumina HiSeq2000	chr10:0-106781190:0;chr10:106781191-106785684:-1;chr10:106785685-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-7272536:0;chr16:7272537-7313781:-1;chr16:7313782-90354753:0;chr17:0-13901959:0;chr17:13901960-14352662:1;chr17:14352663-81195210:0;chr18:0-30390957:0;chr18:30390958-30434395:-1;chr18:30434396-41115065:0;chr18:41115066-41137288:-1;chr18:41137289-54582240:0;chr18:54582241-54601567:-1;chr18:54601568-61151888:0;chr18:61151889-61960835:-1;chr18:61960836-78077248:0;chr19:0-59128983:0;chr1:0-216624610:0;chr1:216624611-216634039:-1;chr1:216634040-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-8612211:0;chr2:8612212-8646334:-1;chr2:8646335-243199373:0;chr3:0-15622615:0;chr3:15622616-15839069:1;chr3:15839070-198022430:0;chr4:0-177288198:0;chr4:177288199-177313813:-1;chr4:177313814-191154276:0;chr5:0-180915260:0;chr6:0-2822663:0;chr6:23340660-24176390:-1;chr6:24176391-30676240:0;chr6:2822664-2825594:-1;chr6:2825595-23340659:0;chr6:30676241-30679025:-1;chr6:30679026-32938466:0;chr6:32938467-32946578:-1;chr6:32946579-171115067:0;chr7:0-44122813:0;chr7:112684470-112965616:-1;chr7:112685216-112735909:1;chr7:112965617-159138663:0;chr7:44122814-44127168:-1;chr7:44127169-112684469:0;chr8:0-111114002:0;chr8:111114003-111115146:-1;chr8:111115147-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:9103916-9103916,hs1:9105932-9105932;hs1:41260951-41260951,hs1:41262403-41262403;hs1:46314569-46314569,hs1:46316968-46316968;hs1:72181667-72181667,hs1:72184200-72184200;hs1:106355204-106355204,hs1:106359919-106359919;hs1:160485624-160485624,hs1:160495808-160495808;hs1:189322814-189322814,hs1:189324518-189324518;hs1:215867806-215867806,hs1:215869113-215869113;hs1:246331007-246331007,hs1:246333198-246333198;hs2:34926198-34926198,hs2:34927805-34927805;hs2:65645820-65645820,hs2:65647159-65647159;hs2:88666373-88666373,hs2:88668047-88668047;hs2:121039959-121039959,hs2:121042150-121042150;hs2:124256294-124256294,hs2:124257977-124257977;hs2:142335927-142335927,hs2:142337316-142337316;hs2:230014680-230014680,hs2:230016584-230016584;hs3:7170392-7170392,hs3:7172139-7172139;hs3:14578606-14578606,hs3:14580585-14580585;hs3:19078063-19078063,hs3:19079225-19079225;hs3:60141928-60141928,hs3:60144283-60144283;hs3:64970323-64970323,hs3:64971706-64971706;hs3:86131944-86131944,hs17:53607639-53607639;hs3:130431512-130431512,hs3:130432525-130432525;hs3:130502238-130502238,hs3:130503796-130503796;hs3:139597755-139597755,hs3:139603775-139603775;hs3:178646484-178646484,hs3:178658686-178658686;hs3:180258303-180258303,hs3:180264172-180264172;hs4:26645648-26645648,hs4:26653984-26653984;hs4:53205731-53205731,hs4:53207716-53207716;hs4:80271113-80271113,hs4:80272412-80272412;hs4:190655481-190655481,hs18:53541704-53541704;hs5:6510129-6510129,hs5:6511947-6511947;hs5:12295358-12295358,hs5:12305745-12305745;hs5:52010150-52010150,hs6:4941869-4941869;hs5:52010187-52010187,hs5:63077745-63077745;hs5:52013478-52013478,hs18:64032844-64032844;hs5:52640908-52640908,hs6:41444152-41444152;hs5:59344334-59344334,hs5:59346298-59346298;hs5:64884778-64884778,hs6:4938688-4938688;hs5:64899153-64899153,hs6:36315354-36315354;hs5:85011971-85011971,hs5:166984875-166984875;hs5:85012160-85012160,hs5:89064338-89064338;hs5:85014203-85014203,hs5:89067723-89067723;hs5:85845011-85845011,hs5:153838798-153838798;hs5:88592503-88592503,hs5:163308447-163308447;hs5:90292079-90292079,hs5:151878477-151878477;hs5:101223742-101223742,hs5:149252355-149252355;hs5:121603274-121603274,hs5:121621910-121621910;hs5:131805363-131805363,hs5:131809549-131809549;hs5:139880940-139880940,hs5:168120778-168120778;hs5:140047467-140047467,hs5:154417681-154417681;hs5:170852697-170852697,hs5:170854057-170854057;hs5:176960992-176960992,hs18:67726295-67726295;hs6:513001-513001,hs6:15338526-15338526;hs6:546895-546895,hs6:13340396-13340396;hs6:1127207-1127207,hs18:63946292-63946292;hs6:1204014-1204014,hs6:2823453-2823453;hs6:1214543-1214543,hs6:8839757-8839757;hs6:1249900-1249900,hs6:10980571-10980571;hs6:1275263-1275263,hs6:12867018-12867018;hs6:1837394-1837394,hs18:35943205-35943205;hs6:1863588-1863588,hs6:9018016-9018016;hs6:2148808-2148808,hs17:14215274-14215274;hs6:2149610-2149610,hs6:10130581-10130581;hs6:2248141-2248141,hs18:61524007-61524007;hs6:2277706-2277706,hs6:4345725-4345725;hs6:2512715-2512715,hs18:64024570-64024570;hs6:2538540-2538540,hs6:10671096-10671096;hs6:2654722-2654722,hs6:4954365-4954365;hs6:2759788-2759788,hs6:9858332-9858332;hs6:2778803-2778803,hs18:34316615-34316615;hs6:2785247-2785247,hs18:64146744-64146744;hs6:2805455-2805455,hs6:17059886-17059886;hs6:2816055-2816055,hs6:17149712-17149712;hs6:2816432-2816432,hs6:10801356-10801356;hs6:3135468-3135468,hs18:48037065-48037065;hs6:3401978-3401978,hs18:48021817-48021817;hs6:3635376-3635376,hs6:17097292-17097292;hs6:3664407-3664407,hs6:10801530-10801530;hs6:3664611-3664611,hs6:10800990-10800990;hs6:3913413-3913413,hs6:1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Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA	Melanoma is notable for its metastatic propensity, lethality in the advanced setting and association with ultraviolet exposure early in life. To obtain a comprehensive genomic view of melanoma in humans, we sequenced the genomes of 25 metastatic melanomas and matched germline DNA. A wide range of point mutation rates was observed: lowest in melanomas whose primaries arose on non-ultraviolet-exposed hairless skin of the extremities (3 and 14 per megabase (Mb) of genome), intermediate in those originating from hair-bearing skin of the trunk (5-55 per Mb), and highest in a patient with a documented history of chronic sun exposure (111 per Mb). Analysis of whole-genome sequence data identified PREX2 (phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 2)--a PTEN-interacting protein and negative regulator of PTEN in breast cancer--as a significantly mutated gene with a mutation frequency of approximately 14% in an independent extension cohort of 107 human melanomas. PREX2 mutations are biologically relevant, as ectopic expression of mutant PREX2 accelerated tumour formation of immortalized human melanocytes in vivo. Thus, whole-genome sequencing of human melanoma tumours revealed genomic evidence of ultraviolet pathogenesis and discovered a new recurrently mutated gene in melanoma.	GRCh37/hg19		phs000452		Yes	ACOT13,C18orf45;C18orf45,DOK6;CAP2,C18orf45;CDH2,CCDC102B;CLIC5,C18orf26;DDR1,ATF6B;DSP,ATF6B;DSP,HLA;DSP,MAK;DSP,NPC1;DTNBP1,KATNAL2;EXOC2,JARID2;F13A1,C18orf26;LY86,LOXHD1;NCR2,SETBP1;PHACTR1,KIAA1012;TAF11,BTBD9;UBR2,SETBP1;UHRF1BP1,BTBD9;WRNIP1,FHOD3
CTDB0341	Research	22622578	Berger MF, Hodis E, Heffernan TP, Deribe YL, Lawrence MS, Protopopov A, Ivanova E, Watson IR, Nickerson E, Ghosh P, Zhang H, Zeid R, Ren X, Cibulskis K, Sivachenko AY, Wagle N, Sucker A, Sougnez C, Onofrio R, Ambrogio L, Auclair D, Fennell T, Carter SL, Drier Y, Stojanov P, Singer MA, Voet D, Jing R, Saksena G, Barretina J, Ramos AH, Pugh TJ, Stransky N, Parkin M, Winckler W, Mahan S, Ardlie K, Baldwin J, Wargo J, Schadendorf D, Meyerson M, Gabriel SB, Golub TR, Wagner SN, Lander ES, Getz G, Chin L, Garraway LA	Melanoma genome sequencing reveals frequent PREX2 mutations	Nature	2012 May 	5,22	Melanoma	Next Generation Sequencing	Homo sapiens	ME035	Illumina HiSeq2000	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-103336094:0;chr14:103336095-103505623:1;chr14:103505624-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-58014519:0;chr17:58014520-58030611:-1;chr17:58030612-58031370:0;chr17:58031371-58033330:-1;chr17:58033331-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-9805643:0;chr1:160610796-160620905:-1;chr1:160620906-249250621:0;chr1:9805644-9983935:-1;chr1:9983936-160610795:0;chr20:0-63025520:0;chr21:0-26545901:0;chr21:26545902-26580567:-1;chr21:26580568-48129895:0;chr22:0-20927907:0;chr22:20927908-20949578:-1;chr22:20949579-23747545:0;chr22:23747546-23966618:-1;chr22:23966619-51304566:0;chr2:0-187180806:0;chr2:187180807-187183014:-1;chr2:187183015-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-54748906:0;chr5:54748907-54971031:1;chr5:54971032-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-124567394:0;chr8:124567395-124569744:-1;chr8:124569745-146364022:0;chr9:0-141213431:0;chrX:0-15409547:0;chrX:15409548-15686130:1;chrX:15668652-15686120:-1;chrX:15684400-15686346:1;chrX:15686347-155270560:0;chrY:0-59373566:0	hs1:8655029-8655029,hs1:8657168-8657168;hs1:49798993-49798993,hs1:49801451-49801451;hs1:53382625-53382625,hs1:53383890-53383890;hs1:64693342-64693342,hs1:64694621-64694621;hs1:101117401-101117401,hs1:101130085-101130085;hs1:143512806-143512806,hs5:38417994-38417994;hs1:144931335-144931335,hs2:46762281-46762281;hs1:144931335-144931335,hs2:46762281-46762281;hs1:176883763-176883763,hs1:181693108-181693108;hs1:185550047-185550047,hs1:185558527-185558527;hs1:210105649-210105649,hs1:210107267-210107267;hs1:240223859-240223859,hs1:240226433-240226433;hs2:53074337-53074337,hs2:53083656-53083656;hs2:72748919-72748919,hs2:72750717-72750717;hs2:115153642-115153642,hs2:115155467-115155467;hs3:81242-81242,hs3:1921867-1921867;hs3:35135645-35135645,hs3:35137473-35137473;hs3:57917588-57917588,hs3:57921021-57921021;hs3:106501624-106501624,hs3:106504144-106504144;hs3:113193251-113193251,hs3:113203874-113203874;hs3:146034612-146034612,hs3:146040410-146040410;hs3:177328083-177328083,hs3:177330243-177330243;hs3:180513096-180513096,hs3:180517204-180517204;hs4:154243429-154243429,hs4:154244692-154244692;hs5:485618-485618,hs22:17206980-17206980;hs5:512468-512468,hs5:28161882-28161882;hs5:518260-518260,hs5:36369866-36369866;hs5:841498-841498,hs5:35478937-35478937;hs5:1057413-1057413,hs5:21221208-21221208;hs5:1075488-1075488,hs22:48659248-48659248;hs5:1075528-1075528,hs22:18341455-18341455;hs5:1146423-1146423,hs5:2797971-2797971;hs5:1153000-1153000,hs5:21472495-21472495;hs5:1181561-1181561,hs5:31251355-31251355;hs5:1182536-1182536,hs22:50780201-50780201;hs5:1254824-1254824,hs22:40248068-40248068;hs5:1271870-1271870,hs5:3872609-3872609;hs5:1272275-1272275,hs5:53662217-53662217;hs5:1287439-1287439,hs5:49815427-49815427;hs5:1307328-1307328,hs22:37421558-37421558;hs5:1308446-1308446,hs5:23210371-23210371;hs5:1310046-1310046,hs5:28779106-28779106;hs5:1311657-1311657,hs22:37038541-37038541;hs5:1316192-1316192,hs5:23303899-23303899;hs5:1323567-1323567,hs5:20043814-20043814;hs5:1549749-1549749,hs22:18925485-18925485;hs5:1668570-1668570,hs22:21071046-21071046;hs5:1675555-1675555,hs22:40242354-40242354;hs5:1675908-1675908,hs22:20951086-20951086;hs5:1676289-1676289,hs5:36682095-36682095;hs5:1680592-1680592,hs5:36635679-36635679;hs5:1687983-1687983,hs22:20970717-20970717;hs5:1689528-1689528,hs5:23307560-23307560;hs5:1690969-1690969,hs5:9395950-9395950;hs5:1698340-1698340,hs5:23287905-23287905;hs5:1717674-1717674,hs22:18084499-18084499;hs5:1723774-1723774,hs5:53657758-53657758;hs5:1748718-1748718,hs22:33919289-33919289;hs5:2799749-2799749,hs22:49946492-49946492;hs5:3872302-3872302,hs5:5351020-5351020;hs5:3884443-3884443,hs5:4128717-4128717;hs5:3886206-3886206,hs22:20862880-20862880;hs5:3890639-3890639,hs5:5121579-5121579;hs5:3929861-3929861,hs5:32074678-32074678;hs5:4098909-4098909,hs5:21264652-21264652;hs5:4117048-4117048,hs22:51005572-51005572;hs5:4124493-4124493,hs5:19903666-19903666;hs5:5092489-5092489,hs5:9512605-9512605;hs5:5352515-5352515,hs5:31246269-31246269;hs5:5359964-5359964,hs5:9488557-9488557;hs5:5383859-5383859,hs22:17905943-17905943;hs5:5385062-5385062,hs22:20962595-20962595;hs5:5392080-5392080,hs22:19901110-19901110;hs5:5399802-5399802,hs5:35711677-35711677;hs5:5401503-5401503,hs5:28160458-28160458;hs5:5402565-5402565,hs22:49974409-49974409;hs5:5568139-5568139,hs5:31911774-31911774;hs5:9502216-9502216,hs5:53661253-53661253;hs5:9502760-9502760,hs5:21405801-21405801;hs5:9509516-9509516,hs5:23457270-23457270;hs5:9554937-9554937,hs22:37416227-37416227;hs5:11444653-11444653,hs5:11446174-11446174;hs5:13162833-13162833,hs5:44084898-44084898;hs5:13400528-13400528,hs5:32078369-32078369;hs5:13401841-13401841,hs22:20880879-20880879;hs5:13556250-13556250,hs5:32078551-32078551;hs5:13563174-13563174,hs5:49804975-49804975;hs5:13564727-13564727,hs5:26928343-26928343;hs5:13569561-13569561,hs5:43561719-43561719;hs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Broad Institute of Harvard and MIT, Cambridge, Massachusetts 02142, USA	Melanoma is notable for its metastatic propensity, lethality in the advanced setting and association with ultraviolet exposure early in life. To obtain a comprehensive genomic view of melanoma in humans, we sequenced the genomes of 25 metastatic melanomas and matched germline DNA. A wide range of point mutation rates was observed: lowest in melanomas whose primaries arose on non-ultraviolet-exposed hairless skin of the extremities (3 and 14 per megabase (Mb) of genome), intermediate in those originating from hair-bearing skin of the trunk (5-55 per Mb), and highest in a patient with a documented history of chronic sun exposure (111 per Mb). Analysis of whole-genome sequence data identified PREX2 (phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 2)--a PTEN-interacting protein and negative regulator of PTEN in breast cancer--as a significantly mutated gene with a mutation frequency of approximately 14% in an independent extension cohort of 107 human melanomas. PREX2 mutations are biologically relevant, as ectopic expression of mutant PREX2 accelerated tumour formation of immortalized human melanocytes in vivo. Thus, whole-genome sequencing of human melanoma tumours revealed genomic evidence of ultraviolet pathogenesis and discovered a new recurrently mutated gene in melanoma.	GRCh37/hg19		phs000452		Yes	ARL15,RBM9;BID,TBX1;CACNA1I,SHANK3;CDH12,HMGXB4;CDH12,SLC1A3;CDH6,MED15;CDH9,EGFLAM;DGCR10,ENTHD1;EGFLAM,BCL2L13;EGFLAM,LIFR;GUSBP1,FAM19A5;IL17RA,ENTHD1;KLHL22,ENTHD1;KLHL22,NCF4;MED15,ENTHD1;MED15,FAM116B;MICAL3,CACNA1I;MICAL3,KLHL22;MICAL3,ZBED4;PDZD2,LARGE;PI4KA,CACNA1I;PPAP2A,SLC38A9;PRODH,MED15;RICTOR,GHR;RNASEN,SPEF2;SLC12A7,MICAL3;TERT,ENTHD1;TOP3B,CACNG2;ZDHHC8P1,C22orf43;ZNF131,ENTHD1
CTDB0342	Research	24819516	Iannelli F, Collino A, Sinha S, Radaelli E, Nicoli P, D'Antiga L, Sonzogni A, Faivre J, Buendia MA, Sturm E, Thompson RJ, Knisely AS, Natoli G, Ghisletti S, Ciccarelli FD	Massive gene amplification drives paediatric hepatocellular carcinoma caused by bile salt export pump deficiency	Nature Communications	2014 May 	4,6	Hepatocellular carcinoma	SNP Array	Homo sapiens	UKT	Illumina HumanOmniExpress-12 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YNPO2;SYT14L;TACR3;TBC1D9;TBCK;TECRL;TET2;TMEM155;TMPRSS11A;TMPRSS11B;TMPRSS11BNL;TMPRSS11D;TMPRSS11F;TNIP3;TRAM1L1;TRDN;TRPC3;TSPAN5;UBA6;UBE2D3;UCP1;UFL1;UGT2A1;UGT2A2;UGT2A3;UGT2B15;UGT2B17;UGT2B4;UGT2B7;UGT8;UNC5C;USP45;USP53;VEGFC;YIPF7;YTHDC1;ZNF330;	European Institute of Oncology (IEO), Department of Experimental Oncology, IFOM-IEO Campus, Via Adamello 16, 20139 Milan, Italy 	Hepatocellular carcinoma (HCC) is almost invariably associated with an underlying inflammatory state, whose direct contribution to the acquisition of critical genomic changes is unclear. Here we map acquired genomic alterations in human and mouse HCCs induced by defects in hepatocyte biliary transporters, which expose hepatocytes to bile salts and cause chronic inflammation that develops into cancer. In both human and mouse cancer genomes, we find few somatic point mutations with no impairment of cancer genes, but massive gene amplification and rearrangements. This genomic landscape differs from that of virus- and alcohol-associated liver cancer. Copy-number gains preferentially occur at late stages of cancer development and frequently target the MAPK signalling pathway, and in particular direct regulators of JNK. The pharmacological inhibition of JNK retards cancer progression in the mouse. Our study demonstrates that intrahepatic cholestasis leading to hepatocyte exposure to bile acids and inflammation promotes cancer through genomic modifications that can be distinguished from those determined by other aetiological factors. 	GRCh37/hg19				Yes	NA
CTDB0343	Research	24819516	Iannelli F, Collino A, Sinha S, Radaelli E, Nicoli P, D'Antiga L, Sonzogni A, Faivre J, Buendia MA, Sturm E, Thompson RJ, Knisely AS, Natoli G, Ghisletti S, Ciccarelli FD	Massive gene amplification drives paediatric hepatocellular carcinoma caused by bile salt export pump deficiency	Nature Communications	2014 May 	19	Hepatocellular carcinoma	Next Generation Sequencing	Mus musculus	60400/1	Illumina Genome Analyzer Iix and Illumina 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Institute of Oncology (IEO), Department of Experimental Oncology, IFOM-IEO Campus, Via Adamello 16, 20139 Milan, Italy 	Hepatocellular carcinoma (HCC) is almost invariably associated with an underlying inflammatory state, whose direct contribution to the acquisition of critical genomic changes is unclear. Here we map acquired genomic alterations in human and mouse HCCs induced by defects in hepatocyte biliary transporters, which expose hepatocytes to bile salts and cause chronic inflammation that develops into cancer. In both human and mouse cancer genomes, we find few somatic point mutations with no impairment of cancer genes, but massive gene amplification and rearrangements. This genomic landscape differs from that of virus- and alcohol-associated liver cancer. Copy-number gains preferentially occur at late stages of cancer development and frequently target the MAPK signalling pathway, and in particular direct regulators of JNK. The pharmacological inhibition of JNK retards cancer progression in the mouse. Our study demonstrates that intrahepatic cholestasis leading to hepatocyte exposure to bile acids and inflammation promotes cancer through genomic modifications that can be distinguished from those determined by other aetiological factors. 	NCBI37/mm9				Yes	NA
CTDB0344	Research	23010713	Zehentner BK, Hartmann L, Johnson KR, Stephenson CF, Chapman DB, de Baca ME, Wells DA, Loken MR, Tirtorahardjo B, Gunn SR, Lim L	Array-based karyotyping in plasma cell neoplasia after plasma cell enrichment increases detection of genomic aberrations	American Journal of Clinical Pathology	2012 Oct	17	Plasma cell neoplasm	Array CGH	Homo sapiens	MA-MMHL-48					Hematologics Inc, 3161 Elliott Ave, Ste 200, Seattle, WA 98121, USA	The discovery of genomic abnormalities present in monoclonal plasma cells has diagnostic, prognostic, and disease-monitoring implications in plasma cell neoplasms (PCNs). However, technical and disease-related limitations hamper the detection of these abnormalities using cytogenetic analysis or fluorescence in situ hybridization (FISH). In this study, 28 bone marrow specimens with known PCNs were examined for the presence of genomic abnormalities using microarray analysis after plasma cell enrichment. Cytogenetic analysis was performed on 15 of 28 samples, revealing disease-related genomic aberrations in only 3 (20%) of 15 cases. FISH analysis was performed on enriched plasma cells and detected aberrations in 84.6% of specimens while array comparative genomic hybridization (aCGH) detected abnormalities in 89.3% of cases. Furthermore, aCGH revealed additional abnormalities in 24 cases compared with FISH alone. We conclude that aCGH after plasma cell enrichment, in combination with FISH, is a valuable approach for routine clinical use in achieving a more complete genetic characterization of patients with PCN.	GRCh37/hg19				Yes	NA
CTDB0345	Research	26017449	Patch AM, Christie EL, Etemadmoghadam D, Garsed DW, George J, Fereday S, Nones K, Cowin P, Alsop K, Bailey PJ, Kassahn KS, Newell F, Quinn MC, Kazakoff S, Quek K, Wilhelm-Benartzi C, Curry E, Leong HS; Australian Ovarian Cancer Study Group, Hamilton A, Mileshkin L, Au-Yeung G, Kennedy C, Hung J, Chiew YE, Harnett P, Friedlander M, Quinn M, Pyman J, Cordner S, O'Brien P, Leditschke J, Young G, Strachan K, Waring P, Azar W, Mitchell C, Traficante N, Hendley J, Thorne H, Shackleton M, Miller DK, Arnau GM, Tothill RW, Holloway TP, Semple T, Harliwong I, Nourse C, Nourbakhsh E, Manning S, Idrisoglu S, Bruxner TJ, Christ AN, Poudel B, Holmes O, Anderson M, Leonard C, Lonie A, Hall N, Wood S, Taylor DF, Xu Q, Fink JL, Waddell N, Drapkin R, Stronach E, Gabra H, Brown R, Jewell A, Nagaraj SH, Markham E, Wilson PJ, Ellul J, McNally O, Doyle MA, Vedururu R, Stewart C, Lengyel E, Pearson JV, Waddell N, deFazio A, Grimmond SM, Bowtell DD	Whole-genome characterization of chemoresistant ovarian cancer	Nature	2015 May	15	Ovarian cancer	Next Generation Sequencing	Homo sapiens	AOCS_097_ICGC_DBPC_20130205_074	Illumina Genome Network				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4067, Australia	Patients with high-grade serous ovarian cancer (HGSC) have experienced little improvement in overall survival, and standard treatment has not advanced beyond platinum-based combination chemotherapy, during the past 30 years. To understand the drivers of clinical phenotypes better, here we use whole-genome sequencing of tumour and germline DNA samples from 92 patients with primary refractory, resistant, sensitive and matched acquired resistant disease. We show that gene breakage commonly inactivates the tumour suppressors RB1, NF1, RAD51B and PTEN in HGSC, and contributes to acquired chemotherapy resistance. CCNE1 amplification was common in primary resistant and refractory disease. We observed several molecular events associated with acquired resistance, including multiple independent reversions of germline BRCA1 or BRCA2 mutations in individual patients, loss of BRCA1 promoter methylation, an alteration in molecular subtype, and recurrent promoter fusion associated with overexpression of the drug efflux pump MDR1. 	GRCh37/hg19	GSE65821			Yes	NA
CTDB0346	Research	26017449	Patch AM, Christie EL, Etemadmoghadam D, Garsed DW, George J, Fereday S, Nones K, Cowin P, Alsop K, Bailey PJ, Kassahn KS, Newell F, Quinn MC, Kazakoff S, Quek K, Wilhelm-Benartzi C, Curry E, Leong HS; Australian Ovarian Cancer Study Group, Hamilton A, Mileshkin L, Au-Yeung G, Kennedy C, Hung J, Chiew YE, Harnett P, Friedlander M, Quinn M, Pyman J, Cordner S, O'Brien P, Leditschke J, Young G, Strachan K, Waring P, Azar W, Mitchell C, Traficante N, Hendley J, Thorne H, Shackleton M, Miller DK, Arnau GM, Tothill RW, Holloway TP, Semple T, Harliwong I, Nourse C, Nourbakhsh E, Manning S, Idrisoglu S, Bruxner TJ, Christ AN, Poudel B, Holmes O, Anderson M, Leonard C, Lonie A, Hall N, Wood S, Taylor DF, Xu Q, Fink JL, Waddell N, Drapkin R, Stronach E, Gabra H, Brown R, Jewell A, Nagaraj SH, Markham E, Wilson PJ, Ellul J, McNally O, Doyle MA, Vedururu R, Stewart C, Lengyel E, Pearson JV, Waddell N, deFazio A, Grimmond SM, Bowtell DD	Whole-genome characterization of chemoresistant ovarian cancer	Nature	2015 May	8	Ovarian cancer	Next Generation Sequencing	Homo sapiens	AOCS_132_ICGC_DBPC_20130205_120	Illumina Genome Network				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4067, Australia	Patients with high-grade serous ovarian cancer (HGSC) have experienced little improvement in overall survival, and standard treatment has not advanced beyond platinum-based combination chemotherapy, during the past 30 years. To understand the drivers of clinical phenotypes better, here we use whole-genome sequencing of tumour and germline DNA samples from 92 patients with primary refractory, resistant, sensitive and matched acquired resistant disease. We show that gene breakage commonly inactivates the tumour suppressors RB1, NF1, RAD51B and PTEN in HGSC, and contributes to acquired chemotherapy resistance. CCNE1 amplification was common in primary resistant and refractory disease. We observed several molecular events associated with acquired resistance, including multiple independent reversions of germline BRCA1 or BRCA2 mutations in individual patients, loss of BRCA1 promoter methylation, an alteration in molecular subtype, and recurrent promoter fusion associated with overexpression of the drug efflux pump MDR1. 	GRCh37/hg19	GSE65821			Yes	NA
CTDB0347	Research	26017449	Patch AM, Christie EL, Etemadmoghadam D, Garsed DW, George J, Fereday S, Nones K, Cowin P, Alsop K, Bailey PJ, Kassahn KS, Newell F, Quinn MC, Kazakoff S, Quek K, Wilhelm-Benartzi C, Curry E, Leong HS; Australian Ovarian Cancer Study Group, Hamilton A, Mileshkin L, Au-Yeung G, Kennedy C, Hung J, Chiew YE, Harnett P, Friedlander M, Quinn M, Pyman J, Cordner S, O'Brien P, Leditschke J, Young G, Strachan K, Waring P, Azar W, Mitchell C, Traficante N, Hendley J, Thorne H, Shackleton M, Miller DK, Arnau GM, Tothill RW, Holloway TP, Semple T, Harliwong I, Nourse C, Nourbakhsh E, Manning S, Idrisoglu S, Bruxner TJ, Christ AN, Poudel B, Holmes O, Anderson M, Leonard C, Lonie A, Hall N, Wood S, Taylor DF, Xu Q, Fink JL, Waddell N, Drapkin R, Stronach E, Gabra H, Brown R, Jewell A, Nagaraj SH, Markham E, Wilson PJ, Ellul J, McNally O, Doyle MA, Vedururu R, Stewart C, Lengyel E, Pearson JV, Waddell N, deFazio A, Grimmond SM, Bowtell DD	Whole-genome characterization of chemoresistant ovarian cancer	Nature	2015 May	13	Ovarian cancer	Next Generation Sequencing	Homo sapiens	AOCS_093_ICGC_DBPC_20130205_064	Illumina Genome Network			BRCA2	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4067, Australia	Patients with high-grade serous ovarian cancer (HGSC) have experienced little improvement in overall survival, and standard treatment has not advanced beyond platinum-based combination chemotherapy, during the past 30 years. To understand the drivers of clinical phenotypes better, here we use whole-genome sequencing of tumour and germline DNA samples from 92 patients with primary refractory, resistant, sensitive and matched acquired resistant disease. We show that gene breakage commonly inactivates the tumour suppressors RB1, NF1, RAD51B and PTEN in HGSC, and contributes to acquired chemotherapy resistance. CCNE1 amplification was common in primary resistant and refractory disease. We observed several molecular events associated with acquired resistance, including multiple independent reversions of germline BRCA1 or BRCA2 mutations in individual patients, loss of BRCA1 promoter methylation, an alteration in molecular subtype, and recurrent promoter fusion associated with overexpression of the drug efflux pump MDR1. 	GRCh37/hg19	GSE65821			Yes	NA
CTDB0348	Research	26017449	Patch AM, Christie EL, Etemadmoghadam D, Garsed DW, George J, Fereday S, Nones K, Cowin P, Alsop K, Bailey PJ, Kassahn KS, Newell F, Quinn MC, Kazakoff S, Quek K, Wilhelm-Benartzi C, Curry E, Leong HS; Australian Ovarian Cancer Study Group, Hamilton A, Mileshkin L, Au-Yeung G, Kennedy C, Hung J, Chiew YE, Harnett P, Friedlander M, Quinn M, Pyman J, Cordner S, O'Brien P, Leditschke J, Young G, Strachan K, Waring P, Azar W, Mitchell C, Traficante N, Hendley J, Thorne H, Shackleton M, Miller DK, Arnau GM, Tothill RW, Holloway TP, Semple T, Harliwong I, Nourse C, Nourbakhsh E, Manning S, Idrisoglu S, Bruxner TJ, Christ AN, Poudel B, Holmes O, Anderson M, Leonard C, Lonie A, Hall N, Wood S, Taylor DF, Xu Q, Fink JL, Waddell N, Drapkin R, Stronach E, Gabra H, Brown R, Jewell A, Nagaraj SH, Markham E, Wilson PJ, Ellul J, McNally O, Doyle MA, Vedururu R, Stewart C, Lengyel E, Pearson JV, Waddell N, deFazio A, Grimmond SM, Bowtell DD	Whole-genome characterization of chemoresistant ovarian cancer	Nature	2015 May	6	Ovarian cancer	Next Generation Sequencing	Homo sapiens	AOCS_160_ICGC_DBDE_20130904_014	Illumina Genome Network				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4067, Australia	Patients with high-grade serous ovarian cancer (HGSC) have experienced little improvement in overall survival, and standard treatment has not advanced beyond platinum-based combination chemotherapy, during the past 30 years. To understand the drivers of clinical phenotypes better, here we use whole-genome sequencing of tumour and germline DNA samples from 92 patients with primary refractory, resistant, sensitive and matched acquired resistant disease. We show that gene breakage commonly inactivates the tumour suppressors RB1, NF1, RAD51B and PTEN in HGSC, and contributes to acquired chemotherapy resistance. CCNE1 amplification was common in primary resistant and refractory disease. We observed several molecular events associated with acquired resistance, including multiple independent reversions of germline BRCA1 or BRCA2 mutations in individual patients, loss of BRCA1 promoter methylation, an alteration in molecular subtype, and recurrent promoter fusion associated with overexpression of the drug efflux pump MDR1. 	GRCh37/hg19	GSE65821			Yes	NA
CTDB0349	Research	26017449	Patch AM, Christie EL, Etemadmoghadam D, Garsed DW, George J, Fereday S, Nones K, Cowin P, Alsop K, Bailey PJ, Kassahn KS, Newell F, Quinn MC, Kazakoff S, Quek K, Wilhelm-Benartzi C, Curry E, Leong HS; Australian Ovarian Cancer Study Group, Hamilton A, Mileshkin L, Au-Yeung G, Kennedy C, Hung J, Chiew YE, Harnett P, Friedlander M, Quinn M, Pyman J, Cordner S, O'Brien P, Leditschke J, Young G, Strachan K, Waring P, Azar W, Mitchell C, Traficante N, Hendley J, Thorne H, Shackleton M, Miller DK, Arnau GM, Tothill RW, Holloway TP, Semple T, Harliwong I, Nourse C, Nourbakhsh E, Manning S, Idrisoglu S, Bruxner TJ, Christ AN, Poudel B, Holmes O, Anderson M, Leonard C, Lonie A, Hall N, Wood S, Taylor DF, Xu Q, Fink JL, Waddell N, Drapkin R, Stronach E, Gabra H, Brown R, Jewell A, Nagaraj SH, Markham E, Wilson PJ, Ellul J, McNally O, Doyle MA, Vedururu R, Stewart C, Lengyel E, Pearson JV, Waddell N, deFazio A, Grimmond SM, Bowtell DD	Whole-genome characterization of chemoresistant ovarian cancer	Nature	2015 May	4	Ovarian cancer	Next Generation Sequencing	Homo sapiens	AOCS_034_ICGC_DBPC_20130205_009	Illumina Genome Network				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4067, Australia	Patients with high-grade serous ovarian cancer (HGSC) have experienced little improvement in overall survival, and standard treatment has not advanced beyond platinum-based combination chemotherapy, during the past 30 years. To understand the drivers of clinical phenotypes better, here we use whole-genome sequencing of tumour and germline DNA samples from 92 patients with primary refractory, resistant, sensitive and matched acquired resistant disease. We show that gene breakage commonly inactivates the tumour suppressors RB1, NF1, RAD51B and PTEN in HGSC, and contributes to acquired chemotherapy resistance. CCNE1 amplification was common in primary resistant and refractory disease. We observed several molecular events associated with acquired resistance, including multiple independent reversions of germline BRCA1 or BRCA2 mutations in individual patients, loss of BRCA1 promoter methylation, an alteration in molecular subtype, and recurrent promoter fusion associated with overexpression of the drug efflux pump MDR1. 	GRCh37/hg19	GSE65821			Yes	NA
CTDB0350	Research	26017449	Patch AM, Christie EL, Etemadmoghadam D, Garsed DW, George J, Fereday S, Nones K, Cowin P, Alsop K, Bailey PJ, Kassahn KS, Newell F, Quinn MC, Kazakoff S, Quek K, Wilhelm-Benartzi C, Curry E, Leong HS; Australian Ovarian Cancer Study Group, Hamilton A, Mileshkin L, Au-Yeung G, Kennedy C, Hung J, Chiew YE, Harnett P, Friedlander M, Quinn M, Pyman J, Cordner S, O'Brien P, Leditschke J, Young G, Strachan K, Waring P, Azar W, Mitchell C, Traficante N, Hendley J, Thorne H, Shackleton M, Miller DK, Arnau GM, Tothill RW, Holloway TP, Semple T, Harliwong I, Nourse C, Nourbakhsh E, Manning S, Idrisoglu S, Bruxner TJ, Christ AN, Poudel B, Holmes O, Anderson M, Leonard C, Lonie A, Hall N, Wood S, Taylor DF, Xu Q, Fink JL, Waddell N, Drapkin R, Stronach E, Gabra H, Brown R, Jewell A, Nagaraj SH, Markham E, Wilson PJ, Ellul J, McNally O, Doyle MA, Vedururu R, Stewart C, Lengyel E, Pearson JV, Waddell N, deFazio A, Grimmond SM, Bowtell DD	Whole-genome characterization of chemoresistant ovarian cancer	Nature	2015 May	12	Ovarian cancer	Next Generation Sequencing	Homo sapiens	AOCS_152_ICGC_DBPC_20130205_174	Illumina Genome Network				Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4067, Australia	Patients with high-grade serous ovarian cancer (HGSC) have experienced little improvement in overall survival, and standard treatment has not advanced beyond platinum-based combination chemotherapy, during the past 30 years. To understand the drivers of clinical phenotypes better, here we use whole-genome sequencing of tumour and germline DNA samples from 92 patients with primary refractory, resistant, sensitive and matched acquired resistant disease. We show that gene breakage commonly inactivates the tumour suppressors RB1, NF1, RAD51B and PTEN in HGSC, and contributes to acquired chemotherapy resistance. CCNE1 amplification was common in primary resistant and refractory disease. We observed several molecular events associated with acquired resistance, including multiple independent reversions of germline BRCA1 or BRCA2 mutations in individual patients, loss of BRCA1 promoter methylation, an alteration in molecular subtype, and recurrent promoter fusion associated with overexpression of the drug efflux pump MDR1. 	GRCh37/hg19	GSE65821			Yes	NA
CTDB0351	Research	25496518	Reimann E, Koks S, Ho XD, Maasalu K, Martson A	Whole exome sequencing of a single osteosarcoma case--integrative analysis with whole transcriptome RNA-seq data	Human Genomics	2014 Dec 	8	Osteosarcoma	Next Generation Sequencing	Homo sapiens	case 1	SOLiD 5500xl	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-77755834:0;chr13:77755835-77756057:1;chr13:77756058-77759236:0;chr13:77759237-77759512:1;chr13:77759513-77760004:0;chr13:77760005-77760198:1;chr13:77760199-77763084:0;chr13:77763085-77763182:1;chr13:77763183-77764385:0;chr13:77764386-77764470:1;chr13:77764471-77765812:0;chr13:77765813-77765948:1;chr13:77765949-77768286:0;chr13:77768287-77768379:1;chr13:77768380-77779389:0;chr13:77779390-77779518:1;chr13:77779519-77779606:0;chr13:77779607-77779733:1;chr13:77779734-77780786:0;chr13:77780787-77780960:1;chr13:77780961-77785300:0;chr13:77785301-77785455:1;chr13:77785456-77786089:0;chr13:77786090-77786295:1;chr13:77786296-77791973:0;chr13:77791974-77792092:1;chr13:77792093-77798584:0;chr13:77798585-77798667:1;chr13:77798668-77799568:0;chr13:77799569-77799689:1;chr13:77799690-77807289:0;chr13:77807290-77807398:1;chr13:77807399-77817192:0;chr13:77817193-77817295:1;chr13:77817296-77817939:0;chr13:77817940-77818086:1;chr13:77818087-77825284:0;chr13:77825285-77825490:1;chr13:77825491-77831804:0;chr13:77831805-77831964:1;chr13:77831965-77834561:0;chr13:77834562-77834727:1;chr13:77834728-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-7058570:0;chr19:10102679-10102724:-1;chr19:10102725-10103501:0;chr19:10103502-10103556:-1;chr19:10103557-10104054:0;chr19:10104055-10104109:-1;chr19:10104110-10104293:0;chr19:10104294-10104348:-1;chr19:10104349-10104427:0;chr19:10104428-10104482:-1;chr19:10104483-10106238:0;chr19:10106239-10106293:-1;chr19:10106294-10106740:0;chr19:10106741-10106795:-1;chr19:10106796-10106880:0;chr19:10106881-10106938:-1;chr19:10106939-10107107:0;chr19:10107108-10107192:-1;chr19:10107193-10108045:0;chr19:10108046-10108109:-1;chr19:10108110-10108658:0;chr19:10108659-10108701:-1;chr19:10108702-10108776:0;chr19:10108777-10108825:-1;chr19:10108826-10112198:0;chr19:10112199-10112346:-1;chr19:10112347-10112442:0;chr19:10112443-10112557:-1;chr19:10112558-10114239:0;chr19:10114240-10114390:-1;chr19:10114391-10114715:0;chr19:10114716-10114821:-1;chr19:10114822-10116232:0;chr19:10116233-10116390:-1;chr19:10116391-10120972:0;chr19:10120973-10121147:-1;chr19:10121148-10127731:0;chr19:10127732-10127891:-1;chr19:10127892-10129405:0;chr19:10129406-10129586:-1;chr19:10129587-12910989:0;chr19:101971714-101971828:-1;chr19:101971829-101999993:0;chr19:101999994-102000164:-1;chr19:12910990-12911113:-1;chr19:12911114-12911425:0;chr19:12911426-12911883:-1;chr19:12911729-12911883:-1;chr19:12911884-12911971:0;chr19:12911972-12912084:-1;chr19:12912085-12912552:0;chr19:12912553-12912694:-1;chr19:12912695-12918018:0;chr19:12918019-12918143:-1;chr19:12918144-12918231:0;chr19:12918232-12918320:-1;chr19:12918321-12920883:0;chr19:12920884-12921022:-1;chr19:12921023-12921129:0;chr19:12921130-12921218:-1;chr19:12921219-12923895:0;chr19:12923896-12924020:-1;chr19:12924021-12924140:0;chr19:12924141-12924462:-1;chr19:12924463-12937587:0;chr19:12937588-12937685:-1;chr19:12937686-12945597:0;chr19:12945598-12945660:-1;chr19:12945661-12949257:0;chr19:12949258-12949469:-1;chr19:12949470-12951258:0;chr19:12951259-12951348:-1;chr19:12951349-12951803:0;chr19:12951804-12951880:-1;chr19:12951881-12954341:0;chr19:12954342-12954421:-1;chr19:12954422-12958102:0;chr19:12958103-12958264:-1;chr19:12958265-12958424:0;chr19:12958425-12958501:-1;chr19:12958502-12958660:0;chr19:12958661-12958871:-1;chr19:12958872-12962746:0;chr19:12962747-12962849:-1;chr19:12962850-12962927:0;chr19:12962928-12963061:-1;chr19:12963062-12963140:0;chr19:12963141-12963209:-1;chr19:12963210-12969174:0;chr19:12969175-12969255:-1;chr19:12969256-12969343:0;chr19:12969344-12969553:-1;chr19:12969554-12975621:0;chr19:12975622-12975761:-1;chr19:12975762-12975858:0;chr19:12975859-12975992:-1;chr19:12975993-12976128:0;chr19:12976129-12976295:-1;chr19:12976296-12976529:0;chr19:12976530-12976632:-1;chr19:12976633-12976792:0;chr19:12976793-12976916:-1;chr19:12976917-12977465:0;chr19:12977466-12977576:-1;chr19:12977577-12978286:0;chr19:12978287-12978466:-1;chr19:12978467-12979455:0;chr19:12979456-12979663:-1;chr19:12979664-12979878:0;chr19:12979879-12980109:-1;chr19:12980110-12981636:0;chr19:12981637-12981760:-1;chr19:12981761-12981848:0;chr19:12981849-12981986:-1;chr19:12981987-12984136:0;chr19:12984137-12984325:-1;chr19:12984326-12989482:0;chr19:12989483-12989648:-1;chr19:12989649-12991614:0;chr19:12991615-12991694:-1;chr19:12991695-12992102:0;chr19:12992103-12992335:-1;chr19:12992336-12997866:0;chr19:12997867-12998017:-1;chr19:12998018-13002299:0;chr19:13002300-13002336:-1;chr19:13002337-13002643:0;chr19:13002644-13002788:-1;chr19:13002789-13002928:0;chr19:13002929-13002992:-1;chr19:13002993-13004295:0;chr19:13004296-13004467:-1;chr19:13004468-13006804:0;chr19:13006805-13006935:-1;chr19:13006936-13007017:0;chr19:13007018-13007235:-1;chr19:13007236-13007722:0;chr19:13007723-13007827:-1;chr19:13007828-13008115:0;chr19:13008116-13008242:-1;chr19:13008243-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Osteosarcoma (OS) is a prevalent primary malignant bone tumour with unknown etiology. These highly metastasizing tumours are among the most frequent causes of cancer-related deaths. Thus, there is an urgent need for different markers, and with our study, we were aiming towards finding novel biomarkers for OS. Methods: For that, we analysed the whole exome of the tumorous and non-tumour bone tissue from the same patient with OS applying next-generation sequencing. For data analysis, we used several softwares and combined the exome data with RNA-seq data from our previous study. Results: In the tumour exome, we found wide genomic rearrangements, which should qualify as chromotripsis-we detected almost 3,000 somatic single nucleotide variants (SNVs) and small indels and more than 2,000 copy number variants (CNVs) in different chromosomes. Furthermore, the somatic changes seem to be associated to bone tumours, whereas germline mutations to cancer in general. We confirmed the previous findings that the most significant pathway involved in OS pathogenesis is probably the WNT/beta-catenin signalling pathway. Also, the IGF1/ IGF2 and IGF1R homodimer signalling and TP53 (including downstream tumour suppressor gene EI24) pathways may have a role. Additionally, the mucin family genes, especially MUC4 and cell cycle controlling gene CDC27 may be considered as potential biomarkers for OS. Conclusions: The genes, in which the mutations were detected, may be considered as targets for finding biomarkers for OS. As the study is based on a single case and only DNA and RNA analysis, further confirmative studies are required.	GRCh37/hg19					NA
CTDB0352	Research	23139213	Cazes A, Louis-Brennetot C, Mazot P, Dingli F, Lombard B, Boeva V, Daveau R, Cappo J, Combaret V, Schleiermacher G, Jouannet S, Ferrand S, Pierron G, Barillot E, Loew D, Vigny M, Delattre O, Janoueix-Lerosey I	Characterization of rearrangements involving the ALK gene reveals a novel truncated form associated with tumor aggressiveness in neuroblastoma	Cancer Research	2013 Jan 	2,3	Neuroblastoma	Next Generation Sequencing	Homo sapiens	CLB-Re	Illumina Genome Analyzer II	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-29344475:0;chr2:29344476-33156045:-1;chr2:29603903-42009571:-1;chr2:29646730-36893802:-1;chr2:42009572-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0	hs2:29344476-29344476,hs2:33156045-33156045;hs2:29603903-29603903,hs2:42009571-42009571;hs2:29646730-29646730,hs2:36893802-36893802;hs2:29423161-29423161,hs3:65157963-65157963;hs2:29557752-29557752,hs3:74605412-74605412;hs2:29346060-29346060,hs3:61180791-61180791	ALK;LTBP1;VIT;	Inserm U830, Institut Curie, Centre de Recherche, Paris, France	Activating mutations of the ALK gene have been identified in sporadic and familial cases of neuroblastoma (NB), a cancer of the peripheral nervous system, and are thought to be the primary mechanism of oncogenic activation of this receptor in this pediatric neoplasm. To address the possibility that ALK activation may occur through genomic rearrangements as detected in other cancers, we first took advantage of high-resolution arraycomparative genomic hybridization to search for ALK rearrangements in NB samples. Using complementary experiments by capture/paired-end sequencing and FISH experiments, various types of rearrangements were fully characterized, including partial gains or amplifications, in several NB cell lines and primary tumors. In the CLB-Bar cell line, we described a genomic rearrangement associated with an amplification of the ALK locus, leading to the expression of a 170 kDa protein lacking part of the extracellular domain encoded by exons 4 to 11, named ALKD4-11. Analysis of genomic DNA from the tumor at diagnosis and relapse revealed that the ALK gene was amplified at diagnosis but that the rearranged ALK allele was observed at the relapse stage only, suggesting that it may be implicated in tumor aggressiveness. Consistently, oncogenic and tumorigenic properties of the ALKD4-11 variant were shown after stable expression in NIH3T3 cells. Moreover, we documented an increased constitutive kinase activity of this variant, as well as an impaired maturation and retention into intracellular compartments. These results indicate that genomic rearrangements constitute an alternative mechanism to ALK point mutations resulting in receptor activation.	NCBI 36/hg18				Yes	ALK,CNTN3;ALK,FHIT;ALK,LTBP1;ALK,VIT
CTDB0354	Research	24147068	Wei JS, Johansson P, Chen L, Song YK, Tolman C, Li S, Hurd L, Patidar R, Wen X, Badgett TC, Cheuk AT, Marshall JC, Steeg PS, Vaque Diez JP, Yu Y, Gutkind JS, Khan J	Massively parallel sequencing reveals an accumulation of de novo mutations and an activating mutation of LPAR1 in a patient with metastatic neuroblastoma	PLoS One	2013 Oct 	1,4,13	Neuroblastoma	Next Generation Sequencing	Homo sapiens	Met2	Complete Genomics	chr10:0-66751984:0;chr10:66751985-66789278:1;chr10:66789279-135534747:0;chr11:0-135006516:0;chr12:0-133577764:0;chr12:133577765-133630336:1;chr12:133630337-133851895:0;chr13:0-43207210:0;chr13:43207211-45534853:1;chr13:43312476-44870674:1;chr13:45534854-115169878:0;chr14:0-26468519:0;chr14:26468520-27412468:1;chr14:27412469-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-38535209:0;chr17:38535210-38696124:1;chr17:38696125-81195210:0;chr18:0-78077248:0;chr19:0-46304183:0;chr19:46304184-46362265:1;chr19:46362266-59128983:0;chr1:0-19684671:0;chr1:19684672-45527083:1;chr1:21258729-36939067:1;chr1:23118056-33564477:1;chr1:25684105-30354775:-1;chr1:29102259-34772072:-1;chr1:34472642-76565404:-1;chr1:76565405-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-19499749:0;chr22:19499750-19707873:1;chr22:19707874-51304566:0;chr2:0-79090239:0;chr2:79090240-79706333:1;chr2:79706334-243199373:0;chr3:0-198022430:0;chr4:0-62315268:0;chr4:62315269-66379523:1;chr4:66379524-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-8772565:0;chr7:8772566-91744804:1;chr7:91744805-159138663:0;chr8:0-73803609:0;chr8:73803610-73803665:1;chr8:73803666-146364022:0;chr9:0-141213431:0;chrX:0-76916705:0;chrX:76916706-76932438:-1;chrX:76932439-155270560:0;chrY:0-59373566:0	hs1:15709415-15709415,hs1:38462152-38462152;hs1:21588867-21588867,hs1:31216791-31216791;hs1:22778291-22778291,hs1:23118846-23118846;hs1:22778291-22778291,hs1:34817224-34817224;hs1:24633158-24633158,hs1:45523914-45523914;hs1:29195642-29195642,hs1:85959093-85959093;hs1:29801030-29801030,hs1:43429062-43429062;hs1:91853148-91853148,hsX:108297835-108297835;hs1:113835948-113835948,hs1:150053653-150053653;hs1:113841722-113841722,hs4:68112150-68112150;hs1:113842344-113842344,hs4:68106267-68106267;hs1:113842677-113842677,hs4:62591576-62591576;hs1:113842740-113842740,hs4:62013582-62013582;hs1:113843257-113843257,hs4:68100833-68100833;hs1:113843282-113843282,hs4:66377763-66377763;hs1:113843298-113843298,hs4:65359600-65359600;hs1:113843411-113843411,hs4:62337136-62337136;hs1:113844354-113844354,hs4:66483003-66483003;hs1:113928797-113928797,hs4:68115985-68115985;hs1:113929632-113929632,hsX:88386784-88386784;hs1:113929764-113929764,hs4:62017959-62017959;hs1:113931614-113931614,hs4:68106604-68106604;hs1:113932103-113932103,hs1:150062096-150062096;hs1:113933436-113933436,hs1:150008218-150008218;hs1:113934553-113934553,hs4:62057325-62057325;hs1:113935655-113935655,hs1:150001425-150001425;hs1:113936130-113936130,hs4:65653764-65653764;hs1:113937594-113937594,hs4:62590597-62590597;hs1:113940793-113940793,hs4:62849618-62849618;hs1:113943479-113943479,hs1:114050846-114050846;hs1:113943660-113943660,hsX:88443338-88443338;hs1:113945298-113945298,hs4:66414608-66414608;hs1:113945397-113945397,hs4:62450837-62450837;hs1:113945941-113945941,hs4:62013440-62013440;hs1:113946026-113946026,hs1:150082718-150082718;hs1:113947399-113947399,hs4:66376686-66376686;hs1:113950971-113950971,hs4:62642505-62642505;hs1:113952218-113952218,hs4:68112287-68112287;hs1:113952548-113952548,hs4:66469482-66469482;hs1:113952775-113952775,hs4:62385455-62385455;hs1:113957585-113957585,hs1:150123509-150123509;hs1:113958567-113958567,hs4:68099716-68099716;hs1:114025815-114025815,hs4:62743097-62743097;hs1:114047339-114047339,hs1:115144218-115144218;hs1:114757940-114757940,hs4:66374994-66374994;hs1:114768743-114768743,hs4:65655134-65655134;hs1:114769641-114769641,hs4:68099839-68099839;hs1:115140410-115140410,hs4:62628181-62628181;hs1:115142025-115142025,hs4:62681547-62681547;hs1:115142684-115142684,hs4:68101875-68101875;hs1:115143745-115143745,hs4:62329357-62329357;hs1:115144218-115144218,hs1:150016216-150016216;hs1:115144218-115144218,hs4:65361603-65361603;hs1:115144237-115144237,hs4:65363110-65363110;hs1:115145868-115145868,hs4:68107760-68107760;hs1:115147404-115147404,hs4:62007917-62007917;hs1:115147404-115147404,hs4:66383970-66383970;hs1:115148786-115148786,hs4:62257823-62257823;hs1:118202326-118202326,hs4:62214589-62214589;hs1:118202917-118202917,hs4:68130589-68130589;hs1:118212065-118212065,hs4:68085547-68085547;hs1:118213100-118213100,hs4:66461586-66461586;hs1:149848864-149848864,hs4:66461122-66461122;hs1:149849107-149849107,hs4:62675345-62675345;hs1:149849397-149849397,hs4:67785141-67785141;hs1:149851969-149851969,hs4:68096639-68096639;hs1:149857304-149857304,hs1:150114821-150114821;hs1:149857606-149857606,hs4:68115132-68115132;hs1:149859337-149859337,hs4:66417295-66417295;hs1:149859793-149859793,hs13:45014739-45014739;hs1:149860562-149860562,hs4:68130487-68130487;hs1:149861374-149861374,hs4:62341741-62341741;hs1:149866964-149866964,hs4:66343595-66343595;hs1:149990170-149990170,hs13:43252566-43252566;hs1:149995285-149995285,hs4:65401213-65401213;hs1:149995946-149995946,hs13:44492215-44492215;hs1:149996435-149996435,hs4:66465174-66465174;hs1:149997366-149997366,hs4:66461038-66461038;hs1:149998608-149998608,hs4:65660854-65660854;hs1:149999602-149999602,hs4:65646567-65646567;hs1:150001035-150001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62-44666462,hs13:44894360-44894360;hs13:44666846-44666846,hs13:44670225-44670225	ADC;CAPZB;CSF3R;CSMD2;DDAH1;DENND2C;ECE1;EIF4G3;ENOX1;EPHA5;EPHB2;FHAD1;FHL3;FLJ32224;HFM1;HIST2H2AB;HIST2H2AC;HIST2H2BE;LAPTM5;LPHN3;MAGI3;NUFIP1;PLEKHO1;ST6GALNAC3;TMEM50A;TSC22D1;VPS45;ZBTB40;ZSWIM5;	Oncogenomics Section, Pediatric Oncology Branch, Advanced Technology Center, National Cancer Institute, Bethesda, Maryland, United States of America	Neuroblastoma is one of the most genomically heterogeneous childhood malignances studied to date, and the molecular events that occur during the course of the disease are not fully understood. Genomic studies in neuroblastoma have showed only a few recurrent mutations and a low somatic mutation burden. However, none of these studies has examined the mutations arising during the course of disease, nor have they systemically examined the expression of mutant genes. Here we performed genomic analyses on tumors taken during a 3.5 years disease course from a neuroblastoma patient (bone marrow biopsy at diagnosis, adrenal primary tumor taken at surgical resection, and a liver metastasis at autopsy). Whole genome sequencing of the index liver metastasis identified 44 non-synonymous somatic mutations in 42 genes (0.85 mutation/MB) and a large hemizygous deletion in the ATRX gene which has been recently reported in neuroblastoma. Of these 45 somatic alterations, 15 were also detected in the primary tumor and bone marrow biopsy, while the other 30 were unique to the index tumor, indicating accumulation of de novo mutations during therapy. Furthermore, transcriptome sequencing on the 3 tumors demonstrated only 3 out of the 15 commonly mutated genes (LPAR1, GATA2, and NUFIP1) had high level of expression of the mutant alleles, suggesting potential oncogenic driver roles of these mutated genes. Among them, the druggable G-protein coupled receptor LPAR1 was highly expressed in all tumors. Cells expressing the LPAR1 R163W mutant demonstrated a significantly increased motility through elevated Rho signaling, but had no effect on growth. Therefore, this study highlights the need for multiple biopsies and sequencing during progression of a cancer and combinatorial DNA and RNA sequencing approach for systematic identification of expressed driver mutations.	GRCh37/hg19				Yes	CAPZB,ZSWIM5;CDC45,SEPT5;CSMD2,ST6GALNAC3;DENND2C,EPHA5;DENND2C,LPHN3;ECE1,LAPTM5;EIF4G3,CSF3R;EPHB2,ADC;FHAD1,FHL3;HIST2H2AB,EPHA5;HIST2H2AB,TSC22D1;HIST2H2AC,TSC22D1;HIST2H2BE,VPS45;LPHN3,EPHA5;MAGI3,DENND2C;MAGI3,EPHA5;MAGI3,LPHN3;MAGI3,PLEKHO1;MAGI3,VPS45;PLEKHO1,EPHA5;PLEKHO1,LPHN3;RSPH6A,SYMPK;SEPT5,GP1BB;VPS45,EPHA5;ZBTB40,EPHB2;ZNF26,ZNF84
CTDB0355	Research	25625332	Castro-Vega LJ, Letouze E, Burnichon N, Buffet A, Disderot PH, Khalifa E, Loriot C, Elarouci N, Morin A, Menara M, Lepoutre-Lussey C, Badoual C, Sibony M, Dousset B, Libe R, Zinzindohoue F, Plouin PF, Bertherat J, Amar L, de Reynies A, Favier J, Gimenez-Roqueplo AP	Multi-omics analysis defines core genomic alterations in pheochromocytomas and paragangliomas	Nature Communications	2015 Jan 	1,5,17	Pheochromocytomas and paragangliomas	SNP Array	Homo sapiens	37	Illumina HumanCNV610-Quad v1.0. Hybridization				INSERM, UMR970, Paris-Cardiovascular Research Center, F-75015 Paris, France 	Pheochromocytomas and paragangliomas (PCCs/PGLs) are neural crest-derived tumours with a very strong genetic component. Here we report the first integrated genomic examination of a large collection of PCC/PGL. SNP array analysis reveals distinct copy-number patterns associated with genetic background. Whole-exome sequencing shows a low mutation rate of 0.3 mutations per megabase, with few recurrent somatic mutations in genes not previously associated with PCC/PGL. DNA methylation arrays and miRNA sequencing identify DNA methylation changes and miRNA expression clusters strongly associated with messenger RNA expression profiling. Overexpression of the miRNA cluster 182/96/183 is specific in SDHB-mutated tumours and induces malignant traits, whereas silencing of the imprinted DLK1-MEG3 miRNA cluster appears as a potential driver in a subgroup of sporadic tumours. Altogether, the complete genomic landscape of PCC/PGL is mainly driven by distinct germline and/or somatic mutations in susceptibility genes and reveals different molecular entities, characterized by a set of unique genomic alterations. 	GRCh37/hg19				Yes	NA
CTDB0356	Research	25625332	Castro-Vega LJ, Letouze E, Burnichon N, Buffet A, Disderot PH, Khalifa E, Loriot C, Elarouci N, Morin A, Menara M, Lepoutre-Lussey C, Badoual C, Sibony M, Dousset B, Libe R, Zinzindohoue F, Plouin PF, Bertherat J, Amar L, de Reynies A, Favier J, Gimenez-Roqueplo AP	Multi-omics analysis defines core genomic alterations in pheochromocytomas and paragangliomas	Nature Communications	2015 Jan 	1,5,17	Pheochromocytomas and paragangliomas	SNP Array	Homo sapiens	49	Illumina HumanCNV610-Quad v1.0. Hybridization				INSERM, UMR970, Paris-Cardiovascular Research Center, F-75015 Paris, France 	Pheochromocytomas and paragangliomas (PCCs/PGLs) are neural crest-derived tumours with a very strong genetic component. Here we report the first integrated genomic examination of a large collection of PCC/PGL. SNP array analysis reveals distinct copy-number patterns associated with genetic background. Whole-exome sequencing shows a low mutation rate of 0.3 mutations per megabase, with few recurrent somatic mutations in genes not previously associated with PCC/PGL. DNA methylation arrays and miRNA sequencing identify DNA methylation changes and miRNA expression clusters strongly associated with messenger RNA expression profiling. Overexpression of the miRNA cluster 182/96/183 is specific in SDHB-mutated tumours and induces malignant traits, whereas silencing of the imprinted DLK1-MEG3 miRNA cluster appears as a potential driver in a subgroup of sporadic tumours. Altogether, the complete genomic landscape of PCC/PGL is mainly driven by distinct germline and/or somatic mutations in susceptibility genes and reveals different molecular entities, characterized by a set of unique genomic alterations. 	GRCh37/hg19				Yes	NA
CTDB0357	Research	25625332	Castro-Vega LJ, Letouze E, Burnichon N, Buffet A, Disderot PH, Khalifa E, Loriot C, Elarouci N, Morin A, Menara M, Lepoutre-Lussey C, Badoual C, Sibony M, Dousset B, Libe R, Zinzindohoue F, Plouin PF, Bertherat J, Amar L, de Reynies A, Favier J, Gimenez-Roqueplo AP	Multi-omics analysis defines core genomic alterations in pheochromocytomas and paragangliomas	Nature Communications	2015 Jan 	1,5,17	Pheochromocytomas and paragangliomas	SNP Array	Homo sapiens	188	Illumina HumanCNV610-Quad v1.0. Hybridization				INSERM, UMR970, Paris-Cardiovascular Research Center, F-75015 Paris, France 	Pheochromocytomas and paragangliomas (PCCs/PGLs) are neural crest-derived tumours with a very strong genetic component. Here we report the first integrated genomic examination of a large collection of PCC/PGL. SNP array analysis reveals distinct copy-number patterns associated with genetic background. Whole-exome sequencing shows a low mutation rate of 0.3 mutations per megabase, with few recurrent somatic mutations in genes not previously associated with PCC/PGL. DNA methylation arrays and miRNA sequencing identify DNA methylation changes and miRNA expression clusters strongly associated with messenger RNA expression profiling. Overexpression of the miRNA cluster 182/96/183 is specific in SDHB-mutated tumours and induces malignant traits, whereas silencing of the imprinted DLK1-MEG3 miRNA cluster appears as a potential driver in a subgroup of sporadic tumours. Altogether, the complete genomic landscape of PCC/PGL is mainly driven by distinct germline and/or somatic mutations in susceptibility genes and reveals different molecular entities, characterized by a set of unique genomic alterations. 	GRCh37/hg19				Yes	NA
CTDB0358	Research	22362584	Natrajan R, Mackay A, Lambros MB, Weigelt B, Wilkerson PM, Manie E, Grigoriadis A, A'hern R, van der Groep P, Kozarewa I, Popova T, Mariani O, Turajlic S, Furney SJ, Marais R, Rodruigues DN, Flora AC, Wai P, Pawar V, McDade S, Carroll J, Stoppa-Lyonnet D, Green AR, Ellis IO, Swanton C, van Diest P, Delattre O, Lord CJ, Foulkes WD, Vincent-Salomon A, Ashworth A, Henri Stern M, Reis-Filho JS	A whole-genome massively parallel sequencing analysis of BRCA1 mutant oestrogen receptor-negative and -positive breast cancers	The Journal of Pathology	2012 May	6,X	Breast cancer	Next Generation Sequencing	Homo sapiens	BRCA1/ER+BC	Complete Genomics				The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London, SW3 6JB, UK	BRCA1 encodes a tumour suppressor protein that plays pivotal roles in homologous recombination (HR) DNA repair, cell-cycle checkpoints, and transcriptional regulation. BRCA1 germline mutations confer a high risk of early-onset breast and ovarian cancer. In more than 80% of cases, tumours arising in BRCA1 germline mutation carriers are oestrogen receptor (ER)-negative; however, up to 15% are ER-positive. It has been suggested that BRCA1 ER-positive breast cancers constitute sporadic cancers arising in the context of a BRCA1 germline mutation rather than being causally related to BRCA1 loss-of-function. Whole-genome massively parallel sequencing of ER-positive and ER-negative BRCA1 breast cancers, and their respective germline DNAs, was used to characterize the genetic landscape of BRCA1 cancers at base-pair resolution. Only BRCA1 germline mutations, somatic loss of the wild-type allele, and TP53 somatic mutations were recurrently found in the index cases. BRCA1 breast cancers displayed a mutational signature consistent with that caused by lack of HR DNA repair in both ER-positive and ER-negative cases. Sequencing analysis of independent cohorts of hereditary BRCA1 and sporadic non-BRCA1 breast cancers for the presence of recurrent pathogenic mutations and/or homozygous deletions found in the index cases revealed that DAPK3, TMEM135, KIAA1797, PDE4D, and GATA4 are potential additional drivers of breast cancers. This study demonstrates that BRCA1 pathogenic germline mutations coupled with somatic loss of the wild-type allele are not sufficient for hereditary breast cancers to display an ER-negative phenotype, and has led to the identification of three potential novel breast cancer genes (ie DAPK3, TMEM135, and GATA4).	GRCh37/hg19				Yes	SUPT6H,ARHGAP12;EXT2,TTC17
CTDB0359	Research	22237106	Zhang J, Ding L, Holmfeldt L, Wu G, Heatley SL, Payne-Turner D, Easton J, Chen X, Wang J, Rusch M, Lu C, Chen SC, Wei L, Collins-Underwood JR, Ma J, Roberts KG, Pounds SB, Ulyanov A, Becksfort J, Gupta P, Huether R, Kriwacki RW, Parker M, McGoldrick DJ, Zhao D, Alford D, Espy S, Bobba KC, Song G, Pei D, Cheng C, Roberts S, Barbato MI, Campana D, Coustan-Smith E, Shurtleff SA, Raimondi SC, Kleppe M, Cools J, Shimano KA, Hermiston ML, Doulatov S, Eppert K, Laurenti E, Notta F, Dick JE, Basso G, Hunger SP, Loh ML, Devidas M, Wood B, Winter S, Dunsmore KP, Fulton RS, Fulton LL, Hong X, Harris CC, Dooling DJ, Ochoa K, Johnson KJ, Obenauer JC, Evans WE, Pui CH, Naeve CW, Ley TJ, Mardis ER, Wilson RK, Downing JR, Mullighan CG	The genetic basis of early T-cell precursor acute lymphoblastic leukaemia	Nature	2012 Jan 	1,11,12	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	STJALL001		chr10:0-135374737:0;chr11:0-61155471:0;chr11:134436401-134452384:0;chr11:61155472-70912249:-1;chr11:70912250-77979119:0;chr11:77979120-79868685:-1;chr11:79868686-80914909:0;chr11:80914910-81015904:1;chr11:81015905-82756272:0;chr11:82756273-83023070:1;chr11:83023071-83642443:0;chr11:83642444-134436400:-1;chr12:0-0:0;chr12:1-4034408:1;chr12:11787382-11852551:-1;chr12:11852551-21227923:-1;chr12:21227923-22066294:1;chr12:22066294-26671330:-1;chr12:26671330-28194413:1;chr12:28194414-132349534:0;chr12:4034408-11787382:-1;chr13:0-36416293:0;chr13:114028001-114142980:0;chr13:36416294-114028000:-1;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-88827254:0;chr17:0-78774742:0;chr18:0-75851817:0;chr18:75851818-76106200:-1;chr18:76106201-76117153:0;chr19:0-63811651:0;chr1:0-635200:0;chr1:183681561-184318407:1;chr1:184318408-185391929:0;chr1:185391930-222493387:1;chr1:222493388-226744537:0;chr1:226744538-232978811:1;chr1:232978812-233022500:0;chr1:233022501-247149600:1;chr1:247149601-247249719:0;chr1:635201-8847300:-1;chr1:8847301-183681560:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-94419549:0;chr6:94419550-95073427:-1;chr6:95073428-170899992:0;chr7:0-99532387:0;chr7:142194036-142205270:0;chr7:142205271-158821462:1;chr7:158821463-158821424:0;chr7:99532388-142194035:1;chr8:0-180567:0;chr8:180568-25681600:1;chr8:25681601-25681600:0;chr8:25681601-89256109:1;chr8:89256110-146274826:0;chr9:0-80097141:0;chr9:103678699-140273252:0;chr9:80097142-103678698:-1;chrX:0-0:0;chrX:1-40412672:1;chrX:40412673-154913754:0;chrY:0-57772954:0	hs1:185391933-185391933,hs1:183681561-183681561;hs1:211055963-211055963,hs1:226744535-226744535;hs1:211056775-211056775,hs1:185394336-185394336;hs1:222493387-222493387,hs1:211057022-211057022;hs4:6947258-6947258,hs4:6960707-6960707;hs4:53945291-53945291,hs7:27172066-27172066;hs4:53945348-53945348,hs8:89256006-89256006;hs6:95073427-95073427,hs11:80914910-80914910;hs7:27171985-27171985,hsX:40412627-40412627;hs10:21278245-21278245,hs10:21279404-21279404;hs11:81015904-81015904,hs6:94419550-94419550;hs11:43874661-43874661,hs11:77957935-77957935;hs11:61155472-61155472,hs11:70912250-70912250;hs11:77979120-77979120,hs11:82756273-82756273;hs11:79868681-79868681,hs11:43875121-43875121;hs11:79873315-79873315,hs11:83007059-83007059;hs11:83023070-83023070,hs12:28194412-28194412;hs12:4034408-4034408,hs12:21227923-21227923;hs12:11787386-11787386,hs12:11852551-11852551;hs12:22066294-22066294,hs12:26671330-26671330;hs14:21977845-21977845,hs14:21988920-21988920;hsX:40412669-40412669,hs8:89256109-89256109	A2M;A2ML1;AASDHPPT;ABCB10;ABCC9;ABCG4;ACAD8;ACAP3;ACAT1;ACOT7;ACRBP;ACRV1;ACSM4;ACTA1;ACTN2;ACTN3;ACTRT2;ACY3;ADAMTS15;ADAMTS8;ADIPOR1;ADIPOR2;ADORA1;ADRBK1;ADSS;AEBP2;AGRN;AGT;AHCTF1;AHNAK;AICDA;AIDA;AIP;AJAP1;AKAP3;ALDH3B1;ALDH3B2;ALG9;ALKBH3;ALKBH8;AMICA1;AMOTL1;ANGEL2;ANGPTL5;ANKK1;ANKRD13D;ANKRD49;ANO1;ANO2;APLP2;APOA1;APOA4;APOA5;APOBEC1;APOC3;APOLD1;ARCN1;ARHGDIB;ARHGEF16;ARID4B;ARL2;ARL8A;ARNTL2;ART4;ARV1;ASPM;ASRGL1;ATAD3A;ATAD3B;ATAD3C;ATF3;ATF7IP;ATG2A;ATL3;ATN1;ATP2B4;ATPGD1;AURKAIP1;AURKAPS1;AVPR1B;B3GALNT2;B3GALT2;B3GALT6;B3GAT3;B4GALNT3;BAD;BANF1;BATF2;BATF3;BBS1;BCAT1;BCL2L14;BHLHE41;BPNT1;BTG2;C12orf11;C12orf32;C12orf36;C12orf39;C12orf4;C12orf5;C12orf53;C12orf57;C12orf59;C12orf60;C12orf67;C12orf69;C12orf70;C12orf71;C12orf77;C1orf100;C1orf101;C1orf106;C1orf107;C1orf115;C1orf116;C1orf124;C1orf131;C1orf150;C1orf159;C1orf170;C1orf174;C1orf198;C1orf229;C1orf31;C1orf57;C1orf70;C1orf86;C1orf96;C1R;C1RL;C1S;C3AR1;C7orf34;C8orf48;C8orf58;C9orf129;C9orf153;C9orf156;C9orf170;CACNA1C;CACNA2D4;CALML6;CAMTA1;CAPN9;CAPZA3;CASC1;CCDC27;CCDC77;CCND2;CD163L1;CDKN1B;CEP170;CHML;CHRM3;CMAS;CNST;COG2;CREBL2;DAD1L;DCP1B;DDX47;DERA;DISC1;DISC2;DLG2;DUSP16;DUSP5P;EDARADD;EFCAB2;EFCAB4B;EGLN1;EMP1;EPS8;ERC1;ERO1LB;ERP27;ETNK1;ETV6;EXO1;EXOC8;FAM138D;FAM36A;FAM89A;FBXL14;FGFR1OP2;FH;FKBP4;FOXM1;GALNT2;GNPAT;GOLT1B;GPR19;GYS2;HMCN1;HSN2;IAPP;IFLTD1;IQSEC3;ITFG2;ITPR2;KCNJ8;KDM5A;KIAA0528;KLHDC5;KRAS;LDHB;LOC100130522;LOC100133893;LOC100292680;LRMP;LRTM2;LYRM5;MED21;MIR920;MRPS35;NINJ2;NVL;ODZ4;PPFIBP1;PTHLH;PYROXD1;RASSF8;RECQL;REP15;RNF187;RPLP0P2;SLCO1A2;SLCO1B1;SOX5;SSPN;ST8SIA1;STK38L;TATDN3;TM7SF3;	Department of Computational Biology and Bioinformatics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA	Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole-genome sequencing of 12 ETP ALL cases and assessed the frequency of the identified somatic mutations in 94 T-cell acute lymphoblastic leukaemia cases. ETP ALL was characterized by activating mutations in genes regulating cytokine receptor and RAS signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF), inactivating lesions disrupting haematopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1 and EP300) and histone-modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of recurrent mutation including DNM2, ECT2L and RELN. The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haematopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL.	NCBI 36/hg18		phs000340		Yes	NA
CTDB0360	Research	22237106	Zhang J, Ding L, Holmfeldt L, Wu G, Heatley SL, Payne-Turner D, Easton J, Chen X, Wang J, Rusch M, Lu C, Chen SC, Wei L, Collins-Underwood JR, Ma J, Roberts KG, Pounds SB, Ulyanov A, Becksfort J, Gupta P, Huether R, Kriwacki RW, Parker M, McGoldrick DJ, Zhao D, Alford D, Espy S, Bobba KC, Song G, Pei D, Cheng C, Roberts S, Barbato MI, Campana D, Coustan-Smith E, Shurtleff SA, Raimondi SC, Kleppe M, Cools J, Shimano KA, Hermiston ML, Doulatov S, Eppert K, Laurenti E, Notta F, Dick JE, Basso G, Hunger SP, Loh ML, Devidas M, Wood B, Winter S, Dunsmore KP, Fulton RS, Fulton LL, Hong X, Harris CC, Dooling DJ, Ochoa K, Johnson KJ, Obenauer JC, Evans WE, Pui CH, Naeve CW, Ley TJ, Mardis ER, Wilson RK, Downing JR, Mullighan CG	The genetic basis of early T-cell precursor acute lymphoblastic leukaemia	Nature	2012 Jan 	2,9	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	STJALL002		chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-8545706:0;chr12:27480227-132349534:0;chr12:8545707-27480226:-1;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-75555812:0;chr16:75555813-75582197:1;chr16:75582198-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-0:0;chr19:1-63793700:1;chr19:63793701-63811651:0;chr1:0-91721921:0;chr1:100818677-103024856:-1;chr1:103024857-247249719:0;chr1:91721922-93409158:-1;chr1:93409159-93589481:0;chr1:93589482-97369434:-1;chr1:97369435-97385719:0;chr1:97385720-97385843:-1;chr1:97385844-100818676:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-0:0;chr22:1-49491400:1;chr22:49491401-49691432:0;chr2:0-206579746:0;chr2:206579747-207028592:1;chr2:207028592-207725565:1;chr2:207725565-209229004:1;chr2:209229004-210601250:1;chr2:210601250-210911367:1;chr2:210911367-211035238:1;chr2:211035238-213106802:1;chr2:213106802-213129128:1;chr2:213129128-242651100:-1;chr2:242651101-242951149:0;chr3:0-199501827:0;chr4:0-191273063:0;chr5:0-180857866:0;chr6:0-30822391:0;chr6:30822392-32895237:-1;chr6:32895238-170899992:0;chr7:0-50144815:0;chr7:50144816-50421851:-1;chr7:50421852-158821424:0;chr8:0-115945867:0;chr8:115945868-116017817:1;chr8:116017818-146274826:0;chr9:0-29999:0;chr9:104248373-105070517:-1;chr9:105070518-118874264:0;chr9:118874265-120461292:-1;chr9:120461293-140273252:0;chr9:21096626-22880450:-1;chr9:22880450-70510800:-1;chr9:30000-21096626:-1;chr9:70510800-70705182:-1;chr9:70705182-72993063:-1;chr9:72993063-73941820:-1;chr9:73941820-76718037:-1;chr9:76718037-77929470:-1;chr9:77929470-78271717:-1;chr9:78271718-78705695:0;chr9:78705696-83900722:-1;chr9:83900723-87880619:0;chr9:87880620-89388052:-1;chr9:89388053-104248372:0;chrX:0-68505335:0;chrX:68505336-69493999:1;chrX:69493999-69701501:1;chrX:69701501-70174245:1;chrX:70174245-70800355:1;chrX:70800356-154913754:0;chrY:0-57772954:0	hs1:91721922-91721922,hs1:97385720-97385720;hs1:93589482-93589482,hs1:100818677-100818677;hs1:97385843-97385843,hs1:97369434-97369434;hs1:103024856-103024856,hs1:93409158-93409158;hs2:213106802-213106802,hs2:207028592-207028592;hs2:213129128-213129128,hs2:207725565-207725565;hs2:209229004-209229004,hsX:68505336-68505336;hs7:50144816-50144816,hs7:50421851-50421851;hs8:116017817-116017817,hs8:115945868-115945868;hs9:21096626-21096626,hs9:118874265-118874265;hs9:72993063-72993063,hs9:78271717-78271717;hs9:76718037-76718037,hs9:105070517-105070517;hs9:83900722-83900722,hs9:70705182-70705182;hs9:87880620-87880620,hs9:89388052-89388052;hs9:104248373-104248373,hs9:120461292-120461292;hs9:126600441-126600441,hs9:126599797-126599797;hs12:11921859-11921859,hs2:206579740-206579740;hs12:91128883-91128883,hs12:27480226-27480226;hs16:75582197-75582197,hs16:75555813-75555813;hsX:69493999-69493999,hs2:210601250-210601250;hsX:70174245-70174245,hs2:211035238-211035238;hsX:70800355-70800355,hs2:206579747-206579747;hsX:70800356-70800356,hs12:11922106-11922106;hsX:69550634-69550634,hsX:69551230-69551230	AAMP;ABCA12;ABCB6;ACADL;ACCN4;ACER2;ACO1;ACSL3;ADAM23;ADAMTSL1;AGAP1;AGFG1;AGXT;AK3;ALDH1A1;ALDH1B1;ALPI;ALPP;ALPPL2;ANKMY1;ANKRD20A1;ANKRD20A2;ANKRD20A3;ANKRD20A4;ANKZF1;ANO7;ANXA1;ANXA2P2;AP1S3;APTX;AQP12A;AQP12B;AQP3;AQP7;AQP7P1;AQP7P2;AQP7P3;ARID3C;ARL4C;ARMC9;ARPC2;ASTN2;B4GALT1;BAG1;BG201338;BNC2;C12orf60;C2orf67;C2orf80;C6orf10;C6orf15;C6orf25;C9orf100;C9orf11;C9orf122;C9orf123;C9orf128;C9orf135;C9orf150;C9orf153;C9orf170;C9orf40;C9orf41;C9orf46;C9orf53;C9orf57;C9orf66;C9orf68;C9orf70;C9orf85;C9orf93;C9orf95;CBWD1;CCNYL1;CD274;CDC37L1;CDKN2A;CDKN2B;CDKN2BAS;CEP78;CER1;CNTLN;CPO;CREB1;CRYGA;CRYGB;CRYGC;CRYGD;CYLC2;DAPK1;DENND4C;DMRT1;DMRT2;DMRT3;DMRTA1;DYTN;EEF1B2;ERBB4;FAM108B1;FAM119A;FAM122A;FAM189A2;FASTKD2;FLJ43859;FLJ43950;FLJ44082;FLJ46321;FOXB2;FXN;FZD5;GAS1;GCNT1;GDA;GNA14;GNAQ;GOLM1;GPR1;IDH1;IFNA1;IFNA10;IFNA13;IFNA14;IFNA16;IFNA17;IFNA2;IFNA21;IFNA4;IFNA5;IFNA6;IFNA7;IFNA8;IFNE;IFNW1;INO80D;ISCA1;KLF7;KLF9;LANCL1;LOC100130426;LOC29034;MAP2;MDH1B;MIR204;MIR548F2;MYL1;NDUFS1;OSTF1;PCSK5;PIKFYVE;PIP5K1B;PLEKHM3;PRKACG;PRUNE2;PSAT1;PTAR1;PTH2R;RFK;RORB;RPE;RPSAP9;SMC5;SNORA70C;SNORD51;TJP2;TLE1;TLE4;TLR4;TMC1;TMEM2;TRPM3;TRPM6;UNC80;VPS13A;ZCCHC6;ZDBF2;ZFAND5;	Department of Computational Biology and Bioinformatics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA	Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole-genome sequencing of 12 ETP ALL cases and assessed the frequency of the identified somatic mutations in 94 T-cell acute lymphoblastic leukaemia cases. ETP ALL was characterized by activating mutations in genes regulating cytokine receptor and RAS signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF), inactivating lesions disrupting haematopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1 and EP300) and histone-modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of recurrent mutation including DNM2, ECT2L and RELN. The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haematopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL.	NCBI 36/hg18		phs000340		Yes	C2orf67,KIF4A;ETV6,INO80D;INO80D,BG201338
CTDB0361	Research	22237106	Zhang J, Ding L, Holmfeldt L, Wu G, Heatley SL, Payne-Turner D, Easton J, Chen X, Wang J, Rusch M, Lu C, Chen SC, Wei L, Collins-Underwood JR, Ma J, Roberts KG, Pounds SB, Ulyanov A, Becksfort J, Gupta P, Huether R, Kriwacki RW, Parker M, McGoldrick DJ, Zhao D, Alford D, Espy S, Bobba KC, Song G, Pei D, Cheng C, Roberts S, Barbato MI, Campana D, Coustan-Smith E, Shurtleff SA, Raimondi SC, Kleppe M, Cools J, Shimano KA, Hermiston ML, Doulatov S, Eppert K, Laurenti E, Notta F, Dick JE, Basso G, Hunger SP, Loh ML, Devidas M, Wood B, Winter S, Dunsmore KP, Fulton RS, Fulton LL, Hong X, Harris CC, Dooling DJ, Ochoa K, Johnson KJ, Obenauer JC, Evans WE, Pui CH, Naeve CW, Ley TJ, Mardis ER, Wilson RK, Downing JR, Mullighan CG	The genetic basis of early T-cell precursor acute lymphoblastic leukaemia	Nature	2012 Jan 	1,4,5,9,10	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	STJALL003		chr10:0-7430589:0;chr10:24920178-63614386:0;chr10:63614387-66275073:-1;chr10:66275074-68176655:0;chr10:68176656-68950041:-1;chr10:68950042-76649371:0;chr10:7430590-24920177:-1;chr10:76649372-78529151:-1;chr10:78529152-80761759:0;chr10:80761760-96821276:-1;chr10:96821277-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-97862275:0;chr14:97862276-98116066:-1;chr14:98116067-106368585:0;chr15:0-100338915:0;chr16:0-84850282:0;chr16:84850283-85033002:-1;chr16:85033003-88827254:0;chr17:0-78774742:0;chr18:0-60008337:0;chr18:60008338-60413979:-1;chr18:60413980-61115803:0;chr18:61115804-61276902:-1;chr18:61276903-76117153:0;chr19:0-63811651:0;chr1:0-65943700:0;chr1:106673274-107678605:-1;chr1:107678606-107716341:0;chr1:107716342-144004701:-1;chr1:144004702-247249719:0;chr1:65943701-77157200:-1;chr1:77157201-78144610:0;chr1:78144611-78755005:-1;chr1:78755006-106673273:0;chr20:0-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-199501827:0;chr4:0-84837682:0;chr4:125893225-135358957:-1;chr4:135358958-191273063:0;chr4:84837683-96243984:-1;chr4:96243985-125893224:0;chr5:0-6776459:0;chr5:116236493-116328132:1;chr5:116328133-117950913:0;chr5:117950914-122015240:-1;chr5:122015241-180857866:0;chr5:13467228-61592429:0;chr5:61592430-67173064:-1;chr5:67173065-116236492:0;chr5:6776460-7052197:-1;chr5:7052198-7070447:0;chr5:7070448-13467227:-1;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-146274826:0;chr9:0-15805305:0;chr9:15805306-15811941:1;chr9:15811942-20310301:0;chr9:20310302-21615196:-1;chr9:21615196-21778860:-1;chr9:21778860-22282780:-1;chr9:22282780-31089571:-1;chr9:31089571-31827466:-1;chr9:31827467-38084084:0;chr9:38084085-38301919:-1;chr9:38301920-38906324:0;chr9:38906325-38993888:-1;chr9:38993889-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0	hs1:78144611-78144611,hs1:65935999-65935999;hs1:107716342-107716342,hs1:77157121-77157121;hs1:163486878-163486878,hs1:163486903-163486903;hs1:65943763-65943763,hs10:24920177-24920177;hs1:107678605-107678605,hs10:66275073-66275073;hs4:84837683-84837683,hs4:135358957-135358957;hs4:159764088-159764088,hs10:7430590-7430590;hs4:159770296-159770296,hs10:24923739-24923739;hs5:67173064-67173064,hs4:135348611-135348611;hs5:6776460-6776460,hs5:7070448-7070448;hs5:117950914-117950914,hs5:116328132-116328132;hs5:7052197-7052197,hs10:66301865-66301865;hs5:61592430-61592430,hs10:96821276-96821276;hs9:21778860-21778860,hs9:38301919-38301919;hs9:38084085-38084085,hs9:22282780-22282780;hs9:38993888-38993888,hs9:21615196-21615196;hs10:66275072-66275072,hs1:107678605-107678605;hs10:80761760-80761760,hs1:78755007-78755007;hs10:63614387-63614387,hs4:96243984-96243984;hs10:66301858-66301858,hs4:125893225-125893225;hs10:24923743-24923743,hs10:68950041-68950041;hs10:76649372-76649372,hs10:78529151-78529151;hs16:84850283-84850283,hs14:98116066-98116066;hs16:66071321-66071321,hs16:66071625-66071625;hs18:60008338-60008338,hs18:61276902-61276902	ABCG2;ACADM;ACBD7;ACTA2;ADAM30;ADAMTS6;ADCY2;ADO;ADORA3;AFF1;AGAP11;AHCYL1;AKNAD1;ALX3;AMIGO1;AMPD1;AMPD2;ANKRD1;ANKRD13C;ANKRD22;ANKRD33B;ANXA11;ANXA2P3;AP4B1;ARHGAP21;ARHGAP24;ARL5B;ARMC3;ASB17;ATAD1;ATOH1;ATP1A1;ATP5C1;ATP5F1;ATXN7L2;BCAS2;BCL2L15;BEND7;BMI1;BMPR1A;BMPR1B;BTAF1;C10orf11;C10orf111;C10orf113;C10orf114;C10orf116;C10orf140;C10orf4;C10orf41;C10orf47;C10orf57;C10orf58;C10orf67;C10orf99;C1orf103;C1orf141;C1orf152;C1orf161;C1orf162;C1orf173;C1orf183;C1QL3;C4orf12;C4orf29;C4orf33;C4orf36;C5orf44;C5orf49;C9orf11;C9orf53;C9orf72;C9orf82;CACNB2;CAMK1D;CCDC3;CCT5;CD180;CDC123;CDKN2A;CDKN2B;CDKN2B-AS1;CDNF;CDS1;CENPK;CEP55;CFLP1;CH25H;CMBL;COMMD3;COMTD1;CPEB3;CRYZ;CTH;CTNNA3;CTNND2;CYP26A1;CYP26C1;CYP2C18;DAP;DEPDC1;DIMT1L;DIRAS3;DMP1;DMRTA1;DMXL1;DNAJB4;DSPP;DTWD2;EGR2;ELAVL2;ERBB2IP;FAM13A;FAM13AOS;FAM159B;FAM170A;FAM173B;FAM190A;FASTKD3;FAT4;FPGT;FTMT;FUBP1;GADD45A;GIPC2;GNG12;GPR177;GPRIN3;GRID2;HERC3;HERC5;HERC6;HHLA3;HPGDS;HSD17B11;HSD17B4;HSPA4L;HTR1A;IFNA1;IFNA10;IFNA13;IFNA14;IFNA16;IFNA17;IFNA2;IFNA21;IFNA4;IFNA5;IFNA6;IFNA7;IFNA8;IFNB1;IFNE;IFNK;IFNW1;IFT74;IL12RB2;IL23R;INSL5;INTU;IPO11;ISCA1L;JMJD1C;KCNMA1;KIAA1797;KIF2A;KLHL9;LARP1B;LHX8;LINGO2;LOC554202;LOC732275;LOC84989;LOX;LRRC19;LRRC40;LRRC7;LRRC70;LRRTM3;MARCH6;MAST4;MFSD8;MGC27382;MIR1296;MIR31;MIR873;MIR876;MOBKL2B;MTAP;MTRR;NCRNA00032;NEXN;NLN;NRBF2;NTNG1;PABPC4L;PCDH10;PGRMC2;PHF17;PLAA;PLK4;POLS;PPWD1;PRMT6;PRR16;PTGFR;REEP3;RGS7BP;RNF180;ROPN1L;RTKN2;RXFP1;SCLT1;SDCCAG10;SEMA5A;SFMBT2;SFRS12IP1;SLC25A31;SNCAIP;SNORD123;SRFBP1;ST6GALNAC5;TAS2R1;TEK;TNFAIP8;TUSC1;VDAC2;ZNF365;ZNF474;ZNF503;	Department of Computational Biology and Bioinformatics, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA	Early T-cell precursor acute lymphoblastic leukaemia (ETP ALL) is an aggressive malignancy of unknown genetic basis. We performed whole-genome sequencing of 12 ETP ALL cases and assessed the frequency of the identified somatic mutations in 94 T-cell acute lymphoblastic leukaemia cases. ETP ALL was characterized by activating mutations in genes regulating cytokine receptor and RAS signalling (67% of cases; NRAS, KRAS, FLT3, IL7R, JAK3, JAK1, SH2B3 and BRAF), inactivating lesions disrupting haematopoietic development (58%; GATA3, ETV6, RUNX1, IKZF1 and EP300) and histone-modifying genes (48%; EZH2, EED, SUZ12, SETD2 and EP300). We also identified new targets of recurrent mutation including DNM2, ECT2L and RELN. The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal and myeloid leukaemia haematopoietic stem cells. These findings suggest that addition of myeloid-directed therapies might improve the poor outcome of ETP ALL.	NCBI 36/hg18		phs000340		Yes	ARHGAP21,RXFP1;CTNNA3,ARHGAP21;NTNG1,ST6GALNAC5;RXFP1,SFMBT2
CTDB0362	Research	22832583	Jones DT, Jager N, Kool M, Zichner T, Hutter B, Sultan M, Cho YJ, Pugh TJ, Hovestadt V, Stutz AM, Rausch T, Warnatz HJ, Ryzhova M, Bender S, Sturm D, Pleier S, Cin H, Pfaff E, Sieber L, Wittmann A, Remke M, Witt H, Hutter S, Tzaridis T, Weischenfeldt J, Raeder B, Avci M, Amstislavskiy V, Zapatka M, Weber UD, Wang Q, Lasitschka B, Bartholomae CC, Schmidt M, von Kalle C, Ast V, Lawerenz C, Eils J, Kabbe R, Benes V, van Sluis P, Koster J, Volckmann R, Shih D, Betts MJ, Russell RB, Coco S, Tonini GP, Schuller U, Hans V, Graf N, Kim YJ, Monoranu C, Roggendorf W, Unterberg A, Herold-Mende C, Milde T, Kulozik AE, von Deimling A, Witt O, Maass E, Rossler J, Ebinger M, Schuhmann MU, Fruhwald MC, Hasselblatt M, Jabado N, Rutkowski S, von Bueren AO, Williamson D, Clifford SC, McCabe MG, Collins VP, Wolf S, Wiemann S, Lehrach H, Brors B, Scheurlen W, Felsberg J, Reifenberger G, Northcott PA, Taylor MD, Meyerson M, Pomeroy SL, Yaspo ML, Korbel JO, Korshunov A, Eils R, Pfister SM, Lichter P	Dissecting the genomic complexity underlying medulloblastoma	Nature	2012 Aug 	10	Medulloblastoma	Next Generation Sequencing	Homo sapiens	ICGC_MB23	Illumina				Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, Heidelberg 69120, Germany	Medulloblastoma is an aggressively growing tumour, arising in the cerebellum or medulla/brain stem. It is the most common malignant brain tumour in children, and shows tremendous biological and clinical heterogeneity. Despite recent treatment advances, approximately 40% of children experience tumour recurrence, and 30% will die from their disease. Those who survive often have a significantly reduced quality of life. Four tumour subgroups with distinct clinical, biological and genetic profiles are currently identified. WNT tumours, showing activated wingless pathway signalling, carry a favourable prognosis under current treatment regimens. SHH tumours show hedgehog pathway activation, and have an intermediate prognosis. Group 3 and 4 tumours are molecularly less well characterized, and also present the greatest clinical challenges. The full repertoire of genetic events driving this distinction, however, remains unclear. Here we describe an integrative deep-sequencing analysis of 125 tumour-normal pairs, conducted as part of the International Cancer Genome Consortium (ICGC) PedBrain Tumor Project. Tetraploidy was identified as a frequent early event in Group 3 and 4 tumours, and a positive correlation between patient age and mutation rate was observed. Several recurrent mutations were identified, both in known medulloblastoma-related genes (CTNNB1, PTCH1, MLL2, SMARCA4) and in genes not previously linked to this tumour (DDX3X, CTDNEP1, KDM6A, TBR1), often in subgroup-specific patterns. RNA sequencing confirmed these alterations, and revealed the expression of what are, to our knowledge, the first medulloblastoma fusion genes identified. Chromatin modifiers were frequently altered across all subgroups. These findings enhance our understanding of the genomic complexity and heterogeneity underlying medulloblastoma, and provide several potential targets for new therapeutics, especially for Group 3 and 4 patients.	GRCh37/hg19				Yes	NA
CTDB0363	Research	22832583	Jones DT, Jager N, Kool M, Zichner T, Hutter B, Sultan M, Cho YJ, Pugh TJ, Hovestadt V, Stutz AM, Rausch T, Warnatz HJ, Ryzhova M, Bender S, Sturm D, Pleier S, Cin H, Pfaff E, Sieber L, Wittmann A, Remke M, Witt H, Hutter S, Tzaridis T, Weischenfeldt J, Raeder B, Avci M, Amstislavskiy V, Zapatka M, Weber UD, Wang Q, Lasitschka B, Bartholomae CC, Schmidt M, von Kalle C, Ast V, Lawerenz C, Eils J, Kabbe R, Benes V, van Sluis P, Koster J, Volckmann R, Shih D, Betts MJ, Russell RB, Coco S, Tonini GP, Schuller U, Hans V, Graf N, Kim YJ, Monoranu C, Roggendorf W, Unterberg A, Herold-Mende C, Milde T, Kulozik AE, von Deimling A, Witt O, Maass E, Rossler J, Ebinger M, Schuhmann MU, Fruhwald MC, Hasselblatt M, Jabado N, Rutkowski S, von Bueren AO, Williamson D, Clifford SC, McCabe MG, Collins VP, Wolf S, Wiemann S, Lehrach H, Brors B, Scheurlen W, Felsberg J, Reifenberger G, Northcott PA, Taylor MD, Meyerson M, Pomeroy SL, Yaspo ML, Korbel JO, Korshunov A, Eils R, Pfister SM, Lichter P	Dissecting the genomic complexity underlying medulloblastoma	Nature	2012 Aug 	2	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MBRep_T53	Illumina			MYCN;GLI2	Division of Pediatric Neurooncology, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, Heidelberg 69120, Germany	Medulloblastoma is an aggressively growing tumour, arising in the cerebellum or medulla/brain stem. It is the most common malignant brain tumour in children, and shows tremendous biological and clinical heterogeneity. Despite recent treatment advances, approximately 40% of children experience tumour recurrence, and 30% will die from their disease. Those who survive often have a significantly reduced quality of life. Four tumour subgroups with distinct clinical, biological and genetic profiles are currently identified. WNT tumours, showing activated wingless pathway signalling, carry a favourable prognosis under current treatment regimens. SHH tumours show hedgehog pathway activation, and have an intermediate prognosis. Group 3 and 4 tumours are molecularly less well characterized, and also present the greatest clinical challenges. The full repertoire of genetic events driving this distinction, however, remains unclear. Here we describe an integrative deep-sequencing analysis of 125 tumour-normal pairs, conducted as part of the International Cancer Genome Consortium (ICGC) PedBrain Tumor Project. Tetraploidy was identified as a frequent early event in Group 3 and 4 tumours, and a positive correlation between patient age and mutation rate was observed. Several recurrent mutations were identified, both in known medulloblastoma-related genes (CTNNB1, PTCH1, MLL2, SMARCA4) and in genes not previously linked to this tumour (DDX3X, CTDNEP1, KDM6A, TBR1), often in subgroup-specific patterns. RNA sequencing confirmed these alterations, and revealed the expression of what are, to our knowledge, the first medulloblastoma fusion genes identified. Chromatin modifiers were frequently altered across all subgroups. These findings enhance our understanding of the genomic complexity and heterogeneity underlying medulloblastoma, and provide several potential targets for new therapeutics, especially for Group 3 and 4 patients.	GRCh37/hg19				Yes	NA
CTDB0364	Research	21892161	Bass AJ, Lawrence MS, Brace LE, Ramos AH, Drier Y, Cibulskis K, Sougnez C, Voet D, Saksena G, Sivachenko A, Jing R, Parkin M, Pugh T, Verhaak RG, Stransky N, Boutin AT, Barretina J, Solit DB, Vakiani E, Shao W, Mishina Y, Warmuth M, Jimenez J, Chiang DY, Signoretti S, Kaelin WG, Spardy N, Hahn WC, Hoshida Y, Ogino S, Depinho RA, Chin L, Garraway LA, Fuchs CS, Baselga J, Tabernero J, Gabriel S, Lander ES, Getz G, Meyerson M	Genomic sequencing of colorectal adenocarcinomas identifies a recurrent VTI1A-TCF7L2 fusion	Nature Genetics	2011 Sep 	1,3,6	Colorectal cancer	Next Generation Sequencing	Homo sapiens	CRC-3	Illumina GA-II	chr10:0-129527237:0;chr10:129527238-129783714:-1;chr10:129783715-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-5683448:0;chr16:5683449-5776175:-1;chr16:5776176-6331356:0;chr16:6331357-7095068:-1;chr16:6523054-6622896:-1;chr16:6749075-6769575:-1;chr16:6860343-6889417:-1;chr16:7095069-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-10754997:0;chr1:10754998-10897669:1;chr1:10897670-49446321:0;chr1:245318786-245412605:-1;chr1:245412606-247249719:0;chr1:49446322-49489944:-1;chr1:49489945-245318785:0;chr20:0-15034058:0;chr20:15034059-15057086:-1;chr20:15057087-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-57109388:0;chr2:57109389-57145561:-1;chr2:57145562-242951149:0;chr3:0-2683189:0;chr3:2683190-2761783:1;chr3:2761784-4787249:0;chr3:4787250-4815954:-1;chr3:4815955-5951263:0;chr3:5951264-5988489:-1;chr3:5988490-6559790:0;chr3:60213356-60616233:-1;chr3:60532986-60541605:1;chr3:60616234-199501827:0;chr3:6559791-7177138:1;chr3:6737767-7245547:1;chr3:6796695-6825146:-1;chr3:7245548-60213355:0;chr4:0-189926790:0;chr4:189926791-189997001:-1;chr4:189997002-190416475:0;chr4:190416476-190601298:-1;chr4:190601299-191273063:0;chr5:0-178065039:0;chr5:178065040-178899590:-1;chr5:178899591-180857866:0;chr6:0-39862556:0;chr6:39862557-40074147:-1;chr6:40074148-170899992:0;chr7:0-110547180:0;chr7:110547181-110729058:-1;chr7:110724998-110927085:1;chr7:110927086-158821424:0;chr8:0-120453229:0;chr8:120453230-120750651:-1;chr8:120750652-123860546:0;chr8:123860547-123862069:-1;chr8:123862070-128170552:0;chr8:128170553-128473966:1;chr8:128473967-146274826:0;chr9:0-10517408:0;chr9:10517409-10571170:1;chr9:10571171-26169649:0;chr9:26169650-26330710:-1;chr9:26330711-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0	hs1:224945390-224945390,hs1:233909251-233909251;hs1:240378413-240378413,hs1:245369879-245369879;hs1:224945525-224945525,hs1:233870037-233870037;hs1:233923401-233923401,hs1:236536122-236536122;hs1:236231922-236231922,hs1:237182872-237182872;hs1:245475793-245475793,hs3:5894391-5894391;hs1:236419236-236419236,hs3:5566303-5566303;hs1:235922389-235922389,hs3:4611675-4611675;hs1:235918361-235918361,hs3:11080171-11080171;hs1:5466610-5466610,hs3:7316755-7316755;hs1:233632828-233632828,hs3:5932076-5932076;hs1:236254591-236254591,hs3:5170554-5170554;hs1:5275710-5275710,hs3:5187100-5187100;hs1:5303622-5303622,hs3:8282035-8282035;hs1:236845686-236845686,hs3:10925011-10925011;hs1:245408838-245408838,hs3:2802655-2802655;hs1:237185816-237185816,hs3:8016594-8016594;hs1:5301538-5301538,hs3:6054295-6054295;hs1:233714631-233714631,hs3:6880142-6880142;hs1:245349054-245349054,hs3:3585460-3585460;hs1:224875793-224875793,hs3:3145867-3145867;hs1:236540834-236540834,hs3:2921314-2921314;hs1:224887091-224887091,hs3:3721322-3721322;hs1:235853269-235853269,hs3:6891109-6891109;hs1:233787690-233787690,hs3:3273593-3273593;hs1:235861396-235861396,hs3:8292875-8292875;hs1:244869048-244869048,hs3:7582747-7582747;hs1:233862655-233862655,hs5:178278887-178278887;hs1:245288005-245288005,hs5:178130481-178130481;hs2:53628330-53628330,hs2:53629451-53629451;hs2:60636921-60636921,hs2:60639951-60639951;hs2:151790755-151790755,hs9:135957853-135957853;hs3:6566468-6566468,hs3:7578764-7578764;hs3:3795729-3795729,hs3:5546204-5546204;hs3:2897939-2897939,hs3:6212189-6212189;hs3:2853112-2853112,hs3:5935342-5935342;hs3:5911194-5911194,hs3:7354302-7354302;hs3:2702507-2702507,hs3:8331278-8331278;hs3:3234820-3234820,hs3:6876658-6876658;hs3:3777596-3777596,hs3:3813752-3813752;hs3:5184088-5184088,hs3:7710801-7710801;hs3:4828423-4828423,hs3:7072509-7072509;hs3:2848467-2848467,hs3:7050326-7050326;hs3:6017124-6017124,hs3:7294182-7294182;hs3:10830132-10830132,hs5:178740539-178740539;hs3:3420430-3420430,hs5:178084387-178084387;hs3:6263160-6263160,hs5:178758089-178758089;hs3:6987679-6987679,hs5:178930532-178930532;hs5:132903613-132903613,hs5:133396590-133396590;hs5:87253239-87253239,hs8:91569923-91569923;hs5:171852562-171852562,hs9:106961714-106961714;hs6:27910367-27910367,hs6:106918619-106918619;hs6:66391721-66391721,hs6:75299704-75299704;hs6:127469925-127469925,hs6:128781514-128781514;hs6:42219015-42219015,hs6:106314863-106314863;hs6:27343409-27343409,hs6:108122202-108122202;hs6:51486682-51486682,hs6:53732426-53732426;hs6:65842350-65842350,hs6:106542981-106542981;hs6:75292810-75292810,hs6:104494212-104494212;hs6:44587618-44587618,hs6:65789992-65789992;hs6:42007977-42007977,hs6:107965922-107965922;hs6:25748686-25748686,hs6:41403970-41403970;hs6:64543890-64543890,hs6:107883335-107883335;hs6:25214697-25214697,hs6:27085335-27085335;hs6:27858841-27858841,hs6:106939044-106939044;hs6:34975611-34975611,hs6:106940055-106940055;hs6:41068797-41068797,hs6:49850765-49850765;hs6:41989443-41989443,hs6:51716875-51716875;hs6:51799583-51799583,hs6:52648225-52648225;hs6:25188883-25188883,hs6:108126806-108126806;hs6:25200375-25200375,hs6:106934554-106934554;hs6:26432414-26432414,hs6:107228180-107228180;hs6:27301141-27301141,hs6:42271311-42271311;hs6:27763751-27763751,hs6:36305598-36305598;hs6:34533687-34533687,hs6:107337718-107337718;hs6:36280941-36280941,hs6:44076259-44076259;hs6:38222706-38222706,hs6:40183593-40183593;hs6:39865154-39865154,hs6:105413847-105413847;hs6:40017876-40017876,hs6:49266572-49266572;hs6:41792828-41792828,hs6:58797510-58797510;hs6:42150556-42150556,hs6:107161417-107161417;hs6:127469928-127469928,hs6:128781518-128781518;hs6:43747579-43747579,hs6:106932132-106932132;hs6:42328572-42328572,hs6:65141693-65141693;hs6:40441124-40441124,hs6:54387076-54387076;hs6:25774577-25774577,hs6:46056103-46056103;hs6:33209107-33209107,hs6:107004069-107004069;hs6:39521662-39521662,hs6:107849873-107849873;hs6:50600569-50600569,hs6:53546383-53546383;hs6:55600617-55600617,hs6:63329817-63329817;hs6:33418159-33418159,hs6:107985099-107985099;hs7:65024392-65024392,hs7:153522286-153522286;hs7:153522268-153522268,hs8:76589412-76589412;hs10:19393206-19393206,hs10:19397392-19397392;hs16:27857950-27857950,hs16:31733613-31733613;hs16:34872868-34872868,hs16:46364585-46364585;hs22:27395596-27395596,hsX:92926657-92926657;hs22:27395907-27395907,hsX:92926675-92926675;	AGBL4;AIM1;ANKS1A;ARL8B;ASB3;ATG5;B3GALNT2;BRPF3;BYSL;C1orf127;C1orf229;C6orf132;C6orf223;C6orf41;CASZ1;CDC5L;CLIC5;CMAH;CNST;CNTN4;COL12A1;CRBN;DAAM2;EDEM1;EYS;FHIT;GCLC;GNG4;GRM7;GUCA1B;GUSBL2;HACE1;HIST1H2AK;HIST1H2BL;HIST1H4H;HMGCLL1;ITPKB;ITPR1;KHDRBS2;KIF6;LMCD1;LOC146481;LOC339535;LOC553137;LRRC1;LRRN1;LYPLA2P1;LYST;MED20;MOCS1;MRPS18A;MUT;NCR2;NPHP4;PACSIN1;PDSS2;PGK2;PKHD1;PLD5;PRDM1;PRSS16;QRSL1;RSPO3;RTN4IP1;RYR2;SCGN;SCML4;SLC6A1;SLC6A11;SOBP;TAF8;TBCE;TDRG1;TFAP2D;TFEB;TINAG;TMEM14A;TRERF1;TRNT1;UNC5CL;VN1R5;ZFAND3;ZNF124;ZNF669;ZNF670;ZP4;	Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA	Prior studies have identified recurrent oncogenic mutations in colorectal adenocarcinoma and have surveyed exons of protein-coding genes for mutations in 11 affected individuals. Here we report whole-genome sequencing from nine individuals with colorectal cancer, including primary colorectal tumors and matched adjacent non-tumor tissues, at an average of 30.7x and 31.9x coverage, respectively. We identify an average of 75 somatic rearrangements per tumor, including complex networks of translocations between pairs of chromosomes. Eleven rearrangements encode predicted in-frame fusion proteins, including a fusion of VTI1A and TCF7L2 found in 3 out of 97 colorectal cancers. Although TCF7L2 encodes TCF4, which cooperates with beta-catenin in colorectal carcinogenesis, the fusion lacks the TCF4 beta-catenin-binding domain. We found a colorectal carcinoma cell line harboring the fusion gene to be dependent on VTI1A-TCF7L2 for anchorage-independent growth using RNA interference-mediated knockdown. This study shows previously unidentified levels of genomic rearrangements in colorectal carcinoma that can lead to essential gene fusions and other oncogenic events.	NCBI 36/hg18		phs000374		Yes	ARL8B,GRM7;B3GALNT2,GRM7;BRPF3,C6orf223;BYSL,SOBP;CNTN4,GRM7;EYS,PDSS2;GRM7,RUFY1;ITPKB,GNG4;ITPR1,GRM7;KIF6,PDSS2;MED20,PKHD1;PKHD1,TMEM14A;RYR2,GRM7;SCGN,CLIC5;TRERF1,EYS
CTDB0365	Research	21892161	Bass AJ, Lawrence MS, Brace LE, Ramos AH, Drier Y, Cibulskis K, Sougnez C, Voet D, Saksena G, Sivachenko A, Jing R, Parkin M, Pugh T, Verhaak RG, Stransky N, Boutin AT, Barretina J, Solit DB, Vakiani E, Shao W, Mishina Y, Warmuth M, Jimenez J, Chiang DY, Signoretti S, Kaelin WG, Spardy N, Hahn WC, Hoshida Y, Ogino S, Depinho RA, Chin L, Garraway LA, Fuchs CS, Baselga J, Tabernero J, Gabriel S, Lander ES, Getz G, Meyerson M	Genomic sequencing of colorectal adenocarcinomas identifies a recurrent VTI1A-TCF7L2 fusion	Nature Genetics	2011 Sep 	4,8,16,20	Colorectal cancer	Next Generation Sequencing	Homo sapiens	CRC-4	Illumina GA-II	chr10:0-133602378:0;chr10:133602379-133603110:-1;chr10:133603111-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-106368585:0;chr15:0-100338915:0;chr16:0-46478965:0;chr16:46478966-46479751:-1;chr16:46479752-88827254:0;chr17:0-78774742:0;chr18:0-3252927:0;chr18:3252928-3667075:-1;chr18:3667076-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-18951205:0;chr20:18951206-18954029:1;chr20:18954030-23952550:0;chr20:23952551-23954112:-1;chr20:23954113-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-125106623:0;chr2:125106624-125349147:-1;chr2:125349148-242951149:0;chr3:0-199501827:0;chr4:0-14254204:0;chr4:127937758-127945196:-1;chr4:127945197-191273063:0;chr4:14254205-14874661:-1;chr4:14874662-60044608:0;chr4:60044609-60059497:1;chr4:60059498-97533520:0;chr4:97533521-97617439:-1;chr4:97617440-127937757:0;chr5:0-180857866:0;chr6:0-48438106:0;chr6:48438107-48604253:-1;chr6:48604254-170899992:0;chr7:0-153554788:0;chr7:153554789-153709348:-1;chr7:153709349-158821424:0;chr8:0-41184493:0;chr8:137736983-138443498:-1;chr8:138443499-146274826:0;chr8:41184494-41861964:-1;chr8:41861965-52186318:0;chr8:52186319-52186587:-1;chr8:52186588-137736982:0;chr9:0-140273252:0;chrX:0-154913754:0;chrY:0-57772954:0	hs18:56258628-56258628,hs18:58362793-58362793;hs18:44496014-44496014,hs18:57443167-57443167;hs18:45023683-45023683,hs18:58380361-58380361;hs8:37328910-37328910,hs20:9561906-9561906;hs8:35575394-35575394,hs20:36595752-36595752;hs20:11072897-11072897,hs20:18064337-18064337;hs20:18085103-18085103,hs20:37021184-37021184;hs8:35357822-35357822,hs8:40866668-40866668;hs20:11078572-11078572,hs20:16865475-16865475;hs8:40564418-40564418,hs8:41258684-41258684;hs8:38794152-38794152,hs20:15734259-15734259;hs8:32575936-32575936,hs20:19499614-19499614;hs20:9579492-9579492,hs20:11068460-11068460;hs8:29956507-29956507,hs8:40870381-40870381;hs8:40568862-40568862,hs8:41210874-41210874;hs8:33309871-33309871,hs20:17303124-17303124;hs8:25088587-25088587,hs20:18210598-18210598;hs8:30408156-30408156,hs20:11069502-11069502;hs20:15506293-15506293,hs20:18142088-18142088;hs20:18162173-18162173,hs20:21266868-21266868;hs8:30530516-30530516,hs8:37326190-37326190;hs20:11072781-11072781,hs20:19498233-19498233;hs20:17295462-17295462,hs20:18952001-18952001;hs20:19302660-19302660,hs20:25291885-25291885;hs8:36058467-36058467,hs8:40512207-40512207;hs8:28227333-28227333,hs20:21270719-21270719;hs8:29865798-29865798,hs20:18083453-18083453;hs8:33311546-33311546,hs20:11068323-11068323;hs4:22195633-22195633,hs16:76386760-76386760;hs8:24974004-24974004,hs8:33314079-33314079;hs8:28228387-28228387,hs8:29283557-29283557;hs8:32575153-32575153,hs20:9577156-9577156;hs5:103343225-103343225,hs5:112990395-112990395;hs20:11400256-11400256,hs20:21285670-21285670;hs8:33311815-33311815,hs20:17847854-17847854;hs8:25090475-25090475,hs8:30527338-30527338;hs8:36160000-36160000,hs20:9372180-9372180;hs8:30014989-30014989,hs8:32555657-32555657;hs8:34922223-34922223,hs8:38798886-38798886;hs20:36536910-36536910,hs20:36621390-36621390;hs8:25100854-25100854,hs8:38798630-38798630;hs8:40498457-40498457,hs8:41622567-41622567;hs8:37454709-37454709,hs20:11070889-11070889;hs8:38628449-38628449,hs8:39830749-39830749;hs8:25102333-25102333,hs20:9397869-9397869;hs20:15333991-15333991,hs20:23960108-23960108;hs5:103343228-103343228,hs5:109521576-109521576;hs8:30538770-30538770,hs8:32581683-32581683;hs8:30530225-30530225,hs20:19302099-19302099;hs20:9567639-9567639,hs20:17892276-17892276;hs4:15431666-15431666,hs4:22709584-22709584;hs4:22197860-22197860,hs16:76377794-76377794;hs8:37458596-37458596,hs20:16855593-16855593;hs14:57321226-57321226,hs21:20491241-20491241;hs8:35244643-35244643,hs8:41402287-41402287;hs16:76376882-76376882,hs16:76386047-76386047;hs4:15322903-15322903,hs16:74907715-74907715;hs4:15425543-15425543,hs4:21193396-21193396;hs4:22195631-22195631,hs16:70665402-70665402;hs8:34921160-34921160,hs20:18953496-18953496;hs11:93716656-93716656,hs11:94163529-94163529;hs11:93716665-93716665,hs11:94163527-94163527;hs8:37340845-37340845,hs8:38794493-38794493;hs16:70024265-70024265,hs16:74933305-74933305;hs4:15473705-15473705,hs4:21781015-21781015;hs4:22192981-22192981,hs16:70670202-70670202;hs3:86038783-86038783,hs3:86047882-86047882;hs2:53141964-53141964,hs13:61689111-61689111;hs4:14479438-14479438,hs4:14481964-14481964;hs4:14543570-14543570,hs16:70665240-70665240;hs10:97093914-97093914,hs20:10987822-10987822;hs8:34934614-34934614,hs20:19302106-19302106;hs20:11064575-11064575,hs20:25287646-25287646;hs16:74937229-74937229,hs16:76382447-76382447;hs10:97093694-97093694,hs20:10987662-10987662;hs8:40398218-40398218,hs20:36806255-36806255;hs7:124026928-124026928,hs14:58290310-58290310	ABCC12;ABHD12;ACTR5;ANK1;ASB3;BTBD3;C1QTNF7;CD38;CNTNAP4;CPEB2;CSRP2BP;DHX35;DOCK5;DUSP4;FAM135B;FUT10;GBA3;GGTLC1;GOLGA7;GPR125;HPR;IDO1;INTU;JAG1;KHDRBS3;LOC286135;LPHN3;MACROD2;NEFL;NKX6-3;NRG1;OTOR;PAK7;PCSK2;PDHA2;PET117;PLCB4;PNOC;PXDNL;RALGAPB;RBPMS;RNF5P1;SFRP1;SLC24A3;SNX5;TACC1;TMEM66;TXNL4B;UNC5D;VAT1L;XRN2;ZMAT4;ZNF133;ZNF23;ZNF703;	Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA	Prior studies have identified recurrent oncogenic mutations in colorectal adenocarcinoma and have surveyed exons of protein-coding genes for mutations in 11 affected individuals. Here we report whole-genome sequencing from nine individuals with colorectal cancer, including primary colorectal tumors and matched adjacent non-tumor tissues, at an average of 30.7x and 31.9x coverage, respectively. We identify an average of 75 somatic rearrangements per tumor, including complex networks of translocations between pairs of chromosomes. Eleven rearrangements encode predicted in-frame fusion proteins, including a fusion of VTI1A and TCF7L2 found in 3 out of 97 colorectal cancers. Although TCF7L2 encodes TCF4, which cooperates with beta-catenin in colorectal carcinogenesis, the fusion lacks the TCF4 beta-catenin-binding domain. We found a colorectal carcinoma cell line harboring the fusion gene to be dependent on VTI1A-TCF7L2 for anchorage-independent growth using RNA interference-mediated knockdown. This study shows previously unidentified levels of genomic rearrangements in colorectal carcinoma that can lead to essential gene fusions and other oncogenic events.	NCBI 36/hg18		phs000374		Yes	BST1,CNTNAP4;CD38,KCNIP4;CNTNAP4,VAT1L;DOCK5,PLCB4;NRG1,PAK7;NRG1,SLC24A3;RBPMS,SLC24A3;SLC24A3,ABHD12;TACC1,MACROD2;UNC5D,RALGAPB
CTDB0366	Research	21892161	Bass AJ, Lawrence MS, Brace LE, Ramos AH, Drier Y, Cibulskis K, Sougnez C, Voet D, Saksena G, Sivachenko A, Jing R, Parkin M, Pugh T, Verhaak RG, Stransky N, Boutin AT, Barretina J, Solit DB, Vakiani E, Shao W, Mishina Y, Warmuth M, Jimenez J, Chiang DY, Signoretti S, Kaelin WG, Spardy N, Hahn WC, Hoshida Y, Ogino S, Depinho RA, Chin L, Garraway LA, Fuchs CS, Baselga J, Tabernero J, Gabriel S, Lander ES, Getz G, Meyerson M	Genomic sequencing of colorectal adenocarcinomas identifies a recurrent VTI1A-TCF7L2 fusion	Nature Genetics	2011 Sep 	5,11,X	Colorectal cancer	Next Generation Sequencing	Homo sapiens	CRC-6	Illumina GA-II	chr10:0-135374737:0;chr11:0-134452384:0;chr12:0-132349534:0;chr13:0-114142980:0;chr14:0-76714076:0;chr14:76714077-76720824:1;chr14:76720825-106368585:0;chr15:0-100338915:0;chr16:0-6526414:0;chr16:6526415-6960093:-1;chr16:6708036-6921294:-1;chr16:6960094-71296250:0;chr16:71296251-71581646:-1;chr16:71581647-88827254:0;chr17:0-78774742:0;chr18:0-76117153:0;chr19:0-63811651:0;chr1:0-247249719:0;chr20:0-14461407:0;chr20:14461408-15021576:-1;chr20:15021577-15267859:0;chr20:15267860-15450481:1;chr20:15450482-62435964:0;chr21:0-46944323:0;chr22:0-49691432:0;chr2:0-242951149:0;chr3:0-59959992:0;chr3:176312186-176314409:1;chr3:176314410-199501827:0;chr3:59959993-59994869:1;chr3:59994870-60693023:0;chr3:60693024-60995416:-1;chr3:60995417-176312185:0;chr4:0-92475037:0;chr4:92475038-92502563:-1;chr4:92502564-92535698:0;chr4:92535699-92625911:-1;chr4:92625912-191273063:0;chr5:0-180857866:0;chr6:0-170899992:0;chr7:0-158821424:0;chr8:0-9981487:0;chr8:10335595-146274826:0;chr8:9981488-10335594:-1;chr9:0-4573927:0;chr9:4573928-4674674:-1;chr9:4674675-140273252:0;chrX:0-7459933:0;chrX:142336499-142429682:1;chrX:142429683-154913754:0;chrX:7459934-7568488:-1;chrX:7568489-142336498:0;chrY:0-57772954:0	hs5:158747640-158747640,hs11:68093742-68093742;hsX:104863865-104863865,hsX:142403712-142403712;hs5:98134842-98134842,hs11:58106127-58106127;hs18:44926172-44926172,hs18:46013514-46013514;hsX:86058035-86058035,hsX:124825414-124825414;hs5:98214924-98214924,hs5:157876135-157876135;hs1:191671679-191671679,hs1:191819910-191819910;hs5:122741029-122741029,hs5:159744189-159744189;hs5:122736211-122736211,hs11:130217878-130217878;hsX:25613574-25613574,hsX:107742244-107742244;hs5:125637905-125637905,hs11:130222298-130222298;hs5:103605949-103605949,hs11:95790285-95790285;hsX:122937829-122937829,hsX:142348044-142348044;hs5:122741036-122741036,hs5:125720100-125720100;hs5:122723838-122723838,hs11:130217949-130217949;hs18:46013512-46013512,hs18:53897496-53897496;hsX:49011736-49011736,hsX:64251170-64251170;hsX:55048491-55048491,hsX:122967449-122967449;hs1:191671680-191671680,hs1:191819913-191819913;hs5:96606058-96606058,hs5:123104889-123104889;hs5:103599978-103599978,hs5:153955365-153955365;hs5:96226634-96226634,hs11:100153009-100153009;hs5:103600037-103600037,hs11:94602050-94602050;hsX:53497999-53497999,hsX:69698863-69698863;hsX:79853797-79853797,hsX:85382306-85382306;hs5:122715537-122715537,hs11:68093742-68093742;hsX:29401569-29401569,hsX:122937035-122937035;hsX:58517184-58517184,hsX:110740735-110740735;hs5:114954407-114954407,hs5:125721276-125721276;hs5:122717021-122717021,hs5:123100394-123100394;hs5:123100570-123100570,hs11:95790329-95790329;hs5:159754284-159754284,hs11:63010998-63010998;hsX:63121602-63121602,hsX:64301050-64301050;hsX:115120846-115120846,hsX:142336327-142336327;hs5:114954403-114954403,hs5:153955467-153955467;hs5:123049468-123049468,hs5:132655097-132655097;hs5:123105121-123105121,hs5:159778023-159778023;hs5:123116543-123116543,hs5:150142920-150142920;hs11:58100154-58100154,hs11:60132932-60132932;hs16:6653874-6653874,hs16:7661265-7661265;hs5:122747926-122747926,hs5:123116614-123116614;hsX:67379720-67379720,hsX:122967037-122967037;hs5:123049810-123049810,hs5:132586703-132586703;hsX:56077983-56077983,hsX:142404171-142404171;hs5:103605990-103605990,hs11:130254634-130254634;hs5:153429264-153429264,hs11:95785181-95785181;hs8:36536789-36536789,hs8:36560279-36560279;hsX:48961667-48961667,hsX:75688815-75688815;hsX:75666948-75666948,hsX:107732123-107732123;hsX:48810100-48810100,hsX:142347898-142347898;hs8:127318815-127318815,hs8:129338694-129338694;hsX:48784377-48784377,hsX:65938205-65938205;hs1:200980692-200980692,hs3:66383929-66383929;hs5:122756417-122756417,hs11:100152883-100152883;hs17:19246777-19246777,hs17:19257957-19257957;hsX:69735999-69735999,hsX:142429612-142429612;hsX:75678097-75678097,hsX:104732644-104732644;hsX:48978268-48978268,hsX:85346286-85346286;hs8:41693481-41693481,hs8:41694385-41694385;hs8:43103766-43103766,hs8:60011734-60011734	AGTR2;ALG13;APEX2;BRWD3;C11orf64;C5orf54;C5orf62;CACNA1F;CCDC120;CCDC22;CEP120;CHD1;COL4A5;CSNK1G3;DACH2;DCAF12L2;EBF1;EDA2R;ERAP2;FLJ32810;FSTL4;GRAMD3;HRASLS5;HSD17B10;IL1RAPL1;IL1RAPL2;JRKL;KLF8;LARP1;LPXN;MAGEB18;MAGEE1;MFAP3;MIR1468;NUDT12;OPHN1;PPP1R3F;RGMB;RIOK2;SAPS3;SESN3;SLU7;SNX19;SPANXN3;STAG2;TEX11;TFE3;TMED7-TICAM2;VCX;ZC4H2;ZFP91;ZXDA;	Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA	Prior studies have identified recurrent oncogenic mutations in colorectal adenocarcinoma and have surveyed exons of protein-coding genes for mutations in 11 affected individuals. Here we report whole-genome sequencing from nine individuals with colorectal cancer, including primary colorectal tumors and matched adjacent non-tumor tissues, at an average of 30.7x and 31.9x coverage, respectively. We identify an average of 75 somatic rearrangements per tumor, including complex networks of translocations between pairs of chromosomes. Eleven rearrangements encode predicted in-frame fusion proteins, including a fusion of VTI1A and TCF7L2 found in 3 out of 97 colorectal cancers. Although TCF7L2 encodes TCF4, which cooperates with beta-catenin in colorectal carcinogenesis, the fusion lacks the TCF4 beta-catenin-binding domain. We found a colorectal carcinoma cell line harboring the fusion gene to be dependent on VTI1A-TCF7L2 for anchorage-independent growth using RNA interference-mediated knockdown. This study shows previously unidentified levels of genomic rearrangements in colorectal carcinoma that can lead to essential gene fusions and other oncogenic events.	NCBI 36/hg18		phs000374		Yes	APEX2,STAG2;C5orf54,HRASLS5;CCDC22,DACH2;CEP120,FLJ32810;CEP120,SAPS3;IL1RAPL1,STAG2;OPHN1,STAG2;RGMB,ZFP91;TEX11,SPANXN3;TMED7,GRAMD3
CTDB0367	Research	23583981	Zhang J, Wu G, Miller CP, Tatevossian RG, Dalton JD, Tang B, Orisme W, Punchihewa C, Parker M, Qaddoumi I, Boop FA, Lu C, Kandoth C, Ding L, Lee R, Huether R, Chen X, Hedlund E, Nagahawatte P, Rusch M, Boggs K, Cheng J, Becksfort J, Ma J, Song G, Li Y, Wei L, Wang J, Shurtleff S, Easton J, Zhao D, Fulton RS, Fulton LL, Dooling DJ, Vadodaria B, Mulder HL, Tang C, Ochoa K, Mullighan CG, Gajjar A, Kriwacki R, Sheer D, Gilbertson RJ, Mardis ER, Wilson RK, Downing JR, Baker SJ, Ellison DW; St. Jude Children's Research Hospital -Washington University Pediatric Cancer Genome Project	Whole-genome sequencing identifies genetic alterations in pediatric low-grade gliomas	Nature Genetics	2013 Jun	5,6	Glioma	Next Generation Sequencing	Homo sapiens	SJLGG005	Illumina Genome Analyzer IIx or HighSeq	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-104635198:0;chr6:104635199-135517619:-1;chr6:135517620-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs5:140843463-140843463,hs6:104664174-104664174;hs6:135517564-135517564,hs5:140857801-140857801	PCDHGB1;MYB	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	The most common pediatric brain tumors are low-grade gliomas (LGGs). We used whole-genome sequencing to identify multiple new genetic alterations involving BRAF, RAF1, FGFR1, MYB, MYBL1 and genes with histone-related functions, including H3F3A and ATRX, in 39 LGGs and low-grade glioneuronal tumors (LGGNTs). Only a single non-silent somatic alteration was detected in 24 of 39 (62%) tumors. Intragenic duplications of the portion of FGFR1 encoding the tyrosine kinase domain (TKD) and rearrangements of MYB were recurrent and mutually exclusive in 53% of grade II diffuse LGGs. Transplantation of Trp53-null neonatal astrocytes expressing FGFR1 with the duplication involving the TKD into the brains of nude mice generated high-grade astrocytomas with short latency and 100% penetrance. FGFR1 with the duplication induced FGFR1 autophosphorylation and upregulation of the MAPK/ERK and PI3K pathways, which could be blocked by specific inhibitors. Focusing on the therapeutically challenging diffuse LGGs, our study of 151 tumors has discovered genetic alterations and potential therapeutic targets across the entire range of pediatric LGGs and LGGNTs.	GRCh37/hg19				Yes	NA
CTDB0368	Research	23583981	Zhang J, Wu G, Miller CP, Tatevossian RG, Dalton JD, Tang B, Orisme W, Punchihewa C, Parker M, Qaddoumi I, Boop FA, Lu C, Kandoth C, Ding L, Lee R, Huether R, Chen X, Hedlund E, Nagahawatte P, Rusch M, Boggs K, Cheng J, Becksfort J, Ma J, Song G, Li Y, Wei L, Wang J, Shurtleff S, Easton J, Zhao D, Fulton RS, Fulton LL, Dooling DJ, Vadodaria B, Mulder HL, Tang C, Ochoa K, Mullighan CG, Gajjar A, Kriwacki R, Sheer D, Gilbertson RJ, Mardis ER, Wilson RK, Downing JR, Baker SJ, Ellison DW; St. Jude Children's Research Hospital -Washington University Pediatric Cancer Genome Project	Whole-genome sequencing identifies genetic alterations in pediatric low-grade gliomas	Nature Genetics	2013 Jun	8	Glioma	Next Generation Sequencing	Homo sapiens	SJLGG033	Illumina Genome Analyzer IIx or HighSeq	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-67490865:0;chr8:67490866-89031536:1;chr8:69654188-67490578:1;chr8:78562383-89031728:-1;chr8:82753337-69654563:1;chr8:89031729-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs8:78562409-78562409,hs8:82753859-82753859	C8orf34;MYBL1;SNX16	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	The most common pediatric brain tumors are low-grade gliomas (LGGs). We used whole-genome sequencing to identify multiple new genetic alterations involving BRAF, RAF1, FGFR1, MYB, MYBL1 and genes with histone-related functions, including H3F3A and ATRX, in 39 LGGs and low-grade glioneuronal tumors (LGGNTs). Only a single non-silent somatic alteration was detected in 24 of 39 (62%) tumors. Intragenic duplications of the portion of FGFR1 encoding the tyrosine kinase domain (TKD) and rearrangements of MYB were recurrent and mutually exclusive in 53% of grade II diffuse LGGs. Transplantation of Trp53-null neonatal astrocytes expressing FGFR1 with the duplication involving the TKD into the brains of nude mice generated high-grade astrocytomas with short latency and 100% penetrance. FGFR1 with the duplication induced FGFR1 autophosphorylation and upregulation of the MAPK/ERK and PI3K pathways, which could be blocked by specific inhibitors. Focusing on the therapeutically challenging diffuse LGGs, our study of 151 tumors has discovered genetic alterations and potential therapeutic targets across the entire range of pediatric LGGs and LGGNTs.	GRCh37/hg19				Yes	C8orf34,MYBL1
CTDB0369	Research	23583981	Zhang J, Wu G, Miller CP, Tatevossian RG, Dalton JD, Tang B, Orisme W, Punchihewa C, Parker M, Qaddoumi I, Boop FA, Lu C, Kandoth C, Ding L, Lee R, Huether R, Chen X, Hedlund E, Nagahawatte P, Rusch M, Boggs K, Cheng J, Becksfort J, Ma J, Song G, Li Y, Wei L, Wang J, Shurtleff S, Easton J, Zhao D, Fulton RS, Fulton LL, Dooling DJ, Vadodaria B, Mulder HL, Tang C, Ochoa K, Mullighan CG, Gajjar A, Kriwacki R, Sheer D, Gilbertson RJ, Mardis ER, Wilson RK, Downing JR, Baker SJ, Ellison DW; St. Jude Children's Research Hospital -Washington University Pediatric Cancer Genome Project	Whole-genome sequencing identifies genetic alterations in pediatric low-grade gliomas	Nature Genetics	2013 Jun	6	Glioma	Next Generation Sequencing	Homo sapiens	SJLGG035	Illumina Genome Analyzer IIx or HighSeq	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-135491704:0;chr6:135491705-136884680:-1;chr6:136882615-135495476:1;chr6:136884681-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs6:135540965-135540965,hs8:89335432-89335432;hs8:88417780-88417780,hs6:136741489-136741489	MAP3K5;MAP7;MMP16;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	The most common pediatric brain tumors are low-grade gliomas (LGGs). We used whole-genome sequencing to identify multiple new genetic alterations involving BRAF, RAF1, FGFR1, MYB, MYBL1 and genes with histone-related functions, including H3F3A and ATRX, in 39 LGGs and low-grade glioneuronal tumors (LGGNTs). Only a single non-silent somatic alteration was detected in 24 of 39 (62%) tumors. Intragenic duplications of the portion of FGFR1 encoding the tyrosine kinase domain (TKD) and rearrangements of MYB were recurrent and mutually exclusive in 53% of grade II diffuse LGGs. Transplantation of Trp53-null neonatal astrocytes expressing FGFR1 with the duplication involving the TKD into the brains of nude mice generated high-grade astrocytomas with short latency and 100% penetrance. FGFR1 with the duplication induced FGFR1 autophosphorylation and upregulation of the MAPK/ERK and PI3K pathways, which could be blocked by specific inhibitors. Focusing on the therapeutically challenging diffuse LGGs, our study of 151 tumors has discovered genetic alterations and potential therapeutic targets across the entire range of pediatric LGGs and LGGNTs.	GRCh37/hg19				Yes	NA
CTDB0370	Research	23583981	Zhang J, Wu G, Miller CP, Tatevossian RG, Dalton JD, Tang B, Orisme W, Punchihewa C, Parker M, Qaddoumi I, Boop FA, Lu C, Kandoth C, Ding L, Lee R, Huether R, Chen X, Hedlund E, Nagahawatte P, Rusch M, Boggs K, Cheng J, Becksfort J, Ma J, Song G, Li Y, Wei L, Wang J, Shurtleff S, Easton J, Zhao D, Fulton RS, Fulton LL, Dooling DJ, Vadodaria B, Mulder HL, Tang C, Ochoa K, Mullighan CG, Gajjar A, Kriwacki R, Sheer D, Gilbertson RJ, Mardis ER, Wilson RK, Downing JR, Baker SJ, Ellison DW; St. Jude Children's Research Hospital -Washington University Pediatric Cancer Genome Project	Whole-genome sequencing identifies genetic alterations in pediatric low-grade gliomas	Nature Genetics	2013 Jun	9	Glioma	Next Generation Sequencing	Homo sapiens	SJLGG038	Illumina Genome Analyzer IIx or HighSeq	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-14731423:0;chr9:14731424-78562970:-1;chr9:21749091-22015572:-1;chr9:22024624-22025145:-1;chr9:37804215-37804296:-1;chr9:78559926-78663080:-1;chr9:78654643-36070277:1;chr9:78663081-78671456:0;chr9:78671457-89348568:-1;chr9:84653505-78666783:1;chr9:89340180-78518260:1;chr9:89348569-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs9:78566224-78566224,hs9:116237623-116237623;hs9:89337633-89337633,hs9:78583405-78583405;hs12:12018549-12018549,hs15:88646889-88646889;hs12:12018559-12018559,hs15:88646886-88646886	CDKN2B-AS1;ETV6;NTRK3;PCSK5;RECK;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	The most common pediatric brain tumors are low-grade gliomas (LGGs). We used whole-genome sequencing to identify multiple new genetic alterations involving BRAF, RAF1, FGFR1, MYB, MYBL1 and genes with histone-related functions, including H3F3A and ATRX, in 39 LGGs and low-grade glioneuronal tumors (LGGNTs). Only a single non-silent somatic alteration was detected in 24 of 39 (62%) tumors. Intragenic duplications of the portion of FGFR1 encoding the tyrosine kinase domain (TKD) and rearrangements of MYB were recurrent and mutually exclusive in 53% of grade II diffuse LGGs. Transplantation of Trp53-null neonatal astrocytes expressing FGFR1 with the duplication involving the TKD into the brains of nude mice generated high-grade astrocytomas with short latency and 100% penetrance. FGFR1 with the duplication induced FGFR1 autophosphorylation and upregulation of the MAPK/ERK and PI3K pathways, which could be blocked by specific inhibitors. Focusing on the therapeutically challenging diffuse LGGs, our study of 151 tumors has discovered genetic alterations and potential therapeutic targets across the entire range of pediatric LGGs and LGGNTs.	GRCh37/hg19				Yes	PCSK5,RECK
CTDB0371	Research	23583981	Zhang J, Wu G, Miller CP, Tatevossian RG, Dalton JD, Tang B, Orisme W, Punchihewa C, Parker M, Qaddoumi I, Boop FA, Lu C, Kandoth C, Ding L, Lee R, Huether R, Chen X, Hedlund E, Nagahawatte P, Rusch M, Boggs K, Cheng J, Becksfort J, Ma J, Song G, Li Y, Wei L, Wang J, Shurtleff S, Easton J, Zhao D, Fulton RS, Fulton LL, Dooling DJ, Vadodaria B, Mulder HL, Tang C, Ochoa K, Mullighan CG, Gajjar A, Kriwacki R, Sheer D, Gilbertson RJ, Mardis ER, Wilson RK, Downing JR, Baker SJ, Ellison DW; St. Jude Children's Research Hospital -Washington University Pediatric Cancer Genome Project	Whole-genome sequencing identifies genetic alterations in pediatric low-grade gliomas	Nature Genetics	2013 Jun	1,3,11,12	Glioma	Next Generation Sequencing	Homo sapiens	SJLGG039	Illumina Genome Analyzer IIx or HighSeq	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-12649233:0;chr3:12649234-46001511:-1;chr3:46001512-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-9539556:0;chr7:6300099-159138663:0;chr7:9539557-6300098:1;chr8:0-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:3643330-3643330,hs11:115411715-115411715;hs1:3643581-3643581,hs11:69538645-69538645;hs1:3649438-3649438,hs22:47557135-47557135;hs1:12582471-12582471,hs12:103110023-103110023;hs1:12584121-12584121,hs11:118491727-118491727;hs3:49168971-49168971,hs11:66966686-66966686;hs3:186716601-186716601,hs4:1899271-1899271;hs4:5039611-5039611,hs3:183723574-183723574;hs10:98887882-98887882,hs16:2158836-2158836;hs11:69540077-69540077,hs1:9555182-9555182;hs11:69541460-69541460,hs12:103111315-103111315;hs12:103110079-103110079,hs10:95588803-95588803;hs12:103112184-103112184,hs3:9662023-9662023;hs12:106295961-106295961,hs1:12581667-12581667;hs16:410315-410315,hs4:5037703-5037703;hs16:2170637-2170637,hs12:103110956-103110956;hs16:2172065-2172065,hs1:1196437-1196437	ABCC5;CYTH3;FYCO1;KDM2A;PHLDB1;PKD1;RAF1;SLIT1;ST6GAL1;TP73;UBE2J2;WHSC1;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	The most common pediatric brain tumors are low-grade gliomas (LGGs). We used whole-genome sequencing to identify multiple new genetic alterations involving BRAF, RAF1, FGFR1, MYB, MYBL1 and genes with histone-related functions, including H3F3A and ATRX, in 39 LGGs and low-grade glioneuronal tumors (LGGNTs). Only a single non-silent somatic alteration was detected in 24 of 39 (62%) tumors. Intragenic duplications of the portion of FGFR1 encoding the tyrosine kinase domain (TKD) and rearrangements of MYB were recurrent and mutually exclusive in 53% of grade II diffuse LGGs. Transplantation of Trp53-null neonatal astrocytes expressing FGFR1 with the duplication involving the TKD into the brains of nude mice generated high-grade astrocytomas with short latency and 100% penetrance. FGFR1 with the duplication induced FGFR1 autophosphorylation and upregulation of the MAPK/ERK and PI3K pathways, which could be blocked by specific inhibitors. Focusing on the therapeutically challenging diffuse LGGs, our study of 151 tumors has discovered genetic alterations and potential therapeutic targets across the entire range of pediatric LGGs and LGGNTs.	GRCh37/hg19				Yes	FYCO1,RAF1;ST6GAL1,WHSC1;UBE2J2,PKD1
CTDB0372	Research	26031834	Norris AL, Kamiyama H, Makohon-Moore A, Pallavajjala A, Morsberger LA, Lee K, Batista D, Iacobuzio-Donahue CA, Lin MT, Klein AP, Hruban RH, Wheelan SJ, Eshleman JR	Transflip mutations produce deletions in pancreatic cancer	Genes, Chromosomes & Cancer	2015 May 	9,18	Pancreatic cancer	SNP Array	Homo sapiens	Pa102C	Illumina Omni2.5 array			C18orf54;CCDC68;DCC;DYNAP;ELAC1;FAM75D1;LINC01539;LOC101927273;MAPK4;MBD2;ME2;MEX3C;MIR4529;MRO;POLI;RAB27B;SMAD4;SNORA37;STARD6;TCF4;	Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins School of Medicine, Baltimore, MD, 21231	Pancreatic ductal adenocarcinoma (PDAC) is driven by the inactivation of the tumor suppressor genes (TSGs), CDKN2A (P16) and SMAD4 (DPC4), commonly by homozygous deletions (HDs). Using a combination of high density single-nucleotide polymorphism (SNP) microarray and whole genome sequencing (WGS), we fine-mapped novel breakpoints surrounding deletions of CDKN2A and SMAD4 and characterized them by their underlying structural variants (SVs). Only one third of CDKN2A and SMAD4 deletions (6 of 18) were simple interstitial deletions, rather, the majority of deletions were caused by complex rearrangements, specifically, a translocation on one side of the TSG in combination with an inversion on the other side. We designate these as TransFlip mutations. Characteristics of TransFlip mutations are: (1) a propensity to target the TSGs CDKN2A and SMAD4 (P < 0.005), (2) not present in the germline of the examined samples, (3) non-recurrent breakpoints, (4) relatively small (47 bp to 3.4 kb) inversions, (5) inversions can be either telomeric or centromeric to the TSG, and (6) non-reciprocal, and non-recurrent translocations. TransFlip mutations are novel complex genomic rearrangements with unique breakpoint signatures in pancreatic cancer. We hypothesize that they are a common but poorly understood mechanism of TSG inactivation in human cancer.	GRCh37/hg19				Yes	NA
CTDB0373	Research	26031834	Norris AL, Kamiyama H, Makohon-Moore A, Pallavajjala A, Morsberger LA, Lee K, Batista D, Iacobuzio-Donahue CA, Lin MT, Klein AP, Hruban RH, Wheelan SJ, Eshleman JR	Transflip mutations produce deletions in pancreatic cancer	Genes, Chromosomes & Cancer	2015 May 	18	Pancreatic cancer	SNP Array	Homo sapiens	Pa227C	Illumina Omni2.5 array			C18orf54;CCDC68;DCC;DYNAP;ELAC1;MBD2;ME2;MEX3C;POLI;RAB27B;SMAD4;SNORA37;STARD6;TCF4;	Department of Pathology, The Sol Goldman Pancreatic Cancer Research Center, Johns Hopkins School of Medicine, Baltimore, MD, 21231	Pancreatic ductal adenocarcinoma (PDAC) is driven by the inactivation of the tumor suppressor genes (TSGs), CDKN2A (P16) and SMAD4 (DPC4), commonly by homozygous deletions (HDs). Using a combination of high density single-nucleotide polymorphism (SNP) microarray and whole genome sequencing (WGS), we fine-mapped novel breakpoints surrounding deletions of CDKN2A and SMAD4 and characterized them by their underlying structural variants (SVs). Only one third of CDKN2A and SMAD4 deletions (6 of 18) were simple interstitial deletions, rather, the majority of deletions were caused by complex rearrangements, specifically, a translocation on one side of the TSG in combination with an inversion on the other side. We designate these as TransFlip mutations. Characteristics of TransFlip mutations are: (1) a propensity to target the TSGs CDKN2A and SMAD4 (P < 0.005), (2) not present in the germline of the examined samples, (3) non-recurrent breakpoints, (4) relatively small (47 bp to 3.4 kb) inversions, (5) inversions can be either telomeric or centromeric to the TSG, and (6) non-reciprocal, and non-recurrent translocations. TransFlip mutations are novel complex genomic rearrangements with unique breakpoint signatures in pancreatic cancer. We hypothesize that they are a common but poorly understood mechanism of TSG inactivation in human cancer.	GRCh37/hg19				Yes	NA
CTDB0377	Research	24413735	Papaemmanuil E, Rapado I, Li Y, Potter NE, Wedge DC, Tubio J, Alexandrov LB, Van Loo P, Cooke SL, Marshall J, Martincorena I, Hinton J, Gundem G, van Delft FW5, Nik-Zainal S, Jones DR, Ramakrishna M, Titley I, Stebbings L, Leroy C, Menzies A, Gamble J, Robinson B, Mudie L, Raine K, O'Meara S, Teague JW, Butler AP, Cazzaniga G, Biondi A, Zuna J, Kempski H, Muschen M, Ford AM, Stratton MR, Greaves M, Campbell PJ	RAG-mediated recombination is the predominant driver of oncogenic rearrangement in ETV6-RUNX1 acute lymphoblastic leukemia	Nature Genetics	2014 Feb	X	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	PD4021a	Illumina GAIIx	chr10:0-111767206:0;chr10:111767207-111868993:-1;chr10:111868994-135534747:0;chr11:0-36619637:0;chr11:36619638-36641928:-1;chr11:36641929-135006516:0;chr12:0-133851895:0;chr13:0-79741019:0;chr13:79741020-80622777:-1;chr13:80622778-115169878:0;chr14:0-20535558:0;chr14:20535559-20669165:1;chr14:20669166-93785332:0;chr14:93785333-93798624:-1;chr14:93798625-107349540:0;chr15:0-102531392:0;chr16:0-81913021:0;chr16:81913022-82023811:-1;chr16:82023812-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-241650825:0;chr1:241650826-241656688:-1;chr1:241656689-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-176913895:0;chr3:176913896-177100751:-1;chr3:177100752-198022430:0;chr4:0-96032247:0;chr4:96032248-96078844:-1;chr4:96078845-191154276:0;chr5:0-22951246:0;chr5:22951247-23013377:-1;chr5:23013378-180915260:0;chr6:0-171115067:0;chr7:0-136958304:0;chr7:136958305-139011263:-1;chr7:139011264-159138663:0;chr8:0-146364022:0;chr9:0-141213431:0;chrX:0-6249420:0;chrX:105962256-109139512:1;chrX:10852341-24782792:1;chrX:120451702-155270560:0;chrX:51132045-74233382:-1;chrX:6249421-11552024:-1;chrX:62711496-104787984:-1;chrX:65752070-67144086:-1;chrX:6669959-107350305:1;chrX:74235850-76566878:-1;chrX:76567692-105963715:1;chrX:76568085-120451701:1;chrY:0-59373566:0	hs1:241650826-241650926,hs1:241656588-241656688;hs3:176913896-176913996,hs3:177100651-177100751;hs4:96032248-96032348,hs4:96078744-96078844;hs5:22951247-22951347,hs5:23013277-23013377;hs7:136958305-136958405,hs7:139011163-139011263;hs10:111767207-111767307,hs10:111868893-111868993;hs11:36619638-36619738,hs11:36641828-36641928;hs13:79741020-79741120,hs13:80622677-80622777;hs14:93785333-93785433,hs14:93798524-93798624;hs16:81913022-81913122,hs16:82023711-82023811;hsX:6249421-6249521,hsX:11551924-11552024;hsX:51132045-51132145,hsX:74233282-74233382;hsX:62711496-62711596,hsX:104787884-104787984;hsX:65752070-65752170,hsX:67143986-67144086;hsX:74235850-74235950,hsX:76566778-76566878	ABCB7;AC002359;AC002365;AC002366;AC002504;AC002981;AC003658;AC003666;AC003684;AC004073;AC004074;AC004386;AC004478;AC004673;AC004998;AC005023;AC005926;AC006062;AC006144;AC008162;AC073488;AC073597;AC073909;AC078993;AC092198;AC112497;AC112778;AC115617;AC117517;AC121344;AC233283;ACA64;ACE2;ACOT9;ACRC;ACSL4;ACTBP1;ACTG1P10;ACTR3P2;AF196779;AF196969;AF196970;AF196972;AF207550;AF238380;AF241726;AGTR2;AKAP14;AKAP16B;AKAP4;AKR1B1P8;AL008708;AL009172;AL022165;AL031115;AL031311;AL035088;AL035422;AL035427;AL035494;AL049610;AL078580;AL096700;AL109750;AL121578;AL121869;AL133512;AL135749;AL136137;AL137845;AL138891;AL139396;AL139809;AL158141;AL158819;AL159987;AL161723;AL161779;AL353691;AL353698;AL353999;AL355852;AL357752;AL359079;AL360224;AL390840;AL390966;AL391315;AL391358;AL391803;AL391821;AL445236;AL445467;AL445523;AL451005;AL513007;AL590069;AL590240;AL590285;AL590407;AL590410;AL590762;AL590763;AL590808;AL591378;AL591394;AL591708;AL592043;AL596268;AL627402;AL670379;AL672138;AL732366;AL772208;AL772284;AL928646;AL929101;ALAS2;ALG13;AMELX;AMMECR1;AMOT;ANKRD58;AP1S2;APEX2;API5P1;APOO;APOOL;AR;ARAF;ARHGAP6;ARHGEF9;ARL13A;ARMCX1;ARMCX2;ARMCX3;ARMCX4;ARMCX5;ARMCX6;ARR3;ARX;ASB11;ASB12;ASB9;ASS1P5;ATG4A;ATP1B4;ATP6AP2;ATP7A;ATRX;ATXN3L;AWAT1;AWAT2;BCOR;BEND2;BEX1;BEX2;BEX4;BEX5;BHLHB9;BMP15;BMP2KL;BMX;BRWD3;BTF3P8;BTK;BX119917;BX119964;BX276092;BX682235;BX842568;C11orf74;C1GALT1C1;CA5B;CA5BP;CACNA1F;CAPN6;CASK;CBX1P1;CBX1P2;CBX1P4;CCDC120;CCDC22;CCNB3;CCT4P2;CDK16;CDKL5;CDX4;CENPI;CENPVL1;CFP;CHIC1;CHM;CHRDL1;CHST7;CITED1;CKS1BP6;CLCN4;CLCN5;CLDN2;CNKSR2;COL4A5;COL4A6;COX7B;CPXCR1;CSTF2;CT47A1;CT47A10;CT47A11;CT47A2;CT47A3;CT47A4;CT47A5;CT47A6;CT47A7;CT47A8;CT47A9;CT47B1;CTD-2225F20;CTD-2230M5;CTD-2234B20;CTD-2267G17;CTD-2522E6;CTD-2542O7;CTPS2;CUL4B;CXCR3;CXorf21;CXorf22;CXorf23;CXorf24;CXorf26;CXorf27;CXorf29;CXorf30;CXorf31;CXorf36;CXorf38;CXorf41;CXorf46;CXorf49;CXorf49B;CXorf56;CXorf57;CXorf58;CXorf59;CXorf61;CXorf65;CXorf67;CXXC1P1;CYBB;CYLC1;CYSLTR1;DACH2;DCAF8L1;DCAF8L2;DCX;DDX3X;DDX53;DGAT2L6;DGKK;DIAPH2;DLG3;DMD;DMRTC1;DMRTC1B;DOCK11;DRP2;DUSP21;DYNLT3;EBP;EDA;EDA2R;EEF1A1P15;EEF1A1P29;EEF1A1P30;EEF1A1P40;EEF1B4;EFHC2;EFNB1;EGFL6;EIF1AX;EIF2S3;EIF4A1P10;EIF4BP7;EIF4BP9;ERAS;ERCC6L;ERVWE2;ESX1;FAAH2;FABP5P15;FAM104B;FAM120C;FAM123B;FAM133A;FAM155B;FAM156A;FAM156B;FAM199X;FAM3C2;FAM46D;FAM47A;FAM47B;FAM47C;FAM47DP;FAM48B1;FAM48B2;FAM70A;FAM9A;FAM9B;FAM9C;FANCB;FDPSP5;FGD1;FGF16;FIGF;FOXO4;FOXP3;FOXR2;FRMPD3;FRMPD4;FTH1P14;FTH1P18;FTH1P19;FTHL17;FTLP16;FTLP2;FTSJ1;FUNDC1;FXYD8;GAGE1;GAGE10;GAGE12B;GAGE12C;GAGE12D;GAGE12E;GAGE12F;GAGE12G;GAGE12H;GAGE12I;GAGE12J;GAGE13;GAGE2A;GAGE2D;GAGE2E;GAPDHP1;GAPDHP65;GATA1;GDPD2;GEMIN8;GEMIN8P3;GHc-1077H7;GHc-210E9;GHc-362H12;GHc-602D8;GJA6P;GJB1;GK;GLA;GLOD5;GLRA2;GLRA4;GLUD1P9;GNG5P2;GNL3L;GPKOW;GPM6B;GPR143;GPR173;GPR174;GPR34;GPR64;GPR82;GPRASP1;GPRASP2;GRIPAP1;GRPR;GSPT2;GUCY2F;H2BFM;H2BFWT;HCCS;HDAC6;HDAC8;HDHD1;HDX;HEPH;HK2P1;HMGA1P1;HMGB1P12;HMGB1P15;HMGB1P16;HMGB1P32;HMGN5;HNRNPH2;HSD17B10;HSPB1P2;HTR2C;HUWE1;IGBP1;IL13RA1;IL13RA2;IL1RAPL1;IL1RAPL2;IL2RG;INE1;INGX;IQSEC2;IRS4;ITGB1BP2;ITIH5L;ITM2A;KAL1;KCND1;KCNE1L;KCTD9P2;KDM5C;KDM6A;KIAA1210;KIAA2022;KIF4A;KLF8;KLHL13;KLHL15;KLHL34;KLHL4;KRT18P49;KRT8P14;LAMP2;LANCL3;LAS1L;LDHBP2;LHFPL1;LL0XNC01-105G4;LL0XNC01-116E7;LL0XNC01-131B10;LL0XNC01-144A10;LL0XNC01-157D4;LL0XNC01-177E8;LL0XNC01-19D8;LL0XNC01-221F2;LL0XNC01-237H1;LL0XNC01-240C2;LL0XNC01-250H12;LL0XNC01-46H11;LL0XNC01-73E8;LONRF3;LPAR4;LRCH2;LUZP4;MAGEB1;MAGEB10;MAGEB16;MAGEB17;MAGEB18;MAGEB2;MAGEB3;MAGEB4;MAGEB5;MAGEB6;MAGEB6B;MAGED1;MAGED2;MAGED4;MAGED4B;MAGEE1;MAGEE2;MAGEH1;MAGIX;MAGT1;MAOA;MAOB;MAP3K15;MAP7D2;MBTPS2;MCART6;MCTS1;MED12;MED14;MID1;MID1IP1;MID2;MIR1277;MIR1298;MIR1468;MIR188;MIR1911;MIR1912;MIR221;MIR222;MIR223;MIR325;MIR361;MIR362;MIR374A;MIR374B;MIR421;MIR448;MIR500A;MIR500B;MIR501;MIR502;MIR532;MIR545;MIR548F5;MIR548I4;MIR548M;MIR651;MIR652;MIR660;MIR764;MIR766;MIR98;MIRLET7F2;MORC4;MORF4L2;MORF4LP5;MOSPD2;MRPL32P1;MRPL35P4;MRPS17P9;MSL3;MSN;MTMR8;MTND2P2;MUM1L1;MYCL2;NAP1L2;NAP1L3;NAP1L6;NCBP2L;NCRNA00182;NCRNA00183;NCRNA00246;NCRNA00269;NDP;NDUFA1;NDUFB11;NGFRAP1;NHS;NHSL2;NKAP;NKAPP1;NKRF;NLGN3;NONO;NOX1;NPM1P8;NR0B1;NRK;NUDT10;NUDT11;NUP62CL;NUS1P1;NXF2;NXF2B;NXF3;NXF4;NXF5;NXT2;NYX;OFD1;OGT;OPHN1;OTC;OTUD5;OTUD6A;P2RY10;P2RY4;PA2G4P1;PABPC1L2A;PABPC1L2B;PABPC1P3;PABPC5;PAGE1;PAGE2;PAGE2B;PAGE3;PAGE4;PAGE5;PAICSP7;PAK3;PCDH11X;PCDH19;PCSK1N;PCYT1B;PDHA1;PDK3;PDZD11;PFKFB1;PGAM4;PGK1;PGRMC1;PHEX;PHF16;PHF8;PHKA1;PHKA2;PIGA;PIM2;PIN4;PIR;PJA1;PLP1;PLP2;PLS3;PNPLA4;POF1B;POLA1;PORCN;POU3F4;PPEF1;PPP1R2P9;PPP1R3F;PQBP1;PRAF2;PRDX4;PRICKLE3;PRPS1;PRPS2;PRRG1;PSMD10;PTCHD1;PYY3;RAB40A;RAB40AL;RAB41;RAB9A;RAB9B;RAI2;RBBP7;RBM10;RBM3;RBM41;RBMXL3;REPS2;RGAG1;RGAG4;RGN;RHOXF1;RHOXF2;RHOXF2B;RIBC1;RIPPLY1;RLIM;RN28S1;RNF113A;RNF128;RNF19BPX;RNU12-2P;RNU6-50P;RNU7-56P;RNU7-7P;RP2;RP5-1000K24;RP5-1055C14;RP5-1059E7;RP5-1091N2;RP5-1100E15;RP5-1139I1;RP5-1145L23;RP5-1158B12;RP5-1158E12;RP5-1158H2;RP5-1168A5;RP5-1170D6;RP5-1172N10;RP5-1174J21;RP5-820B18;RP5-834A16;RP5-839M11;RP5-849L7;RP5-878I13;RP5-928E24;RP5-944N9;RP5-958B3;RP5-961K14;RP5-964N17;RP5-972B16;RP5-998G20;RP6-105D16;RP6-113J7;RP6-127F18;RP6-145B8;RP6-149D17;RP6-159A1;RP6-162O13;RP6-186E3;RP6-191P20;RP6-1O2;RP6-204F4;RP6-218J18;RP6-227L5;RP6-22P16;RP6-24A23;RP6-29D12;RP6-60B16;RP6-99M1;RPA4;RPGR;RPL36A;RPL39;RPL9P7;RPS15AP40;RPS26P11;RPS4X;RPS6KA3;RPS6KA6;RRAGB;RRM2P3;RS1;S100G;SALL1P1;SAR1AP4;SAT1;SATL1;SCARNA23;SCML1;SCML2;SEPT6;SERPINA7;SH3BGRL;SH3KBP1;SHC1P1;SHROOM2;SHROOM4;SIAH1L;SLC16A2;SLC25A43;SLC25A5;SLC35A2;SLC38A5;SLC6A14;SLC7A3;SLC9A7;SMC1A;SMEK3P;SMPX;SMS;SNORA11C;SNORA11D;SNORA11E;SNORA35;SNORA64;SNORA68;SNORA7;SNORA9;SNORD112;SNORD30;SNORD96B;snosnR60_Z15;snoU2_19;SNX12;SPACA5;SPACA5B;SPANXN5;SPIN2A;SPIN2B;SPIN3;SPIN4;SRIP2;SRPX;SRPX2;SSX1;SSX10;SSX2;SSX2B;SSX3;SSX4;SSX4B;SSX5;SSX6;SSX7;SSX8;SSX9;ST13P18;STARD8;STS;SUV39H1;SYAP1;SYN1;SYP;SYTL4;SYTL5;TAB3;TAF1;TAF7L;TAF9B;TBC1D25;TBC1D8B;TBL1X;TBX22;TCEAL1;TCEAL2;TCEAL3;TCEAL4;TCEAL5;TCEAL6;TCEAL7;TCEAL8;TCEANC;TDGF3;TERF1P4;TEX11;TEX13A;TEX13B;TEX16P;TFE3;TGIF2LX;TIMM17B;TIMM8A;TIMP1;TLR7;TLR8;TMEM164;TMEM27;TMEM31;TMEM35;TMEM47;TMSB15A;TMSB15B;TMSB4X;TNMD;TRAPPC2;TRMT2B;TRNAE37P;TRO;TRPC5;TSC22D3;TSPAN6;TSPAN7;TSPYL2;TSR2;TTC3P1;TXLNG;U5;U70984;UBA1;UBE2A;UBQLN2;UPF3B;UPRT;UQCRBP1;USMG5P1;USP11;USP12PX;USP27X;USP51;USP9X;UXT;VCX;VCX2;VCX3A;VCX3B;VDAC1P1;VDAC1P2;VENTXP1;VN1R110P;VSIG1;VSIG4;VTRNA3P;WAS;WBP5;WDR13;WDR44;WDR45;WNK3;WWC3;XAGE1A;XAGE1B;XAGE1C;XAGE1D;XAGE2;XAGE2B;XAGE3;XAGE5;XIST;XK;XKRX;XX-FW87585A5;XXyac-YR12DB5;Y10196;YAP1P2;YIPF6;YWHAZP7;YWHAZP8;YY2;Z68873;Z73964;Z80107;Z82216;Z83745;Z97356;Z97985;Z98304;ZBTB33;ZC3H12B;ZC4H2;ZCCHC12;ZCCHC13;ZCCHC16;ZCCHC5;ZDHHC15;ZFRP1;ZFX;ZMAT1;ZMYM3;ZNF157;ZNF182;ZNF41;ZNF630;ZNF645;ZNF673;ZNF674;ZNF711;ZNF81;ZRSR2;ZXDA;ZXDB;	Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, UK	The ETV6-RUNX1 fusion gene, found in 25% of childhood acute lymphoblastic leukemia (ALL) cases, is acquired in utero but requires additional somatic mutations for overt leukemia. We used exome and low-coverage whole-genome sequencing to characterize secondary events associated with leukemic transformation. RAG-mediated deletions emerge as the dominant mutational process, characterized by recombination signal sequence motifs near breakpoints, incorporation of non-templated sequence at junctions, ~30-fold enrichment at promoters and enhancers of genes actively transcribed in B cell development and an unexpectedly high ratio of recurrent to non-recurrent structural variants. Single-cell tracking shows that this mechanism is active throughout leukemic evolution, with evidence of localized clustering and reiterated deletions. Integration of data on point mutations and rearrangements identifies ATF7IP and MGA as two new tumor-suppressor genes in ALL. Thus, a remarkably parsimonious mutational process transforms ETV6-RUNX1-positive lymphoblasts, targeting the promoters, enhancers and first exons of genes that normally regulate B cell differentiation.	GRCh37/hg19				Yes	NA
CTDB0378	Research	25790038	Kovac M, Navas C, Horswell S, Salm M, Bardella C, Rowan A, Stares M, Castro-Giner F, Fisher R, de Bruin EC, Kovacova M, Gorman M, Makino S, Williams J, Jaeger E, Jones A, Howarth K, Larkin J, Pickering L, Gore M, Nicol DL, Hazell S, Stamp G, O'Brien T, Challacombe B, Matthews N, Phillimore B, Begum S, Rabinowitz A, Varela I, Chandra A, Horsfield C, Polson A, Tran M, Bhatt R, Terracciano L, Eppenberger-Castori S, Protheroe A, Maher E, El Bahrawy M, Fleming S, Ratcliffe P, Heinimann K, Swanton C, Tomlinson I	Recurrent chromosomal gains and heterogeneous driver mutations characterise papillary renal cancer evolution	Nature Communications	2015 Mar 	2	Renal cancer	Next Generation Sequencing	Homo sapiens	P09	Complete 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and Population Genetics Laboratory, Wellcome Trust Centre for Human Genetics, Nuffield Department of Clinical Medicine, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK 	Papillary renal cell carcinoma (pRCC) is an important subtype of kidney cancer with a problematic pathological classification and highly variable clinical behaviour. Here we sequence the genomes or exomes of 31 pRCCs, and in four tumours, multi-region sequencing is undertaken. We identify BAP1, SETD2, ARID2 and Nrf2 pathway genes (KEAP1, NHE2L2 and CUL3) as probable drivers, together with at least eight other possible drivers. However, only ~10% of tumours harbour detectable pathogenic changes in any one driver gene, and where present, the mutations are often predicted to be present within cancer sub-clones. We specifically detect parallel evolution of multiple SETD2 mutations within different sub-regions of the same tumour. By contrast, large copy number gains of chromosomes 7, 12, 16 and 17 are usually early, monoclonal changes in pRCC evolution. The predominance of large copy number variants as the major drivers for pRCC highlights an unusual mode of tumorigenesis that may challenge precision medicine approaches. 	GRCh37/hg19			PRJEB7875;ERP008861	Yes	NA
CTDB0379	Research	24703847	Chen X, Bahrami A, Pappo A, Easton J, Dalton J, Hedlund E, Ellison D, Shurtleff S, Wu G, Wei L, Parker M, Rusch M, Nagahawatte P, Wu J, Mao S, Boggs K, Mulder H, Yergeau D, Lu C, Ding L, Edmonson M, Qu C, Wang J, Li Y, Navid F, Daw NC, Mardis ER, Wilson RK, Downing JR, Zhang J, Dyer MA	Recurrent somatic structural variations contribute to tumorigenesis in pediatric osteosarcoma	Cell Reports	2014 Apr 	14	Osteosarcoma	Next Generation Sequencing	Homo sapiens	SJOS002_D	Illumina 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of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA	Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue in a discovery cohort, as well as 14 samples in a validation cohort. Single-nucleotide variations (SNVs) exhibited a pattern of localized hypermutation called kataegis in 50% of the tumors. We identified p53 pathway lesions in all tumors in the discovery cohort, nine of which were translocations in the first intron of the TP53 gene. Beyond TP53, the RB1, ATRX, and DLG2 genes showed recurrent somatic alterations in 29%-53% of the tumors. These data highlight the power of whole-genome sequencing for identifying recurrent somatic alterations in cancer genomes that may be missed using other methods. 	GRCh37/hg19				Yes	NA
CTDB0380	Research	24703847	Chen X, Bahrami A, Pappo A, Easton J, Dalton J, Hedlund E, Ellison D, Shurtleff S, Wu G, Wei L, Parker M, Rusch M, Nagahawatte P, Wu J, Mao S, Boggs K, Mulder H, Yergeau D, Lu C, Ding L, Edmonson M, Qu C, Wang J, Li Y, Navid F, Daw NC, Mardis ER, Wilson RK, Downing JR, Zhang J, Dyer MA	Recurrent somatic structural variations contribute to tumorigenesis in pediatric osteosarcoma	Cell Reports	2014 Apr 	17	Osteosarcoma	Next Generation Sequencing	Homo sapiens	SJOS003_D	Illumina 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of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA	Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue in a discovery cohort, as well as 14 samples in a validation cohort. Single-nucleotide variations (SNVs) exhibited a pattern of localized hypermutation called kataegis in 50% of the tumors. We identified p53 pathway lesions in all tumors in the discovery cohort, nine of which were translocations in the first intron of the TP53 gene. Beyond TP53, the RB1, ATRX, and DLG2 genes showed recurrent somatic alterations in 29%-53% of the tumors. These data highlight the power of whole-genome sequencing for identifying recurrent somatic alterations in cancer genomes that may be missed using other methods. 	GRCh37/hg19				Yes	NA
CTDB0381	Research	24703847	Chen X, Bahrami A, Pappo A, Easton J, Dalton J, Hedlund E, Ellison D, Shurtleff S, Wu G, Wei L, Parker M, Rusch M, Nagahawatte P, Wu J, Mao S, Boggs K, Mulder H, Yergeau D, Lu C, Ding L, Edmonson M, Qu C, Wang J, Li Y, Navid F, Daw NC, Mardis ER, Wilson RK, Downing JR, Zhang J, Dyer MA	Recurrent somatic structural variations contribute to tumorigenesis in pediatric osteosarcoma	Cell Reports	2014 Apr 	6	Osteosarcoma	Next Generation Sequencing	Homo sapiens	SJOS005_D	Illumina 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of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA	Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue in a discovery cohort, as well as 14 samples in a validation cohort. Single-nucleotide variations (SNVs) exhibited a pattern of localized hypermutation called kataegis in 50% of the tumors. We identified p53 pathway lesions in all tumors in the discovery cohort, nine of which were translocations in the first intron of the TP53 gene. Beyond TP53, the RB1, ATRX, and DLG2 genes showed recurrent somatic alterations in 29%-53% of the tumors. These data highlight the power of whole-genome sequencing for identifying recurrent somatic alterations in cancer genomes that may be missed using other methods. 	GRCh37/hg19				Yes	NA
CTDB0382	Research	24703847	Chen X, Bahrami A, Pappo A, Easton J, Dalton J, Hedlund E, Ellison D, Shurtleff S, Wu G, Wei L, Parker M, Rusch M, Nagahawatte P, Wu J, Mao S, Boggs K, Mulder H, Yergeau D, Lu C, Ding L, Edmonson M, Qu C, Wang J, Li Y, Navid F, Daw NC, Mardis ER, Wilson RK, Downing JR, Zhang J, Dyer MA	Recurrent somatic structural variations contribute to tumorigenesis in pediatric osteosarcoma	Cell Reports	2014 Apr 	13	Osteosarcoma	Next Generation Sequencing	Homo sapiens	SJOS010_M	Illumina 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of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN 38105, USA	Pediatric osteosarcoma is characterized by multiple somatic chromosomal lesions, including structural variations (SVs) and copy number alterations (CNAs). To define the landscape of somatic mutations in pediatric osteosarcoma, we performed whole-genome sequencing of DNA from 20 osteosarcoma tumor samples and matched normal tissue in a discovery cohort, as well as 14 samples in a validation cohort. Single-nucleotide variations (SNVs) exhibited a pattern of localized hypermutation called kataegis in 50% of the tumors. We identified p53 pathway lesions in all tumors in the discovery cohort, nine of which were translocations in the first intron of the TP53 gene. Beyond TP53, the RB1, ATRX, and DLG2 genes showed recurrent somatic alterations in 29%-53% of the tumors. These data highlight the power of whole-genome sequencing for identifying recurrent somatic alterations in cancer genomes that may be missed using other methods. 	GRCh37/hg19				Yes	NA
CTDB0383	Research	22833442	Stevens-Kroef M, Weghuis DO, Croockewit S, Derksen L, Hooijer J, Elidrissi-Zaynoun N, Siepman A, Simons A, Kessel AG	High detection rate of clinically relevant genomic abnormalities in plasma cells enriched from patients with multiple myeloma	Genes, Chromosomes & Cancer	2012 Nov	13	Multiple myeloma	SNP Array	Homo sapiens	case 34	Affymetrix GeneChip 250k				Department of Human Genetics, Radboud University Nijmegen Medical Centre, The Netherlands	Multiple myeloma is a heterogeneous disease, which is characterized by the occurrence of specific genomic abnormalities that are both of diagnostic and prognostic relevance. Since the detection of these abnormalities through molecular-genetic techniques is hampered by the overall low percentage of plasma cells present in primary bone marrow aspirates, we assessed the efficacy of these techniques in enriched plasma cell fractions from 61 multiple myeloma patients. Using interphase FISH, genomic abnormalities could be detected in 96% of the enriched samples as compared to 61% in the cultured whole bone marrow samples. We also found that microarray-based genomic profiling of enriched plasma samples facilitates the detection of additional, possibly clinically relevant, genomic abnormalities. We conclude that the genomic delineation of enriched plasma cells from multiple myeloma patients results in a significantly increased detection rate of clinically relevant genomic abnormalities. In order to facilitate molecular-genetic data interpretation, we recommend morphological assessment of plasma cell purity after enrichment.					Yes	NA
CTDB0384	Research	25186909	Inaki K, Menghi F, Woo XY, Wagner JP, Jacques PE, Lee YF, Shreckengast PT, Soon WW, Malhotra A, Teo AS, Hillmer AM, Khng AJ, Ruan X, Ong SH, Bertrand D, Nagarajan N, Karuturi RK, Miranda AH, Liu ET	Systems consequences of amplicon formation in human breast cancer	Genome Research	2014 Oct	22	Breast cancer	Next Generation Sequencing	Homo sapiens	BT55	AB SOLiD 3 Plus System	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-26477557:0;chr17:26477558-53167545:-1;chr17:35327718-44040832:-1;chr17:35484752-32471649:1;chr17:35511432-35114153:1;chr17:44577064-47997384:-1;chr17:48218299-19265756:1;chr17:48761811-35187023:1;chr17:53167546-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs17:43485798-43485798,hs17:46036716-46036716;hs17:35336616-35336616,hs17:45874398-45874398;hs17:34388439-34388439,hs17:44664869-44664869;hs17:46780169-46780169,hs17:48815995-48815995;hs8:82011394-82011394,hs8:86729758-86729758;hs13:58728264-58728264,hs17:45198558-45198558		Cancer Therapeutics and Stratified Oncology, Genome Institute of Singapore, Genome, Singapore 138672, Singapore	Chromosomal structural variations play an important role in determining the transcriptional landscape of human breast cancers. To assess the nature of these structural variations, we analyzed eight breast tumor samples with a focus on regions of gene amplification using mate-pair sequencing of long-insert genomic DNA with matched transcriptome profiling. We found that tandem duplications appear to be early events in tumor evolution, especially in the genesis of amplicons. In a detailed reconstruction of events on chromosome 17, we found large unpaired inversions and deletions connect a tandemly duplicated ERBB2 with neighboring 17q21.3 amplicons while simultaneously deleting the intervening BRCA1 tumor suppressor locus. This series of events appeared to be unusually common when examined in larger genomic data sets of breast cancers albeit using approaches with lesser resolution. Using siRNAs in breast cancer cell lines, we showed that the 17q21.3 amplicon harbored a significant number of weak oncogenes that appeared consistently coamplified in primary tumors. Down-regulation of BRCA1 expression augmented the cell proliferation in ERBB2-transfected human normal mammary epithelial cells. Coamplification of other functionally tested oncogenic elements in other breast tumors examined, such as RIPK2 and MYC on chromosome 8, also parallel these findings. Our analyses suggest that structural variations efficiently orchestrate the gain and loss of cancer gene cassettes that engage many oncogenic pathways simultaneously and that such oncogenic cassettes are favored during the evolution of a cancer.	GRCh37/hg19	GSE57914			Yes	MYH9,TTC28;CABIN1,BRD1;DESI1,EIF3L
CTDB0385	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	4	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG003_A	Illumina Genome Analyzer IIx or HiSeq	chr10:0-319616:0;chr10:135524701-135534747:0;chr10:25879812-25885000:1;chr10:25885001-25885000:0;chr10:25885001-25889198:1;chr10:25889199-25889198:0;chr10:25889199-25894119:1;chr10:25894120-25894119:0;chr10:25894120-25897300:1;chr10:25897301-25897400:0;chr10:25897401-25897500:1;chr10:25897501-42753900:0;chr10:319617-320400:1;chr10:320401-320400:0;chr10:320401-408027:1;chr10:408028-408027:0;chr10:408028-710869:1;chr10:42753901-135524700:-1;chr10:710870-710869:0;chr10:710870-711300:1;chr10:711301-711300:0;chr10:711301-776100:1;chr10:776101-25879811:0;chr11:0-133700:0;chr11:13221610-13221609:0;chr11:13221610-13223467:-1;chr11:13223468-13223467:0;chr11:13223468-84279022:-1;chr11:133701-13221609:-1;chr11:134946401-135006516:0;chr11:84279023-84279022:0;chr11:84279023-84309912:-1;chr11:84309913-134946400:-1;chr11:84309913-84309912:0;chr12:0-57948297:0;chr12:122248387-124310873:1;chr12:124310874-133851895:0;chr12:57948298-57953600:1;chr12:57953601-57953600:0;chr12:57953601-57963600:1;chr12:57963601-57963600:0;chr12:57963601-58158690:1;chr12:58158691-58158690:0;chr12:58158691-58310360:1;chr12:58310361-58310360:0;chr12:58310361-58310600:1;chr12:58310601-58310600:0;chr12:58310601-58557840:1;chr12:58557841-58557840:0;chr12:58557841-58558200:1;chr12:58558201-58558200:0;chr12:58558201-58561515:1;chr12:58561516-58561515:0;chr12:58561516-58569000:1;chr12:58569001-58569000:0;chr12:58569001-58569700:1;chr12:58569701-58569700:0;chr12:58569701-58570000:1;chr12:58570001-58570000:0;chr12:58570001-58611116:1;chr12:58611117-58611116:0;chr12:58611117-58611438:1;chr12:58611439-58611438:0;chr12:58611439-58615200:1;chr12:58615201-58615200:0;chr12:58615201-58618300:1;chr12:58618301-58618300:0;chr12:58618301-58619700:1;chr12:58619701-58619700:0;chr12:58619701-58621800:1;chr12:58621801-122248386:0;chr13:0-115169878:0;chr14:0-19964300:0;chr14:107289501-107349540:0;chr14:19964301-22352300:-1;chr14:22352301-22352300:0;chr14:22352301-22974800:1;chr14:22974801-30217076:0;chr14:30217077-30350303:-1;chr14:30350304-107289500:-1;chr14:30350304-30350303:0;chr15:0-21885800:0;chr15:102521201-102531392:0;chr15:21885801-102521200:-1;chr16:0-74531130:0;chr16:74531131-74532821:-1;chr16:74532822-90354753:0;chr17:0-0:0;chr17:1-14258442:-1;chr17:14258443-57825593:0;chr17:57825594-58210400:1;chr17:58210401-58210400:0;chr17:58210401-58264300:1;chr17:58264301-58264400:0;chr17:58264401-58405372:1;chr17:58405373-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-161160900:0;chr1:161160901-161173000:-1;chr1:161173001-243265700:0;chr1:243265701-245044000:1;chr1:245044001-249250621:0;chr20:0-39609281:0;chr20:39609282-39788000:1;chr20:39788001-39788000:0;chr20:39788001-39804900:1;chr20:39804901-39804900:0;chr20:39804901-40217500:1;chr20:40217501-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-10500:0;chr4:10484201-10484200:0;chr4:10484201-10501699:1;chr4:10501-8158568:-1;chr4:10501700-10501699:0;chr4:10501700-19042264:-1;chr4:19042265-19042264:0;chr4:19042265-19043000:1;chr4:19043001-19043000:0;chr4:19043001-19049946:1;chr4:19049947-19049946:0;chr4:19049947-19054823:1;chr4:19054824-19054823:0;chr4:19054824-19055600:1;chr4:19055601-19055600:0;chr4:19055601-19088800:1;chr4:19088801-19088800:0;chr4:19088801-19089300:1;chr4:19089301-19089300:0;chr4:19089301-19093940:1;chr4:19093941-19093940:0;chr4:19093941-19094330:1;chr4:19094331-19094330:0;chr4:19094331-19094500:1;chr4:19094501-19094500:0;chr4:19094501-19102604:1;chr4:19102605-19102604:0;chr4:19102605-19115421:1;chr4:191043901-191154276:0;chr4:19115422-19115421:0;chr4:19115422-32457739:-1;chr4:32457740-32457739:0;chr4:32457740-32458805:1;chr4:32458806-32458805:0;chr4:32458806-33005500:-1;chr4:33005501-33005730:0;chr4:33005731-33012600:1;chr4:33012601-33012600:0;chr4:33012601-33013782:1;chr4:33013783-33013782:0;chr4:33013783-34569129:-1;chr4:34569130-34569129:0;chr4:34569130-34640647:1;chr4:34640648-34640647:0;chr4:34640648-34640657:1;chr4:34640658-34640657:0;chr4:34640658-34653188:1;chr4:34653189-34653188:0;chr4:34653189-34658100:1;chr4:34658101-34658100:0;chr4:34658101-34675530:1;chr4:34675531-34675530:0;chr4:34675531-35616000:1;chr4:35616001-35616000:0;chr4:35616001-36989108:-1;chr4:36989109-36989108:0;chr4:36989109-36992396:1;chr4:36992397-53595100:0;chr4:53595101-54513083:1;chr4:54513084-54513083:0;chr4:54513084-54513200:1;chr4:54513201-54513200:0;chr4:54513201-54562900:1;chr4:54562901-54562900:0;chr4:54562901-54565100:1;chr4:54565101-54565100:0;chr4:54565101-54565500:1;chr4:54565501-54565500:0;chr4:54565501-54568102:1;chr4:54568103-54568102:0;chr4:54568103-54575669:1;chr4:54575670-54575669:0;chr4:54575670-54576083:1;chr4:54576084-54576083:0;chr4:54576084-54576195:1;chr4:54576196-54576195:0;chr4:54576196-54577438:1;chr4:54577439-54577438:0;chr4:54577439-54862394:1;chr4:54862395-54862394:0;chr4:54862395-54863600:1;chr4:54863601-54863600:0;chr4:54863601-54864000:1;chr4:54864001-54864000:0;chr4:54864001-54868081:1;chr4:54868082-54868081:0;chr4:54868082-54872475:1;chr4:54872476-54872475:0;chr4:54872476-54876900:1;chr4:54876901-54876900:0;chr4:54876901-54879647:1;chr4:54879648-54879647:0;chr4:54879648-54881882:1;chr4:54881883-54881882:0;chr4:54881883-55040002:1;chr4:55040003-55040002:0;chr4:55040003-55139437:1;chr4:55139438-55139437:0;chr4:55139438-55140416:1;chr4:55140417-55140416:0;chr4:55140417-55212164:1;chr4:55212165-55212164:0;chr4:55212165-55358161:1;chr4:55358162-57015374:0;chr4:57015375-57025500:1;chr4:57025501-57259600:0;chr4:57259601-64706666:-1;chr4:64706667-64706666:0;chr4:64706667-64710500:1;chr4:64710501-64710500:0;chr4:64710501-64713100:1;chr4:64713101-64713500:0;chr4:64713501-64717100:1;chr4:64717101-64717100:0;chr4:64717101-64717400:1;chr4:64717401-64717400:0;chr4:64717401-64722629:1;chr4:64722630-64722629:0;chr4:64722630-69463216:-1;chr4:69463217-69463216:0;chr4:69463217-69491400:1;chr4:69491401-69491500:0;chr4:69491501-69493000:1;chr4:69493001-69493100:0;chr4:69493101-69495900:1;chr4:69495901-69495975:0;chr4:69495976-69503400:1;chr4:69503401-69503460:0;chr4:69503461-69505866:1;chr4:69505867-191043900:-1;chr4:69505867-69505866:0;chr4:8158569-8158568:0;chr4:8158569-8184900:1;chr4:8184901-8184900:0;chr4:8184901-8185264:1;chr4:8185265-10484200:-1;chr4:8185265-8185264:0;chr5:0-110271009:0;chr5:110271010-137498900:-1;chr5:137498901-138227100:0;chr5:138227101-145626781:-1;chr5:145626782-180915260:0;chr6:0-57623682:0;chr6:171050901-171115067:0;chr6:57623683-58075900:-1;chr6:58075901-61880300:0;chr6:61880301-171050900:-1;chr7:0-117407779:0;chr7:117407780-117408436:-1;chr7:117408437-135306487:0;chr7:135306488-135306625:-1;chr7:135306626-159138663:0;chr8:0-123740009:0;chr8:123740010-124433923:1;chr8:124433924-146364022:0;chr9:0-141213431:0;chrX:0-2699500:0;chrX:124406301-124406300:0;chrX:124406301-124414700:-1;chrX:124414701-124414700:0;chrX:124414701-144898200:1;chrX:144898201-144898200:0;chrX:144898201-144913900:1;chrX:144913901-144913900:0;chrX:144913901-154930300:1;chrX:154930301-155270560:0;chrX:2699501-124406300:1;chrY:0-2649500:0;chrY:26446401-59373566:0;chrY:2649501-26446400:-1	hs3:160202262-160202262,hs2:159281315-159281315;hs4:19115422-19115422,hs4:55358162-55358162;hs4:33005731-33005731,hs10:25879812-25879812;hs4:55140417-55140417,hs10:710870-710870;hs4:8185265-8185265,hs4:33013781-33013781;hs4:34569130-34569130,hs4:32457740-32457740;hs4:88005070-88005070,hs4:64706667-64706667;hs4:55140417-55140417,hs10:710870-710870;hs4:8158569-8158569,hs10:319617-319617;hs4:55139438-55139438,hs11:98307129-98307129;hs4:54872476-54872476,hs4:54513084-54513084;hs4:34675531-34675531,hs4:55212165-55212165;hs6:57623683-57623683,hs17:14258443-14258443;hs10:8040140-8040140,hs10:22018846-22018846;hs10:8040140-8040140,hs10:22018846-22018846;hs10:408028-408028,hs4:69491436-69491436;hs10:776144-776144,hs4:10501696-10501696;hs12:58614957-58614957,hs12:58614760-58614760;hs12:58158691-58158691,hs4:54868080-54868080;hs13:91558653-91558653,hs13:89295341-89295341	ABLIM2;ACOX3;AFAP1;AFF1;ARAP2;ARL9;BOD1L;C1orf101;C4orf14;C8orf76;CCKAR;CENPC1;CHIC2;CLNK;CXorf51;DCAF16;DEFB131;DRD5;DTHD1;DUX2;DUX4;DUX4L2;DUX4L3;DUX4L4;DUX4L5;DUX4L6;DUX4L7;EPHA5;FAM184B;FIP1L1;GBA3;GPCRLTM7;GPR125;GPR78;GRPEL1;GSX2;HOPX;HS3ST1;HTRA3;IGFBP7;LCORL;LNX1;LOC100288413;LOC144776;LOC653486;LPHN3;MED28;METTL19;NCAPG;NKX3-2;PACRGL;PAICS;PCDH7;PDGFRA;POLR2B;PPAT;PSAPL1;RAB28;RASL11B;RBPJ;REST;SCFD2;SH3TC1;SLC2A9;SORCS2;SRP72;STAP1;STIM2;TBC1D19;TECRL;TMPRSS11B;UBA6;UGT2A3;UGT2B10;UGT2B11;UGT2B15;UGT2B17;UGT2B7;WDR1;YTHDC1;ZNF518B;ZNF595;ZNF718;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	DIP2C,PDGFRA
CTDB0386	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	15	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG004_D	Illumina Genome Analyzer IIx or HiSeq	chr10:0-42355000:0;chr10:135476901-135534747:0;chr10:42355001-52665706:-1;chr10:52665707-52665706:0;chr10:52665707-69909310:-1;chr10:69909311-69909310:0;chr10:69909311-85091787:-1;chr10:85091788-85091787:0;chr10:85091788-85095874:-1;chr10:85095875-85095874:0;chr10:85095875-85101400:-1;chr10:85101401-85101645:0;chr10:85101646-85107120:-1;chr10:85107121-85107120:0;chr10:85107121-85121200:-1;chr10:85121201-85121745:0;chr10:85121746-85158900:-1;chr10:85158901-85158900:0;chr10:85158901-89580853:-1;chr10:89580854-89580853:0;chr10:89580854-89693652:-1;chr10:89693653-135476900:-1;chr10:89693653-89693652:0;chr11:0-168400:0;chr11:134946401-135006516:0;chr11:168401-2466500:-1;chr11:2466501-134946400:-1;chr11:2466501-2466500:0;chr12:0-133851895:0;chr13:0-19020700:0;chr13:115109801-115169878:0;chr13:19020701-115109800:-1;chr14:0-19191600:0;chr14:107289501-107349540:0;chr14:19191601-22033026:1;chr14:22033027-22033026:0;chr14:22033027-22034100:-1;chr14:22034101-22034200:0;chr14:22034201-22073565:1;chr14:22073566-107289500:-1;chr14:22073566-22073565:0;chr15:0-20000000:0;chr15:20000001-82664400:-1;chr15:82664401-83229106:0;chr15:83229107-83234500:1;chr15:83234501-83234500:0;chr15:83234501-83305857:1;chr15:83305858-83305857:0;chr15:83305858-83609926:1;chr15:83609927-83609926:0;chr15:83609927-83709380:1;chr15:83709381-83709380:0;chr15:83709381-83833182:1;chr15:83833183-83833182:0;chr15:83833183-83886500:1;chr15:83886501-83886500:0;chr15:83886501-84958300:1;chr15:84958301-85080346:0;chr15:85080347-86293000:1;chr15:86293001-86293000:0;chr15:86293001-86313100:1;chr15:86313101-86313100:0;chr15:86313101-86656300:1;chr15:86656301-86656300:0;chr15:86656301-86674945:1;chr15:86674946-86674945:0;chr15:86674946-87172300:1;chr15:87172301-87172300:0;chr15:87172301-87177448:1;chr15:87177449-87177448:0;chr15:87177449-87531100:1;chr15:87531101-87531100:0;chr15:87531101-87659900:1;chr15:87659901-87659900:0;chr15:87659901-88288100:1;chr15:88288101-88288100:0;chr15:88288101-88660093:1;chr15:88660094-88660093:0;chr15:88660094-89676083:1;chr15:89676084-89676083:0;chr15:89676084-89804637:1;chr15:89804638-89804637:0;chr15:89804638-90278566:1;chr15:90278567-96729370:0;chr15:96729371-96770681:1;chr15:96770682-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-25583775:0;chr18:25583776-25705352:-1;chr18:25705353-78077248:0;chr19:0-158500:0;chr19:11485901-19965815:1;chr19:158501-7996700:-1;chr19:19965816-19965815:0;chr19:19965816-24453400:-1;chr19:24453401-27731800:0;chr19:27731801-59118800:-1;chr19:59118801-59128983:0;chr19:7996701-11485900:0;chr1:0-249250621:0;chr20:0-60000:0;chr20:18439844-18439843:0;chr20:18439844-18983600:1;chr20:18983601-19284572:0;chr20:19284573-22770329:-1;chr20:22770330-63025520:0;chr20:60001-18439843:-1;chr21:0-14338400:0;chr21:14338401-48119800:-1;chr21:48119801-48129895:0;chr22:0-17039000:0;chr22:17039001-17652692:-1;chr22:17652693-17657900:0;chr22:17657901-17804279:-1;chr22:17804280-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-90700:0;chr6:53410001-98489375:0;chr6:90701-53410000:-1;chr6:98489376-98642109:-1;chr6:98642110-171115067:0;chr7:0-159138663:0;chr8:0-74565145:0;chr8:74565146-74754778:1;chr8:74754779-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs15:85864830-85864830,hs15:86160094-86160094;hs14:22033027-22033027,hs14:22073566-22073566;hs20:18439844-18439844,hs14:22034083-22034083;hs19:33121294-33121294,hs10:3446375-3446375;hs15:85865305-85865305,hs15:89250459-89250459;hs19:19965816-19965816,hsX:1781376-1781376;hs15:95610288-95610288,hs15:99346209-99346209;hs3:169746022-169746022,hs15:95592769-95592769;hs10:85091788-85091788,hs10:85120150-85120150;hs15:86674946-86674946,hs15:87177449-87177449;hs15:89408289-89408289,hs15:88945062-88945062;hs15:86185075-86185075,hs15:84313872-84313872;hs15:89804638-89804638,hs15:88977330-88977330;hs15:85357531-85357531,hs15:89292296-89292296;hs15:85167984-85167984,hs15:83709381-83709381	ABHD2;ACAN;ADAMTSL3;AEN;AGBL1;AKAP13;ALPK3;AP3B2;BNC1;BTBD1;C10orf99;C15orf40;C15orf42;C19orf12;CPEB1;DET1;EFTUD1;FAM103A1;FAM154B;FANCI;FSD2;GOLGA6L10;GOLGA6L6;HAPLN3;HDGFRP3;HOMER2;IGF1R;ISG20;KIF7;KLHL25;LOC100128496;LOC645781;LOC653486;MEX3B;MFGE8;MRPL46;MRPS11;NMB;NTRK3;OR4M2;OR4N4;PDE8A;PEX11A;PLIN1;POLG;POTEB;RHCG;RLBP1;SEC11A;SH3GL3;SLC28A1;TM6SF1;TMC3;WDR73;WDR93;WHAMM;ZNF592;ZSCAN2;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	ABHD2,AKAP13;BTBD1,CPEB1;BTBD1,NTRK3;CPEB1,NTRK3;UBE2Q2P1,HDGFRP3
CTDB0387	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	X	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG007_A	Illumina Genome Analyzer IIx or HiSeq	chr10:0-135534747:0;chr11:0-55362900:0;chr11:106865708-106866660:-1;chr11:106866661-106880100:0;chr11:106880101-116354984:-1;chr11:116354985-135006516:0;chr11:55362901-63762408:-1;chr11:63762409-68314700:0;chr11:68314701-70395737:-1;chr11:70395738-106865707:0;chr12:0-34485100:0;chr12:34485101-34505100:-1;chr12:34505101-64597831:0;chr12:64597832-64597915:1;chr12:64597916-133851895:0;chr13:0-19338000:0;chr13:19338001-70111100:-1;chr13:70111101-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-20271200:0;chr17:20271201-22262900:1;chr17:22262901-29683303:0;chr17:29683304-29684973:1;chr17:29684974-81195210:0;chr18:0-78077248:0;chr19:0-158500:0;chr19:158501-397400:1;chr19:397401-551800:0;chr19:551801-572300:1;chr19:572301-59128983:0;chr1:0-144454200:0;chr1:144454201-249240500:1;chr1:249240501-249250621:0;chr20:0-60000:0;chr20:26317701-63025520:0;chr20:60001-26317700:-1;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-133825295:0;chr6:133825296-135577686:-1;chr6:135577687-171115067:0;chr7:0-124170500:0;chr7:124170501-124278903:1;chr7:124278904-124305859:0;chr7:124305860-141747700:1;chr7:141747701-141747840:0;chr7:141747841-141775645:1;chr7:141775646-141775645:0;chr7:141775646-146953908:1;chr7:146953909-146953908:0;chr7:146953909-147164300:1;chr7:147164301-147164300:0;chr7:147164301-147294114:1;chr7:147294115-147294171:0;chr7:147294172-147329892:1;chr7:147329893-147329892:0;chr7:147329893-147344346:1;chr7:147344347-147344346:0;chr7:147344347-159128500:-1;chr7:159128501-159138663:0;chr8:0-146364022:0;chr9:0-10000:0;chr9:10001-39638800:-1;chr9:39638801-89558853:0;chr9:89558854-89560838:-1;chr9:89560839-141213431:0;chrX:0-127371980:0;chrX:127371981-127381000:1;chrX:127381001-127929013:0;chrX:127929014-127929393:1;chrX:127929394-128870386:0;chrX:128870387-128870533:1;chrX:128870534-128870533:0;chrX:128870534-128870818:1;chrX:128870819-128870818:0;chrX:128870819-128870853:1;chrX:128870854-128870853:0;chrX:128870854-128870958:1;chrX:128870959-128870958:0;chrX:128870959-128871109:1;chrX:128871110-128871109:0;chrX:128871110-128871248:1;chrX:128871249-128871248:0;chrX:128871249-128871276:1;chrX:128871277-128871276:0;chrX:128871277-128871421:1;chrX:128871422-128871421:0;chrX:128871422-128871484:1;chrX:128871485-128871484:0;chrX:128871485-128871563:1;chrX:128871564-128871563:0;chrX:128871564-128871902:1;chrX:128871903-128871902:0;chrX:128871903-128871966:1;chrX:128871967-128942253:0;chrX:128942254-129069878:1;chrX:129069879-131390128:0;chrX:131390129-131412063:1;chrX:131412064-131413081:0;chrX:131413082-131438243:1;chrX:131438244-131438243:0;chrX:131438244-131438265:1;chrX:131438266-131438265:0;chrX:131438266-131438518:1;chrX:131438519-131438518:0;chrX:131438519-131438569:1;chrX:131438570-131438569:0;chrX:131438570-131438697:1;chrX:131438698-131438697:0;chrX:131438698-131438816:1;chrX:131438817-131438816:0;chrX:131438817-131439360:1;chrX:131439361-131441477:0;chrX:131441478-131443085:1;chrX:131443086-131443085:0;chrX:131443086-131444117:1;chrX:131444118-131447200:0;chrX:131447201-131447284:1;chrX:131447285-131447284:0;chrX:131447285-131447478:1;chrX:131447479-131447478:0;chrX:131447479-131447600:1;chrX:131447601-131447600:0;chrX:131447601-131448419:1;chrX:131448420-131454500:0;chrX:131454501-131456182:1;chrX:131456183-134229769:0;chrX:134229770-134230082:1;chrX:134230083-134235682:0;chrX:134235683-134235780:1;chrX:134235781-134235780:0;chrX:134235781-134236334:1;chrX:134236335-134236334:0;chrX:134236335-134236561:1;chrX:134236562-134246828:0;chrX:134246829-134246894:1;chrX:134246895-134246894:0;chrX:134246895-134247016:1;chrX:134247017-134247016:0;chrX:134247017-134247216:1;chrX:134247217-135480500:0;chrX:135480501-135503157:1;chrX:135503158-142667655:0;chrX:142667656-142689555:1;chrX:142689556-142689555:0;chrX:142689556-142689760:1;chrX:142689761-142689760:0;chrX:142689761-142689892:1;chrX:142689893-142689892:0;chrX:142689893-142690042:1;chrX:142690043-143256900:0;chrX:143256901-143310858:1;chrX:143310859-143310858:0;chrX:143310859-143311096:1;chrX:143311097-143311096:0;chrX:143311097-144354565:1;chrX:144354566-144355187:0;chrX:144355188-152989100:1;chrX:152989101-152989100:0;chrX:152989101-153076600:1;chrX:153076601-153076600:0;chrX:153076601-154930300:1;chrX:154930301-155270560:0;chrY:0-2649500:0;chrY:2649501-28817600:-1;chrY:28817601-59373566:0	hs17:29684974-29684974,hs11:99252689-99252689;hs11:99252874-99252874,hs17:29683304-29683304;hsX:128870472-128870472,hsX:131438519-131438519;hsX:131448163-131448163,hsX:131438484-131438484;hsX:131447601-131447601,hsX:131438266-131438266;hsX:131438437-131438437,hsX:128870472-128870472;hsX:128871527-128871527,hsX:131438750-131438750;hsX:128871110-128871110,hsX:128870670-128870670;hsX:129069879-129069879,hsX:131412064-131412064;hsX:127921466-127921466,hsX:128870979-128870979;hsX:134247205-134247205,hsX:128870976-128870976;hsX:143311097-143311097,hsX:142667656-142667656;hsX:128870625-128870625,hsX:131438842-131438842;hsX:134233095-134233095,hsX:131447151-131447151;hsX:128871359-128871359,hsX:128870800-128870800;hsX:131438655-131438655,hsX:142689893-142689893;hsX:128871563-128871563,hsX:134230174-134230174;hsX:131443086-131443086,hsX:142690043-142690043;hs11:70395738-70395738,hs11:63762409-63762409;hsX:127921323-127921323,hsX:128871432-128871432;hsX:131438266-131438266,hsX:131390129-131390129	ABCD1;ARHGAP4;AVPR2;BCAP31;C12orf66;C17orf51;C9orf66;CLIC2;CXorf1;CXorf51;DUSP9;FAM58A;FMR1;FMR1NB;GPR112;H2AFB2;IDH3G;L1CAM;LOC154872;LOC646627;NAA10;PDZD4;PLXNB3;PNCK;RAB39B;SLC6A8;SLITRK2;SPANXN1;SRPK3;SSR4;TMLHE;UTP14A;VBP1;ZDHHC9;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	NA
CTDB0388	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	7	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG009_A	Illumina Genome Analyzer IIx or HiSeq	chr10:0-71700:0;chr10:135476901-135534747:0;chr10:39154801-42397500:0;chr10:42397501-135476900:1;chr10:71701-39154800:1;chr11:0-133700:0;chr11:133701-33358870:1;chr11:134923601-134946400:-1;chr11:134946401-135006516:0;chr11:33358871-33358870:0;chr11:33358871-33499500:1;chr11:33499501-33499500:0;chr11:33499501-36302000:1;chr11:36302001-36302000:0;chr11:36302001-36402368:1;chr11:36402369-36402368:0;chr11:36402369-42060600:1;chr11:42060601-42060600:0;chr11:42060601-42229819:1;chr11:42229820-42268811:0;chr11:42268812-43804586:1;chr11:43804587-43804586:0;chr11:43804587-44203059:1;chr11:44203060-44203059:0;chr11:44203060-49718400:1;chr11:49718401-68164538:0;chr11:68164539-68656400:1;chr11:68656401-68656400:0;chr11:68656401-71229300:1;chr11:71229301-134923600:0;chr12:0-60700:0;chr12:133841501-133851895:0;chr12:38173487-38173486:0;chr12:38173487-38173907:1;chr12:38173908-38173907:0;chr12:38173908-38312286:1;chr12:38312287-38312286:0;chr12:38312287-38314476:1;chr12:38314477-38314476:0;chr12:38314477-38316609:1;chr12:38316610-38316609:0;chr12:38316610-38507400:1;chr12:38507401-38507400:0;chr12:38507401-38792988:1;chr12:38792989-38792988:0;chr12:38792989-38853764:1;chr12:38853765-38853764:0;chr12:38853765-38854563:1;chr12:38854564-38854563:0;chr12:38854564-38856100:1;chr12:38856101-38856200:0;chr12:38856201-39610824:1;chr12:39610825-39610824:0;chr12:39610825-39620400:1;chr12:39620401-39620400:0;chr12:39620401-39627046:1;chr12:39627047-39627046:0;chr12:39627047-39629862:1;chr12:39629863-39629862:0;chr12:39629863-39639529:1;chr12:39639530-39639529:0;chr12:39639530-39712373:1;chr12:39712374-39712373:0;chr12:39712374-39717962:1;chr12:39717963-39717962:0;chr12:39717963-39745127:1;chr12:39745128-39745127:0;chr12:39745128-39745406:1;chr12:39745407-39745406:0;chr12:39745407-39803052:1;chr12:39803053-39803052:0;chr12:39803053-39803797:1;chr12:39803798-39803797:0;chr12:39803798-39847187:1;chr12:39847188-39847187:0;chr12:39847188-39999826:1;chr12:39999827-39999826:0;chr12:39999827-40212630:1;chr12:40212631-40212630:0;chr12:40212631-40688681:1;chr12:40688682-40688681:0;chr12:40688682-40713320:1;chr12:40713321-40713320:0;chr12:40713321-40770415:1;chr12:40770416-40770415:0;chr12:40770416-40929589:1;chr12:40929590-40929589:0;chr12:40929590-41056798:1;chr12:41056799-41056798:0;chr12:41056799-41155666:1;chr12:41155667-41155666:0;chr12:41155667-41160013:1;chr12:41160014-41160013:0;chr12:41160014-41263446:1;chr12:41263447-41263446:0;chr12:41263447-41569417:1;chr12:41569418-41569417:0;chr12:41569418-41598772:1;chr12:41598773-41598772:0;chr12:41598773-41607583:1;chr12:41607584-133841500:1;chr12:41607584-41607583:0;chr12:60701-38173486:1;chr13:0-19020700:0;chr13:115109801-115169878:0;chr13:19020701-115109800:1;chr14:0-107349540:0;chr15:0-20000000:0;chr15:102465301-102531392:0;chr15:20000001-35297736:1;chr15:35297737-35297736:0;chr15:35297737-35309792:1;chr15:35309793-35309792:0;chr15:35309793-35315716:1;chr15:35315717-35315716:0;chr15:35315717-69109900:1;chr15:69109901-102465300:1;chr15:69109901-69109900:0;chr16:0-60000:0;chr16:60001-90292700:1;chr16:90292701-90354753:0;chr17:0-15472400:0;chr17:15472401-16531563:1;chr17:16531564-16531563:0;chr17:16531564-17419160:1;chr17:17419161-17419160:0;chr17:17419161-19701431:1;chr17:19701432-19701431:0;chr17:19701432-19750042:1;chr17:19750043-19750042:0;chr17:19750043-21563400:1;chr17:21563401-21670200:0;chr17:21670201-81195100:1;chr17:81195101-81195210:0;chr18:0-78077248:0;chr19:0-158500:0;chr19:158501-59118800:1;chr19:59118801-59128983:0;chr1:0-10100:0;chr1:10101-54171200:1;chr1:102242625-102242666:0;chr1:102242667-149035800:1;chr1:149035801-149035800:0;chr1:149035801-149204100:-1;chr1:149204101-149646000:0;chr1:149646001-249240500:1;chr1:249240501-249250621:0;chr1:54171201-54171200:0;chr1:54171201-54241609:1;chr1:54241610-54241609:0;chr1:54241610-56062273:1;chr1:56062274-56062273:0;chr1:56062274-56194700:1;chr1:56194701-56194800:0;chr1:56194801-57287043:1;chr1:57287044-102242624:1;chr1:57287044-57287043:0;chr20:0-60000:0;chr20:19669501-19669500:0;chr20:19669501-19685417:1;chr20:19685418-19685417:0;chr20:19685418-19784054:1;chr20:19784055-19924774:0;chr20:19924775-19946227:1;chr20:19946228-19946227:0;chr20:19946228-19946309:1;chr20:19946310-19946309:0;chr20:19946310-19946798:1;chr20:19946799-19946798:0;chr20:19946799-19967000:1;chr20:19967001-19967000:0;chr20:19967001-62918900:1;chr20:60001-19669500:1;chr20:62918901-63025520:0;chr21:0-14338400:0;chr21:14338401-33496500:1;chr21:33496501-33496500:0;chr21:33496501-33520100:1;chr21:33520101-33520200:0;chr21:33520201-34785736:1;chr21:34785737-34785736:0;chr21:34785737-34786036:1;chr21:34786037-34786036:0;chr21:34786037-48119800:1;chr21:48119801-48129895:0;chr22:0-16847900:0;chr22:16847901-49254240:1;chr22:49254241-49254240:0;chr22:49254241-49335475:1;chr22:49335476-49335475:0;chr22:49335476-51234500:1;chr22:51234501-51304566:0;chr2:0-10000:0;chr2:10001-115940300:1;chr2:115940301-116003600:0;chr2:116003601-243094700:1;chr2:243094701-243199373:0;chr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6019-117406019,hs7:157991199-157991199;hs12:38166571-38166571,hs7:108112775-108112775;hs11:18782557-18782557,hs11:14061845-14061845;hs7:88468475-88468475,hs12:39745128-39745128;hs12:38314477-38314477,hs7:108131272-108131272;hs5:40488800-40488800,hs5:40903036-40903036;hs12:41263008-41263008,hs7:113581438-113581438;hs6:69586179-69586179,hs11:42268812-42268812;hs20:19946228-19946228,hs20:19924775-19924775;hs7:93536941-93536941,hs7:92874371-92874371;hs1:57287044-57287044,hs7:86646669-86646669;hs17:19701432-19701432,hs17:19750043-19750043;hs12:39601641-39601641,hs7:88636338-88636338;hs12:40212631-40212631,hs7:113050032-113050032;hs7:113365729-113365729,hs12:40929590-40929590;hs12:39607882-39607882,hs7:88413777-88413777;hs7:116815626-116815626,hs21:34785737-34785737;hs20:19946799-19946799,hs20:19946223-19946223;hs21:34786037-34786037,hs7:100248747-100248747;hs7:90915962-90915962,hs7:90969953-90969953;hs7:108129790-108129790,hs12:38312287-38312287;hs15:68083464-68083464,hs15:99162473-99162473;hs7:86703321-86703321,hs7:86644073-86644073;hs7:91067762-91067762,hs12:39627047-39627047;hs1:56194701-56194701,hs7:92242202-92242202;hs7:116465984-116465984,hs12:40652829-40652829;hs11:36402369-36402369,hs11:68689001-68689001;hs10:45293715-45293715,hs1:76310109-76310109;hs21:34786037-34786037,hs7:100248747-100248747;hs7:84152311-84152311,hs12:39803798-39803798;hs20:19946228-19946228,hs20:19924775-19924775;hs7:88468475-88468475,hs12:39745128-39745128;hs12:38507372-38507372,hs12:38173431-38173431;hs7:88414617-88414617,hs7:88625420-88625420;hs9:82697356-82697356,hs9:94005095-94005095;hs18:40045135-40045135,hs5:31998216-31998216;hs7:88414440-88414440,hs7:88623990-88623990;hs7:93536941-93536941,hs7:92874371-92874371;hs7:117406019-117406019,hs7:157991199-157991199;hs20:19946799-19946799,hs20:19946223-19946223;hs7:88622690-88622690,hs12:39639530-39639530;hs7:157989631-157989631,hs12:41598773-41598773;hs7:84152122-84152122,hs12:39610825-39610825;hs7:157989631-157989631,hs12:41598773-41598773;hs7:88468475-88468475,hs12:39745128-39745128;hs12:40770416-40770416,hs12:41155667-41155667;hs5:31225486-31225486,hs5:32654333-32654333;hs7:108131315-108131315,hs12:41261949-41261949;hs4:67403436-67403436,hs5:1957113-1957113;hs1:68995754-68995754,hs10:48424974-48424974;hs7:90920686-90920686,hs12:39717963-39717963;hs1:111319853-111319853,hs7:99598937-99598937;hs12:39712374-39712374,hs12:39803053-39803053;hs22:44963845-44963845,hs10:129335123-129335123;hs20:19946799-19946799,hs20:19946223-19946223;hs7:113581568-113581568,hs12:40928739-40928739;hs11:36402369-36402369,hs11:68689001-68689001;hs12:41569418-41569418,hs12:41607584-41607584;hs7:108131315-108131315,hs12:41261949-41261949;hs7:92873779-92873779,hs7:92904864-92904864;hs11:77494008-77494008,hs5:151134882-151134882;hs7:92873779-92873779,hs7:92904864-92904864;hs7:117406019-117406019,hs7:157991199-157991199;hs7:91912720-91912720,hs7:66494424-66494424;hs7:157989631-157989631,hs12:41598773-41598773;hs18:11776823-11776823,hs10:95623582-95623582;hs8:75751494-75751494,hs8:75754424-75754424;hs7:90972509-90972509,hs7:88560802-88560802;hs12:40688682-40688682,hs7:117013151-117013151;hs1:54241610-54241610,hs7:96773436-96773436;hs7:91912720-91912720,hs7:66494424-66494424;hs12:39626877-39626877,hs7:88623643-88623643;hs20:19946799-19946799,hs20:19946223-19946223;hs15:68453333-68453333,hs15:35297737-35297737;hs10:46004233-46004233,hs7:86972930-86972930;hs7:93536941-93536941,hs7:92874371-92874371;hs12:40688682-40688682,hs7:117013151-117013151	ABCB1;ABCB4;ACN9;ACTL6B;ADAM22;AGFG2;AIMP2;AKAP9;AMPH;ANKIB1;ANKRD7;ASL;ASNS;ASZ1;BET1;C11orf74;C11orf96;C12orf40;C15orf41;C17orf51;C1orf123;C1orf168;C4orf33;C7orf23;C7orf36;C7orf42;C7orf47;C7orf50;C7orf51;C7orf53;C7orf60;C7orf61;C7orf62;C7orf63;C7orf64;C7orf66;C7orf70;C8orf33;C8orf34;C9orf66;CACNA2D1;CAPZA2;CASD1;CAV1;CAV2;CCDC132;CDK14;CDK6;CFTR;CHCHD2;CHN2;CLDN12;COL1A2;COX19;CPVL;CRCP;CREB5;CROT;CTTNBP2;CYP2W1;CYP51A1;CYTH3;DBF4;DLD;DLX5;DLX6;DMTF1;DNAJB6;DNAJB9;EIF2AK1;EPDR1;EPO;ESYT2;FAM133B;FBXO24;FLJ42280;FOXP2;FZD1;GAL3ST4;GATAD1;GATS;GIGYF1;GNB2;GNG11;GNGT1;GPC2;GPCRLTM7;GPER;GPR146;GPR85;GRM3;GTPBP10;GUSB;HEPACAM2;HGF;HIBADH;IFRD1;IMMP2L;INTS1;JAZF1;KCND2;KCTD7;KIAA1324L;KRIT1;LAMB1;LAMB4;LMTK2;LOC100128496;LOC100288524;LOC120824;LOC283116;LOC389493;LOC646627;LOC647589;LOC653486;LRCH4;LRRD1;MAFK;MDFIC;MEPCE;MICALL2;MNX1;MOSPD3;MTERF;NCAPG2;NOM1;NRCAM;OCM2;PCLO;PCOLCE;PDGFA;PEX1;PHKG1;PILRA;PILRB;PMS2;PNPLA8;POP7;POU6F2;PPP1R3A;PRKAR1B;PRR15;PTPRN2;PVRIG;RABGEF1;RAC1;RALA;RSPH10B;RSPH10B2;SAMD9;SAMD9L;SAP25;SBDS;SEMA3A;SEMA3D;SEMA3E;SFRP4;SHFM1;SLC26A3;SPDYE3;SRI;ST7;STAG3;STAG3L4;STARD3NL;STEAP1;STEAP2;STEAP4;TAC1;TAX1BP1;TES;TFEC;TFR2;THAP5;TMEM168;TP53TG1;TPST1;TRIL;TSC22D4;TSPAN12;TXNDC3;TYW1;UBE3C;UNCX;USP42;VIPR2;VPS41;WDR60;WIPF3;WNT2;ZCWPW1;ZFAND2A;ZNF479;ZNF679;ZNF680;ZNF716;ZNF727;ZNF735;ZNF736;ZNF804B;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	CCDC132,GNGT1;PTPRN2,PDZRN4;ST7,ACTL6B;ST7,IFNGR2;ZNF804B,KIF21A
CTDB0389	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	4	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG011_D	Illumina Genome Analyzer IIx or 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high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19					C4orf37,CUL2;C4orf37,OXNAD1;CUL2,C4orf37;CUL2,OXNAD1;DPH3,C4orf37;KIAA1530,CSN1S2AP;KIAA1530,VEGFC
CTDB0390	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	19	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG017_D	Illumina Genome Analyzer IIx or HiSeq	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-51025700:0;chr17:51025701-81160200:1;chr17:81160201-81195210:0;chr18:0-78077248:0;chr19:0-42798400:0;chr19:42798401-42890591:-1;chr19:42890592-45876123:0;chr19:45876124-45876822:-1;chr19:45876823-45876822:0;chr19:45876823-47930700:-1;chr19:47930701-47930700:0;chr19:47930701-55103700:-1;chr19:55103701-55103700:0;chr19:55103701-55669739:-1;chr19:55669740-55669739:0;chr19:55669740-59118800:-1;chr19:59118801-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-155288619:0;chr2:155288620-155288700:1;chr2:155288701-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-53103600:0;chr8:146303801-146364022:0;chr8:53103601-146303800:1;chr9:0-10000:0;chr9:10001-140772668:1;chr9:140772669-140773505:0;chr9:140773506-141102500:1;chr9:141102501-141213431:0;chrX:0-155270560:0;chrY:0-2649500:0;chrY:2649501-28817600:-1;chrY:28817601-59373566:0	hs19:40936318-40936318,hs19:40490842-40490842;hs19:55668538-55668538,hs19:47930726-47930726;hs19:55664092-55664092,hs10:121613523-121613523;hs10:130144300-130144300,hs19:46258672-46258672;hs19:55664092-55664092,hs10:121613523-121613523;hs19:38422818-38422818,hs19:55669249-55669249;hs19:37197984-37197984,hs19:37095913-37095913;hs19:37219530-37219530,hs19:37003614-37003614;hs19:46432959-46432959,hs19:45846358-45846358	C19orf51;C5AR1;C8orf33;C9orf66;CD3EAP;CHMP2A;CIC;DHX34;EPS8L1;ERCC1;FOSB;GLTSCR1;GPR77;KLC3;KPTN;LILRA1;LOC388553;MEGF8;MEIS3;MZF1;NAPA;PAFAH1B3;PPP1R12C;PPP1R13L;PPP6R1;PRR19;PRR24;PTPRH;RTN2;SIPA1L3;SLC8A2;SYT5;TMEM145;TMEM86B;TNNI3;TNNT1;TRIM28;UBE2M;ZBTB45;ZNF529;ZNF541;ZNF567;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	ZNF529,ZNF567
CTDB0391	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	7	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG019_E	Illumina Genome Analyzer IIx or HiSeq	chr10:0-29724120:0;chr10:29724121-29725468:-1;chr10:29725469-135534747:0;chr11:0-54951600:0;chr11:134946401-135006516:0;chr11:54951601-57527368:-1;chr11:57527369-82843400:0;chr11:82843401-134946400:-1;chr12:0-146200:0;chr12:132129601-132130400:0;chr12:132130401-133841500:1;chr12:133841501-133851895:0;chr12:146201-132129600:1;chr13:0-19125100:0;chr13:19125101-20016700:-1;chr13:20016701-115169878:0;chr14:0-19964300:0;chr14:107289501-107349540:0;chr14:19964301-22313700:-1;chr14:22313701-22981000:0;chr14:22981001-69670528:-1;chr14:69670529-69678041:0;chr14:69678042-107289500:-1;chr15:0-25313000:0;chr15:102521201-102531392:0;chr15:25313001-76622300:1;chr15:76622301-76640100:0;chr15:76640101-102521200:1;chr16:0-491380:0;chr16:32579628-32602840:-1;chr16:32602841-57021623:0;chr16:491381-5306900:1;chr16:5306901-32579627:0;chr16:57021624-70844000:-1;chr16:70844001-70862600:0;chr16:70862601-71202500:-1;chr16:71202501-71202500:0;chr16:71202501-90292700:-1;chr16:90292701-90354753:0;chr17:0-0:0;chr17:1-9152635:-1;chr17:10472147-10472146:0;chr17:10472147-12553016:1;chr17:12553017-12553016:0;chr17:12553017-12556411:1;chr17:12556412-12556411:0;chr17:12556412-21547300:1;chr17:21547301-21685300:0;chr17:21685301-22244500:1;chr17:22244501-47563225:0;chr17:47563226-54457337:-1;chr17:54457338-54475403:0;chr17:54475404-81195100:1;chr17:81195101-81195210:0;chr17:9152636-9152635:0;chr17:9152636-9156674:1;chr17:9156675-10472146:1;chr17:9156675-9156674:0;chr18:0-10000:0;chr18:10001-611800:1;chr18:10175701-10175900:0;chr18:10175901-10572600:1;chr18:10572601-10578600:0;chr18:10578601-10667800:1;chr18:10667801-10667800:0;chr18:10667801-15133800:1;chr18:1076501-1076500:0;chr18:1076501-1095200:1;chr18:1095201-1095200:0;chr18:1095201-1106353:1;chr18:1106354-1106353:0;chr18:1106354-9968351:1;chr18:15133801-78077248:0;chr18:611801-611800:0;chr18:611801-835400:1;chr18:835401-835600:0;chr18:835601-903595:1;chr18:903596-1076500:1;chr18:903596-903595:0;chr18:9968352-10175700:1;chr18:9968352-9968351:0;chr19:0-51211400:0;chr19:51211401-59118800:-1;chr19:59118801-59128983:0;chr1:0-819600:0;chr1:15548770-15548769:0;chr1:15548770-16786988:1;chr1:16786989-16786988:0;chr1:16786989-34461945:1;chr1:193727004-193860372:0;chr1:193860373-194088940:1;chr1:194088941-194088940:0;chr1:194088941-194169600:1;chr1:194169601-194171400:0;chr1:194171401-195495654:1;chr1:195495655-195552586:0;chr1:195552587-195552837:1;chr1:195552838-195552864:0;chr1:195552865-249240500:1;chr1:249240501-249250621:0;chr1:34461946-34461945:0;chr1:34461946-55959700:1;chr1:55959701-55963200:0;chr1:55963201-193727003:1;chr1:819601-15548769:1;chr20:0-24961256:0;chr20:24961257-26319500:-1;chr20:26319501-42178022:0;chr20:42178023-42312177:-1;chr20:42312178-43648400:0;chr20:43648401-43683190:-1;chr20:43683191-43683190:0;chr20:43683191-43685448:1;chr20:43685449-43685448:0;chr20:43685449-43734200:-1;chr20:43734201-43734977:0;chr20:43734978-44779160:-1;chr20:44779161-44779160:0;chr20:44779161-44779459:1;chr20:44779460-44821200:0;chr20:44821201-45052769:-1;chr20:45052770-55921500:0;chr20:55921501-56241001:-1;chr20:56241002-56241290:0;chr20:56241291-56416900:-1;chr20:56416901-56426355:0;chr20:56426356-56426519:1;chr20:56426520-56427143:0;chr20:56427144-56427397:1;chr20:56427398-56427397:0;chr20:56427398-62965000:-1;chr20:62965001-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-10000:0;chr2:10001-3964064:1;chr2:14341477-14342747:0;chr2:14342748-89890400:1;chr2:176927801-177065200:0;chr2:177065201-243183600:1;chr2:243183601-243199373:0;chr2:3964065-3965113:0;chr2:3965114-5661024:1;chr2:5661025-5661216:0;chr2:5661217-6209834:1;chr2:6209835-6209834:0;chr2:6209835-6210152:1;chr2:6210153-14341476:1;chr2:6210153-6210152:0;chr2:89890401-95328000:0;chr2:95328001-176927800:1;chr3:0-60200:0;chr3:60201-90504800:-1;chr3:90504801-198022430:0;chr4:0-10500:0;chr4:10501-6625400:-1;chr4:111277369-117199152:-1;chr4:117199153-134597500:0;chr4:134597501-139135082:-1;chr4:139135083-139135772:0;chr4:139135773-139135939:-1;chr4:139135940-151010360:0;chr4:151010361-191043900:-1;chr4:191043901-191154276:0;chr4:28785401-41628800:0;chr4:41628801-48836200:-1;chr4:48836201-111277368:0;chr4:6625401-28785400:-1;chr4:6625401-6625400:0;chr5:0-39732051:0;chr5:156635001-156635583:1;chr5:156635584-158483014:0;chr5:158483015-180736100:1;chr5:180736101-180915260:0;chr5:39732052-40087311:1;chr5:40087312-156635000:0;chr6:0-171115067:0;chr7:0-10000:0;chr7:10001-6705600:1;chr7:142329001-142329000:0;chr7:142329001-142494000:1;chr7:142494001-142494000:0;chr7:142494001-159128500:1;chr7:159128501-159138663:0;chr7:20822801-20838700:0;chr7:20838701-54773922:1;chr7:54773923-54773922:0;chr7:54773923-54779600:1;chr7:54779601-54779600:0;chr7:54779601-54782520:1;chr7:54782521-54782520:0;chr7:54782521-54784298:1;chr7:54784299-54784298:0;chr7:54784299-54784400:1;chr7:54784401-54784400:0;chr7:54784401-54785900:1;chr7:54785901-54785900:0;chr7:54785901-54786000:1;chr7:54786001-54786000:0;chr7:54786001-54789800:1;chr7:54789801-54789800:0;chr7:54789801-54790449:1;chr7:54790450-54790449:0;chr7:54790450-54799600:1;chr7:54799601-54799600:0;chr7:54799601-54879471:1;chr7:54879472-54879471:0;chr7:54879472-54880958:1;chr7:54880959-54880958:0;chr7:54880959-54881840:1;chr7:54881841-54881840:0;chr7:54881841-54894665:1;chr7:54894666-54894665:0;chr7:54894666-54895600:1;chr7:54895601-54895600:0;chr7:54895601-54902699:1;chr7:54902700-54902699:0;chr7:54902700-54906701:1;chr7:54906702-54906701:0;chr7:54906702-54907100:1;chr7:54907101-54907100:0;chr7:54907101-54908000:1;chr7:54908001-54908000:0;chr7:54908001-54908078:1;chr7:54908079-54908078:0;chr7:54908079-54916540:1;chr7:54916541-54916540:0;chr7:54916541-54916600:1;chr7:54916601-54916600:0;chr7:54916601-54952744:1;chr7:54952745-54952744:0;chr7:54952745-54959954:1;chr7:54959955-54959954:0;chr7:54959955-54963734:1;chr7:54963735-54963734:0;chr7:54963735-54963959:1;chr7:54963960-54963959:0;chr7:54963960-54980294:1;chr7:54980295-54980294:0;chr7:54980295-55052400:1;chr7:55052401-55052400:0;chr7:55052401-55053900:1;chr7:55053901-55053900:0;chr7:55053901-55058700:1;chr7:55058701-55058700:0;chr7:55058701-55081919:1;chr7:55081920-55081919:0;chr7:55081920-55085400:1;chr7:55085401-55085400:0;chr7:55085401-55092300:1;chr7:55092301-55092300:0;chr7:55092301-55123400:1;chr7:55123401-55123400:0;chr7:55123401-55129251:1;chr7:55129252-55129251:0;chr7:55129252-55161900:1;chr7:55161901-55161900:0;chr7:55161901-55163646:1;chr7:55163647-55163646:0;chr7:55163647-55164300:1;chr7:55164301-55164300:0;chr7:55164301-55168181:1;chr7:55168182-55168181:0;chr7:55168182-55168362:1;chr7:55168363-55168362:0;chr7:55168363-55169572:1;chr7:55169573-55169572:0;chr7:55169573-55169903:1;chr7:55169904-55169903:0;chr7:55169904-55170121:1;chr7:55170122-55170121:0;chr7:55170122-55190400:1;chr7:55190401-55190400:0;chr7:55190401-55205018:1;chr7:55205019-55205018:0;chr7:55205019-55220004:1;chr7:55220005-55220004:0;chr7:55220005-55221881:1;chr7:55221882-55221881:0;chr7:55221882-55226820:1;chr7:55226821-55226820:0;chr7:55226821-55232583:1;chr7:55232584-55232583:0;chr7:55232584-55301500:1;chr7:55301501-55301500:0;chr7:55301501-55309600:1;chr7:55309601-55309600:0;chr7:55309601-55318500:1;chr7:55318501-55318800:0;chr7:55318801-55319600:1;chr7:55319601-55319600:0;chr7:55319601-55319652:1;chr7:55319653-55319652:0;chr7:55319653-55324034:1;chr7:55324035-55324034:0;chr7:55324035-55469200:1;chr7:55469201-55470200:0;chr7:55470201-62496438:1;chr7:62496439-62496438:0;chr7:62496439-62496509:1;chr7:62496510-62496509:0;chr7:62496510-62498600:1;chr7:62498601-62498600:0;chr7:62498601-62499395:1;chr7:62499396-62499395:0;chr7:62499396-62499809:1;chr7:62499810-62499809:0;chr7:62499810-62500611:1;chr7:62500612-62500611:0;chr7:62500612-62501322:1;chr7:62501323-62501322:0;chr7:62501323-62514100:1;chr7:62514101-62514100:0;chr7:62514101-62514200:1;chr7:62514201-62514200:0;chr7:62514201-62549040:1;chr7:62549041-62549040:0;chr7:62549041-62549700:1;chr7:62549701-62549700:0;chr7:62549701-62554400:1;chr7:62554401-62554400:0;chr7:62554401-62556900:1;chr7:62556901-62556900:0;chr7:62556901-62564588:1;chr7:62564589-62564588:0;chr7:62564589-62570000:1;chr7:62570001-62570000:0;chr7:62570001-62578000:1;chr7:62578001-62578000:0;chr7:62578001-62584786:1;chr7:62584787-62584786:0;chr7:62584787-62616843:1;chr7:62616844-62616843:0;chr7:62616844-62616900:1;chr7:62616901-62616900:0;chr7:62616901-62623500:1;chr7:62623501-62623500:0;chr7:62623501-62625000:1;chr7:62625001-62625000:0;chr7:62625001-62649300:1;chr7:62649301-62649400:0;chr7:62649401-88783140:1;chr7:6705601-20822800:1;chr7:6705601-6705600:0;chr7:88783141-88783140:0;chr7:88783141-89103703:1;chr7:89103704-89103703:0;chr7:89103704-89627796:1;chr7:89627797-89627796:0;chr7:89627797-89628673:1;chr7:89628674-89628673:0;chr7:89628674-89635623:1;chr7:89635624-89635623:0;chr7:89635624-89794190:1;chr7:89794191-89794190:0;chr7:89794191-89970196:1;chr7:89970197-89970196:0;chr7:89970197-90023082:1;chr7:90023083-90023082:0;chr7:90023083-90023600:1;chr7:90023601-90023600:0;chr7:90023601-90026621:1;chr7:90026622-90026621:0;chr7:90026622-90027100:1;chr7:90027101-90027100:0;chr7:90027101-90035500:1;chr7:90035501-90035500:0;chr7:90035501-90036400:1;chr7:90036401-90036400:0;chr7:90036401-90039500:1;chr7:90039501-90039500:0;chr7:90039501-90040018:1;chr7:90040019-90040018:0;chr7:90040019-90045854:1;chr7:90045855-90045854:0;chr7:90045855-90058500:1;chr7:90058501-90058500:0;chr7:90058501-90059200:1;chr7:90059201-90059200:0;chr7:90059201-90059354:1;chr7:90059355-90059354:0;chr7:90059355-90059663:1;chr7:90059664-90059663:0;chr7:90059664-90059800:1;chr7:90059801-90059800:0;chr7:90059801-90061200:1;chr7:90061201-90061200:0;chr7:90061201-90089100:1;chr7:90089101-90089100:0;chr7:90089101-90089600:1;chr7:90089601-90089600:0;chr7:90089601-90446306:1;chr7:90446307-90446306:0;chr7:90446307-90447301:1;chr7:90447302-90447301:0;chr7:90447302-90447684:1;chr7:90447685-90447684:0;chr7:90447685-90858766:1;chr7:90858767-90858766:0;chr7:90858767-90859121:1;chr7:90859122-90859121:0;chr7:90859122-90860791:1;chr7:90860792-90860791:0;chr7:90860792-90861357:1;chr7:90861358-90861357:0;chr7:90861358-90861902:1;chr7:90861903-90861902:0;chr7:90861903-90862044:1;chr7:90862045-90862044:0;chr7:90862045-90919529:1;chr7:90919530-90919529:0;chr7:90919530-90922323:1;chr7:90922324-90922323:0;chr7:90922324-90922566:1;chr7:90922567-90922566:0;chr7:90922567-90948578:1;chr7:90948579-90948578:0;chr7:90948579-91001636:1;chr7:91001637-91001636:0;chr7:91001637-91002500:1;chr7:91002501-91002500:0;chr7:91002501-91035291:1;chr7:91035292-91035291:0;chr7:91035292-91078093:1;chr7:91078094-91078093:0;chr7:91078094-91104306:1;chr7:91104307-91104306:0;chr7:91104307-91106000:1;chr7:91106001-91111700:0;chr7:91111701-91205687:1;chr7:91205688-91205687:0;chr7:91205688-91882897:1;chr7:91882898-91882897:0;chr7:91882898-91886139:1;chr7:91886140-91886139:0;chr7:91886140-91968332:1;chr7:91968333-91968332:0;chr7:91968333-92161106:1;chr7:92161107-92161106:0;chr7:92161107-92412562:1;chr7:92412563-92412562:0;chr7:92412563-92459422:1;chr7:92459423-92459422:0;chr7:92459423-92464998:1;chr7:92464999-92464998:0;chr7:92464999-92518631:1;chr7:92518632-92518631:0;chr7:92518632-92519100:1;chr7:92519101-92519100:0;chr7:92519101-92526180:1;chr7:92526181-92526180:0;chr7:92526181-92547989:1;chr7:92547990-92547989:0;chr7:92547990-92548092:1;chr7:92548093-92548092:0;chr7:92548093-92568133:1;chr7:92568134-92568133:0;chr7:92568134-92576500:1;chr7:92576501-92576500:0;chr7:92576501-92590729:1;chr7:92590730-92590729:0;chr7:92590730-92929683:1;chr7:92929684-92929683:0;chr7:92929684-93044577:1;chr7:93044578-93044577:0;chr7:93044578-93064458:1;chr7:93064459-93064458:0;chr7:93064459-93129715:1;chr7:93129716-93129715:0;chr7:93129716-93275426:1;chr7:93275427-93275426:0;chr7:93275427-93290724:1;chr7:93290725-93290724:0;chr7:93290725-93296700:1;chr7:93296701-93296700:0;chr7:93296701-93296800:1;chr7:93296801-93296800:0;chr7:93296801-93324800:1;chr7:93324801-93324800:0;chr7:93324801-93337970:1;chr7:93337971-93337970:0;chr7:93337971-93359788:1;chr7:93359789-93359788:0;chr7:93359789-93455399:1;chr7:93455400-93455399:0;chr7:93455400-93477576:1;chr7:93477577-93477576:0;chr7:93477577-93496100:1;chr7:93496101-93496100:0;chr7:93496101-93634225:1;chr7:93634226-93634225:0;chr7:93634226-93634279:1;chr7:93634280-93634279:0;chr7:93634280-93634400:1;chr7:93634401-93634400:0;chr7:93634401-93638700:1;chr7:93638701-93638700:0;chr7:93638701-93638900:1;chr7:93638901-93638900:0;chr7:93638901-93639700:1;chr7:93639701-93639700:0;chr7:93639701-93641920:1;chr7:93641921-93641920:0;chr7:93641921-93648000:1;chr7:93648001-93648000:0;chr7:93648001-93648700:1;chr7:93648701-93649400:0;chr7:93649401-93676169:1;chr7:93676170-142329000:1;chr7:93676170-93676169:0;chr8:0-107064781:0;chr8:107064782-107064882:1;chr8:107064883-139372300:0;chr8:139372301-139401500:-1;chr8:139401501-146364022:0;chr9:0-140191022:0;chr9:140191023-141102500:-1;chr9:141102501-141213431:0;chrX:0-32683343:0;chrX:124406001-124412100:-1;chrX:124412101-155270560:0;chrX:32683344-32688542:1;chrX:32688543-124406000:0;chrY:0-2649500:0;chrY:26446401-59373566:0;chrY:2649501-26446400:-1	hs7:91008052-91008052,hs7:55230736-55230736;hs17:12553017-12553017,hs17:12556412-12556412;hs9:140191023-140191023,hs5:156635001-156635001;hs20:43428357-43428357,hs20:56426519-56426519;hs7:55294526-55294526,hs7:93064459-93064459;hs20:56426242-56426242,hs20:44779161-44779161;hs7:62629233-62629233,hs7:55058683-55058683;hs13:61154634-61154634,hs13:96154380-96154380;hs17:10472147-10472147,hs17:10475143-10475143;hs7:54826618-54826618,hs7:54962436-54962436;hs7:62577951-62577951,hs7:55363719-55363719;hs2:3964065-3964065,hs2:6209835-6209835;hs1:194044706-194044706,hs1:195495655-195495655;hs17:9156675-9156675,hs17:9152636-9152636	ABCB5;ADAM22;AKAP9;ANKIB1;BET1;C11orf31;C15orf27;C16orf89;C17orf51;C19orf48;C1GALT1;C1orf168;C1orf94;C20orf85;C3orf38;C4orf32;C7orf26;C7orf28B;C7orf34;C7orf62;C7orf63;C7orf64;CALCR;CASD1;CCDC132;CDCA7L;CDK14;CDK6;CHCHD2;CLDN12;CLEC5A;COBL;COL1A2;CYP51A1;DDC;DNAH11;EGFR;ESYT2;FAM133B;FZD1;GATAD1;GNG11;GNGT1;GPCRLTM7;GRB10;GRID2IP;GTPBP10;HEPACAM2;ITGB8;KDELR2;KRIT1;LANCL2;LOC100288524;LOC389493;LOC646627;LOC647589;LRRD1;MACC1;MRPS17;MTERF;NCAPG2;OR9A4;PDGFA;PEG10;PEX1;PHKG1;POM121L12;PPP1R9A;PRKAR1B;PRSS2;PTPRN2;RAPGEF5;RSPH10B;RSPH10B2;SAMD9;SAMD9L;SEC61G;SEPT14;SGCE;SP4;SP8;SRI;STEAP1;STEAP1B;STEAP2;STEAP4;TAS2R38;TFPI2;TMEM196;TRPV6;VIPR2;VOPP1;VSTM2A;WDR60;ZDHHC4;ZNF12;ZNF479;ZNF679;ZNF680;ZNF713;ZNF716;ZNF727;ZNF735;ZNF736;ZNF804B;ZNF853;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	NA
CTDB0392	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	8	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG019_S	Illumina Genome Analyzer IIx or HiSeq	chr10:0-17221872:0;chr10:135524701-135534747:0;chr10:17221873-17221959:-1;chr10:17221960-37345400:0;chr10:37345401-38192500:1;chr10:38192501-42397400:0;chr10:42397401-58847981:1;chr10:58847982-58847981:0;chr10:58847982-58848265:-1;chr10:58848266-58848265:0;chr10:58848266-84029641:1;chr10:84029642-84029641:0;chr10:84029642-84029794:1;chr10:84029795-135524700:1;chr10:84029795-84029794:0;chr11:0-133700:0;chr11:133701-17226760:1;chr11:134946401-135006516:0;chr11:17226761-17226760:0;chr11:17226761-87552907:1;chr11:87552908-87552907:0;chr11:87552908-92215404:1;chr11:92215405-134946400:1;chr11:92215405-92215404:0;chr12:0-187600:0;chr12:102303201-102303200:0;chr12:102303201-133841500:1;chr12:133841501-133851895:0;chr12:15816523-15816522:0;chr12:15816523-15976421:1;chr12:15976422-15976421:0;chr12:15976422-73334844:1;chr12:187601-15816522:1;chr12:73334845-73334844:0;chr12:73334845-73335347:1;chr12:73335348-102303200:1;chr12:73335348-73335347:0;chr13:0-19020700:0;chr13:115109801-115169878:0;chr13:19020701-84759402:1;chr13:84759403-84759402:0;chr13:84759403-84759665:1;chr13:84759666-115109800:1;chr13:84759666-84759665:0;chr14:0-20160900:0;chr14:107289501-107349540:0;chr14:20160901-22314500:1;chr14:22314501-22314500:0;chr14:22314501-22973300:1;chr14:22973301-22973500:0;chr14:22973501-41517904:1;chr14:41517905-41517904:0;chr14:41517905-41517995:-1;chr14:41517996-41517995:0;chr14:41517996-86016606:1;chr14:86016607-87381885:0;chr14:87381886-107289500:1;chr15:0-20000000:0;chr15:100797601-100797600:0;chr15:100797601-102465300:1;chr15:102465301-102531392:0;chr15:20000001-20112000:1;chr15:20112001-20113600:0;chr15:20113601-20195100:1;chr15:20195101-35116500:0;chr15:35116501-35231000:1;chr15:35231001-36528500:0;chr15:36528501-36867536:1;chr15:36867537-36869238:0;chr15:36869239-36873388:1;chr15:36873389-36873388:0;chr15:36873389-36873787:1;chr15:36873788-36873787:0;chr15:36873788-36882500:1;chr15:36882501-42151795:0;chr15:42151796-42157409:1;chr15:42157410-42161525:0;chr15:42161526-56072428:1;chr15:56072429-56072428:0;chr15:56072429-88756068:1;chr15:88756069-88756068:0;chr15:88756069-95148800:1;chr15:95148801-95148800:0;chr15:95148801-96034976:1;chr15:96034977-96034976:0;chr15:96034977-99776023:1;chr15:99776024-100797600:1;chr15:99776024-99776023:0;chr16:0-60000:0;chr16:32579628-32602840:0;chr16:32602841-47817562:1;chr16:47817563-47817562:0;chr16:47817563-56970744:1;chr16:56970745-56970744:0;chr16:56970745-56970761:1;chr16:56970762-56970761:0;chr16:56970762-57021623:1;chr16:57021624-70883400:0;chr16:60001-32579627:1;chr16:70883401-71202600:1;chr16:71202601-90354753:0;chr17:0-9152635:0;chr17:10472147-10472146:0;chr17:10472147-12553016:1;chr17:12553017-12553016:0;chr17:12553017-12556411:1;chr17:12556412-12556411:0;chr17:12556412-21547300:1;chr17:21547301-21666600:0;chr17:21666601-22244500:1;chr17:22244501-25341900:0;chr17:25341901-47563457:1;chr17:47563458-54461900:0;chr17:54461901-54475403:1;chr17:54475404-54475403:0;chr17:54475404-81195100:1;chr17:81195101-81195210:0;chr17:9152636-9156674:1;chr17:9156675-10472146:1;chr17:9156675-9156674:0;chr18:0-46100:0;chr18:15390901-18510900:0;chr18:18510901-33125000:1;chr18:33125001-33125000:0;chr18:33125001-33730996:1;chr18:33730997-33730996:0;chr18:33730997-33732118:1;chr18:33732119-33732118:0;chr18:33732119-78017200:1;chr18:46101-15390900:1;chr18:78017201-78077248:0;chr19:0-89200:0;chr19:51211401-51211400:0;chr19:51211401-59118800:1;chr19:59118801-59128983:0;chr19:89201-51211400:1;chr1:0-10100:0;chr1:10101-15548769:1;chr1:104103501-104103500:0;chr1:104103501-109840900:1;chr1:109840901-109840900:0;chr1:109840901-181461280:1;chr1:15548770-15548769:0;chr1:15548770-16786988:1;chr1:16786989-16786988:0;chr1:16786989-57814198:1;chr1:181461281-181461280:0;chr1:181461281-181561000:1;chr1:181561001-181561000:0;chr1:181561001-181716968:1;chr1:181716969-181716968:0;chr1:181716969-181786100:1;chr1:181786101-181786100:0;chr1:181786101-221362400:1;chr1:221362401-221362400:0;chr1:221362401-221443535:1;chr1:221443536-221443535:0;chr1:221443536-249240500:1;chr1:249240501-249250621:0;chr1:57814199-57814198:0;chr1:57814199-58253800:1;chr1:58253801-58253800:0;chr1:58253801-65425645:1;chr1:65425646-65425645:0;chr1:65425646-74159348:1;chr1:74159349-74159348:0;chr1:74159349-74160442:1;chr1:74160443-74160442:0;chr1:74160443-74173368:1;chr1:74173369-74173368:0;chr1:74173369-89020239:1;chr1:89020240-89020239:0;chr1:89020240-91330205:1;chr1:91330206-91330205:0;chr1:91330206-97525031:1;chr1:97525032-104103500:1;chr1:97525032-97525031:0;chr20:0-60000:0;chr20:24961257-24963319:0;chr20:24963320-24963563:1;chr20:24963564-29804200:0;chr20:29804201-42178022:1;chr20:42178023-42312200:0;chr20:42312201-43428141:1;chr20:43428142-43428141:0;chr20:43428142-43428356:1;chr20:43428357-43428356:0;chr20:43428357-43432880:1;chr20:43432881-43432880:0;chr20:43432881-43648400:1;chr20:43648401-43683190:0;chr20:43683191-43685448:1;chr20:43685449-44779160:0;chr20:44779161-44779459:1;chr20:44779460-44779459:0;chr20:44779460-44821300:1;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S8;KCNU1;KCNV1;KIAA0196;KIAA1429;LOC100287718;LOC100288524;LOC342918;LOC389493;LOC389676;LOC646627;LOC647589;LOC653486;LOC653550;LOC728379;LOC728393;LRRC69;MAK16;MCPH1;MFHAS1;MMP16;MSRA;MTDH;MTERFD1;MTFR1;MYC;MYOM2;NBN;NSMCE2;OR4F21;OSGIN2;PDE7A;PDP1;PGCP;PKHD1L1;PLEKHF2;POU5F1B;PPP1R3B;PROSC;PRSS55;PTDSS1;PVT1;RAD21;RAD54B;RBM12B;RIPK2;RNF122;RP1L1;RUNX1T1;SDC2;SGK223;SLC26A7;SOX7;SQLE;SYBU;TMEM67;TNKS;TP53INP1;TRIB1;TRIM55;TRPS1;TSPYL5;TTPA;UNC5D;UQCRB;UTP23;XKR5;YTHDF3;ZNF16;ZNF250;ZNF572;ZNF596;ZNF7;ZNF703;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	MMP16,TRAPPC9
CTDB0393	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	11	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG033_D	Illumina Genome Analyzer IIx or HiSeq	chr10:0-71700:0;chr10:133126601-133126600:0;chr10:133126601-133615420:-1;chr10:133615421-133615420:0;chr10:133615421-135524700:-1;chr10:135524701-135534747:0;chr10:71701-133126600:-1;chr11:0-133700:0;chr11:133701-43535100:-1;chr11:43535101-43803997:0;chr11:43803998-43806013:-1;chr11:43806014-44233709:0;chr11:44233710-44256240:-1;chr11:44256241-44309731:0;chr11:44309732-44311714:-1;chr11:44311715-44490058:0;chr11:44490059-44491110:-1;chr11:44491111-49321300:0;chr11:49321301-49324802:-1;chr11:49324803-49342700:0;chr11:49342701-49344600:-1;chr11:49344601-49469784:0;chr11:49469785-49473400:-1;chr11:49473401-49709800:0;chr11:49709801-49709900:-1;chr11:49709901-49872900:0;chr11:49872901-49873797:-1;chr11:49873798-50039400:0;chr11:50039401-50783300:-1;chr11:50783301-51478200:0;chr11:51478201-51479700:-1;chr11:51479701-56855245:0;chr11:56855246-56856221:-1;chr11:56856222-57196584:0;chr11:57196585-57199328:-1;chr11:57199329-78658239:0;chr11:78658240-78661352:-1;chr11:78661353-78757193:0;chr11:78757194-78776707:-1;chr11:78776708-78789380:0;chr11:78789381-78789707:-1;chr11:78789708-79224347:0;chr11:79224348-79235886:-1;chr11:79235887-80667820:0;chr11:80667821-80669032:-1;chr11:80669033-80904687:0;chr11:80904688-80905811:-1;chr11:80905812-80942176:0;chr11:80942177-80943341:-1;chr11:80943342-81112000:0;chr11:81112001-81119896:-1;chr11:81119897-81122119:0;chr11:81122120-81123236:-1;chr11:81123237-81160000:0;chr11:81160001-81164674:-1;chr11:81164675-81199018:0;chr11:81199019-81229211:-1;chr11:81229212-81456001:0;chr11:81456002-81458951:-1;chr11:81458952-81489473:0;chr11:81489474-81494346:-1;chr11:81494347-81520322:0;chr11:81520323-81592978:-1;chr11:81592979-81605192:0;chr11:81605193-81610465:-1;chr11:81610466-81687160:0;chr11:81687161-81707288:-1;chr11:81707289-81739100:0;chr11:81739101-81852600:-1;chr11:81852601-81919900:0;chr11:81919901-81938638:-1;chr11:81938639-81950281:0;chr11:81950282-81951632:1;chr11:81951633-81982600:0;chr11:81982601-82054200:-1;chr11:82054201-82066681:0;chr11:82066682-82071205:-1;chr11:82071206-82117676:0;chr11:82117677-82119116:-1;chr11:82119117-82129510:0;chr11:82129511-82130653:-1;chr11:82130654-82256487:0;chr11:82256488-82258654:-1;chr11:82258655-82266651:0;chr11:82266652-82273666:-1;chr11:82273667-82341040:0;chr11:82341041-82341400:-1;chr11:82341401-82359753:0;chr11:82359754-82362251:-1;chr11:82362252-82415113:0;chr11:82415114-82428443:-1;chr11:82428444-82479476:0;chr11:82479477-82481098:-1;chr11:82481099-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-247833258:0;chr1:247833259-248280226:-1;chr1:248280227-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-10000:0;chr2:10001-243183600:1;chr2:243183601-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-11700:0;chr5:11701-1237096:-1;chr5:1237097-1302234:0;chr5:1302235-1303753:-1;chr5:1303754-1336451:0;chr5:1336452-1337151:-1;chr5:1337152-1383086:0;chr5:1383087-1604200:-1;chr5:14514082-14514313:1;chr5:14514314-26870466:0;chr5:1604201-1706671:0;chr5:1706672-1707434:-1;chr5:1707435-1727784:0;chr5:1727785-1729176:-1;chr5:1729177-1817305:0;chr5:1817306-1819919:-1;chr5:1819920-14514081:0;chr5:26870467-26871530:-1;chr5:26871531-27288159:0;chr5:27288160-27290181:-1;chr5:27290182-27297282:0;chr5:27297283-27297778:-1;chr5:27297779-27434368:0;chr5:27434369-27435554:-1;chr5:27435555-27442287:0;chr5:27442288-27443958:-1;chr5:27443959-27462573:0;chr5:27462574-27463904:-1;chr5:27463905-27545232:0;chr5:27545233-27546306:-1;chr5:27546307-27547179:0;chr5:27547180-27551462:-1;chr5:27551463-27741690:0;chr5:27741691-27742981:-1;chr5:27742982-27802800:0;chr5:27802801-27827200:-1;chr5:27827201-27905811:0;chr5:27905812-31416789:-1;chr5:31416790-31465404:0;chr5:31465405-31501808:-1;chr5:31501809-31521054:0;chr5:31521055-31543284:-1;chr5:31543285-31577003:0;chr5:31577004-31578807:-1;chr5:31578808-31579608:0;chr5:31579609-31580016:-1;chr5:31580017-31585352:0;chr5:31585353-31594600:-1;chr5:31594601-31667400:0;chr5:31667401-31667639:-1;chr5:31667640-31669032:0;chr5:31669033-31673193:-1;chr5:31673194-31679937:0;chr5:31679938-31683039:-1;chr5:31683040-32316983:0;chr5:32316984-32318500:-1;chr5:32318501-180915260:0;chr6:0-171115067:0;chr7:0-22573900:0;chr7:142327601-142494500:1;chr7:142494501-159138663:0;chr7:22573901-23074600:-1;chr7:23074601-142327600:0;chr8:0-146364022:0;chr9:0-21815670:0;chr9:21815671-21873127:-1;chr9:21873128-21873638:0;chr9:21873639-22208701:-1;chr9:22208702-38642890:0;chr9:38642891-38643842:1;chr9:38643843-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs5:31579609-31579609,hs11:57199329-57199329;hs5:31416790-31416790,hs5:1237097-1237097;hs5:1302235-1302235,hs11:82481099-82481099;hs5:31579609-31579609,hs11:57199330-57199330;hs8:114833218-114833218,hs8:114832069-114832069;hs9:38643843-38643843,hs9:44357162-44357162;hs11:78904762-78904762,hs11:78776708-78776708;hs11:55258222-55258222,hs5:32316984-32316984;hs11:56856222-56856222,hs11:49840025-49840025;hs11:49324803-49324803,hs11:44491111-44491111;hs11:78904762-78904762,hs11:78776708-78776708;hs11:79022285-79022285,hs5:31502398-31502398;hs11:49835295-49835295,hs11:81605193-81605193;hs11:57196585-57196585,hs5:27434367-27434367;hs11:49732378-49732378,hs5:31673194-31673194;hs11:82342498-82342498,hs11:81164675-81164675;hs11:79022285-79022285,hs5:31502398-31502398;hs11:79022285-79022285,hs5:31502398-31502398;hs11:81687161-81687161,hs5:31577004-31577004;hs11:44490059-44490059,hs11:80667821-80667821	ALX4;API5;BET1L;C11orf74;C5orf22;EXT2;GAB2;HSD17B12;LOC653486;LRRC4C;ODF3;ODZ4;RAG2;RIC8A;SCGB1C1;TTC17;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	DROSHA,ODZ4;ODZ4,GAB2
CTDB0394	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	11	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG033_R	Illumina Genome Analyzer IIx or HiSeq	chr10:0-135534747:0;chr11:0-44309731:0;chr11:44309732-44311714:-1;chr11:44311715-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-14514081:0;chr5:14514082-14514313:1;chr5:14514314-27664485:0;chr5:27664486-27667031:-1;chr5:27667032-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-21815670:0;chr9:21815671-21873127:-1;chr9:21873128-21873638:0;chr9:21873639-22208701:-1;chr9:22208702-38668798:0;chr9:38668799-38668900:-1;chr9:38668901-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:59487649-59487649,hs1:59486603-59486603;hs5:27741691-27741691,hs11:81950282-81950282;hs5:31501809-31501809,hs5:27290182-27290182;hs5:1817306-1817306,hs11:78661353-78661353;hs5:26871531-26871531,hs11:80669033-80669033;hs5:27545233-27545233,hs11:78684758-78684758;hs5:27664486-27664486,hs11:43546379-43546379;hs5:31579055-31579055,hs5:27742982-27742982;hs6:37112618-37112618,hs6:37113534-37113534;hs9:38668799-38668799,hs9:40612047-40612047;hs9:21815270-21815270,hs9:45680204-45680204;hs9:22208702-22208702,hs9:21873128-21873128;hs9:38668945-38668945,hs9:38642891-38642891;hs9:7747590-7747590,hs9:7748055-7748055;hs11:81520323-81520323,hs11:82117677-82117677;hs11:79224348-79224348,hs11:82359754-82359754;hs11:57196585-57196585,hs5:27434369-27434369;hs11:82273667-82273667,hs11:78385377-78385377;hs11:51477878-51477878,hs5:27443959-27443959;hs11:81458952-81458952,hs11:81256568-81256568;hs11:78776708-78776708,hs11:78904762-78904762;hs11:82055697-82055697,hs11:43806014-43806014;hs11:81592979-81592979,hs11:82341655-82341655;hs11:79021519-79021519,hs11:49473546-49473546;hs11:82341041-82341041,hs5:31667640-31667640;hs11:51419319-51419319,hs11:82129511-82129511;hs11:78776708-78776708,hs11:78904762-78904762;hs11:79022285-79022285,hs5:31502397-31502397;hs11:79022285-79022285,hs5:31502397-31502397;hs11:78336914-78336914,hs5:31502387-31502387;hs11:80905812-80905812,hs11:50013811-50013811;hs11:80667821-80667821,hs11:44490059-44490059;hs11:81164675-81164675,hs11:82342498-82342498;hs22:34760397-34760397,hs22:34758774-34758774	ALX4;HSD17B12;ODZ4;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	DROSHA,ODZ4
CTDB0395	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	11	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG044_D	Illumina Genome Analyzer IIx or HiSeq	chr10:0-590762:0;chr10:113717960-113718856:1;chr10:113718857-135534747:0;chr10:36216901-36217358:1;chr10:36217359-113717959:0;chr10:590763-591339:1;chr10:591340-36216900:0;chr11:0-9381932:0;chr11:117147124-117147229:1;chr11:117147230-117147229:0;chr11:117147230-117147293:1;chr11:117147294-117147293:0;chr11:117147294-117147526:1;chr11:117147527-117147526:0;chr11:117147527-117147599:1;chr11:117147600-117147599:0;chr11:117147600-117148260:1;chr11:117148261-124892738:0;chr11:12354327-12362307:1;chr11:12362308-15418488:0;chr11:124892739-124897028:1;chr11:124897029-126878541:0;chr11:126878542-126879135:1;chr11:126879136-126916300:0;chr11:126916301-126929040:1;chr11:126929041-128385963:0;chr11:128385964-128388667:-1;chr11:128388668-130212881:0;chr11:130212882-130213472:1;chr11:130213473-130538031:0;chr11:130538032-130538363:1;chr11:130538364-135006516:0;chr11:15418489-15423585:1;chr11:15423586-16391702:0;chr11:16391703-16392069:1;chr11:16392070-44181815:0;chr11:44181816-44181892:1;chr11:44181893-44181892:0;chr11:44181893-44182032:1;chr11:44182033-44182032:0;chr11:44182033-44182102:1;chr11:44182103-44182102:0;chr11:44182103-44182185:1;chr11:44182186-44182185:0;chr11:44182186-44182305:1;chr11:44182306-45025344:0;chr11:45025345-45026288:1;chr11:45026289-56495916:0;chr11:56495917-56496156:1;chr11:56496157-56496156:0;chr11:56496157-56497019:1;chr11:56497020-57401772:0;chr11:57401773-57417606:1;chr11:57417607-64784205:0;chr11:64784206-64784263:1;chr11:64784264-64784263:0;chr11:64784264-64784443:1;chr11:64784444-64784443:0;chr11:64784444-64784493:1;chr11:64784494-66641858:0;chr11:66641859-66646647:1;chr11:66646648-68441694:0;chr11:68441695-68441948:1;chr11:68441949-68441948:0;chr11:68441949-68442034:1;chr11:68442035-68803684:0;chr11:68803685-69625651:1;chr11:69625652-69625651:0;chr11:69625652-69625909:1;chr11:69625910-73868933:0;chr11:73868934-73869921:1;chr11:73869922-75448865:0;chr11:75448866-75459377:1;chr11:75459378-75694533:0;chr11:75694534-75694846:1;chr11:75694847-75694846:0;chr11:75694847-75694948:1;chr11:75694949-75694948:0;chr11:75694949-75695031:1;chr11:75695032-75695031:0;chr11:75695032-75695167:1;chr11:75695168-75695167:0;chr11:75695168-75695300:1;chr11:75695301-75695300:0;chr11:75695301-75695358:1;chr11:75695359-76368659:0;chr11:76368660-76637659:1;chr11:76637660-77549723:0;chr11:77549724-77563766:1;chr11:77563767-85374187:0;chr11:85374188-85421163:1;chr11:85421164-117147123:0;chr11:9381933-9382228:1;chr11:9382229-9382228:0;chr11:9382229-9382400:-1;chr11:9382401-12354326:0;chr12:0-45141200:0;chr12:108708115-108717873:1;chr12:108717874-113323370:0;chr12:113323371-113503543:1;chr12:113503544-118963800:0;chr12:118963801-119034600:1;chr12:119034601-119035200:0;chr12:119035201-119083417:1;chr12:119083418-119654924:0;chr12:119654925-119662873:1;chr12:119662874-120405746:0;chr12:120405747-120549727:1;chr12:120549728-126054474:0;chr12:126054475-126223551:1;chr12:126223552-127222411:0;chr12:127222412-127338633:1;chr12:127338634-130372721:0;chr12:130372722-130437775:1;chr12:130437776-130437775:0;chr12:130437776-130493366:1;chr12:130493367-131752277:0;chr12:131752278-131782900:1;chr12:131782901-133851895:0;chr12:45141201-45147518:1;chr12:45147519-76829559:0;chr12:76829560-76992418:1;chr12:76992419-83849732:0;chr12:83849733-83929456:1;chr12:83929457-83929456:0;chr12:83929457-84078000:-1;chr12:84078001-84078400:0;chr12:84078401-84078700:1;chr12:84078701-86339044:0;chr12:86339045-86554000:1;chr12:86554001-86554000:0;chr12:86554001-86612079:-1;chr12:86612080-89082652:0;chr12:89082653-89116200:1;chr12:89116201-97937921:0;chr12:97937922-97972400:1;chr12:97972401-108708114:0;chr13:0-19344100:0;chr13:115109801-115169878:0;chr13:19344101-95179510:-1;chr13:95179511-95181927:0;chr13:95181928-115109800:-1;chr14:0-19964300:0;chr14:107289501-107349540:0;chr14:19964301-22470700:-1;chr14:22470701-22470700:0;chr14:22470701-22964200:-1;chr14:22964201-22964300:0;chr14:22964301-67872582:-1;chr14:67872583-67872582:0;chr14:67872583-67872847:1;chr14:67872848-67872847:0;chr14:67872848-67873011:1;chr14:67873012-67876556:0;chr14:67876557-74378955:-1;chr14:74378956-74382777:0;chr14:74382778-107289500:-1;chr15:0-35025841:0;chr15:35025842-35028678:1;chr15:35028679-48982996:0;chr15:48982997-48985588:1;chr15:48985589-102531392:0;chr16:0-4713600:0;chr16:34195701-35261153:-1;chr16:35261154-50939904:0;chr16:4713601-4716997:1;chr16:4716998-34195700:0;chr16:50939905-55068138:-1;chr16:55068139-55068138:0;chr16:55068139-55068219:1;chr16:55068220-55068219:0;chr16:55068220-55068526:1;chr16:55068527-55068526:0;chr16:55068527-55068604:1;chr16:55068605-55068604:0;chr16:55068605-55068661:1;chr16:55068662-55068661:0;chr16:55068662-55068962:1;chr16:55068963-55068962:0;chr16:55068963-55069142:1;chr16:55069143-55069142:0;chr16:55069143-55069368:1;chr16:55069369-55069368:0;chr16:55069369-70881800:-1;chr16:70881801-70881800:0;chr16:70881801-71202500:-1;chr16:71202501-71202500:0;chr16:71202501-90292700:-1;chr16:90292701-90354753:0;chr17:0-0:0;chr17:1-8533822:-1;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of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	ACER3,RNF214;ACER3,SBF2;ACER3,UVRAG;ARL2-SNX15,CCDC15;ARL2,CCDC15;C11orf67,CCDC15;ELP4,TOLLIP;EXT2,CCDC15;EXT2,RNF214;EXT2,UVRAG;NRXN2,C2CD3
CTDB0396	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	1	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG052_A	Illumina Genome Analyzer IIx or HiSeq	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-88770568:0;chr16:88770569-88775128:-1;chr16:88775129-90354753:0;chr17:0-0:0;chr17:1-53752100:-1;chr17:53752101-81195210:0;chr18:0-4799362:0;chr18:4799363-4800722:1;chr18:4800723-78077248:0;chr19:0-59128983:0;chr1:0-160184572:0;chr1:160184573-160250709:1;chr1:160250710-164413579:0;chr1:164413580-164942182:1;chr1:164942183-179645200:0;chr1:179645201-179672902:1;chr1:179672903-189845500:0;chr1:189845501-190084826:1;chr1:190084827-191539361:0;chr1:191539362-191840800:1;chr1:191840801-213590917:0;chr1:213590918-213806500:1;chr1:213806501-213806600:0;chr1:213806601-213826652:1;chr1:213826653-213826652:0;chr1:213826653-214099100:1;chr1:214099101-215150731:0;chr1:215150732-215383700:1;chr1:215383701-215383700:0;chr1:215383701-215438700:1;chr1:215438701-217011100:0;chr1:217011101-217011649:1;chr1:217011650-223845282:0;chr1:223845283-223864287:1;chr1:223864288-224159300:0;chr1:224159301-224433800:1;chr1:224433801-226111380:0;chr1:226111381-226130723:1;chr1:226130724-226299312:0;chr1:226299313-226307700:1;chr1:226307701-231617388:0;chr1:231617389-231617502:-1;chr1:231617503-243631700:0;chr1:243631701-243666411:1;chr1:243666412-243666411:0;chr1:243666412-244255809:1;chr1:244255810-244255809:0;chr1:244255810-244258832:1;chr1:244258833-244258832:0;chr1:244258833-244456847:1;chr1:244456848-244456847:0;chr1:244456848-244483720:1;chr1:244483721-244483720:0;chr1:244483721-244613600:1;chr1:244613601-244613600:0;chr1:244613601-244639300:1;chr1:244639301-244639300:0;chr1:244639301-244775604:1;chr1:244775605-244775604:0;chr1:244775605-244791274:1;chr1:244791275-244791274:0;chr1:244791275-244810891:1;chr1:244810892-244810891:0;chr1:244810892-244824391:1;chr1:244824392-244824391:0;chr1:244824392-244912500:1;chr1:244912501-248575282:0;chr1:248575283-248841426:1;chr1:248841427-249250621:0;chr20:0-7958500:0;chr20:30504301-30504600:1;chr20:30504601-30504600:0;chr20:30504601-30875100:1;chr20:30875101-63025520:0;chr20:7958501-8357700:1;chr20:8357701-8847000:0;chr20:8847001-8848000:1;chr20:8848001-8848000:0;chr20:8848001-9430500:1;chr20:9430501-30504300:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-16271700:0;chr2:154222901-232427800:1;chr2:16271701-16273700:1;chr2:16273701-154222900:0;chr2:232427801-232427800:0;chr2:232427801-232454600:1;chr2:232454601-232454600:0;chr2:232454601-243183600:1;chr2:243183601-243199373:0;chr3:0-71141292:0;chr3:71141293-71142503:1;chr3:71142504-198022430:0;chr4:0-66028885:0;chr4:66028886-66078980:-1;chr4:66078981-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-81250209:0;chr7:81250210-81494866:-1;chr7:81494867-159138663:0;chr8:0-146364022:0;chr9:0-125778877:0;chr9:125778878-125813203:1;chr9:125813204-125858274:0;chr9:125858275-125932429:1;chr9:125932430-126014933:0;chr9:126014934-126372978:1;chr9:126372979-141213431:0;chrX:0-155270560:0;chrY:0-2649500:0;chrY:2649501-59033300:-1;chrY:59033301-59373566:0	hs1:179271743-179271743,hs1:217011514-217011514;hs1:213806462-213806462,hs1:213977967-213977967;hs1:181415623-181415623,hs2:16059652-16059652;hs1:244085168-244085168,hs2:16158764-16158764;hs1:244015023-244015023,hs2:15779022-15779022;hs1:244257689-244257689,hs2:16109043-16109043;hs1:243666412-243666412,hs1:213826653-213826653;hs1:160250710-160250710,hs2:16080516-16080516;hs1:226130724-226130724,hs2:16194175-16194175;hs1:243637600-243637600,hs2:16125188-16125188;hs1:224137797-224137797,hs2:16397105-16397105;hs1:160250710-160250710,hs2:16080516-16080516;hs1:244456848-244456848,hs1:244810892-244810892;hs1:248774822-248774822,hs2:16027731-16027731;hs1:244791275-244791275,hs1:244483721-244483721;hs1:248575283-248575283,hs1:223845283-223845283;hs1:244349557-244349557,hs2:16246164-16246164;hs1:189136623-189136623,hs1:189115741-189115741;hs1:244871886-244871886,hs1:243855104-243855104;hs2:15841330-15841330,hs2:49631766-49631766;hs2:15951349-15951349,hs2:15903825-15903825;hs2:16148785-16148785,hs2:15939326-15939326;hs2:16055176-16055176,hs9:126014934-126014934;hs2:25962331-25962331,hs2:8807104-8807104;hs2:19947861-19947861,hs2:19860821-19860821;hs2:16035150-16035150,hs1:243948145-243948145;hs2:234728796-234728796,hs2:218858882-218858882;hs2:8880748-8880748,hs2:15934069-15934069;hs2:19859431-19859431,hs2:19898110-19898110;hs2:16150007-16150007,hs1:215150732-215150732;hs2:19783472-19783472,hs2:15892291-15892291;hs2:39118884-39118884,hs2:20100857-20100857;hs2:16366647-16366647,hs2:39127050-39127050;hs2:8787891-8787891,hs2:15748741-15748741;hs2:15822080-15822080,hs2:25907992-25907992;hs2:15778713-15778713,hs2:19849548-19849548;hs2:15779268-15779268,hs2:16397698-16397698;hs2:8487264-8487264,hs2:39223318-39223318;hs3:192845451-192845451,hs4:68648092-68648092;hs8:110370886-110370886,hs2:204851878-204851878;hs9:117975339-117975339,hs11:23122707-23122707;hs11:23123086-23123086,hs9:117975343-117975343;hs13:73474991-73474991,hs13:67519164-67519164;hs22:39487230-39487230,hs10:128526501-128526501;hsX:42602326-42602326,hs6:19983013-19983013	1-Dec;ADSS;C1orf100;C1orf101;C2orf57;CAPN8;DCAF8;DEGS1;ESRRG;FAM5C;FBXO28;KCNK2;LEFTY2;NVL;OR2G6;OR2T10;OR2T11;OR2T27;OR2T29;OR2T34;OR2T35;PBX1;PEA15;PEX19;PPPDE1;PYCR2;SOAT1;TDRD5;ZNF238;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	C1orf101,PPPDE1;SOAT1,ESRRG;ZNF238,C1orf101
CTDB0397	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	4	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG075_A	Illumina Genome Analyzer IIx or HiSeq	chr10:0-135534747:0;chr11:0-67279338:0;chr11:67279339-67280708:1;chr11:67280709-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-60000:0;chr16:12847041-12847051:1;chr16:12847052-12847051:0;chr16:12847052-12852092:1;chr16:12852093-12852092:0;chr16:12852093-12852270:1;chr16:12852271-12852270:0;chr16:12852271-12865559:1;chr16:12865560-23725353:0;chr16:1476601-12847040:0;chr16:23725354-23725554:1;chr16:23725555-23725554:0;chr16:23725555-23725875:1;chr16:23725876-23725875:0;chr16:23725876-23726002:1;chr16:23726003-27236089:0;chr16:27236090-27236335:1;chr16:27236336-48236182:0;chr16:48236183-48236335:1;chr16:48236336-48236731:0;chr16:48236732-48236759:1;chr16:48236760-48236759:0;chr16:48236760-48237019:1;chr16:48237020-48237019:0;chr16:48237020-48237212:1;chr16:48237213-48237212:0;chr16:48237213-48237315:1;chr16:48237316-52292205:0;chr16:52292206-52292278:1;chr16:52292279-52292278:0;chr16:52292279-52292488:1;chr16:52292489-52292488:0;chr16:52292489-52292653:1;chr16:52292654-52301591:0;chr16:52301592-52301829:1;chr16:52301830-52301829:0;chr16:52301830-52302040:1;chr16:52302041-52302040:0;chr16:52302041-52302225:1;chr16:52302226-52303496:0;chr16:52303497-52304379:1;chr16:52304380-52837006:0;chr16:52837007-52837286:1;chr16:52837287-52837286:0;chr16:52837287-52837444:1;chr16:52837445-52837444:0;chr16:52837445-52837567:1;chr16:52837568-52837567:0;chr16:52837568-52837843:1;chr16:52837844-52837843:0;chr16:52837844-52837896:1;chr16:52837897-65015521:0;chr16:60001-1476600:-1;chr16:65015522-65016184:1;chr16:65016185-65016184:0;chr16:65016185-65016814:1;chr16:65016815-65016814:0;chr16:65016815-65016956:1;chr16:65016957-69969014:0;chr16:69969015-69969228:1;chr16:69969229-71010800:0;chr16:71010801-71010882:1;chr16:71010883-71010882:0;chr16:71010883-71011006:1;chr16:71011007-71011006:0;chr16:71011007-71011157:1;chr16:71011158-71011157:0;chr16:71011158-71011311:1;chr16:71011312-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-854400:0;chr1:1574301-249250621:0;chr1:854401-1574300:-1;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-54561948:0;chr4:111066306-111085094:1;chr4:111085095-114496373:0;chr4:114496374-114496630:1;chr4:114496631-114496630:0;chr4:114496631-114496790:1;chr4:114496791-114496790:0;chr4:114496791-114497040:1;chr4:114497041-114500638:0;chr4:114500639-114500709:1;chr4:114500710-114500709:0;chr4:114500710-114500941:1;chr4:114500942-114500941:0;chr4:114500942-114501140:1;chr4:114501141-114501140:0;chr4:114501141-114501220:1;chr4:114501221-114505714:0;chr4:114505715-114505802:1;chr4:114505803-114505802:0;chr4:114505803-114505952:1;chr4:114505953-115105647:0;chr4:115105648-115105821:1;chr4:115105822-115105821:0;chr4:115105822-115105913:1;chr4:115105914-115105913:0;chr4:115105914-115105992:1;chr4:115105993-115105992:0;chr4:115105993-115106200:1;chr4:115106201-135555464:0;chr4:135555465-135555730:1;chr4:135555731-157014670:0;chr4:157014671-157014847:1;chr4:157014848-157014847:0;chr4:157014848-157014853:1;chr4:157014854-157014853:0;chr4:157014854-157015417:1;chr4:157015418-157015417:0;chr4:157015418-157015648:1;chr4:157015649-157015648:0;chr4:157015649-157015689:1;chr4:157015690-157544075:0;chr4:157544076-157544318:1;chr4:157544319-167367680:0;chr4:167367681-167368117:1;chr4:167368118-167368117:0;chr4:167368118-167368238:1;chr4:167368239-167368238:0;chr4:167368239-167368475:1;chr4:167368476-167368475:0;chr4:167368476-167368722:1;chr4:167368723-191154276:0;chr4:54561949-55998274:1;chr4:55998275-86545800:0;chr4:86545801-86552058:1;chr4:86552059-111066305:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-139218400:0;chr9:139218401-140360200:-1;chr9:140360201-141213431:0;chrX:0-124406000:0;chrX:124406001-124415000:-1;chrX:124415001-155270560:0;chrY:0-59373566:0	hs1:160522842-160522842,hs2:147291273-147291273;hs2:35056944-35056944,hs20:23093718-23093718;hs2:104989746-104989746,hs8:137701896-137701896;hs4:157015690-157015690,hs16:48237211-48237211;hs4:111066306-111066306,hs16:12847050-12847050;hs4:114500710-114500710,hs16:48236760-48236760;hs4:114505953-114505953,hs16:52837568-52837568;hs4:111066306-111066306,hs16:12847050-12847050;hs4:114505953-114505953,hs16:52837572-52837572;hs4:115105822-115105822,hs4:114496744-114496744;hs4:86552059-86552059,hs4:111085095-111085095;hs4:86552059-86552059,hs4:111085095-111085095;hs4:115105914-115105914,hs4:114496405-114496405;hs4:111066306-111066306,hs16:12847050-12847050;hs4:111066306-111066306,hs16:12847050-12847050;hs4:114500710-114500710,hs16:48236760-48236760;hs4:111066306-111066306,hs16:12847050-12847050;hs4:86552059-86552059,hs4:111085095-111085095;hs4:111066306-111066306,hs16:12847050-12847050;hs4:111066306-111066306,hs16:12847050-12847050;hs4:86552059-86552059,hs4:111085095-111085095;hs4:114500710-114500710,hs16:48236760-48236760;hs4:86552059-86552059,hs4:111085095-111085095;hs4:114500710-114500710,hs16:48236760-48236760;hs4:178006250-178006250,hs4:177283845-177283845;hs4:86552059-86552059,hs4:111085095-111085095;hs4:111066307-111066307,hs16:12847050-12847050;hs4:111066306-111066306,hs16:12847050-12847050;hs4:114501141-114501141,hs16:52837287-52837287;hs4:114500710-114500710,hs16:48236760-48236760;hs6:94179585-94179585,hs9:100907845-100907845;hs6:71020488-71020488,hs9:5586122-5586122;hs8:137701896-137701896,hs5:5695845-5695845;hs9:28911555-28911555,hs6:94179602-94179602;hs15:57861466-57861466,hs15:97800496-97800496;hs15:79594850-79594850,hs2:235864474-235864474;hs16:48236336-48236336,hs16:48237316-48237316;hs16:65016734-65016734,hs4:114496791-114496791;hs16:12852271-12852271,hs16:12865560-12865560;hs16:65016738-65016738,hs4:114496791-114496791;hs16:71011340-71011340,hs4:114500750-114500750;hs16:71011340-71011340,hs4:114500754-114500754;hs16:52837897-52837897,hs4:115105648-115105648;hs16:48237171-48237171,hs4:114505803-114505803;hs16:65016815-65016815,hs4:114496374-114496374;hs16:48237213-48237213,hs4:157015690-157015690;hs16:48236336-48236336,hs16:48237316-48237316;hs16:23725964-23725964,hs4:135555725-135555725;hs16:12852271-12852271,hs16:12865560-12865560;hs16:12847052-12847052,hs4:111066306-111066306;hs16:12852271-12852271,hs16:12865560-12865560;hs16:48237171-48237171,hs4:114505807-114505807;hs16:48237167-48237167,hs4:157544070-157544070;hs16:12852271-12852271,hs16:12865560-12865560;hs16:48236336-48236336,hs16:48237316-48237316;hs16:48237167-48237167,hs4:157544077-157544077;hs16:52304380-52304380,hs4:157014854-157014854;hs16:48237167-48237167,hs4:157544076-157544076;hs16:48237171-48237171,hs4:114505803-114505803;hs16:12852271-12852271,hs16:12865560-12865560;hs16:52304380-52304380,hs4:157014853-157014853;hs16:12852271-12852271,hs16:12865560-12865560;hs16:48237171-48237171,hs4:114505715-114505715;hs16:69969141-69969141,hs4:167368339-167368339;hs16:48237171-48237171,hs4:114505715-114505715;hs16:65016813-65016813,hs4:114496374-114496374;hs20:23093720-23093720,hs2:35056942-35056942	ARHGAP24;C16orf91;CAMK2D;CHIC2;ELOVL6;GSX2;KDR;KIT;LOC643988;PDGFRA;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	ARHGAP24,CPPED1;ARHGAP24,ELOVL6;ARHGAP24,VKORC1;CAMK2D,ABCC11;CAMK2D,CDH11;ELOVL6,CPPED1;ELOVL6,VKORC1
CTDB0398	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	4	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG078_A	Illumina Genome Analyzer IIx or 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30;SCRG1;SEL1L3;SH3BP2;SH3TC1;SLBP;SLC10A6;SLC2A9;SLC34A2;SNCA;SORCS2;SPP1;STK32B;STX18;TACC3;TADA2B;TAPT1;TBC1D14;TIGD2;TMEM128;TMEM129;TNIP2;TRIML1;TRIML2;UBE2K;UGT2A3;UGT2B10;UGT2B15;UGT2B17;WDR1;WFS1;ZBTB49;ZFYVE28;ZNF141;ZNF518B;ZNF595;ZNF718;ZNF721;ZNF732;ZNF876P;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	ABLIM2,CRMP1;AFAP1,CTBP1;AFAP1,GAK;C1QTNF7,SORCS2;CC2D2A,SLC2A9;CTBP1,RGS12;EVC2,CTBP1;EVC2,GAK;FAM190A,PTPN13;GAK,CTBP1;GAK,GAK;HTT,HTT;HTT,STK32B;METTL19,EVC;MMRN1,FAM190A;SORCS2,CTBP1;SORCS2,EVC2;SORCS2,GAK;STK32B,HTT;TAPT1,LDB2
CTDB0399	Research	24705251	Wu G, Diaz AK, Paugh BS, Rankin SL, Ju B, Li Y, Zhu X, Qu C, Chen X, Zhang J, Easton J, Edmonson M, Ma X, Lu C, Nagahawatte P, Hedlund E, Rusch M, Pounds S, Lin T, Onar-Thomas A, Huether R, Kriwacki R, Parker M, Gupta P, Becksfort J, Wei L, Mulder HL, Boggs K, Vadodaria B, Yergeau D, Russell JC, Ochoa K, Fulton RS, Fulton LL, Jones C, Boop FA, Broniscer A, Wetmore C, Gajjar A, Ding L, Mardis ER, Wilson RK, Taylor MR, Downing JR, Ellison DW, Zhang J, Baker SJ	The genomic landscape of diffuse intrinsic pontine glioma and pediatric non-brainstem high-grade glioma	Nature Genetics	2014 May	8	Glioma	Next Generation Sequencing	Homo sapiens	SJHGG102_D	Illumina Genome Analyzer IIx or HiSeq	chr10:0-135534747:0;chr11:0-168400:0;chr11:168401-494000:-1;chr11:20127589-50038678:-1;chr11:494001-20127588:0;chr11:50038679-135006516:0;chr12:0-60700:0;chr12:26585601-26598431:0;chr12:26598432-26707500:-1;chr12:26707501-45876957:0;chr12:45876958-45877154:-1;chr12:45877155-133851895:0;chr12:60701-26585600:-1;chr13:0-19258900:0;chr13:19258901-63669725:-1;chr13:63669726-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-60000:0;chr16:53839945-53839944:0;chr16:53839945-54055500:-1;chr16:54055501-54055500:0;chr16:54055501-70885700:-1;chr16:60001-53839944:-1;chr16:70885701-70885700:0;chr16:70885701-71203200:-1;chr16:71203201-71203200:0;chr16:71203201-90292700:-1;chr16:90292701-90354753:0;chr17:0-81195210:0;chr18:0-46100:0;chr18:15401401-78077248:0;chr18:46101-15401400:-1;chr19:0-158500:0;chr19:158501-18524013:1;chr19:18524014-40580700:0;chr19:40580701-59118800:-1;chr19:59118801-59128983:0;chr1:0-72071933:0;chr1:144858001-233905930:1;chr1:233905931-233906010:0;chr1:233906011-249240500:1;chr1:249240501-249250621:0;chr1:72071934-72086469:-1;chr1:72086470-144858000:0;chr20:0-62402290:0;chr20:62402291-62402433:1;chr20:62402434-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-141631967:0;chr2:141631968-141636539:-1;chr2:141636540-243199373:0;chr3:0-181449282:0;chr3:181449283-181451362:-1;chr3:181451363-198022430:0;chr4:0-20698782:0;chr4:20698783-21280082:-1;chr4:21280083-191154276:0;chr5:0-23162974:0;chr5:23162975-23171910:-1;chr5:23171911-180915260:0;chr6:0-1416736:0;chr6:101075198-101368872:-1;chr6:101368873-171115067:0;chr6:1416737-1416804:1;chr6:1416805-101075197:0;chr7:0-159138663:0;chr8:0-33500:0;chr8:101839998-101839997:0;chr8:101839998-101943345:1;chr8:101943346-101943345:0;chr8:101943346-103133592:-1;chr8:103133593-103133592:0;chr8:103133593-106817517:1;chr8:106817518-106817517:0;chr8:106817518-107163457:-1;chr8:107163458-107163457:0;chr8:107163458-108656775:1;chr8:108656776-108656775:0;chr8:108656776-108659146:1;chr8:108659147-108659146:0;chr8:108659147-108659161:1;chr8:108659162-108659161:0;chr8:108659162-112017267:1;chr8:112017268-117328528:0;chr8:117328529-120150971:1;chr8:120150972-120150971:0;chr8:120150972-120152079:1;chr8:120152080-120152079:0;chr8:120152080-122407264:1;chr8:122407265-122407264:0;chr8:122407265-125730559:1;chr8:125730560-125730559:0;chr8:125730560-126291344:1;chr8:126291345-126291344:0;chr8:126291345-129575905:1;chr8:129575906-129575905:0;chr8:129575906-129873396:1;chr8:129873397-129873396:0;chr8:129873397-136422622:1;chr8:136422623-136422622:0;chr8:136422623-146303800:1;chr8:146303801-146364022:0;chr8:33501-39505783:-1;chr8:39505784-39505783:0;chr8:39505784-39506268:1;chr8:39506269-39506268:0;chr8:39506269-43820800:-1;chr8:43820801-46856500:0;chr8:46856501-51010673:1;chr8:51010674-51010673:0;chr8:51010674-52811277:1;chr8:52811278-52811277:0;chr8:52811278-57828923:1;chr8:57828924-57828923:0;chr8:57828924-57829510:-1;chr8:57829511-57829510:0;chr8:57829511-59576285:1;chr8:59576286-101839997:-1;chr8:59576286-59576285:0;chr9:0-141213431:0;chrX:0-29360200:0;chrX:124406301-124414800:-1;chrX:124414801-155270560:0;chrX:29360201-29453392:-1;chrX:29453393-124406300:0;chrY:0-2649500:0;chrY:2649501-59033300:-1;chrY:59033301-59373566:0	hs1:35091533-35091533,hs1:35090329-35090329;hs1:72071934-72071934,hs14:90264461-90264461;hs1:72071934-72071934,hs14:90264461-90264461;hs2:195687849-195687849,hs2:148240980-148240980;hs3:67944284-67944284,hs6:46985711-46985711;hs8:103133593-103133593,hs8:101839998-101839998;hs8:129873397-129873397,hs8:108656776-108656776;hs8:39506269-39506269,hs8:106817518-106817518;hs8:108659162-108659162,hs8:129575906-129575906;hs10:3914053-3914053,hs1:233763481-233763481;hs10:3914020-3914020,hs1:233763490-233763490;hs15:69804520-69804520,hs17:78660946-78660946;hs19:18524014-18524014,hs19:40580585-40580585	ABRA;ADCY8;ANGPT1;ANKRD46;ASAP1;C8orf22;C8orf33;C8orf4;C8orf42;C8orf85;CA8;CEBPD;CHCHD7;CHD7;CLVS1;COL14A1;COL22A1;COLEC10;COMMD5;CYP7A1;DEPTOR;DERL1;DPYS;DSCC1;EBAG9;EFCAB1;EFR3A;EIF3E;EIF3H;ENPP2;ENY2;EXT1;FAM110B;FAM135B;FAM150A;FAM49B;FAM83A;FAM84B;FBXO25;FNTA;GRHL2;GSDMC;HAS2;HGSNAT;HOOK3;HTRA4;IDO1;IDO2;IMPAD1;KCNK9;KCNV1;KHDRBS3;KIAA0146;KIAA0196;KLF10;LOC283116;LOC646627;LOC653486;LRP12;MAL2;MCM4;MED30;MOS;MRPL13;MTBP;MTSS1;MYC;NCALD;NDRG1;NDUFB9;NOV;NPBWR1;NSMAF;NSMCE2;ODF1;OR4F21;OXR1;PABPC1;PCMTD1;PENK;PKHD1L1;PLAG1;POTEA;POU5F1B;PRKDC;PXDNL;RAB2A;RAD21;RB1CC1;RIMS2;RNF139;RNF19A;RRM2B;RSPO2;SAMD12;SDCBP;SDR16C5;SGK196;SLA;SLC30A8;SNAI2;SNTB1;SNTG1;SNX31;SPAG1;SQLE;ST18;ST3GAL1;SYBU;TAF2;TATDN1;TM2D2;TM7SF4;TMEM74;TNFRSF11B;TOX;TRAPPC9;TRHR;TRIB1;TRMT12;TTC35;UBE2V2;UBR5;UBXN2B;UTP23;WDR67;WISP1;YWHAZ;ZFAT;ZFPM2;ZHX2;ZNF16;ZNF250;ZNF572;ZNF596;ZNF7;ZNF706;	Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, Tennessee, USA	Pediatric high-grade glioma (HGG) is a devastating disease with a less than 20% survival rate 2 years after diagnosis. We analyzed 127 pediatric HGGs, including diffuse intrinsic pontine gliomas (DIPGs) and non-brainstem HGGs (NBS-HGGs), by whole-genome, whole-exome and/or transcriptome sequencing. We identified recurrent somatic mutations in ACVR1 exclusively in DIPGs (32%), in addition to previously reported frequent somatic mutations in histone H3 genes, TP53 and ATRX, in both DIPGs and NBS-HGGs. Structural variants generating fusion genes were found in 47% of DIPGs and NBS-HGGs, with recurrent fusions involving the neurotrophin receptor genes NTRK1, NTRK2 and NTRK3 in 40% of NBS-HGGs in infants. Mutations targeting receptor tyrosine kinase-RAS-PI3K signaling, histone modification or chromatin remodeling, and cell cycle regulation were found in 68%, 73% and 59% of pediatric HGGs, respectively, including in DIPGs and NBS-HGGs. This comprehensive analysis provides insights into the unique and shared pathways driving pediatric HGG within and outside the brainstem. 	GRCh37/hg19				Yes	NA
CTDB0400	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_100246	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0401	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_100221	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0402	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_100171	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0403	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_100161	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0404	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_100229	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0405	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_100241	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0406	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_90150	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0407	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_90892	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0408	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_90769	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0409	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_90779	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0410	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_100187	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0411	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_90123	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0412	Research	25770156	Watkins J, Weekes D, Shah V, Gazinska P, Joshi S, Sidhu B, Gillett C, Pinder S, Vanoli F, Jasin M, Mayrhofer M, Isaksson A, Cheang MC, Mirza H, Frankum J, Lord CJ, Ashworth A, Vinayak S, Ford JM, Telli ML, Grigoriadis A, Tutt AN	Genomic Complexity Profiling Reveals That HORMAD1 Overexpression Contributes to Homologous Recombination Deficiency in Triple-Negative Breast Cancers	Cancer Discovery	2015 May	1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,X	Breast cancer	SNP Array	Homo sapiens	P_90178	Affymetrix SNP6.0				Breakthrough Breast Cancer Research Unit, King's College London, London, United Kingdom	Triple-negative breast cancers (TNBC) are characterized by a wide spectrum of genomic alterations, some of which might be caused by defects in DNA repair processes such as homologous recombination (HR). Despite this understanding, associating particular patterns of genomic instability with response to therapy has been challenging. Here, we show that allelic-imbalanced copy-number aberrations (AiCNA) are more prevalent in TNBCs that respond to platinum-based chemotherapy, thus providing a candidate predictive biomarker for this disease. Furthermore, we show that a high level of AiCNA is linked with elevated expression of a meiosis-associated gene, HORMAD1. Elevated HORMAD1 expression suppresses RAD51-dependent HR and drives the use of alternative forms of DNA repair, the generation of AiCNAs, as well as sensitizing cancer cells to HR-targeting therapies. Our data therefore provide a mechanistic association between HORMAD1 expression, a specific pattern of genomic instability, and an association with response to platinum-based chemotherapy in TNBC. SIGNIFICANCE: Previous studies have shown correlation between mutational scars and sensitivity to platinums extending beyond associations with BRCA1/2 mutation, but do not elucidate the mechanism. Here, a novel allele-specific copy-number characterization of genome instability identifies and functionally validates the inappropriate expression of the meiotic gene HORMAD1 as a driver of HR deficiency in TNBC, acting to induce allelic imbalance and moderate platinum and PARP inhibitor sensitivity with implications for the use of such scars and expression of meiotic genes as predictive biomarkers. 		GSE40267			Yes	NA
CTDB0413	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	8	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0004	Illumina HiSeq 2000	chr10:0-69623992:0;chr10:69623993-90200293:-1;chr10:90200294-135534747:0;chr11:0-135006516:0;chr12:0-38096966:0;chr12:38096967-38924661:-1;chr12:38924662-52370131:0;chr12:52370132-52370409:-1;chr12:52370410-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-10849116:0;chr21:10849117-10944185:-1;chr21:10944186-48129895:0;chr22:0-51304566:0;chr2:0-112307636:0;chr2:112307637-112647111:-1;chr2:112647112-243199373:0;chr3:0-198022430:0;chr4:0-160974802:0;chr4:160974803-161098962:-1;chr4:161098963-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-5499065:0;chr8:122709151-129674654:0;chr8:129674655-130526331:-1;chr8:130526332-136409771:0;chr8:136409772-137426384:-1;chr8:137426385-146364022:0;chr8:53079435-108692391:-1;chr8:5499066-5628772:-1;chr8:5628773-53079434:0;chr8:87581785-122709150:-1;chr9:0-9170699:0;chr9:9170700-9523598:-1;chr9:9523599-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:33183391-33183391,hs1:33260864-33260864;hs1:38432796-38432796,hs6:28863604-28863604;hs1:49491351-49491351,hs1:49494430-49494430;hs1:174962536-174962536,hs1:174928636-174928636;hs2:12369960-12369960,hs2:12372645-12372645;hs2:40555062-40555062,hs2:78686837-78686837;hs2:63900644-63900644,hs2:176179133-176179133;hs2:63900646-63900646,hs2:176179119-176179119;hs2:78685414-78685414,hs2:40555062-40555062;hs2:102379496-102379496,hs2:109355974-109355974;hs2:172448061-172448061,hs2:173637622-173637622;hs2:172448061-172448061,hs2:173637622-173637622;hs2:176179132-176179132,hs2:63900634-63900634;hs2:186672954-186672954,hs2:186654331-186654331;hs3:3834568-3834568,hs3:3820326-3820326;hs3:121013940-121013940,hs3:121014043-121014043;hs3:122200142-122200142,hs3:122200197-122200197;hs4:72714689-72714689,hs22:50158256-50158256;hs4:132283261-132283261,hs4:132297084-132297084;hs4:144317983-144317983,hs4:144317891-144317891;hs5:35305661-35305661,hs10:114205128-114205128;hs7:40850149-40850149,hs7:41846253-41846253;hs7:40850149-40850149,hs7:41846253-41846253;hs8:10022420-10022420,hs8:135029870-135029870;hs8:19817022-19817022,hs8:3489795-3489795;hs8:32797612-32797612,hs8:33003443-33003443;hs8:32797615-32797615,hs8:32801119-32801119;hs8:33003449-33003449,hs8:52593586-52593586;hs8:33003553-33003553,hs8:32801124-32801124;hs8:33565022-33565022,hs8:42751079-42751079;hs8:33802316-33802316,hs8:41389673-41389673;hs8:33802606-33802606,hs8:42740151-42740151;hs8:33938890-33938890,hs8:38383664-38383664;hs8:34363629-34363629,hs8:40439288-40439288;hs8:34738487-34738487,hs8:41349058-41349058;hs8:35152145-35152145,hs8:40457135-40457135;hs8:35425128-35425128,hs8:43030916-43030916;hs8:35425132-35425132,hs8:43030916-43030916;hs8:35518102-35518102,hs8:38726593-38726593;hs8:36018492-36018492,hs8:43491062-43491062;hs8:36092475-36092475,hs8:40439881-40439881;hs8:36905668-36905668,hs8:39138168-39138168;hs8:37962219-37962219,hs8:42650011-42650011;hs8:38383468-38383468,hs8:39137712-39137712;hs8:38406501-38406501,hs8:39434675-39434675;hs8:39005932-39005932,hs8:42750641-42750641;hs8:40456981-40456981,hs8:35518290-35518290;hs8:41690105-41690105,hs8:33940233-33940233;hs8:41981041-41981041,hs8:42053399-42053399;hs8:42717762-42717762,hs8:42590038-42590038;hs8:42820001-42820001,hs8:40131819-40131819;hs8:43030477-43030477,hs8:43098475-43098475;hs8:47009554-47009554,hs8:110862767-110862767;hs8:76083913-76083913,hs8:78682752-78682752;hs8:78220523-78220523,hs8:78124580-78124580;hs8:80126508-80126508,hs8:80039302-80039302;hs8:83233679-83233679,hs8:117921027-117921027;hs8:85916753-85916753,hs8:89436223-89436223;hs8:104500556-104500556,hs8:106574934-106574934;hs8:104715306-104715306,hs8:10039759-10039759;hs8:110321690-110321690,hs8:114907572-114907572;hs8:113323346-113323346,hs8:113333495-113333495;hs8:114367382-114367382,hs8:115137397-115137397;hs8:117072421-117072421,hs8:116982986-116982986;hs8:137590138-137590138,hs8:139591703-139591703;hs10:59924521-59924521,hs10:59929757-59929757;hs10:59929863-59929863,hs10:59934682-59934682;hs10:59930284-59930284,hs10:59928967-59928967;hs10:59930284-59930284,hs10:59928967-59928967;hs10:77810044-77810044,hs10:78522769-78522769;hs10:77810044-77810044,hs10:78522769-78522769;hs10:77810044-77810044,hs10:78522769-78522769;hs10:88402703-88402703,hs10:32507525-32507525;hs12:23542591-23542591,hs14:88593733-88593733;hs12:38953236-38953236,hs12:21529818-21529818;hs17:35499733-35499733,hs17:35617124-35617124;hs19:36686497-36686497,hs10:11230133-11230133;hs20:60521456-60521456,hs20:60520564-60520564;hs23:144263583-144263583,hs23:144472906-144472906	FGFR1;	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	ADAM32,RNF170;C8orf86,ADAM32;RIMS2,MSRA
CTDB0414	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	3	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0059	Illumina HiSeq 2000	chr10:0-127389287:0;chr10:127389288-128439429:-1;chr10:128439430-135534747:0;chr11:0-135006516:0;chr12:0-25872245:0;chr12:25872246-34414441:-1;chr12:34414442-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-21334777:0;chr2:21334778-22001683:-1;chr2:217915725-217993867:-1;chr2:217993868-243199373:0;chr2:22001684-217915724:0;chr3:0-78131967:0;chr3:118877415-80820129:1;chr3:172220462-171989369:1;chr3:172429136-172412681:1;chr3:172476665-82780298:1;chr3:190045000-190048756:-1;chr3:190113509-198022430:0;chr3:78131968-118881483:-1;chr3:83014922-82821204:1;chr3:83114349-190113508:-1;chr4:0-94332899:0;chr4:126686846-127536820:-1;chr4:127536821-140683203:0;chr4:140683204-153459905:-1;chr4:153459906-191154276:0;chr4:94332900-94857806:-1;chr4:94857807-126686845:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-9301697:0;chr9:9301698-9304495:-1;chr9:9304496-9458671:0;chr9:9458672-9684823:-1;chr9:9684824-141213431:0;chrX:0-102271590:0;chrX:102271591-102805328:-1;chrX:102805329-155270560:0;chrY:0-59373566:0	hs1:64103531-64103531,hs1:64023910-64023910;hs1:64850193-64850193,hs10:101600019-101600019;hs1:195973597-195973597,hs1:195973710-195973710;hs1:233962189-233962189,hs1:233963570-233963570;hs2:49854729-49854729,hs2:49864604-49864604;hs2:49862912-49862912,hs2:49872200-49872200;hs2:49865156-49865156,hs2:49865297-49865297;hs2:49865285-49865285,hs2:49872459-49872459;hs2:49867360-49867360,hs2:49860931-49860931;hs2:49872466-49872466,hs2:49865156-49865156;hs2:65859142-65859142,hs2:65858353-65858353;hs2:91937048-91937048,hs12:123873688-123873688;hs3:71415647-71415647,hs3:71413720-71413720;hs3:80971636-80971636,hs3:88407861-88407861;hs3:82817946-82817946,hs3:82828356-82828356;hs3:82830567-82830567,hs3:83015805-83015805;hs3:103627503-103627503,hs3:176341661-176341661;hs3:109924632-109924632,hs3:118615145-118615145;hs3:171997544-171997544,hs3:172384802-172384802;hs3:172072843-172072843,hs3:172238199-172238199;hs3:172235616-172235616,hs3:172438821-172438821;hs3:172385039-172385039,hs3:172433676-172433676;hs3:172475562-172475562,hs3:190530068-190530068;hs3:176538679-176538679,hs3:178048958-178048958;hs3:178952270-178952270,hs3:177916024-177916024;hs4:81239840-81239840,hs8:107752651-107752651;hs5:28652072-28652072,hs14:55618593-55618593;hs5:175733376-175733376,hs18:55381811-55381811;hs6:159046794-159046794,hs6:158969449-158969449;hs7:46595607-46595607,hs7:46595695-46595695;hs8:100916474-100916474,hs8:100895469-100895469;hs10:90368359-90368359,hs10:90368699-90368699;hs10:122628942-122628942,hs18:57150108-57150108;hs12:25660742-25660742,hs12:25130148-25130148;hs12:27023810-27023810,hs12:28180373-28180373;hs12:28103905-28103905,hs12:28211218-28211218;hs12:33211553-33211553,hs12:30979763-30979763;hs13:75213414-75213414,hs14:55618883-55618883;hs13:111852488-111852488,hs13:112019145-112019145;hs14:55618496-55618496,hs14:55618780-55618780;hs14:55618740-55618740,hs6:66526378-66526378;hs14:75581765-75581765,hs14:75581818-75581818;hs15:48101016-48101016,hs15:48101268-48101268;hs17:50197629-50197629,hs12:81391487-81391487;hs17:60807430-60807430,hs17:60807294-60807294;hs19:816668-816668,hs19:816426-816426;hs24:16975482-16975482,hs17:57707528-57707528	BZW1P1;CCT6P4;CLDN16;GCNT1P3;GHSR;NCEH1;SLC31A1P1;TNFSF10;	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	FNDC3B,NCEH1;FNDC3B,TNFSF10
CTDB0415	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	15	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0069	Illumina HiSeq 2000	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-74903578:0;chr15:62553529-88218199:0;chr15:74903579-62553528:1;chr15:81504848-102531392:0;chr15:88218200-81504847:1;chr16:0-6733751:0;chr16:6733752-6746153:-1;chr16:6746154-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-18719933:0;chr4:18719934-18734248:-1;chr4:18734249-191154276:0;chr5:0-17603583:0;chr5:17603377-180915260:0;chr5:17603584-17603376:1;chr6:0-171115067:0;chr7:0-44105123:0;chr7:44105124-55782353:-1;chr7:55782354-159138663:0;chr8:0-52122989:0;chr8:111320246-146364022:0;chr8:52122990-52558645:-1;chr8:52130274-55083438:-1;chr8:55080109-52128202:1;chr8:55083439-75672293:0;chr8:75672294-111320245:-1;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:142787688-142787688,hs15:96397373-96397373;hs1:187947763-187947763,hs1:187954812-187954812;hs1:187947874-187947874,hs1:187982378-187982378;hs1:211502242-211502242,hs1:211502184-211502184;hs1:227467579-227467579,hs1:227473100-227473100;hs1:231607793-231607793,hsX:48977124-48977124;hs2:199710953-199710953,hs2:199713112-199713112;hs3:37718635-37718635,hs11:33288559-33288559;hs4:92925961-92925961,hs4:92873309-92873309;hs5:20547860-20547860,hs14:58706090-58706090;hs5:158687077-158687077,hs6:36247111-36247111;hs6:64769003-64769003,hs6:64768847-64768847;hs6:146323409-146323409,hs6:146298596-146298596;hs7:139819169-139819169,hs9:33002774-33002774;hs7:140173603-140173603,hs7:140143717-140143717;hs8:60467589-60467589,hs8:139995367-139995367;hs8:90023956-90023956,hs8:90023845-90023845;hs8:113825306-113825306,hs8:113825791-113825791;hs8:118508994-118508994,hs8:144025317-144025317;hs8:118509173-118509173,hs8:144025398-144025398;hs8:131988002-131988002,hs8:131988363-131988363;hs8:133124731-133124731,hs8:133115405-133115405;hs8:139995354-139995354,hs8:60470377-60470377;hs9:9145661-9145661,hs9:9178310-9178310;hs9:22043338-22043338,hs9:22126816-22126816;hs9:77543231-77543231,hs14:36281163-36281163;hs10:35640895-35640895,hs10:31753837-31753837;hs10:38115409-38115409,hsX:36047768-36047768;hs10:53679561-53679561,hs10:53679308-53679308;hs10:127948245-127948245,hs10:127948104-127948104;hs11:33342098-33342098,hs3:37617555-37617555;hs12:15370630-15370630,hs4:44547855-44547855;hs14:36117834-36117834,hs14:36119384-36119384;hs14:36266813-36266813,hs14:36267359-36267359;hs15:60193482-60193482,hs15:61077249-61077249;hs15:62809305-62809305,hs15:77985573-77985573;hs15:63895421-63895421,hs15:70393108-70393108;hs15:67977261-67977261,hs15:79859530-79859530;hs15:73776062-73776062,hs15:77985774-77985774;hs15:73777897-73777897,hs15:88462273-88462273;hs15:74903299-74903299,hs15:81506142-81506142;hs15:74903835-74903835,hs15:84689610-84689610;hs15:75247135-75247135,hs15:75274351-75274351;hs15:76701227-76701227,hs15:81784703-81784703;hs15:81505406-81505406,hs15:81506956-81506956;hs15:82016551-82016551,hs15:82142753-82142753;hs15:83786247-83786247,hs15:81783495-81783495;hs15:85885730-85885730,hs15:96290030-96290030;hs15:86069395-86069395,hs15:95884178-95884178;hs15:87493382-87493382,hs15:82146848-82146848;hs15:87501351-87501351,hs15:82127312-82127312;hs15:95843285-95843285,hs15:95843736-95843736;hs15:95877591-95877591,hs1:142798913-142798913;hs15:96310320-96310320,hs15:96440775-96440775;hs15:96429613-96429613,hs15:96518482-96518482;hs16:1339821-1339821,hs16:1339966-1339966;hs17:21548442-21548442,hs20:26079438-26079438;hs17:41110532-41110532,hs11:118225545-118225545;hs17:55291966-55291966,hs17:55281492-55281492;hs17:80583762-80583762,hs17:80592511-80592511;hs17:80604418-80604418,hs14:33002460-33002460;hs18:53870184-53870184,hs18:53839900-53839900;hs19:42002896-42002896,hs17:21726667-21726667;hs20:21770031-21770031,hs20:23883452-23883452;hs20:22543146-22543146,hs20:24109800-24109800;hs20:22545819-22545819,hs20:24109799-24109799;hs20:24108704-24108704,hs20:24108764-24108764;hs20:24123371-24123371,hs20:22542678-22542678;hs22:45334390-45334390,hs22:45336237-45336237;hsX:22672575-22672575,hsX:22672930-22672930;hsX:145181974-145181974,hsX:145167812-145167812	AKAP13;BTBD1;HMGN1P26;KLHL25;	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	C15orf60,LINGO1
CTDB0416	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	14	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0131	Illumina HiSeq 2000	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-30736165:0;chr14:30717638-32201370:0;chr14:30736166-30717637:1;chr14:32201371-50990242:-1;chr14:32240974-31010651:1;chr14:32931626-76186652:-1;chr14:37060590-87020375:0;chr14:39493660-32300903:1;chr14:41277629-77774897:0;chr14:46710304-37983249:1;chr14:46710339-107349540:0;chr14:47617843-46350387:1;chr14:50886218-36399382:1;chr14:76186653-76661699:0;chr14:76450454-78505173:0;chr14:76661700-41277628:1;chr14:77585522-78515648:0;chr14:77774898-76450453:1;chr14:78505174-77585521:1;chr14:78515649-37060589:1;chr14:87020376-46710338:1;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-11049112:0;chr17:11049113-11049360:-1;chr17:11049361-43688024:0;chr17:43688025-45520025:-1;chr17:45520026-81195210:0;chr18:0-78077248:0;chr19:0-1062883:0;chr19:1062884-1248605:-1;chr19:1248606-50292185:0;chr19:50292186-50366076:-1;chr19:50366077-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-14745280:0;chr6:14745281-14745698:-1;chr6:14745699-171115067:0;chr7:0-61829245:0;chr7:110601757-110691241:-1;chr7:110691242-159138663:0;chr7:61829246-61829354:-1;chr7:61829355-110601756:0;chr8:0-3583336:0;chr8:3583337-3597576:-1;chr8:3597577-43444523:0;chr8:41138999-146364022:0;chr8:43444524-43448041:-1;chr8:43448042-43536332:0;chr8:43536333-41138998:1;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:11954514-11954514,hs21:39050074-39050074;hs1:178716640-178716640,hs1:178716693-178716693;hs2:80222459-80222459,hs2:80222650-80222650;hs2:86640837-86640837,hs2:86640892-86640892;hs2:131969113-131969113,hs6:11809179-11809179;hs2:140049049-140049049,hs2:140049479-140049479;hs2:161931745-161931745,hs2:161931253-161931253;hs3:59999981-59999981,hs3:61096854-61096854;hs3:146002981-146002981,hs3:146003064-146003064;hs3:151146128-151146128,hs18:65405909-65405909;hs3:151146520-151146520,hs18:65405921-65405921;hs4:19521427-19521427,hs4:19522043-19522043;hs4:57279732-57279732,hs4:57279631-57279631;hs4:91192146-91192146,hs4:91169877-91169877;hs4:91222774-91222774,hs4:91171457-91171457;hs4:117913141-117913141,hs4:117919231-117919231;hs4:130170961-130170961,hs14:79739674-79739674;hs4:160534224-160534224,hs4:160453026-160453026;hs4:174788390-174788390,hs4:174789046-174789046;hs5:45664516-45664516,hs2:147020927-147020927;hs5:140563527-140563527,hs5:140573649-140573649;hs6:529086-529086,hs6:528889-528889;hs6:3635254-3635254,hs9:21981015-21981015;hs6:27277783-27277783,hs6:27315562-27315562;hs6:28795495-28795495,hs6:28797390-28797390;hs6:30009588-30009588,hs6:30009687-30009687;hs6:30009588-30009588,hs6:30009687-30009687;hs6:69092656-69092656,hs22:29066425-29066425;hs6:137032520-137032520,hs6:137001570-137001570;hs6:165799869-165799869,hs6:165800027-165800027;hs7:6122062-6122062,hs13:26816255-26816255;hs7:56156974-56156974,hs7:56157331-56157331;hs7:56405153-56405153,hs7:56405505-56405505;hs7:84425628-84425628,hs7:84425682-84425682;hs7:90827334-90827334,hs7:90839050-90839050;hs8:37734921-37734921,hs8:43565999-43565999;hs8:41145404-41145404,hs20:26174848-26174848;hs8:41145407-41145407,hs20:26214817-26214817;hs8:43500445-43500445,hs8:43526143-43526143;hs9:73897323-73897323,hs9:73896989-73896989;hs9:96668254-96668254,hs9:96668330-96668330;hs10:77788790-77788790,hs14:74666901-74666901;hs10:101587566-101587566,hs8:140475594-140475594;hs11:13023333-13023333,hs18:53590744-53590744;hs14:19494321-19494321,hs19:19632149-19632149;hs14:21053497-21053497,hs14:20347986-20347986;hs14:21230084-21230084,hs14:21230288-21230288;hs14:21230253-21230253,hs14:22308469-22308469;hs14:23065372-23065372,hs14:36139860-36139860;hs14:29255148-29255148,hs14:49317840-49317840;hs14:29297657-29297657,hs14:48427020-48427020;hs14:29299826-29299826,hs14:48418411-48418411;hs14:29299914-29299914,hs14:29300177-29300177;hs14:31207400-31207400,hs14:34780066-34780066;hs14:31792425-31792425,hs14:77571384-77571384;hs14:31924403-31924403,hs14:32887898-32887898;hs14:32031755-32031755,hs14:53401721-53401721;hs14:32081588-32081588,hs14:78337991-78337991;hs14:32234403-32234403,hs14:78505185-78505185;hs14:32234554-32234554,hs14:37989959-37989959;hs14:32540107-32540107,hs14:78787608-78787608;hs14:36667226-36667226,hs14:53258916-53258916;hs14:37061176-37061176,hs14:46365854-46365854;hs14:39658225-39658225,hs14:45789061-45789061;hs14:40512548-40512548,hs14:39070240-39070240;hs14:44019855-44019855,hs14:50098927-50098927;hs14:46365654-46365654,hs14:87019882-87019882;hs14:48426422-48426422,hs14:87018854-87018854;hs14:49319884-49319884,hs22:46335540-46335540;hs14:53584736-53584736,hs14:76627967-76627967;hs14:54580071-54580071,hs14:76435482-76435482;hs14:63028197-63028197,hs13:98223904-98223904;hs14:74941307-74941307,hs14:77124207-77124207;hs14:75009783-75009783,hs14:54277712-54277712;hs14:75437756-75437756,hs14:75423484-75423484;hs14:76615806-76615806,hs14:77715188-77715188;hs14:76859227-76859227,hs14:78506179-78506179;hs14:77234985-77234985,hs14:77319561-77319561;hs14:77676832-77676832,hs14:88358037-88358037;hs14:77887374-77887374,hs14:86551780-86551780;hs14:78249717-78249717,hs14:78250208-78250208;hs14:78505502-78505502,hs14:87019472-87019472;hs14:88358034-88358034,hs14:72952921-72952921;hs14:106813931-106813931,hs14:106814760-106814760;hs15:20106601-20106601,hs15:20106665-20106665;hs15:30127612-30127612,hs15:30100605-30100605;hs15:51569450-51569450,hs15:51569601-51569601;hs15:74778904-74778904,hs15:74923611-74923611;hs17:26252860-26252860,hs17:41376874-41376874;hs17:26846669-26846669,hs17:26848927-26848927;hs17:26849170-26849170,hs17:37769728-37769728;hs17:26864246-26864246,hs17:80378758-80378758;hs17:26866035-26866035,hs17:61981595-61981595;hs17:27322757-27322757,hs17:58210234-58210234;hs17:27323697-27323697,hs17:80329037-80329037;hs17:36024323-36024323,hs17:40996155-40996155;hs17:36049132-36049132,hs17:80330608-80330608;hs17:37372138-37372138,hs17:40998803-40998803;hs17:37373211-37373211,hs17:40198293-40198293;hs17:40143259-40143259,hs17:41364138-41364138;hs17:40145402-40145402,hs17:80332278-80332278;hs17:40621840-40621840,hs17:41374562-41374562;hs17:40622334-40622334,hs17:73537478-73537478;hs17:41024036-41024036,hs17:41024136-41024136;hs17:41430509-41430509,hs17:58224027-58224027;hs17:43205641-43205641,hs17:43212078-43212078;hs17:43637655-43637655,hs17:43644554-43644554;hs17:43637665-43637665,hs17:43644449-43644449;hs17:46224160-46224160,hs17:58226044-58226044;hs17:46529425-46529425,hs17:62084488-62084488;hs17:48016598-48016598,hs17:36027667-36027667;hs17:58225045-58225045,hs17:73588404-73588404;hs17:61988018-61988018,hs17:40147827-40147827;hs17:62083458-62083458,hs17:73535878-73535878;hs17:80328730-80328730,hs17:80379064-80379064;hs18:20657881-20657881,hs18:20659634-20659634;hs19:40615761-40615761,hs2:65138905-65138905;hs20:26163239-26163239,hs20:26222143-26222143;hs20:26213566-26213566,hs20:26221817-26221817;hs21:11054622-11054622,hs24:59027440-59027440;hs22:29065554-29065554,hs22:29066001-29066001;hs22:29066021-29066021,hs6:69092643-69092643;hs23:121135127-121135127,hs23:121378138-121378138;hs23:121376636-121376636,hs23:121378167-121378167	ADCK1;AHSA1;ALKBH1;ANGEL1;AP4S1;ARF6;ARHGAP42P4;ARHGAP42P5;ATP5S;BAZ1A;C14orf166B;C14orf178;C14orf182;C14orf183;C14orf28;CFL2;CLEC14A;DNAAF2;DPPA3P2;DTD2;EAPP;ERO1L;FAM177A1;FAM179B;FANCM;FCF1;FERMT2;FKBP3;FKSG61;FSCB;G2E3;GEMIN2;GNPNAT1;GPR137C;GPR33;GSTZ1;HEATR5A;HECTD1;HIGD1AP17;IFT43;IGBP1P1;INSM2;IRF2BPL;ISCA2;ISM2;KLHDC1;KLHDC2;KLHL28;KRT18P6;KRT8P2;L2HGDH;LRFN5;LTBP2;MBIP;MDGA2;METTL21D;MGAT2;MIPOL1;MIS18BP1;NEMF;NF1P4;NFKBIA;NGB;NKX2-1;NKX2-8;NOXRED1;NPC2;NUBPL;OR11H12;OR11H13P;OR11H2;OR11K2P;OR4H12P;OR4K1;OR4K16P;OR4K2;OR4K3;OR4K5;OR4K6P;OR4M1;OR4N2;OR4Q3;PAX9;PHKBP2;PNN;POLE2;POTEG;POTEM;PPP2R3C;PRKD1;PRPF39;PSMA6;PSMC6;PTCSC3;QRSL1P3;RAP1AP;RHOQP1;RN7SL1;RN7SL2;RNA5SP384;RNA5SP388;RPA2P;RPL10L;RPL13AP2;RPL21P10;RPL21P5;RPL29P3;RPL32P29;RPL36AL;RPS15AP3;RPS19P3;RPS29;RPS3AP4;SAMD15;SEC23A;SLIRP;SNW1;SNX6;SOS2;SPTLC2;SPTSSA;SRP54;SSTR1;STYX;TGFB3;TMED8;TMEM63C;TRAPPC6B;UBE2CP1;VASH1;ZDHHC22;	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	AKAP6,TTLL5;DDHD1,GPATCH2L;DTD2,AKAP6;HEATR5A,KIAA1737;NUBPL,ADCK1;NUBPL,FERMT2;RP11-176H8.1,AKAP6
CTDB0417	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0154	Illumina HiSeq 2000	chr10:0-135534747:0;chr11:0-62647962:0;chr11:62647963-64550175:-1;chr11:64550176-79066110:0;chr11:68853851-135006516:0;chr11:79066111-68853850:1;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-10268628:0;chr18:10268629-11260768:-1;chr18:11260769-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-15979994:0;chr21:15979995-16139697:-1;chr21:16139698-39214982:0;chr21:39214983-47284002:-1;chr21:47284003-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-109860790:0;chr8:109860791-126920998:-1;chr8:126920999-126934938:0;chr8:126934939-127099671:-1;chr8:127099672-146364022:0;chr9:0-21842702:0;chr9:21842703-22047656:-1;chr9:22047657-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:192749594-192749594,hs6:18869815-18869815;hs4:18830687-18830687,hs4:18830763-18830763;hs4:41072750-41072750,hs4:41074456-41074456;hs4:190559871-190559871,hs18:58850148-58850148;hs5:21567041-21567041,hs5:33501106-33501106;hs5:24545507-24545507,hs22:42599855-42599855;hs5:113247176-113247176,hs19:24587974-24587974;hs5:113496069-113496069,hs22:25955548-25955548;hs6:75534095-75534095,hs21:11054315-11054315;hs8:10093410-10093410,hs8:10096202-10096202;hs8:42224568-42224568,hs5:40520773-40520773;hs8:95279094-95279094,hs22:47422451-47422451;hs8:95279591-95279591,hs22:47422075-47422075;hs8:95280341-95280341,hs22:40476239-40476239;hs8:107283500-107283500,hs8:112852147-112852147;hs8:107380443-107380443,hs8:106650799-106650799;hs8:108926849-108926849,hs8:107283570-107283570;hs8:109063583-109063583,hs8:109064538-109064538;hs8:109897015-109897015,hs8:110355271-110355271;hs8:111611664-111611664,hs8:111612482-111612482;hs8:111611664-111611664,hs8:111612482-111612482;hs8:111901730-111901730,hs8:111901818-111901818;hs8:111929739-111929739,hs8:108890548-108890548;hs8:115756851-115756851,hs8:121073502-121073502;hs8:118348670-118348670,hs8:118793307-118793307;hs8:119321539-119321539,hs8:119322723-119322723;hs8:126914696-126914696,hs8:130646395-130646395;hs8:127085791-127085791,hs8:130606405-130606405;hs8:130606060-130606060,hs8:126914532-126914532;hs9:19090081-19090081,hs9:19089825-19089825;hs11:77917875-77917875,hs11:81682531-81682531;hs11:81638858-81638858,hs11:81291300-81291300;hs11:81681062-81681062,hs11:81686570-81686570;hs12:33538777-33538777,hs12:39769603-39769603;hs12:38852808-38852808,hs12:39666732-39666732;hs14:58472424-58472424,hs23:11732036-11732036;hs18:5700895-5700895,hs18:43447835-43447835;hs18:6067752-6067752,hs18:67162206-67162206;hs18:6086302-6086302,hs18:58826878-58826878;hs18:6540031-6540031,hs18:54121994-54121994;hs18:8329567-8329567,hs18:33486002-33486002;hs18:8383800-8383800,hs18:54129354-54129354;hs18:11356902-11356902,hs18:67197176-67197176;hs18:18643142-18643142,hs18:40066128-40066128;hs18:22339305-22339305,hs18:22352839-22352839;hs18:26119477-26119477,hs21:18541134-18541134;hs18:33262431-33262431,hs21:19652837-19652837;hs18:35173973-35173973,hs18:54128946-54128946;hs18:35193393-35193393,hs18:44309448-44309448;hs18:40076857-40076857,hs18:13650258-13650258;hs18:58785908-58785908,hs21:15886805-15886805;hs18:58839106-58839106,hs21:18551324-18551324;hs18:60998180-60998180,hs18:30824859-30824859;hs18:62158707-62158707,hs18:57207252-57207252;hs18:67189037-67189037,hs18:8230489-8230489;hs18:76777013-76777013,hs18:76774346-76774346;hs18:76854054-76854054,hs21:28861248-28861248;hs19:56817730-56817730,hs19:56818508-56818508;hs20:25760369-25760369,hs22:24724822-24724822;hs21:26530221-26530221,hs21:47030004-47030004;hs21:30692690-30692690,hs21:10932393-10932393;hs21:31558887-31558887,hs18:60996277-60996277;hs21:47052950-47052950,hs18:24416200-24416200;hs22:17312856-17312856,hs22:40481905-40481905;hs22:17399026-17399026,hs22:17920312-17920312;hs22:17404618-17404618,hs22:19692098-19692098;hs22:21808336-21808336,hs22:21947710-21947710;hs22:21959775-21959775,hs22:23068182-23068182;hs22:42073403-42073403,hs22:42087567-42087567;hs22:42567363-42567363,hs22:42568119-42568119;hs22:44488406-44488406,hs22:44489267-44489267;hs23:44763368-44763368,hs23:44810110-44810110;hs23:96640614-96640614,hs23:96729973-96729973	GATA6;	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	DOK6,PTPRM;GALNT1,TMPRSS15;KDSR,CCDC178;L3MBTL4,DOK6
CTDB0418	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	2	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0214	Illumina HiSeq 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263,hs20:34954960-34954960;hs22:48428556-48428556,hs22:48428721-48428721;hs23:31455136-31455136,hs23:32385887-32385887;hs23:68764724-68764724,hs2:124651616-124651616;hs23:68766113-68766113,hs23:68866391-68866391;hs23:77580270-77580270,hs23:77800638-77800638;hs23:78199893-78199893,hs23:78200448-78200448;hs23:98103899-98103899,hs23:144304403-144304403;hs23:102744799-102744799,hs23:144291914-144291914;hs23:102825032-102825032,hs23:122165455-122165455;hs23:122143065-122143065,hs23:153199462-153199462;hs23:144247547-144247547,hs23:153723917-153723917;hs23:144247714-144247714,hs23:154466372-154466372;hs23:144260306-144260306,hs23:144242091-144242091;hs23:148148091-148148091,hs23:148147703-148147703;hs23:153212911-153212911,hs23:153709970-153709970	CIR1;HOXD10;HOXD11;HOXD12;HOXD13;HOXD9;SCRN3;	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	C2orf88,SPAG16;CCT4,NRXN1;DPY30,GALNT14;FAM171B,SPAG16;GALNT14,NRXN1;HPCAL1,NRXN1;ITGAV,TM4SF20;MREG,HIBCH;MYT1L,B3GNT2;NRXN1,GALNT14;SPAG16,VWC2L;SPAST,NRXN1;TPO,DPY30
CTDB0419	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	15	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0242	Illumina HiSeq 2000	chr10:0-83677439:0;chr10:83677440-83993433:-1;chr10:83993434-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-24015124:0;chr15:24015125-24019302:-1;chr15:24019303-25234380:0;chr15:25234381-84031593:-1;chr15:25438273-94740245:-1;chr15:28215971-28219152:-1;chr15:94740246-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-105893411:0;chr1:105893412-105893532:-1;chr1:105893533-249250621:0;chr20:0-63025520:0;chr21:0-11121763:0;chr21:11121764-11130259:-1;chr21:11130260-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-42831559:0;chr3:103697747-198022430:0;chr3:103720395-103697746:1;chr3:42831560-66481263:-1;chr3:60425664-60427126:-1;chr3:66481264-103720394:0;chr4:0-137134729:0;chr4:137134730-137138118:-1;chr4:137138119-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-64245079:0;chr7:107512123-76040784:1;chr7:107676297-159138663:0;chr7:64245080-69414325:-1;chr7:69414326-76038334:0;chr7:76038335-107676296:-1;chr7:76041976-68169942:1;chr7:80850077-81213827:-1;chr8:0-81130493:0;chr8:81130494-81131443:-1;chr8:81131444-146364022:0;chr9:0-7210195:0;chr9:7210196-7210633:-1;chr9:7210634-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:117384844-117384844,hs1:117384777-117384777;hs1:120603720-120603720,hs1:120603591-120603591;hs1:149858214-149858214,hs1:149818151-149818151;hs1:218158248-218158248,hs1:218122840-218122840;hs1:246056323-246056323,hs1:246012028-246012028;hs2:11902837-11902837,hs2:11855181-11855181;hs2:60807404-60807404,hs2:60811687-60811687;hs2:60811536-60811536,hs2:60839859-60839859;hs2:101854561-101854561,hs2:101811284-101811284;hs2:174999623-174999623,hs2:174996895-174996895;hs2:181881108-181881108,hs2:181857808-181857808;hs2:193759771-193759771,hs2:193652545-193652545;hs2:195947791-195947791,hs2:195915537-195915537;hs2:204683460-204683460,hs2:204685171-204685171;hs2:208614784-208614784,hs2:208626111-208626111;hs2:208688103-208688103,hs2:208607411-208607411;hs2:234580982-234580982,hs2:234444869-234444869;hs3:47714610-47714610,hs3:47668365-47668365;hs3:81764449-81764449,hs3:81711619-81711619;hs3:88684295-88684295,hs3:88701566-88701566;hs3:88701106-88701106,hs3:88704281-88704281;hs3:106682233-106682233,hs3:106655286-106655286;hs3:110126528-110126528,hs3:110131405-110131405;hs3:110130732-110130732,hs3:110139586-110139586;hs3:116491223-116491223,hs3:116457131-116457131;hs3:116550903-116550903,hs3:116809391-116809391;hs3:170231654-170231654,hs3:170231503-170231503;hs3:174513956-174513956,hs3:174507396-174507396;hs3:175486846-175486846,hs3:175482720-175482720;hs4:18799-18799,hs4:191034022-191034022;hs4:24154925-24154925,hs4:24130380-24130380;hs4:133256150-133256150,hs4:133251378-133251378;hs4:191042352-191042352,hs15:40493080-40493080;hs5:11233276-11233276,hs5:11172452-11172452;hs5:136056618-136056618,hs5:136026092-136026092;hs5:179681482-179681482,hs5:179611720-179611720;hs6:8320580-8320580,hs6:44423199-44423199;hs6:10356405-10356405,hs6:10346713-10346713;hs6:20684219-20684219,hs6:44256981-44256981;hs6:40145563-40145563,hs6:40146918-40146918;hs6:50075469-50075469,hs6:50053681-50053681;hs6:169008548-169008548,hs6:169008460-169008460;hs7:8190915-8190915,hs7:8190862-8190862;hs7:28050835-28050835,hs7:28052410-28052410;hs7:28054629-28054629,hs7:28054869-28054869;hs7:28089326-28089326,hs7:28042996-28042996;hs7:68169139-68169139,hs23:64126024-64126024;hs7:68173671-68173671,hs7:76977289-76977289;hs7:70907446-70907446,hs7:76978056-76978056;hs7:71065850-71065850,hs23:8715825-8715825;hs7:71080181-71080181,hs7:107553891-107553891;hs7:76976273-76976273,hs23:57007690-57007690;hs7:80877376-80877376,hs7:80961799-80961799;hs7:80961995-80961995,hs7:81214376-81214376;hs7:106860301-106860301,hs7:107512583-107512583;hs7:107202170-107202170,hs23:56844976-56844976;hs7:108539773-108539773,hs23:64568051-64568051;hs7:109775375-109775375,hs23:9861435-9861435;hs7:110252583-110252583,hs23:9859576-9859576;hs7:125433572-125433572,hs7:125433888-125433888;hs7:125438029-125438029,hs7:125371388-125371388;hs7:133832518-133832518,hs7:133866002-133866002;hs7:151084996-151084996,hs7:151038374-151038374;hs8:3615089-3615089,hs8:3617067-3617067;hs8:3616934-3616934,hs8:3629563-3629563;hs8:3618478-3618478,hs8:3619453-3619453;hs8:3618693-3618693,hs8:3620311-3620311;hs8:3628698-3628698,hs8:3634307-3634307;hs8:49115924-49115924,hs8:49058935-49058935;hs8:61458505-61458505,hs8:61487845-61487845;hs8:61483122-61483122,hs8:61490494-61490494;hs8:81153027-81153027,hs6:21291589-21291589;hs8:101425725-101425725,hs8:101436386-101436386;hs8:101429035-101429035,hs8:101436069-101436069;hs8:101468965-101468965,hs8:101429357-101429357;hs8:101719225-101719225,hs8:101721361-101721361;hs9:21964433-21964433,hs9:21969775-21969775;hs9:21964438-21964438,hs9:22450624-22450624;hs9:70988414-70988414,hs9:70959068-70959068;hs9:88565290-88565290,hs9:88544343-88544343;hs9:88574650-88574650,hs9:88565808-88565808;hs10:68939011-68939011,hs10:68876425-68876425;hs10:127190418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Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	BTBD1,MEF2A;OTUD7A,SLC28A1
CTDB0420	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	14	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0285	Illumina HiSeq 2000	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-115169878:0;chr14:0-22748346:0;chr14:22748347-70039551:-1;chr14:28806200-33253161:-1;chr14:46359233-70177736:-1;chr14:61969520-88787111:-1;chr14:76557977-79122197:-1;chr14:88787112-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-58346598:0;chr2:58346599-58391370:-1;chr2:58391371-243199373:0;chr3:0-60320947:0;chr3:60320948-60590043:-1;chr3:60464067-60587666:-1;chr3:60590044-198022430:0;chr4:0-118436189:0;chr4:118436190-118877701:-1;chr4:118877702-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:15028823-15028823,hs11:75631514-75631514;hs1:115389342-115389342,hs1:115389430-115389430;hs1:142674675-142674675,hs4:49220939-49220939;hs2:130822609-130822609,hs2:130823277-130823277;hs2:240217012-240217012,hs17:36169343-36169343;hs3:60665998-60665998,hs3:60668750-60668750;hs3:73630866-73630866,hs3:73630782-73630782;hs6:25361937-25361937,hs6:25462390-25462390;hs6:163814221-163814221,hs8:75184915-75184915;hs7:16963033-16963033,hs7:16848770-16848770;hs7:76144766-76144766,hs7:76648272-76648272;hs7:100875539-100875539,hs12:7032418-7032418;hs8:119222600-119222600,hs12:3072473-3072473;hs8:131734707-131734707,hs13:113037519-113037519;hs8:139754789-139754789,hs8:139754514-139754514;hs10:47621515-47621515,hs10:47683110-47683110;hs11:130835147-130835147,hsX:11732700-11732700;hs11:130835585-130835585,hsX:11731377-11731377;hs12:503368-503368,hs12:506384-506384;hs12:2136299-2136299,hs12:2137198-2137198;hs12:2136302-2136302,hs12:2137072-2137072;hs12:4914054-4914054,hs12:4916494-4916494;hs12:5056660-5056660,hs12:5058136-5058136;hs12:7027858-7027858,hs12:7032386-7032386;hs12:14863361-14863361,hs12:73102548-73102548;hs13:49533344-49533344,hs13:49536625-49536625;hs13:90904631-90904631,hs13:90905841-90905841;hs14:20567119-20567119,hs14:70765261-70765261;hs14:20570529-20570529,hs14:104201816-104201816;hs14:25911556-25911556,hs14:25939492-25939492;hs14:25939239-25939239,hs14:25952440-25952440;hs14:28946711-28946711,hs14:89795007-89795007;hs14:28991980-28991980,hs14:60785597-60785597;hs14:37754429-37754429,hs14:70765870-70765870;hs14:47474391-47474391,hs14:93673586-93673586;hs14:50832570-50832570,hs14:79121478-79121478;hs14:53308020-53308020,hs14:47475441-47475441;hs14:55933286-55933286,hs14:75180469-75180469;hs14:59459822-59459822,hs14:77493487-77493487;hs14:60729531-60729531,hs14:83807231-83807231;hs14:70177409-70177409,hs14:90423041-90423041;hs14:73101069-73101069,hs14:97720809-97720809;hs14:75180523-75180523,hs14:75181867-75181867;hs14:75690551-75690551,hs14:75691743-75691743;hs14:76113998-76113998,hs16:31205301-31205301;hs14:76558319-76558319,hs14:91152317-91152317;hs14:77491801-77491801,hs14:25304825-25304825;hs14:79541771-79541771,hs14:79546183-79546183;hs14:79566785-79566785,hs14:79568348-79568348;hs14:79566820-79566820,hs14:79568791-79568791;hs14:79569115-79569115,hs14:87262838-87262838;hs14:83897092-83897092,hs14:96836537-96836537;hs14:91148147-91148147,hs14:28806596-28806596;hs14:91148148-91148148,hs14:28806715-28806715;hs14:96083512-96083512,hs14:96083457-96083457;hs14:96258975-96258975,hs14:28947810-28947810;hs14:97718173-97718173,hs14:45813125-45813125;hs14:99381415-99381415,hs14:61367574-61367574;hs15:24853619-24853619,hs15:24865097-24865097;hs15:72389131-72389131,hs22:41726727-41726727;hs15:72396048-72396048,hs22:30936193-30936193;hs15:93389841-93389841,hs15:93340422-93340422;hs16:24353297-24353297,hs16:24354566-24354566;hs16:33952705-33952705,hs16:33953695-33953695;hs16:78910362-78910362,hs16:78917807-78917807;hs17:3802553-3802553,hs1:242227150-242227150;hs17:27224031-27224031,hs17:43351838-43351838;hs17:43349269-43349269,hs17:46700561-46700561;hs19:30574825-30574825,hs11:74975891-74975891;hs20:14547529-14547529,hs20:14549049-14549049;hs20:35020897-35020897,hs20:35020993-35020993;hs22:37355133-37355133,hs3:140910140-140910140;hs22:43549345-43549345,hs22:43549653-43549653;hs22:47211171-47211171,hs22:47211234-47211234		Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	CDKL1,NRXN3;IRF2BPL,STXBP6;KIAA0247,TDP1;MDGA2,RP11-371E8.4;MDGA2,UBR7
CTDB0421	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	1	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0300	Illumina HiSeq 2000	chr10:0-24861537:0;chr10:24861538-32060125:-1;chr10:31962055-36634117:-1;chr10:36634118-135534747:0;chr11:0-135006516:0;chr12:0-133851895:0;chr13:0-23519126:0;chr13:23519127-27784262:-1;chr13:27784263-35147450:0;chr13:35147451-46013185:-1;chr13:35148053-115169878:0;chr13:35555829-33276227:1;chr13:46013186-46067163:0;chr13:46067164-35148052:1;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-81195210:0;chr18:0-78077248:0;chr19:0-59128983:0;chr1:0-16448880:0;chr1:146953171-147013988:-1;chr1:147013989-161043318:0;chr1:161043319-162812008:-1;chr1:162812009-164707019:0;chr1:16448881-16825689:-1;chr1:164707020-223309227:-1;chr1:16825690-43752712:0;chr1:170186635-201274599:-1;chr1:171432473-227249607:-1;chr1:174989280-172994699:1;chr1:180354551-179035249:1;chr1:180634533-234997230:-1;chr1:180634660-249250621:0;chr1:180636656-180634185:1;chr1:180639580-189302029:-1;chr1:229653882-238186131:-1;chr1:238186132-238187955:0;chr1:238187956-180634659:1;chr1:43752713-44196704:-1;chr1:44196705-146953170:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-66252186:0;chr4:66252187-66691404:-1;chr4:66691405-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-20973150:0;chr9:20973151-32231383:-1;chr9:27384096-28104309:-1;chr9:28386112-32637207:-1;chr9:32637208-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs1:44629872-44629872,hs1:145211144-145211144;hs1:46416637-46416637,hs1:236773470-236773470;hs1:120679380-120679380,hs12:93771899-93771899;hs1:151236474-151236474,hs1:151295285-151295285;hs1:153158652-153158652,hs1:190789771-190789771;hs1:165970033-165970033,hs1:234537355-234537355;hs1:171270695-171270695,hs1:239139224-239139224;hs1:172344237-172344237,hs1:175298952-175298952;hs1:175270747-175270747,hs1:176846371-176846371;hs1:176849248-176849248,hs1:176850451-176850451;hs1:180634124-180634124,hs1:234818350-234818350;hs1:180638958-180638958,hs1:229653506-229653506;hs1:186942630-186942630,hs1:234701944-234701944;hs1:186942893-186942893,hs1:191110727-191110727;hs1:190789608-190789608,hs1:190789758-190789758;hs1:200506286-200506286,hs1:208027250-208027250;hs1:206872695-206872695,hs1:207695080-207695080;hs1:223131595-223131595,hs1:171273271-171273271;hs1:225952133-225952133,hs1:171343521-171343521;hs1:229650108-229650108,hs1:41444007-41444007;hs1:231951031-231951031,hs1:218857562-218857562;hs1:234668836-234668836,hs1:240774472-240774472;hs1:242100869-242100869,hs1:31670934-31670934;hs2:13428696-13428696,hs5:145554181-145554181;hs2:82557847-82557847,hs2:82561311-82561311;hs2:185744146-185744146,hs22:29065829-29065829;hs3:1062579-1062579,hs22:29065775-29065775;hs3:100577155-100577155,hs3:113784681-113784681;hs3:101386193-101386193,hs3:114341392-114341392;hs6:32592405-32592405,hs6:32592536-32592536;hs8:33978043-33978043,hs20:21232971-21232971;hs9:26383599-26383599,hs13:52612486-52612486;hs9:26663709-26663709,hs13:44214501-44214501;hs9:32983897-32983897,hs13:52822182-52822182;hs9:32983998-32983998,hs13:52822178-52822178;hs9:38433266-38433266,hs13:46780225-46780225;hs10:36599399-36599399,hs10:26670112-26670112;hs10:37118755-37118755,hs18:20361720-20361720;hs10:131039151-131039151,hs10:131039421-131039421;hs11:31034639-31034639,hs22:29066114-29066114;hs11:31034640-31034640,hs22:29065466-29065466;hs11:40954283-40954283,hs11:40954390-40954390;hs12:75485425-75485425,hs22:29065435-29065435;hs13:27875958-27875958,hs13:35562754-35562754;hs13:33282781-33282781,hs13:42327476-42327476;hs13:34193537-34193537,hs13:52774139-52774139;hs13:34266700-34266700,hs13:34857815-34857815;hs13:35200485-35200485,hs13:46009631-46009631;hs13:52154612-52154612,hs13:52154409-52154409;hs15:85706213-85706213,hs16:27705000-27705000;hs18:20486904-20486904,hs10:35315815-35315815;hs18:22097962-22097962,hs10:33020151-33020151;hs22:29065904-29065904,hs12:75485444-75485444;hs22:29066066-29066066,hs3:1062570-1062570;hs23:12468357-12468357,hs23:72594491-72594491;hs23:12553888-12553888,hs23:12555125-12555125;hs23:27228798-27228798,hs23:27229315-27229315;hs23:31308303-31308303,hs23:31020428-31020428	ACTA1;ACTBP11;ADAM15;ADAMTSL4;ADAR;AIM2;ANKRD34A;ANKRD35;ANKRD45;ANP32E;ANXA9;APCS;APH1A;APOA1BP;AQP10;ARF1;ARHGEF11;ARHGEF2;ARNT;ASH1L;ATP6V1E1P1;ATP8B2;AXDND1;BANF1P4;BCAN;BGLAP;BNIPL;BOLA1;BTNL10;C1orf110;C1orf138;C1orf145;C1orf148;C1orf189;C1orf35;C1orf43;C1orf51;C1orf54;C1orf56;C1orf61;C1orf85;CA14;CACYBP;CADM3;CAPN2;CCSAP;CCT3;CCT8P1;CD160;CD1A;CD1B;CD1C;CD1D;CD1E;CD5L;CDC42SE1;CENPL;CERS2;CHD1L;CHRNB2;CHTOP;CICP5;CKS1B;CLK2;CNIH4;COX5BP8;CRABP2;CREB3L4;CRP;CRPP1;CRTC2;CTSK;CTSS;CYCSP52;DAP3;DAP3P1;DARC;DARS2;DCST1;DCST2;DEGS1;DENND4B;DPM3;DRD5P2;DUSP5P1;ECM1;EFNA1;EFNA3;EFNA4;EIF4A1P11;ELL2P1;EMBP1;ENAH;ENSA;ETV3;ETV3L;FAM108A2;FAM108A3P;FAM63A;FAM72B;FAM72C;FAM91A2;FAM96AP2;FBXO28;FCER1A;FCGR1A;FCGR1B;FCGR1C;FCRL1;FCRL2;FCRL3;FCRL4;FCRL5;FDPS;FLAD1;FMO5;FTH1P2;GABPB2;GAS5;GBAP1;GJA8;GJC2;GM2AP2;GNRHR2;GON4L;GOT2P2;GPATCH4;GPR52;GPR89A;GPR89B;GPR89C;GUK1;HAPLN2;HAX1;HCN3;HDGF;HFE2;HIST2H2AA3;HIST2H2AA4;HIST2H2AB;HIST2H2AC;HIST2H2BA;HIST2H2BB;HIST2H2BC;HIST2H2BD;HIST2H2BE;HIST2H2BF;HIST2H3A;HIST2H3C;HIST2H3D;HIST2H3DP1;HIST2H3PS2;HIST2H4A;HIST2H4B;HIST3H2A;HIST3H2BA;HIST3H2BB;HIST3H3;HMGB3P6;HMGN1P5;HMGN2P18;HORMAD1;HYDIN2;IBA57;IFI16;IFRG15;IL6R;ILF2;INSRR;INTS3;IQGAP3;ISG20L2;ITGA10;JMJD4;JTB;KCNN3;KIRREL;KLHL20;KRT8P45;KRTCAP2;LAMTOR2;LBR;LENEP;LHX4;LIX1L;LMNA;LRRC71;MCL1;MEF2AP1;MEF2D;MEX3A;MLLT11;MNDA;MRPL24;MRPL55;MRPS14;MRPS21;MRPS21P2;MSTO1;MTMR11;MTX1;MTX1P1;MUC1;NBPF10;NBPF11;NBPF12;NBPF14;NBPF15;NBPF16;NBPF20;NBPF23;NBPF24;NES;NKAIN1P1;NOTCH2NL;NPHS2;NPR1;NTRK1;NUDT17;NUDT4P1;NUF2;NUP210L;NVL;OBSCN;OR10AA1P;OR10J1;OR10J2P;OR10J3;OR10J4;OR10J5;OR10J6P;OR10J7P;OR10J8P;OR10J9P;OR10K1;OR10K2;OR10R1P;OR10R2;OR10R3P;OR10T1P;OR10T2;OR10X1;OR10Z1;OR13Z1P;OR2AQ1P;OR6K1P;OR6K2;OR6K3;OR6K4P;OR6K5P;OR6K6;OR6N1;OR6N2;OR6P1;OR6Y1;OTUD7B;PAQR6;PBXIP1;PDIA3P;PDZK1;PDZK1P1;PDZK1P2;PEAR1;PEX11B;PFN1P12;PFN1P3;PFN1P4;PFN1P5;PFN1P6;PFN1P7;PFN1P8;PHBP11;PIAS3;PKLR;PLEKHO1;PMF1;PMVK;POLR3C;POLR3GL;POU5F1P4;PPIAL4A;PPIAL4C;PPIAL4D;PPIAL4E;PPIAL4F;PRCC;PRDX6;PRKAB2;PRPF3;PRSS38;PRUNE;PTPN2P1;PYGO2;PYHIN1;RAB13;RAB25;RAB4A;RABGAP1L-IT1;RBM8A;RC3H1;RFWD2;RGS4;RGS5;RHBG;RHOU;RIT1;RNA5S1;RNA5S10;RNA5S11;RNA5S12;RNA5S13;RNA5S14;RNA5S15;RNA5S16;RNA5S17;RNA5S2;RNA5S3;RNA5S4;RNA5S5;RNA5S6;RNA5S7;RNA5S8;RNA5S9;RNA5SP18;RNA5SP19;RNA5SP57;RNA5SP58;RNA5SP59;RNA5SP60;RNA5SP62;RNA5SP63;RNA5SP67;RNA5SP68;RNA5SP77;RNF115;RNF187;RPRD2;RPS27;RPS7P2;RRNAD1;RUSC1;RXFP4;S100A1;S100A13;S100A14;S100A16;S100A2;S100A3;S100A4;S100A5;S100A6;SCARNA3;SEC22B;SEMA4A;SERPINC1;SETDB1;SETP10;SF3B4;SH2D2A;SHC1;SHE;SLC25A44;SLC27A3;SLC39A1;SLC50A1;SMG5;SNAP47;SNAPIN;SOAT1;SPHAR;SPRR2A;SPRR2B;SPRR2C;SPRR2E;SPRR2F;SPRR2G;SPTA1;SRGAP2C;SSR2;SV2A;SYT11;TARS2;TDRD10;TDRD5;THBS3;TMEM78;TMEM79;TNFSF18;TNFSF4;TOR1AIP1;TOR3A;TP53BP2;TPM3;TRIM11;TRIM17;TRIM46;TSACC;TTC24;TXNIP;UBAP2L;UBE2D3P3;UBE2Q1;UBQLN4;VDAC1P9;VHLL;VPS45;WDR26;WNT3A;WNT9A;YY1AP1;ZBTB37;ZBTB7B;ZNF678;ZNF847P;	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	DNM3,TNR;MAPKAPK2,CR1;XPR1,ABCB10
CTDB0422	Research	25719666	Waddell N, Pajic M, Patch AM, Chang DK, Kassahn KS, Bailey P, Johns AL, Miller D, Nones K, Quek K, Quinn MC, Robertson AJ, Fadlullah MZ, Bruxner TJ, Christ AN, Harliwong I, Idrisoglu S, Manning S, Nourse C, Nourbakhsh E, Wani S, Wilson PJ, Markham E, Cloonan N, Anderson MJ, Fink JL, Holmes O, Kazakoff SH, Leonard C, Newell F, Poudel B, Song S, Taylor D, Waddell N, Wood S, Xu Q, Wu J, Pinese M, Cowley MJ, Lee HC, Jones MD, Nagrial AM, Humphris J, Chantrill LA, Chin V, Steinmann AM, Mawson A, Humphrey ES, Colvin EK, Chou A, Scarlett CJ, Pinho AV, Giry-Laterriere M, Rooman I, Samra JS, Kench JG, Pettitt JA, Merrett ND, Toon C, Epari K, Nguyen NQ, Barbour A, Zeps N, Jamieson NB, Graham JS, Niclou SP, Bjerkvig R, Grutzmann R, Aust D, Hruban RH, Maitra A, Iacobuzio-Donahue CA, Wolfgang CL, Morgan RA, Lawlor RT, Corbo V, Bassi C, Falconi M, Zamboni G, Tortora G, Tempero MA; Australian Pancreatic Cancer Genome Initiative, Gill AJ, Eshleman JR, Pilarsky C, Scarpa A, Musgrove EA, Pearson JV, Biankin AV, Grimmond SM	Whole genomes redefine the mutational landscape of pancreatic cancer	Nature	2015 Feb 	18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	ICGC_0326	Illumina HiSeq 2000	chr10:0-135534747:0;chr11:0-135006516:0;chr12:0-128127609:0;chr12:117790616-133851895:0;chr12:128127610-117790615:1;chr13:0-115169878:0;chr14:0-107349540:0;chr15:0-102531392:0;chr16:0-90354753:0;chr17:0-79134247:0;chr17:79134248-79214069:-1;chr17:79214070-81195210:0;chr18:0-20697044:0;chr18:20681228-78077248:0;chr18:20697045-21046735:-1;chr18:20719999-22239764:-1;chr18:20732881-21406056:-1;chr18:20887353-25658851:-1;chr18:21414908-30397351:-1;chr18:22243538-30370126:-1;chr18:25632536-33728583:-1;chr18:25653477-35230964:-1;chr18:28401869-38193019:-1;chr18:33735244-20638703:1;chr18:33740209-20733068:1;chr18:38193020-75018808:0;chr18:75018809-20681227:1;chr19:0-59128983:0;chr1:0-249250621:0;chr20:0-63025520:0;chr21:0-48129895:0;chr22:0-51304566:0;chr2:0-243199373:0;chr3:0-198022430:0;chr4:0-191154276:0;chr5:0-180915260:0;chr6:0-171115067:0;chr7:0-159138663:0;chr8:0-146364022:0;chr9:0-14072345:0;chr9:14072346-22636514:-1;chr9:20510368-22994820:-1;chr9:22994821-27608641:0;chr9:27608642-34592116:-1;chr9:28008731-28173749:-1;chr9:34592117-141213431:0;chrX:0-155270560:0;chrY:0-59373566:0	hs2:54847169-54847169,hs19:7590836-7590836;hs3:129885829-129885829,hs4:9081729-9081729;hs3:174937457-174937457,hs3:175415198-175415198;hs4:53810-53810,hs18:21427413-21427413;hs4:10631567-10631567,hs11:7236366-7236366;hs4:69555074-69555074,hs17:79050328-79050328;hs4:113035328-113035328,hs4:113035254-113035254;hs4:134782520-134782520,hs4:134782375-134782375;hs5:17900859-17900859,hs11:101256794-101256794;hs5:46164109-46164109,hs5:46164440-46164440;hs5:114990579-114990579,hs5:114990653-114990653;hs6:29332294-29332294,hs6:29332596-29332596;hs7:69907547-69907547,hs7:69964700-69964700;hs7:90260231-90260231,hs13:97252597-97252597;hs9:69006947-69006947,hs9:69007000-69007000;hs9:101897142-101897142,hs9:101898952-101898952;hs11:101903472-101903472,hs5:164468879-164468879;hs12:68339430-68339430,hs12:68341279-68341279;hs12:68340568-68340568,hs12:68339929-68339929;hs12:68343433-68343433,hs12:68343786-68343786;hs12:69758688-69758688,hs12:69759079-69759079;hs12:69758688-69758688,hs12:69759079-69759079;hs12:73647739-73647739,hs12:117789872-117789872;hs12:73745584-73745584,hs12:117799233-117799233;hs12:73746388-73746388,hs12:111332021-111332021;hs12:73921918-73921918,hs12:90846317-90846317;hs12:76686883-76686883,hs12:126699944-126699944;hs12:111332528-111332528,hs12:117809273-117809273;hs12:111333499-111333499,hs12:127774324-127774324;hs12:112964664-112964664,hs15:87156445-87156445;hs12:114200447-114200447,hs12:114201706-114201706;hs12:114987615-114987615,hs12:114988503-114988503;hs12:117755004-117755004,hs12:117755581-117755581;hs12:117790000-117790000,hs12:128128138-128128138;hs12:117790477-117790477,hs12:90845657-90845657;hs12:117790510-117790510,hs12:117790961-117790961;hs12:126553969-126553969,hs12:128290870-128290870;hs12:126780558-126780558,hs15:87005783-87005783;hs17:30313708-30313708,hs17:30298564-30298564;hs17:79047868-79047868,hs17:79213515-79213515;hs17:79131869-79131869,hs17:79131919-79131919;hs17:79196200-79196200,hs17:79202843-79202843;hs17:79197281-79197281,hs4:69554919-69554919;hs17:79205201-79205201,hs17:79240391-79240391;hs17:79240113-79240113,hs17:79242305-79242305;hs17:79241381-79241381,hs17:79211948-79211948;hs18:14184199-14184199,hs18:14184304-14184304;hs18:20675454-20675454,hs4:52076-52076;hs18:20728913-20728913,hs20:2726372-2726372;hs18:20737560-20737560,hs18:21051200-21051200;hs18:20766669-20766669,hs18:30390118-30390118;hs18:20837847-20837847,hs18:38194838-38194838;hs18:20839309-20839309,hs18:29412406-29412406;hs18:20851132-20851132,hs18:20861023-20861023;hs18:20855382-20855382,hs18:33721335-33721335;hs18:20860679-20860679,hs18:33739194-33739194;hs18:20874050-20874050,hs18:37605772-37605772;hs18:21051072-21051072,hs20:2740178-2740178;hs18:21062083-21062083,hs18:35246182-35246182;hs18:21419721-21419721,hs18:29412626-29412626;hs18:21420215-21420215,hs20:2727045-2727045;hs18:22242856-22242856,hs18:29413131-29413131;hs18:22244047-22244047,hs18:75019000-75019000;hs18:22248527-22248527,hs20:2734612-2734612;hs18:22278409-22278409,hs20:15310884-15310884;hs18:24945149-24945149,hs18:20851798-20851798;hs18:25644475-25644475,hs18:29406344-29406344;hs18:29351939-29351939,hs18:30402921-30402921;hs18:29394121-29394121,hs18:35194427-35194427;hs18:29413322-29413322,hs18:74979776-74979776;hs18:29441240-29441240,hs18:20710291-20710291;hs18:30396881-30396881,hs18:20839771-20839771;hs18:33719460-33719460,hs18:75015039-75015039;hs18:33741177-33741177,hs18:33741370-33741370;hs18:38211746-38211746,hs18:75018543-75018543;hs18:38216053-38216053,hs18:29335634-29335634;hs18:74996219-74996219,hs18:22243121-22243121;hs18:75018454-75018454,hs18:33721579-33721579;hs19:6807280-6807280,hs19:6808621-6808621;hs19:7130220-7130220,hs19:7131734-7131734;hs19:58720136-58720136,hs19:58721041-58721041;hs19:58721058-58721058,hs19:58721270-58721270;hs20:20482581-20482581,hs20:23059829-23059829;hs20:23053857-23053857,hs20:23099475-23099475;hs20:23087477-23087477,hs20:23090028-23090028;hs20:29593601-29593601,hs20:29599334-29599334;hs21:16418269-16418269,hs21:17406126-17406126;hs21:16418269-16418269,hs21:17406126-17406126;hs21:27975131-27975131,hs21:26978205-26978205;hs21:41460081-41460081,hs21:41401622-41401622	ARIH2P1;CELF4;FHOD3;TPGS2;	Queensland Centre for Medical Genomics, Institute for Molecular Bioscience, The University of Queensland, St Lucia, Brisbane, Queensland 4072, Australia	Pancreatic cancer remains one of the most lethal of malignancies and a major health burden. We performed whole-genome sequencing and copy number variation (CNV) analysis of 100 pancreatic ductal adenocarcinomas (PDACs). Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2). Patterns of structural variation (variation in chromosomal structure) classified PDACs into 4 subtypes with potential clinical utility: the subtypes were termed stable, locally rearranged, scattered and unstable. A significant proportion harboured focal amplifications, many of which contained druggable oncogenes (ERBB2, MET, FGFR1, CDK6, PIK3R3 and PIK3CA), but at low individual patient prevalence. Genomic instability co-segregated with inactivation of DNA maintenance genes (BRCA1, BRCA2 or PALB2) and a mutational signature of DNA damage repair deficiency. Of 8 patients who received platinum therapy, 4 of 5 individuals with these measures of defective DNA maintenance responded. 	GRCh37/hg19				Yes	CABLES1,LAMA3;CABLES1,TRAPPC8;ELP2,CABLES1;LAMA3,TRAPPC8;TMEM241,CDH2;TMEM241,ELP2;TRAPPC8,GALR1
CTDB0423	Research	26305789	Salaverria I, Martin-Garcia D, Lopez C, Clot G, Garcia-Aragones M, Navarro A, Delgado J, Baumann T, Pinyol M, Martin-Guerrero I, Carrio A, Costa D, Queiros AC, Jayne S, Aymerich M, Villamor N, Colomer D, Gonzalez M, Lopez-Guillermo A, Campo E, Dyer MJ, Siebert R, Armengol L, Bea S	Detection of chromothripsis-like patterns with a custom array platform for chronic lymphocytic leukemia	Genes Chromosomes Cancer	2015 Nov	10	Chronic lymphocytic leukemia	Array CGH	Homo sapiens	36	qChip Hemo array	chr10:19322471-20590077:-1;chr10:23733538-25127913:-1;chr10:31647733-36030348:-1;chr10:42418957-46617713:-1;chr10:68811448-75236059:-1;chr10:86477031-86941847:-1;chr10:92351887-94425619:-1;chr10:98597009-112387473:-1;chr10:112829155-114159955:-1;chr10:116716050-118484839:-1;chr10:119239140-124047569:-1		GBF1;NFKB2;PSD;FBXL5;SUFU	Hematopathology Unit, Hospital Clinic Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Barcelona, Spain	Chronic lymphocytic leukemia (CLL) is a common disease with highly variable clinical course. Several recurrent chromosomal alterations are associated with prognosis and may guide risk-adapted therapy. We have developed a targeted genome-wide array to provide a robust tool for ascertaining abnormalities in CLL and to overcome limitations of the 4-marker fluorescence in situ hybridization (FISH). DNA from 180 CLL patients were hybridized to the qChip Hemo array with a high density of probes covering commonly altered loci in CLL (11q22-q23, 13q14, and 17p13), nine focal regions (2p15-p16.1, 2p24.3, 2q13, 2q36.3-q37.1, 3p21.31, 8q24.21, 9p21.3, 10q24.32, and 18q21.32-q21.33) and two larger regions (6q14.1-q22.31 and 7q31.33-q33). Overall, 86% of the cases presented copy number alterations (CNA) by array. There was a high concordance of array findings with FISH (84% sensitivity, 100% specificity); all discrepancies corresponded to subclonal alterations detected only by FISH. A chromothripsis-like pattern was detected in eight cases. Three showed concomitant shattered 5p with gain of TERT along with isochromosome 17q. Presence of 11q loss was associated with shorter time to first treatment (P = 0.003), whereas 17p loss, increased genomic complexity, and chromothripsis were associated with shorter overall survival (P < 0.001, P = 0.001, and P = 0.02, respectively). In conclusion, we have validated a targeted array for the diagnosis of CLL that accurately detects, in a single experiment, all relevant CNAs, genomic complexity, chromothripsis, copy number neutral loss of heterozygosity, and CNAs not covered by the FISH panel. This test may be used as a practical tool to stratify CLL patients for routine diagnostics or clinical trials.	GRCh37/hg19	GSE66923			Yes	NA
CTDB0424	Research	26305789	Salaverria I, Martin-Garcia D, Lopez C, Clot G, Garcia-Aragones M, Navarro A, Delgado J, Baumann T, Pinyol M, Martin-Guerrero I, Carrio A, Costa D, Queiros AC, Jayne S, Aymerich M, Villamor N, Colomer D, Gonzalez M, Lopez-Guillermo A, Campo E, Dyer MJ, Siebert R, Armengol L, Bea S	Detection of chromothripsis-like patterns with a custom array platform for chronic lymphocytic leukemia	Genes Chromosomes Cancer	2015 Nov	5	Chronic lymphocytic leukemia	Array CGH	Homo sapiens	94	qChip Hemo array	chr5:0-1635135:1;chr5:1635135-16113045:-1;chr5:16113045-21741262:1;chr5:21741262-22716680:-1;chr5:22716680-23640589:1;chr5:23640589-24563866:-1;chr5:24563866-29286182:1;chr5:29286182-30221099:-1;chr5:30221099-33065344:1;chr5:33065344-180915260:0		TERT	Hematopathology Unit, Hospital Clinic Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Barcelona, Spain	Chronic lymphocytic leukemia (CLL) is a common disease with highly variable clinical course. Several recurrent chromosomal alterations are associated with prognosis and may guide risk-adapted therapy. We have developed a targeted genome-wide array to provide a robust tool for ascertaining abnormalities in CLL and to overcome limitations of the 4-marker fluorescence in situ hybridization (FISH). DNA from 180 CLL patients were hybridized to the qChip Hemo array with a high density of probes covering commonly altered loci in CLL (11q22-q23, 13q14, and 17p13), nine focal regions (2p15-p16.1, 2p24.3, 2q13, 2q36.3-q37.1, 3p21.31, 8q24.21, 9p21.3, 10q24.32, and 18q21.32-q21.33) and two larger regions (6q14.1-q22.31 and 7q31.33-q33). Overall, 86% of the cases presented copy number alterations (CNA) by array. There was a high concordance of array findings with FISH (84% sensitivity, 100% specificity); all discrepancies corresponded to subclonal alterations detected only by FISH. A chromothripsis-like pattern was detected in eight cases. Three showed concomitant shattered 5p with gain of TERT along with isochromosome 17q. Presence of 11q loss was associated with shorter time to first treatment (P = 0.003), whereas 17p loss, increased genomic complexity, and chromothripsis were associated with shorter overall survival (P < 0.001, P = 0.001, and P = 0.02, respectively). In conclusion, we have validated a targeted array for the diagnosis of CLL that accurately detects, in a single experiment, all relevant CNAs, genomic complexity, chromothripsis, copy number neutral loss of heterozygosity, and CNAs not covered by the FISH panel. This test may be used as a practical tool to stratify CLL patients for routine diagnostics or clinical trials.	GRCh37/hg19	GSE66923			Yes	NA
CTDB0425	Research	26305789	Salaverria I, Martin-Garcia D, Lopez C, Clot G, Garcia-Aragones M, Navarro A, Delgado J, Baumann T, Pinyol M, Martin-Guerrero I, Carrio A, Costa D, Queiros AC, Jayne S, Aymerich M, Villamor N, Colomer D, Gonzalez M, Lopez-Guillermo A, Campo E, Dyer MJ, Siebert R, Armengol L, Bea S	Detection of chromothripsis-like patterns with a custom array platform for chronic lymphocytic leukemia	Genes Chromosomes Cancer	2015 Nov	5,12	Chronic lymphocytic leukemia	Array CGH	Homo sapiens	D1016	qChip Hemo array	chr5:0-4932247:1;chr5:4932248-10467303:0;chr5:10467304-24206970:-1;chr5:24206971-40463864:1;chr5:40463865-40549635:0;chr5:40549636-46350808:-1;chr5:46350807-71514596:0;chr5:71514597-87578797:-1;chr5:87578798-89720410:1;chr5:89720409-89725809:0;chr5:89725810-107092989:-1;chr5:107092989-108797097:1;chr5:108797098-109788754:0;chr5:109788755-111844602:-1;chr5:111844603-113899732:0;chr5:113899733-119403621:-1;chr5:119403622-180915260:0;chr12:0-3916043:1;chr12:3916043-6894818:1;chr12:6894818-7074306:1;chr12:7074306-7266926:0;chr12:7266927-8246697:-1;chr12:8246698-8566721:0;chr12:8566722-16265843:-1;chr12:16265843-16441845:1;chr12:16441845-17785834:1;chr12:17785834-17998159:1;chr12:17998160-18506525:0;chr12:18506526-20500890:-1;chr12:20500890-21052802:1;chr12:21052803-22316053:0;chr12:22316054-22846206:1;chr12:22846206-25044343:1;chr12:25044344-133851895:0		TERT	Hematopathology Unit, Hospital Clinic Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Barcelona, Spain	Chronic lymphocytic leukemia (CLL) is a common disease with highly variable clinical course. Several recurrent chromosomal alterations are associated with prognosis and may guide risk-adapted therapy. We have developed a targeted genome-wide array to provide a robust tool for ascertaining abnormalities in CLL and to overcome limitations of the 4-marker fluorescence in situ hybridization (FISH). DNA from 180 CLL patients were hybridized to the qChip Hemo array with a high density of probes covering commonly altered loci in CLL (11q22-q23, 13q14, and 17p13), nine focal regions (2p15-p16.1, 2p24.3, 2q13, 2q36.3-q37.1, 3p21.31, 8q24.21, 9p21.3, 10q24.32, and 18q21.32-q21.33) and two larger regions (6q14.1-q22.31 and 7q31.33-q33). Overall, 86% of the cases presented copy number alterations (CNA) by array. There was a high concordance of array findings with FISH (84% sensitivity, 100% specificity); all discrepancies corresponded to subclonal alterations detected only by FISH. A chromothripsis-like pattern was detected in eight cases. Three showed concomitant shattered 5p with gain of TERT along with isochromosome 17q. Presence of 11q loss was associated with shorter time to first treatment (P = 0.003), whereas 17p loss, increased genomic complexity, and chromothripsis were associated with shorter overall survival (P < 0.001, P = 0.001, and P = 0.02, respectively). In conclusion, we have validated a targeted array for the diagnosis of CLL that accurately detects, in a single experiment, all relevant CNAs, genomic complexity, chromothripsis, copy number neutral loss of heterozygosity, and CNAs not covered by the FISH panel. This test may be used as a practical tool to stratify CLL patients for routine diagnostics or clinical trials.	GRCh37/hg19	GSE66923			Yes	NA
CTDB0426	Research	26305789	Salaverria I, Martin-Garcia D, Lopez C, Clot G, Garcia-Aragones M, Navarro A, Delgado J, Baumann T, Pinyol M, Martin-Guerrero I, Carrio A, Costa D, Queiros AC, Jayne S, Aymerich M, Villamor N, Colomer D, Gonzalez M, Lopez-Guillermo A, Campo E, Dyer MJ, Siebert R, Armengol L, Bea S	Detection of chromothripsis-like patterns with a custom array platform for chronic lymphocytic leukemia	Genes Chromosomes Cancer	2015 Nov	5	Chronic lymphocytic leukemia	Array CGH	Homo sapiens	D1089	qChip Hemo array	chr5:0-1473747:1;chr5:1473747-10467304:-1;chr5:10467304-11923754:1;chr5:11923754-14080860:-1;chr5:14080860-17066497:1;chr5:17066498-18571708:0;chr5:18571709-20893807:-1;chr5:20893807-24247917:1;chr5:24247917-25034495:-1;chr5:25034496-27272147:0;chr5:27272148-31572967:-1;chr5:31572968-42882592:0;chr5:42882593-46350808:-1;chr5:46350809-180915260:0		TERT	Hematopathology Unit, Hospital Clinic Institut d'Investigacions Biomediques August Pi i Sunyer (IDIBAPS), Barcelona, Spain	Chronic lymphocytic leukemia (CLL) is a common disease with highly variable clinical course. Several recurrent chromosomal alterations are associated with prognosis and may guide risk-adapted therapy. We have developed a targeted genome-wide array to provide a robust tool for ascertaining abnormalities in CLL and to overcome limitations of the 4-marker fluorescence in situ hybridization (FISH). DNA from 180 CLL patients were hybridized to the qChip Hemo array with a high density of probes covering commonly altered loci in CLL (11q22-q23, 13q14, and 17p13), nine focal regions (2p15-p16.1, 2p24.3, 2q13, 2q36.3-q37.1, 3p21.31, 8q24.21, 9p21.3, 10q24.32, and 18q21.32-q21.33) and two larger regions (6q14.1-q22.31 and 7q31.33-q33). Overall, 86% of the cases presented copy number alterations (CNA) by array. There was a high concordance of array findings with FISH (84% sensitivity, 100% specificity); all discrepancies corresponded to subclonal alterations detected only by FISH. A chromothripsis-like pattern was detected in eight cases. Three showed concomitant shattered 5p with gain of TERT along with isochromosome 17q. Presence of 11q loss was associated with shorter time to first treatment (P = 0.003), whereas 17p loss, increased genomic complexity, and chromothripsis were associated with shorter overall survival (P < 0.001, P = 0.001, and P = 0.02, respectively). In conclusion, we have validated a targeted array for the diagnosis of CLL that accurately detects, in a single experiment, all relevant CNAs, genomic complexity, chromothripsis, copy number neutral loss of heterozygosity, and CNAs not covered by the FISH panel. This test may be used as a practical tool to stratify CLL patients for routine diagnostics or clinical trials.	GRCh37/hg19	GSE66923			Yes	NA
CTDB0427	Research	26337081	Kovtun IV, Murphy SJ, Johnson SH, Cheville JC, Vasmatzis G	Chromosomal catastrophe is a frequent event in clinically insignificant prostate cancer	Oncotarget	2015 Oct	4	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR3					Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota, USA	Massive genomic rearrangements, a result of single catastrophic event termed chromothrispsis or chromosomal catastrophe, have been identified in a variety of human cancers. In a few cancer types, chromothripsis was found to be associated with poor prognosis. We performed mate-pair sequencing and analysis of structural rearrangements in 132 prostate cancer cases which included clinically insignificant Gleason score 6 tumors, clinically significant tumors of higher grade (7+) and high grade prostatic intraepithelial neoplasia. Chromothripsis was observed at least 30 per cent of the samples across different grades. Surprisingly, it was frequently observed in clinically insignificant Gleason score 6 tumors, indicating that chromothripsis does not define more aggressive phenotype. The degree of chromothripsis did not increase significantly in tumors of advanced grades and did not appear to contribute to tumor progression. Our data showed that distribution of chromothriptic rearrangements differed from that of fragile sites but correlated with the size of chromosomes. We also provided evidence that rearrangements resulting from chromothripsis were present in the cells of neighboring Gleason patterns of the same tumor. Our data suggest that that chromothripsis plays role in prostate cancer initiation.	GRCh37/hg19				Yes	NA
CTDB0428	Research	26337081	Kovtun IV, Murphy SJ, Johnson SH, Cheville JC, Vasmatzis G	Chromosomal catastrophe is a frequent event in clinically insignificant prostate cancer	Oncotarget	2015 Oct	5	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR119					Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota, USA	Massive genomic rearrangements, a result of single catastrophic event termed chromothrispsis or chromosomal catastrophe, have been identified in a variety of human cancers. In a few cancer types, chromothripsis was found to be associated with poor prognosis. We performed mate-pair sequencing and analysis of structural rearrangements in 132 prostate cancer cases which included clinically insignificant Gleason score 6 tumors, clinically significant tumors of higher grade (7+) and high grade prostatic intraepithelial neoplasia. Chromothripsis was observed at least 30 per cent of the samples across different grades. Surprisingly, it was frequently observed in clinically insignificant Gleason score 6 tumors, indicating that chromothripsis does not define more aggressive phenotype. The degree of chromothripsis did not increase significantly in tumors of advanced grades and did not appear to contribute to tumor progression. Our data showed that distribution of chromothriptic rearrangements differed from that of fragile sites but correlated with the size of chromosomes. We also provided evidence that rearrangements resulting from chromothripsis were present in the cells of neighboring Gleason patterns of the same tumor. Our data suggest that that chromothripsis plays role in prostate cancer initiation.	GRCh37/hg19				Yes	NA
CTDB0429	Research	26337081	Kovtun IV, Murphy SJ, Johnson SH, Cheville JC, Vasmatzis G	Chromosomal catastrophe is a frequent event in clinically insignificant prostate cancer	Oncotarget	2015 Oct	1	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR27					Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota, USA	Massive genomic rearrangements, a result of single catastrophic event termed chromothrispsis or chromosomal catastrophe, have been identified in a variety of human cancers. In a few cancer types, chromothripsis was found to be associated with poor prognosis. We performed mate-pair sequencing and analysis of structural rearrangements in 132 prostate cancer cases which included clinically insignificant Gleason score 6 tumors, clinically significant tumors of higher grade (7+) and high grade prostatic intraepithelial neoplasia. Chromothripsis was observed at least 30 per cent of the samples across different grades. Surprisingly, it was frequently observed in clinically insignificant Gleason score 6 tumors, indicating that chromothripsis does not define more aggressive phenotype. The degree of chromothripsis did not increase significantly in tumors of advanced grades and did not appear to contribute to tumor progression. Our data showed that distribution of chromothriptic rearrangements differed from that of fragile sites but correlated with the size of chromosomes. We also provided evidence that rearrangements resulting from chromothripsis were present in the cells of neighboring Gleason patterns of the same tumor. Our data suggest that that chromothripsis plays role in prostate cancer initiation.	GRCh37/hg19				Yes	NA
CTDB0430	Research	26337081	Kovtun IV, Murphy SJ, Johnson SH, Cheville JC, Vasmatzis G	Chromosomal catastrophe is a frequent event in clinically insignificant prostate cancer	Oncotarget	2015 Oct	2	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR64					Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota, USA	Massive genomic rearrangements, a result of single catastrophic event termed chromothrispsis or chromosomal catastrophe, have been identified in a variety of human cancers. In a few cancer types, chromothripsis was found to be associated with poor prognosis. We performed mate-pair sequencing and analysis of structural rearrangements in 132 prostate cancer cases which included clinically insignificant Gleason score 6 tumors, clinically significant tumors of higher grade (7+) and high grade prostatic intraepithelial neoplasia. Chromothripsis was observed at least 30 per cent of the samples across different grades. Surprisingly, it was frequently observed in clinically insignificant Gleason score 6 tumors, indicating that chromothripsis does not define more aggressive phenotype. The degree of chromothripsis did not increase significantly in tumors of advanced grades and did not appear to contribute to tumor progression. Our data showed that distribution of chromothriptic rearrangements differed from that of fragile sites but correlated with the size of chromosomes. We also provided evidence that rearrangements resulting from chromothripsis were present in the cells of neighboring Gleason patterns of the same tumor. Our data suggest that that chromothripsis plays role in prostate cancer initiation.	GRCh37/hg19				Yes	NA
CTDB0431	Research	26337081	Kovtun IV, Murphy SJ, Johnson SH, Cheville JC, Vasmatzis G	Chromosomal catastrophe is a frequent event in clinically insignificant prostate cancer	Oncotarget	2015 Oct	4	Prostate cancer	Next Generation Sequencing	Homo sapiens	PR6				ANXA5;AP1AR;ARSJ;ATHGEF38;BANK1;BBS12;BBS7;BDH2;CAMK2D;CASP6;CCRN4L;CENPE;CFI;Col25A1;CXXC4;CYP2U1;DKK2;EGF;ELF2;ELMOD2;ELOVL5;ENPEP;EXOSC9;FABP2;FABPC4L;FAT4;FGF2;FLK4;FREM3;GAB1;GAR1;GSTCD;GYPA;GYPB;GYPE;HADH;LRIT3;MAD2L1;MAML3;MANBA;METL14;MFSD8;MGARP;MGST2;NAA15;NDNF;NDST4;NDUFC1;NEUROG2;NFKB;NPNT;NUDT6;OSTC;OTUD4;PAPSS2;PCDH18;PDE5A;PGRMC;PHF17;PITX2;PLA2G12A;PRDM5;PRSS12;QRFPR;RAB33B;RNF150;RPL34;RRH;SCL1T;SCOC;SEC24B;SEC24D;SETD7;SPRY1;SYNPO2;TACR3;TBC1D9;TBCK;TET2;TIFA;TMEM155;TNIP3;TRAM1L1;TRPC3;UBE2D3;UCP1;UGT8;USP38;USP53	Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, Minnesota, USA	Massive genomic rearrangements, a result of single catastrophic event termed chromothrispsis or chromosomal catastrophe, have been identified in a variety of human cancers. In a few cancer types, chromothripsis was found to be associated with poor prognosis. We performed mate-pair sequencing and analysis of structural rearrangements in 132 prostate cancer cases which included clinically insignificant Gleason score 6 tumors, clinically significant tumors of higher grade (7+) and high grade prostatic intraepithelial neoplasia. Chromothripsis was observed at least 30 per cent of the samples across different grades. Surprisingly, it was frequently observed in clinically insignificant Gleason score 6 tumors, indicating that chromothripsis does not define more aggressive phenotype. The degree of chromothripsis did not increase significantly in tumors of advanced grades and did not appear to contribute to tumor progression. Our data showed that distribution of chromothriptic rearrangements differed from that of fragile sites but correlated with the size of chromosomes. We also provided evidence that rearrangements resulting from chromothripsis were present in the cells of neighboring Gleason patterns of the same tumor. Our data suggest that that chromothripsis plays role in prostate cancer initiation.	GRCh37/hg19				Yes	NA
CTDB0432	Research	26168399	George J, Lim JS, Jang SJ, Cun Y, Ozretic L, Kong G, Leenders F, Lu X, Fernandez-Cuesta L, Bosco G, Muller C, Dahmen I, Jahchan NS, Park KS, Yang D, Karnezis AN, Vaka D, Torres A, Wang MS, Korbel JO, Menon R, Chun SM, Kim D, Wilkerson M, Hayes N, Engelmann D, Putzer B, Bos M, Michels S, Vlasic I, Seidel D, Pinther B, Schaub P, Becker C, Altmuller J, Yokota J, Kohno T, Iwakawa R, Tsuta K, Noguchi M, Muley T, Hoffmann H, Schnabel PA, Petersen I, Chen Y, Soltermann A, Tischler V, Choi CM, Kim YH, Massion PP, Zou Y, Jovanovic D, Kontic M, Wright GM, Russell PA, Solomon B, Koch I, Lindner M, Muscarella LA, la Torre A, Field JK, Jakopovic M, Knezevic J, Castanos-Velez E, Roz L, Pastorino U, Brustugun OT, Lund-Iversen M, Thunnissen E, Kohler J, Schuler M, Botling J, Sandelin M, Sanchez-Cespedes M, Salvesen HB, Achter V, Lang U, Bogus M, Schneider PM, Zander T, Ansen S, Hallek M, Wolf J, Vingron M, Yatabe Y, Travis WD, Nurnberg P, Reinhardt C, Perner S, Heukamp L, Buttner R, Haas SA, Brambilla E, Peifer M, Sage J, Thomas RK	Comprehensive genomic profiles of small cell lung cancer	Nature	2015 Aug	3,11	Small cell lung cancer	Next Generation Sequencing	Homo sapiens	S02297	Illumina HiSeq 2000		hs1:20723373-20723373,hs11:121660894-121660894;hs1:20738817-20738817,hs1:26956531-26956531;hs1:27101463-27101463,hs11:121026214-121026214;hs1:188615933-188615933,hs18:25019920-25019920;hs3:1174556-1174556,hs3:24628811-24628811;hs3:1254115-1254115,hs3:124877003-124877003;hs3:1263663-1263663,hs3:155832004-155832004;hs3:1289250-1289250,hs3:178243878-178243878;hs3:1302810-1302810,hs11:35725103-35725103;hs3:1342076-1342076,hs3:64531030-64531030;hs3:1342553-1342553,hs3:89167031-89167031;hs3:1633950-1633950,hs11:114476322-114476322;hs3:1686204-1686204,hs11:75840211-75840211;hs3:1797296-1797296,hs3:7395839-7395839;hs3:1906582-1906582,hs11:34095624-34095624;hs3:1961173-1961173,hs3:7991553-7991553;hs3:1967957-1967957,hs3:185346908-185346908;hs3:2070431-2070431,hs11:39388938-39388938;hs3:2072521-2072521,hs11:97444115-97444115;hs3:2103287-2103287,hs3:55498995-55498995;hs3:2105311-2105311,hs3:63030396-63030396;hs3:2134951-2134951,hs3:160557563-160557563;hs3:2202783-2202783,hs3:3777590-3777590;hs3:2223685-2223685,hs11:94728013-94728013;hs3:2270947-2270947,hs3:192946446-192946446;hs3:2277074-2277074,hs11:48932216-48932216;hs3:2281289-2281289,hs3:5605318-5605318;hs3:2299611-2299611,hs11:16323254-16323254;hs3:2353943-2353943,hs3:38503194-38503194;hs3:2391721-2391721,hs3:124962949-124962949;hs3:2403100-2403100,hs11:62971420-62971420;hs3:2416857-2416857,hs11:21742046-21742046;hs3:2432670-2432670,hs3:133364168-133364168;hs3:2473536-2473536,hs3:131504467-131504467;hs3:2774240-2774240,hs11:92704906-92704906;hs3:2823849-2823849,hs11:129616464-129616464;hs3:2876434-2876434,hs3:148402466-148402466;hs3:2953576-2953576,hs3:59626472-59626472;hs3:2970413-2970413,hs11:87487406-87487406;hs3:3014343-3014343,hs3:48997436-48997436;hs3:3165645-3165645,hs3:131355079-131355079;hs3:3348933-3348933,hs3:35878299-35878299;hs3:3354236-3354236,hs3:119555915-119555915;hs3:3354584-3354584,hs3:193187542-193187542;hs3:3364921-3364921,hs11:51398785-51398785;hs3:3757402-3757402,hs11:18313688-18313688;hs3:3793167-3793167,hs3:164510523-164510523;hs3:3832386-3832386,hs11:42085961-42085961;hs3:3968328-3968328,hs11:63561177-63561177;hs3:4289239-4289239,hs3:162350021-162350021;hs3:4387673-4387673,hs3:111374669-111374669;hs3:4388465-4388465,hs11:27705537-27705537;hs3:4401003-4401003,hs3:124943124-124943124;hs3:4421095-4421095,hs3:18057730-18057730;hs3:4427031-4427031,hs11:105713067-105713067;hs3:4429505-4429505,hs3:155841325-155841325;hs3:4446606-4446606,hs3:23643044-23643044;hs3:4464579-4464579,hs3:52816448-52816448;hs3:4464923-4464923,hs11:122699920-122699920;hs3:4484718-4484718,hs3:145610828-145610828;hs3:4499742-4499742,hs3:197734108-197734108;hs3:4631569-4631569,hs11:29545791-29545791;hs3:4780002-4780002,hs11:73363590-73363590;hs3:5056686-5056686,hs3:65629641-65629641;hs3:5062118-5062118,hs11:106414655-106414655;hs3:5086481-5086481,hs11:49265869-49265869;hs3:5178838-5178838,hs11:48052864-48052864;hs3:5184250-5184250,hs3:46590368-46590368;hs3:5226576-5226576,hs3:176757382-176757382;hs3:5231358-5231358,hs11:63797010-63797010;hs3:5272058-5272058,hs3:61778797-61778797;hs3:5284124-5284124,hs11:42758262-42758262;hs3:5316290-5316290,hs3:34641617-34641617;hs3:5316290-5316290,hs3:34641617-34641617;hs3:5332679-5332679,hs3:51579692-51579692;hs3:5472743-5472743,hs3:152927722-152927722;hs3:5474838-5474838,hs3:95911935-95911935;hs3:5477705-5477705,hs3:127406262-127406262;hs3:5536687-5536687,hs3:11110582-11110582;hs3:5588722-5588722,hs3:137137796-137137796;hs3:5604156-5604156,hs11:22234630-22234630;hs3:5613215-5613215,hs11:62762864-62762864;hs3:5623235-5623235,hs3:37423348-37423348;hs3:5808999-5808999,hs3:116817440-116817440;hs3:5863050-5863050,hs3:65204306-65204306;hs3:5894443-5894443,hs3:95365551-95365551;hs3:5923970-5923970,hs3:109951257-109951257;hs3:5933928-5933928,hs3:49068489-49068489;hs3:5956126-5956126,hs11:96209185-96209185;hs3:5959657-5959657,hs3:99903676-99903676;hs3:6032546-6032546,hs11:123780812-123780812;hs3:6278094-6278094,hs11:40356594-40356594;hs3:6514422-6514422,hs3:85513337-85513337;hs3:6570367-6570367,hs3:187994582-187994582;hs3:7014607-7014607,hs11:86900358-86900358;hs3:7172850-7172850,hs3:179094844-179094844;hs3:7174786-7174786,hs3:58340914-58340914;hs3:7217275-7217275,hs11:38918624-38918624;hs3:7217799-7217799,hs3:65255637-65255637;hs3:7401353-7401353,hs11:101608878-101608878;hs3:7450475-7450475,hs3:121188779-121188779;hs3:7922341-7922341,hs11:111567107-111567107;hs3:7951926-7951926,hs3:51034102-51034102;hs3:7971276-7971276,hs3:134159155-134159155;hs3:8011601-8011601,hs3:43217255-43217255;hs3:8025849-8025849,hs11:46036655-46036655;hs3:8145920-8145920,hs3:53102476-53102476;hs3:8211029-8211029,hs3:112526886-112526886;hs3:9188341-9188341,hs3:89456681-89456681;hs3:9203666-9203666,hs11:16049899-16049899;hs3:9389709-9389709,hs3:172998898-172998898;hs3:9399648-9399648,hs3:101229309-101229309;hs3:9401903-9401903,hs11:117385104-117385104;hs3:9421510-9421510,hs3:98155884-98155884;hs3:9428412-9428412,hs11:45939455-45939455;hs3:9471933-9471933,hs3:120834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have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73DeltaEx2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer.	GRCh37/hg19					NA
CTDB0433	Research	26168399	George J, Lim JS, Jang SJ, Cun Y, Ozretic L, Kong G, Leenders F, Lu X, Fernandez-Cuesta L, Bosco G, Muller C, Dahmen I, Jahchan NS, Park KS, Yang D, Karnezis AN, Vaka D, Torres A, Wang MS, Korbel JO, Menon R, Chun SM, Kim D, Wilkerson M, Hayes N, Engelmann D, Putzer B, Bos M, Michels S, Vlasic I, Seidel D, Pinther B, Schaub P, Becker C, Altmuller J, Yokota J, Kohno T, Iwakawa R, Tsuta K, Noguchi M, Muley T, Hoffmann H, Schnabel PA, Petersen I, Chen Y, Soltermann A, Tischler V, Choi CM, Kim YH, Massion PP, Zou Y, Jovanovic D, Kontic M, Wright GM, Russell PA, Solomon B, Koch I, Lindner M, Muscarella LA, la Torre A, Field JK, Jakopovic M, Knezevic J, Castanos-Velez E, Roz L, Pastorino U, Brustugun OT, Lund-Iversen M, Thunnissen E, Kohler J, Schuler M, Botling J, Sandelin M, Sanchez-Cespedes M, Salvesen HB, Achter V, Lang U, Bogus M, Schneider PM, Zander T, Ansen S, Hallek M, Wolf J, Vingron M, Yatabe Y, Travis WD, Nurnberg P, Reinhardt C, Perner S, Heukamp L, Buttner R, Haas SA, Brambilla E, Peifer M, Sage J, Thomas RK	Comprehensive genomic profiles of small cell lung cancer	Nature	2015 Aug	3,11	Small cell lung cancer	Next Generation Sequencing	Homo sapiens	S02353	Illumina HiSeq 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11:128905331-128905331;hs11:128982637-128982637,hs11:133677455-133677455;hs14:53778126-53778126,hs15:95055625-95055625			We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73DeltaEx2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer.	GRCh37/hg19					ABI3BP,CAT;ABTB2,CNTN5;ABTB2,TPCN2;ACER3,DLG2;ACOX2,PTDSS2;ACPP,KLHL24;ADAMTS9,FXR1;ADCY5,CPB1;ADCY5,DYNC2H1;ALCAM,FCHSD2;ALDH1L1,FGF12;ANKRD28,NELL1;ANO10,NEK11;ANO10,PIK3CA;ARHGAP31,PLEKHA7;ARHGEF26,CPT1A;ARHGEF26,DKK3;ARHGEF3,AP2M1;ARHGEF3,CAPRIN1;ARHGEF3,GTF2H1;ARHGEF3,MB21D2;ARHGEF3,TOPBP1;ARID1A,TECTA;ARIH2,PACS1;ARL8B,LRRC2;ARL8B,PTPRJ;ARNTL,SIK3;ATG3,CPSF7;ATP1B3,FXYD2;ATP2C1,PTPRJ;B4GALT4,FOXRED1;BBX,PLEKHA7;BSN,RNF13;BTD,PLD1;C11orf49,EML3;C11orf49,PRCP;C11orf80,KIAA1731;C11orf80,MAML2;C3orf20,LMLN;C3orf26,ARAP1;C3orf26,ARNTL;C3orf26,IFT80;C3orf26,SLC17A6;C3orf26;FILIP1L,GPR156;C3orf37,TOPBP1;C3orf67,C11orf30;C3orf67,DLG2;CACNA1D,ACP2;CACNA1D,ARHGAP32;CACNA1D,C11orf30;CACNA1D,CADPS;CACNA1D,CSTF3;CACNA1D,EEF1G;CACNA2D3,ARHGAP31;CACNA2D3,C3orf26;CACNA2D3,CADM2;CACNA2D3,DLG2;CACNA2D3,DYNC2H1;CACNA2D3,GSTP1;CACNA2D3,HYOU1;CACNA2D3,LDLRAD3;CACNA2D3,MAGI1;CACNA2D3,MAML2;CACNA2D3,NUP98;CACNA2D3,RTN3;CADM2,C11orf73;CADM2,EPHB1;CADM2,PHC3;CADM2,POU2F3;CADM2,PTPRJ;CADM2,RIC3;CADPS,EPHA6;CADPS,MYNN;CADPS,TMEM132A;CADPS,VWCE;CAND2,ATP2C1;CAPN5,INTS4;CAPRIN1,FADS2;CBLB,TMEM126A;CBLB,TMEM135;CBLB,TP63;CCDC37,MGLL;CD6,LRP5;CD86,VSTM5;CELSR3,TOMM70A;CHCHD6,ARHGAP32;CHDH,FAM131A;CHEK1,FAM118B;CLPB,DLG2;CLSTN2,APLP2;CMC1,FHIT;CMTM8,FGF12;CNTN4,ARIH2;CNTN4,MTNR1B;CNTN5,C11orf57;CNTN5,NPAT;CNTN5,ZBTB16;CNTN6,ADAMTS9;CNTN6,EPHA3;CNTN6,SLC12A8;CNTN6,TRIM44;COL6A6,NELL1;COLQ,PLXNB1;CPNE4,DDB2;CPNE4,PACS1;CPNE4,POLA2;CSRP3,EEF1G;CTSW,DSCAML1;CTSW,OPCML;DDX10,OPCML;DEAF1,PVRL1;DGKG,ALX4;DIRC2,RNF214;DLG1,TNFRSF21;DLG2,AMOTL1;DNAH1,LSAMP;DNAH1,PTDSS2;DNHD1,LTBP3;DOCK3,CLSTN2;DOCK3,FAM43A;DOCK3,MPPED2;DOCK3,PARP15;DOCK3,PLD1;DOCK3,PLEKHA7;DOCK3,TFDP2;DOCK3,VPS8;DRD3,ROPN1;DSCAML1,NTM;ECT2,C11orf30;EDEM1,MACROD1;EEFSEC,CHKA;EIF4E3,TECTA;EIF4E3,TMEM108;ELP4,ABTB2;EPHA3,TNIK;EPHA3,VEPH1;EPHA6,SOX6;EPHA6,ZW10;EPHB1,ALG8;EPHB1,KIRREL3;EPHB1,SLC1A2;EPHB1,TP63;ERC2,ACY3;ERC2,CADPS;ERC2,GPR156;ERC2,HSD17B12;ERC2,LDLRAD3;ERC2,LUZP2;ERC2,MYLK;ERC2,NELL1;ERC2,PAMR1;ETV5,TEAD1;EXOSC7,CADPS;FAM107A,ALG8;FAM19A1,CSTF3;FAM19A1,PGAP2;FAM19A4,KCNMB2;FAM19A4,RNF13;FANCD2,TSEN2;FBLN2,LRP5;FBXL2,LPP;FBXL2,PARL;FHIT,AMBRA1;FHIT,FXR1;FHIT,GAB2;FLNB,CLPB;FLNB,OPCML;FLNB,SLC43A1;FRMD4B,ALCAM;FRMD4B,ROBO2;FXYD2,POU2F3;FYCO1,ZDHHC5;FYCO1,ZNF148;GADL1,F2;GALNTL4,CCDC73;GALNTL4,CPT1A;GAS2,FAM118B;GBE1,C3orf26;GOLGA4,CACNA1D;GOLGA4,TRAK1;GPR128,ATP13A5;GPR128,CNTN5;GPR128,DLG1;GPR156,TNIK;GRM2,GNB4;GRM7,MFN1;GRM7,POLQ;GRM7,PXK;GRM7,TMEM135;GSK3B,DLG2;GSK3B,TEAD1;HACL1,LMLN;HEG1,STIM1;HHATL,NAV2;HPS3,NOX4;HRASLS5,DDX10;HSD17B12,KIRREL3;IFT122,ABTB2;IFT122,DLG2;IGF2BP2,AP2A2;IGSF11,NLGN1;IL20RA,GRM1;IQCJ,MPPED2;IQSEC1,PVRL1;ITGA9,EPHA6;ITIH1,USP13;ITPR1,PLEKHB1;KALRN,DLG2;KALRN,FADS2;KALRN,GNB4;KALRN,SLC9A9;KAT2B,CADPS;KCNH8,C11orf70;KCNH8,CTR9;KCNH8,FHIT;KCNH8,MYLK;KCNH8,RAB6A;KCNH8,RNF13;KCNH8,SBF2;KCNH8,SLC9A9;KCNQ1,PVRL1;KDM2A,GLB1L2;KIF15,CACNA2D3;KIF9,MAGI1;KIF9,TMEM9B;KLHL18,NEK11;KLHL6,OPCML;KY,APLP2;LAMA2,ODZ1;LARS2,CHMP2B;LARS2,LPP;LDHA,APLP2;LDLRAD3,NTM;LHFPL4,SHISA5;LPP,GALNTL4;LPP,LGR4;LRIG1,SUV420H1;LRIG1,TRA2B;LRP5,MAML2;LRRC2,LEPREL1;LRRC34,NARS2;LRRFIP2,KCNQ1;LSAMP,POLA2;MAGI1,EHBP1L1;MAGI1,IGHMBP2;MAGI1,RNF121;MAGI1,SLC3A2;MAP4,MB21D2;MARK2,DCPS;MCM2,LGR4;MINA,MAP3K11;MITF,MCF2L2;MLF1,ARAP1;MLL,JAM3;MME,DLG2;MYRIP,EPHA6;NAA50,NAV2;NAALADL2,EXT2;NAALADL2,ZNF214;NAV2,CSTF3;NAV2,TTC17;NELL1,NPAT;NELL1,PDGFD;NISCH,PRDM11;NLGN1,CDC42BPG;NLGN1,HSD17B12;NLGN1,SYT9;NLGN1,VPS8;NMD3,USP28;NR1I2,PDE3B;NRXN2,KIRREL3;NRXN2,VPS26B;NUP210,DLG2;NUP210,FBXO3;OGG1,PLEKHA7;OPA1,DLG2;OSBPL10,EIF4G2;OSBPL10,ULK4;OXSR1,RAB6A;P4HTM,PANX1;PACS1,SESN3;PAK2,ELP4;PARVA,BTBD10;PBRM1,CCDC67;PBRM1,PPFIA1;PDDC1,SNX19;PDIA5,MAML2;PDIA5,NDUFB5;PDZRN3,MED12L;PDZRN3,ROBO2;PDZRN3,TBL1XR1;PEX5L,MAML2;PHC3,MACROD1;PHF21A,MAML2;PHF21A,NRXN2;PIK3CB,NAALADL2;PIK3CB,PANX1;PIK3R4,PAK2;PLCD1,CORO1B;PLCH1,PACS1;PLCXD2,NAALADL2;PLEKHA7,PHLDB1;POLR2L,CFL1;PRDM11,MTA2;PRKAR2A,MYH15;PRKAR2A,NAALADL2;PRKAR2A,TMEM135;PRKRIR,PGR;PRMT3,NTM;PRRG4,TM7SF2;PRSS42,CD86;PSMC3,MYO7A;PTPLB,ALDH1L1;PTPLB,POU2F3;PTPRG,ABI3BP;PTPRG,ARRB1;PTPRG,CLPB;PTPRG,EXT2;PTPRG,PARP15;PTPRG,SDHAF2;PTPRG,SLC25A26;PTPRG,TNIK;PTPRJ,DAGLA;PTPRJ,GRIA4;RAB43,SIK3;RAB6B,AP2A2;RAB6B,TEAD1;RASA2,CDHR5;RASA2,LDLRAD3;RBM6,CPA3;RBM6,GUCY1A2;RFTN1,UBP1;RHOA,PPFIA1;RIC3,OPCML;RNF13,APLP2;RNF13,POLA2;RNF169,ZBTB16;ROBO1,TSPAN18;ROBO2,CADM1;ROBO2,CD200R1;ROBO2,DLG2;ROBO2,FAM118B;ROBO2,MAML2;ROBO2,NSUN3;ROBO2,PGM2L1;ROBO2,PLS1;ROBO2,SIDT1;ROBO2,ZBTB16;RSRC1,C11orf49;RSRC1,NELL1;SACM1L,DLG2;SACM1L,PTPRG;SBF2,LRP4;SBF2,NAV2;SCN10A,NARS2;SCN11A,AHNAK;SCN11A,PRDM11;SCN5A,TNK2;SEC22A,NRIP3;SEC61A1,LPP;SEMA3G,PTPLB;SETD2,AHNAK;SETD2,ATP11B;SETD2,SKIL;SETD5,STXBP5L;SIGIRR,SLCO2B1;SIRT3,DSCAML1;SLC12A8,CKAP5;SLC1A2,GRIK4;SLC22A25,C11orf85;SLC25A26,ZW10;SLC33A1,DLG2;SLC3A2,ARHGAP32;SLC3A2,PVRL1;SLC43A1,NTM;SLC4A7,CPNE4;SLC6A11,DSCAML1;SLC6A11,NAV2;SLC9A9,CCDC50;SLC9A9,LDLRAD3;SLCO2A1,SBF2;SLMAP,CPNE4;SLMAP,PARP15;SMARCC1,TFDP2;SPATA16,DLG2;SRGAP3,EPHA3;SRGAP3,SOX6;ST6GAL1,GRM1;ST6GAL1,IL20RA;STAB1,TNIK;STAC,FLNB;STARD10,PKNOX2;STIM1,DLG2;STT3B,CCDC81;STT3B,MAP3K11;STT3B,MYRIP;STXBP5L,GANAB;STXBP5L,IQCJ;STXBP5L,RDX;STXBP5L,VPS8;SUCLG2,MS4A4A;SUMF1,GRIA4;SUMF1,ITIH1;SUMF1,KCNAB1;SUMF1,LMLN;TBC1D5,VPS8;TEAD1,PTPRJ;TGFBR2,AP2A2;TGFBR2,TNK2;THRB,NLGN1;TMEM108,APOC3;TMEM216,BSCL2;TMEM89,SLC22A18;TNIK,DSCAML1;TNIK,LDLRAD3;TOMM70A,DLG2;TOPBP1,NTM;TP63,GRM5;TRANK1,CPNE4;TRANK1,EPHA3;TRANK1,FRMD4B;TRANK1,GRIK4;TRIM44,RDX;TSEN2,NAALADL2;TSPAN18,C11orf49;TSPAN4,SIDT2;U2SURP,SHOX2;UBE2E1,TMEM135;UBE2E2,STXBP5L;ULK4,SIRT3;UMPS,MAML2;VPS8,DLG2;VSTM5,ACSL4;VWA5B2,KIRREL3;WDR53,MPPED2;WDR74,FAM55B;WNT7A,VSTM5;XXYLT1,PGAP2;XXYLT1,TEAD1;ZBTB11,ILDR1;ZDHHC13,KIRREL3;ZMAT3,LUZP2;ZNF148,AHNAK;ZNF589,LSAMP;ZNF589,SLMAP
CTDB0434	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	12,22	hTERT RPE-1 cell line	Next Generation Sequencing	Homo sapiens	BM178	Illumina HiSeq 2000, MiSeq or NextSeq			RASSF3;RASSF9	European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19			PRJEB8037	No	NA
CTDB0435	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	8,15	hTERT RPE-1 cell line	Next Generation Sequencing	Homo sapiens	BM175	Illumina HiSeq 2000, MiSeq or NextSeq			BUBR1;CASC5	European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19			PRJEB8037	No	NA
CTDB0436	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	12	hTERT RPE-1 cell line	Next Generation Sequencing	Homo sapiens	BM237	Illumina HiSeq 2000, MiSeq or NextSeq				European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19			PRJEB8037	No	NA
CTDB0437	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	14	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB34					European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19				Yes	NA
CTDB0438	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	15	Medulloblastoma	Next Generation Sequencing	Homo sapiens	MB243					European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19				Yes	NA
CTDB0439	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	14	hTERT RPE-1 cell line	Next Generation Sequencing	Homo sapiens	BM694	Illumina HiSeq 2000, MiSeq or NextSeq				European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19			PRJEB8037	No	NA
CTDB0440	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	17	hTERT RPE-1 cell line	Next Generation Sequencing	Homo sapiens	BM173	Illumina HiSeq 2000, MiSeq or NextSeq				European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19			PRJEB8037	No	NA
CTDB0441	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	10,X	hTERT RPE-1 cell line	Next Generation Sequencing	Homo sapiens	BM1142	Illumina HiSeq 2000, MiSeq or NextSeq				European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19			PRJEB8037	No	NA
CTDB0442	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	6	hTERT RPE-1 cell line	Next Generation Sequencing	Homo sapiens	BM780	Illumina HiSeq 2000, MiSeq or NextSeq				European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19			PRJEB8037	No	NA
CTDB0443	Methodology	26415501	Mardin BR, Drainas AP, Waszak SM, Weischenfeldt J, Isokane M, Stutz AM, Raeder B, Efthymiopoulos T, Buccitelli C, Segura-Wang M, Northcott P, Pfister SM, Lichter P, Ellenberg J, Korbel JO	A cell-based model system links chromothripsis with hyperploidy	Molecular Systems Biology	2015 Sep	6	hTERT RPE-1 cell line	Next Generation Sequencing	Homo sapiens	BM605	Illumina HiSeq 2000, MiSeq or NextSeq				European Molecular Biology Laboratory, Genome Biology Unit, Heidelberg, Germany	A remarkable observation emerging from recent cancer genome analyses is the identification of chromothripsis as a one-off genomic catastrophe, resulting in massive somatic DNA structural rearrangements (SRs). Largely due to lack of suitable model systems, the mechanistic basis of chromothripsis has remained elusive. We developed an integrative method termed complex alterations after selection and transformation (CAST), enabling efficient in vitro generation of complex DNA rearrangements including chromothripsis, using cell perturbations coupled with a strong selection barrier followed by massively parallel sequencing. We employed this methodology to characterize catastrophic SR formation processes, their temporal sequence, and their impact on gene expression and cell division. Our in vitro system uncovered a propensity of chromothripsis to occur in cells with damaged telomeres, and in particular in hyperploid cells. Analysis of primary medulloblastoma cancer genomes verified the link between hyperploidy and chromothripsis in vivo. CAST provides the foundation for mechanistic dissection of complex DNA rearrangement processes.	GRCh37/hg19			PRJEB8037	No	NA
CTDB0444	Research	26328271	Furgason JM, Koncar RF, Michelhaugh SK, Sarkar FH, Mittal S, Sloan AE, Barnholtz-Sloan JS, Bahassi el M	Whole genome sequence analysis links chromothripsis to EGFR, MDM2, MDM4, and CDK4 amplification in glioblastoma	Oncoscience	2015 Jul	6,7,12	Glioblastoma	Next Generation Sequencing	Homo sapiens	TCGA-06-0686				MDM2;CDK4;VEGFA	Department of Internal Medicine, Division of Hematology/Oncology and UC Brain Tumor Center, University of Cincinnati, Cincinnati OH, USA	BACKGROUND: Findings based on recent advances in next-generation sequence analysis suggest that, in some tumors, a single catastrophic event, termed chromothripsis, results in several simultaneous tumorigenic alterations. Previous studies have suggested that glioblastoma (GBM) may exhibit chromothripsis at a higher rate (39%) than other tumors (9%). Primary glioblastoma is an aggressive form of brain cancer that typically appears suddenly in older adults. With aggressive treatment, the median survival time is only 15 months. Their acute onset and widespread genomic instability indicates that chromothripsis may play a key role in their initiation and progression. GBMs are often characterized by EGFR amplification, CDKN2A and PTEN deletion, although approximately 20% of GBMs harbor additional amplifications in MDM2 or MDM4 with CDK4. METHODS: We used the chromothripsis prediction tool, Shatterproof, in conjunction with a custom whole genome sequence analysis pipeline in order to generate putative regions of chromothripsis. The data derived from this study was further expanded on using fluorescence in situ hybridization (FISH) analysis and susceptibility studies with colony formation assays. RESULTS: We show that primary GBMs are associated with higher chromothripsis scores and establish a link between chromothripsis and gene amplification of receptor tyrosine kinases (RTKs), as well as modulators of the TP53 and RB1 pathways. CONCLUSIONS: Utilizing a newly introduced bioinformatic tool, we provide evidence that chromothripsis is associated with the formation of amplicons containing several oncogenes involved in key pathways that are likely essential for post-chromothriptic cell survival.					Yes	NA
CTDB0445	Research	26328271	Furgason JM, Koncar RF, Michelhaugh SK, Sarkar FH, Mittal S, Sloan AE, Barnholtz-Sloan JS, Bahassi el M	Whole genome sequence analysis links chromothripsis to EGFR, MDM2, MDM4, and CDK4 amplification in glioblastoma	Oncoscience	2015 Jul	1,4,12	Glioblastoma	Next Generation Sequencing	Homo sapiens	TCGA-02-2485				CDK4;PDGFRA	Department of Internal Medicine, Division of Hematology/Oncology and UC Brain Tumor Center, University of Cincinnati, Cincinnati OH, USA	BACKGROUND: Findings based on recent advances in next-generation sequence analysis suggest that, in some tumors, a single catastrophic event, termed chromothripsis, results in several simultaneous tumorigenic alterations. Previous studies have suggested that glioblastoma (GBM) may exhibit chromothripsis at a higher rate (39%) than other tumors (9%). Primary glioblastoma is an aggressive form of brain cancer that typically appears suddenly in older adults. With aggressive treatment, the median survival time is only 15 months. Their acute onset and widespread genomic instability indicates that chromothripsis may play a key role in their initiation and progression. GBMs are often characterized by EGFR amplification, CDKN2A and PTEN deletion, although approximately 20% of GBMs harbor additional amplifications in MDM2 or MDM4 with CDK4. METHODS: We used the chromothripsis prediction tool, Shatterproof, in conjunction with a custom whole genome sequence analysis pipeline in order to generate putative regions of chromothripsis. The data derived from this study was further expanded on using fluorescence in situ hybridization (FISH) analysis and susceptibility studies with colony formation assays. RESULTS: We show that primary GBMs are associated with higher chromothripsis scores and establish a link between chromothripsis and gene amplification of receptor tyrosine kinases (RTKs), as well as modulators of the TP53 and RB1 pathways. CONCLUSIONS: Utilizing a newly introduced bioinformatic tool, we provide evidence that chromothripsis is associated with the formation of amplicons containing several oncogenes involved in key pathways that are likely essential for post-chromothriptic cell survival.					Yes	NA
CTDB0446	Research	26328271	Furgason JM, Koncar RF, Michelhaugh SK, Sarkar FH, Mittal S, Sloan AE, Barnholtz-Sloan JS, Bahassi el M	Whole genome sequence analysis links chromothripsis to EGFR, MDM2, MDM4, and CDK4 amplification in glioblastoma	Oncoscience	2015 Jul	7,12	Glioblastoma	Next Generation Sequencing	Homo sapiens	TCGA-19-2624				EGFR;MDM2;CDK4	Department of Internal Medicine, Division of Hematology/Oncology and UC Brain Tumor Center, University of Cincinnati, Cincinnati OH, USA	BACKGROUND: Findings based on recent advances in next-generation sequence analysis suggest that, in some tumors, a single catastrophic event, termed chromothripsis, results in several simultaneous tumorigenic alterations. Previous studies have suggested that glioblastoma (GBM) may exhibit chromothripsis at a higher rate (39%) than other tumors (9%). Primary glioblastoma is an aggressive form of brain cancer that typically appears suddenly in older adults. With aggressive treatment, the median survival time is only 15 months. Their acute onset and widespread genomic instability indicates that chromothripsis may play a key role in their initiation and progression. GBMs are often characterized by EGFR amplification, CDKN2A and PTEN deletion, although approximately 20% of GBMs harbor additional amplifications in MDM2 or MDM4 with CDK4. METHODS: We used the chromothripsis prediction tool, Shatterproof, in conjunction with a custom whole genome sequence analysis pipeline in order to generate putative regions of chromothripsis. The data derived from this study was further expanded on using fluorescence in situ hybridization (FISH) analysis and susceptibility studies with colony formation assays. RESULTS: We show that primary GBMs are associated with higher chromothripsis scores and establish a link between chromothripsis and gene amplification of receptor tyrosine kinases (RTKs), as well as modulators of the TP53 and RB1 pathways. CONCLUSIONS: Utilizing a newly introduced bioinformatic tool, we provide evidence that chromothripsis is associated with the formation of amplicons containing several oncogenes involved in key pathways that are likely essential for post-chromothriptic cell survival.					Yes	NA
CTDB0447	Research	27108385	Ortega V, Chaubey A, Mendiola C, Ehman W Jr, Vadlamudi K, Dupont B, Velagaleti G	Complex Chromosomal Rearrangements in B-Cell Lymphoma: Evidence of Chromoanagenesis? A Case Report	Neoplasia	2016 Apr	3,7,12,14,22	Diffuse large B-cell lymphoma	SNP array	Homo sapiens	27108385_1	Affymetrix CytoScan HD			BCL2;BCL6;IGH	Department of Pathology, University of Texas Health Science Center, San Antonio, TX	Genomic instability is a well-known hallmark of cancer. Recent genome sequencing studies have led to the identification of novel phenomena called chromothripsis and chromoanasynthesis in which complex genomic rearrangements are thought to be derived from a single catastrophic event rather than by several incremental steps. A new term chromoanagenesis or chromosomal rebirth was coined recently to group these two one-step catastrophic events together. These phenomena suggest an evolutionary modality for cancer cells to circumvent individual mutational events with one simultaneous shattering of chromosomes resulting in the random reassembling of segmented genetic material to form complex derivative chromosomes. We report a case of possible chromoanagenesis in a patient with diffuse large B-cell lymphoma. Chromosome analysis from the biopsy showed a complex karyotype with multiple numerical and structural rearrangements including a translocation of chromosomes 3 and 7 involving the BCL6 gene region, with the derivative chromosome further rearranging with chromosomes 14, 7, and 22 with involvement of the IGH gene region. Fluorescence in situ hybridization studies confirmed these findings. Chromosomal microarray studies showed multiple complex copy number variations including a chromosome 12 abnormality, the complexity of which appears to suggest the phenomenon of chromoanagenesis. Our case further illustrates that lymphomagenesis can be complex and may arise from a catastrophic event resulting in multiple complex chromosome rearrangements.					Yes	NA
CTDB0448	Research	26993771	Schutze DM, Krijgsman O, Snijders PJ, Ylstra B, Weischenfeldt J, Mardin BR, Stutz AM, Korbel JO, de Winter JP, Meijer CJ, Quint WG, Bosch L, Wilting SM, Steenbergen RD	Immortalization capacity of HPV types is inversely related to chromosomal instability	Oncotarget	2016 Mar	8	HPV transducted human foreskin keratinocytes cell line	Next Generation Sequencing	Homo sapiens	donorI_HPV16_passage40	Illumina HiSeq			MYC	Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands	High-risk human papillomavirus (hrHPV) types induce immortalization of primary human epithelial cells. Previously we demonstrated that immortalization of human foreskin keratinocytes (HFKs) is HPV type dependent, as reflected by the presence or absence of a crisis period before reaching immortality. This study determined how the immortalization capacity of ten hrHPV types relates to DNA damage induction and overall genomic instability in HFKs.Twenty five cell cultures obtained by transduction of ten hrHPV types (i.e. HPV16/18/31/33/35/45/51/59/66/70 E6E7) in two or three HFK donors each were studied.All hrHPV-transduced HFKs showed an increased number of double strand DNA breaks compared to controls, without exhibiting significant differences between types. However, immortal descendants of HPV-transduced HFKs that underwent a prior crisis period (HPV45/51/59/66/70-transduced HFKs) showed significantly more chromosomal aberrations compared to those without crisis (HPV16/18/31/33/35-transduced HFKs). Notably, the hTERT locus at 5p was exclusively gained in cells with a history of crisis and coincided with increased expression. Chromothripsis was detected in one cell line in which multiple rearrangements within chromosome 8 resulted in a gain of MYC.Together we demonstrated that upon HPV-induced immortalization, the number of chromosomal aberrations is inversely related to the viral immortalization capacity. We propose that hrHPV types with reduced immortalization capacity in vitro, reflected by a crisis period, require more genetic host cell aberrations to facilitate immortalization than types that can immortalize without crisis. This may in part explain the observed differences in HPV-type prevalence in cervical cancers and emphasizes that changes in the host cell genome contribute to HPV-induced carcinogenesis.				PRJEB9176	No	NA
CTDB0449	Research	26993771	Schutze DM, Krijgsman O, Snijders PJ, Ylstra B, Weischenfeldt J, Mardin BR, Stutz AM, Korbel JO, de Winter JP, Meijer CJ, Quint WG, Bosch L, Wilting SM, Steenbergen RD	Immortalization capacity of HPV types is inversely related to chromosomal instability	Oncotarget	2016 Mar	8	HPV transducted human foreskin keratinocytes cell line	array CGH	Homo sapiens	donorI_HPV16_passage100	Agilent 2x105K arrayCGH			MYC	Department of Pathology, VU University Medical Center, Amsterdam, The Netherlands	High-risk human papillomavirus (hrHPV) types induce immortalization of primary human epithelial cells. Previously we demonstrated that immortalization of human foreskin keratinocytes (HFKs) is HPV type dependent, as reflected by the presence or absence of a crisis period before reaching immortality. This study determined how the immortalization capacity of ten hrHPV types relates to DNA damage induction and overall genomic instability in HFKs.Twenty five cell cultures obtained by transduction of ten hrHPV types (i.e. HPV16/18/31/33/35/45/51/59/66/70 E6E7) in two or three HFK donors each were studied.All hrHPV-transduced HFKs showed an increased number of double strand DNA breaks compared to controls, without exhibiting significant differences between types. However, immortal descendants of HPV-transduced HFKs that underwent a prior crisis period (HPV45/51/59/66/70-transduced HFKs) showed significantly more chromosomal aberrations compared to those without crisis (HPV16/18/31/33/35-transduced HFKs). Notably, the hTERT locus at 5p was exclusively gained in cells with a history of crisis and coincided with increased expression. Chromothripsis was detected in one cell line in which multiple rearrangements within chromosome 8 resulted in a gain of MYC.Together we demonstrated that upon HPV-induced immortalization, the number of chromosomal aberrations is inversely related to the viral immortalization capacity. We propose that hrHPV types with reduced immortalization capacity in vitro, reflected by a crisis period, require more genetic host cell aberrations to facilitate immortalization than types that can immortalize without crisis. This may in part explain the observed differences in HPV-type prevalence in cervical cancers and emphasizes that changes in the host cell genome contribute to HPV-induced carcinogenesis.		GSE72063			No	NA
CTDB0450	Research	26929209	Nazaryan-Petersen L, Bertelsen B, Bak M, Jonson L, Tommerup N, Hancks DC, Tumer Z	Germline Chromothripsis Driven by L1-Mediated Retrotransposition and Alu/Alu Homologous Recombination	Hum Mutat	2016 Apr	3,5	Congenital abnormality	Next Generation Sequencing	Homo sapiens	26929209_1	Illumina HiSeq 2500				Applied Human Molecular Genetics, Kennedy Center, Department of Clinical Genetics, Copenhagen University Hospital, Rigshospitalet, Glostrup, 2600, Denmark	Chromothripsis (CTH) is a phenomenon where multiple localized double-stranded DNA breaks result in complex genomic rearrangements. Although the DNA-repair mechanisms involved in CTH have been described, the mechanisms driving the localized "shattering" process remain unclear. High-throughput sequence analysis of a familial germline CTH revealed an inserted SVAE retrotransposon associated with a 110-kb deletion displaying hallmarks of L1-mediated retrotransposition. Our analysis suggests that the SVAE insertion did not occur prior to or after, but concurrent with the CTH event. We also observed L1-endonuclease potential target sites in other breakpoints. In addition, we found four Alu elements flanking the 110-kb deletion and associated with an inversion. We suggest that chromatin looping mediated by homologous Alu elements may have brought distal DNA regions into close proximity facilitating DNA cleavage by catalytically active L1-endonuclease. Our data provide the first evidence that active and inactive human retrotransposons can serve as endogenous mutagens driving CTH in the germline.	GRCh37/hg19				No	NA
CTDB0451	Research	27255164	Lee JC, Lu TP, Changou CA, Liang CW, Huang HN, Lauria A, Huang HY, Lin CY, Chiang YC, Davidson B, Lin MC, Kuo KT	Genomewide copy number analysis of Mullerian adenosarcoma identified chromosomal instability in the aggressive subgroup	Mod Pathol	2016 Jun	12	Mullerian adenosarcoma	Inversion probe array	Homo sapiens	S1	Affymetrix OncoScan FFPE Assay Kit			CDK4;MDM2	Department and Graduate Institute of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan	Mullerian adenosarcomas are malignant gynecologic neoplasms. Advanced staging and sarcomatous overgrowth predict poor prognosis. Because the genomic landscape remains poorly understood, we conducted this study to characterize the genomewide copy number variations in adenosarcomas. Sixteen tumors, including eight with and eight without sarcomatous overgrowth, were subjected to a molecular inversion probe array analysis. Copy number variations, particularly losses, were significantly higher in cases with sarcomatous overgrowth. Frequent gains of chromosomal 12q were noted, often involving cancer-associated genes CDK4 (six cases), MDM2, CPM, YEATS4, DDIT3, GLI1 (five each), HMGA2 and STAT6 (four), without association with sarcomatous overgrowth status. The most frequent losses involved chromosomes 13q (five cases), 9p, 16q and 17q (four cases each) and were almost limited to cases with sarcomatous overgrowth. MDM2 and CDK4 amplification, as well as losses of RB1 (observed in two cases) and CDKN2A/B (one case), was verified by FISH. By immunohistochemistry, all MDM2/CDK4-coamplified cases were confirmed to overexpress both encoded proteins, whereas all four cases with (plus an additional four without) gain of HMGA2 overexpressed the HMGA2 protein. Both cases with RB1 loss were negative for the immunostaining of the encoded protein. Chromothripsis-like copy number profiles involving chromosome 12 or 14 were observed in three fatal cases, all of which harbored sarcomatous overgrowth. With whole chromosome painting and deconvolution fluorescent microscopy, dividing tumor cells in all three cases were shown to have scattered extrachromosomal materials derived from chromosomes involved by chromothripsis, suggesting that this phenomenon may serve as visual evidence for chromothripsis in paraffin tissue. In conclusion, we identified frequent chromosome 12q amplifications, including loci containing potential pharmacological targets. Global chromosomal instability and chromothripsis were more frequent in cases with sarcomatous overgrowth. To our knowledge, this is the first time that evidence of chromothripsis has been demonstrated in paraffin-embedded clinical tissues and in adenosarcomas.		GSE67107			Yes	NA
CTDB0452	Research	27255164	Lee JC, Lu TP, Changou CA, Liang CW, Huang HN, Lauria A, Huang HY, Lin CY, Chiang YC, Davidson B, Lin MC, Kuo KT	Genomewide copy number analysis of Mullerian adenosarcoma identified chromosomal instability in the aggressive subgroup	Mod Pathol	2016 Jun	14	Mullerian adenosarcoma	Inversion probe array	Homo sapiens	S5	Affymetrix OncoScan FFPE Assay Kit				Department and Graduate Institute of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan	Mullerian adenosarcomas are malignant gynecologic neoplasms. Advanced staging and sarcomatous overgrowth predict poor prognosis. Because the genomic landscape remains poorly understood, we conducted this study to characterize the genomewide copy number variations in adenosarcomas. Sixteen tumors, including eight with and eight without sarcomatous overgrowth, were subjected to a molecular inversion probe array analysis. Copy number variations, particularly losses, were significantly higher in cases with sarcomatous overgrowth. Frequent gains of chromosomal 12q were noted, often involving cancer-associated genes CDK4 (six cases), MDM2, CPM, YEATS4, DDIT3, GLI1 (five each), HMGA2 and STAT6 (four), without association with sarcomatous overgrowth status. The most frequent losses involved chromosomes 13q (five cases), 9p, 16q and 17q (four cases each) and were almost limited to cases with sarcomatous overgrowth. MDM2 and CDK4 amplification, as well as losses of RB1 (observed in two cases) and CDKN2A/B (one case), was verified by FISH. By immunohistochemistry, all MDM2/CDK4-coamplified cases were confirmed to overexpress both encoded proteins, whereas all four cases with (plus an additional four without) gain of HMGA2 overexpressed the HMGA2 protein. Both cases with RB1 loss were negative for the immunostaining of the encoded protein. Chromothripsis-like copy number profiles involving chromosome 12 or 14 were observed in three fatal cases, all of which harbored sarcomatous overgrowth. With whole chromosome painting and deconvolution fluorescent microscopy, dividing tumor cells in all three cases were shown to have scattered extrachromosomal materials derived from chromosomes involved by chromothripsis, suggesting that this phenomenon may serve as visual evidence for chromothripsis in paraffin tissue. In conclusion, we identified frequent chromosome 12q amplifications, including loci containing potential pharmacological targets. Global chromosomal instability and chromothripsis were more frequent in cases with sarcomatous overgrowth. To our knowledge, this is the first time that evidence of chromothripsis has been demonstrated in paraffin-embedded clinical tissues and in adenosarcomas.		GSE67107			Yes	NA
CTDB0453	Research	27255164	Lee JC, Lu TP, Changou CA, Liang CW, Huang HN, Lauria A, Huang HY, Lin CY, Chiang YC, Davidson B, Lin MC, Kuo KT	Genomewide copy number analysis of Mullerian adenosarcoma identified chromosomal instability in the aggressive subgroup	Mod Pathol	2016 Jun	12	Mullerian adenosarcoma	Inversion probe array	Homo sapiens	S6	Affymetrix OncoScan FFPE Assay Kit			CDK4;MDM2	Department and Graduate Institute of Pathology, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan	Mullerian adenosarcomas are malignant gynecologic neoplasms. Advanced staging and sarcomatous overgrowth predict poor prognosis. Because the genomic landscape remains poorly understood, we conducted this study to characterize the genomewide copy number variations in adenosarcomas. Sixteen tumors, including eight with and eight without sarcomatous overgrowth, were subjected to a molecular inversion probe array analysis. Copy number variations, particularly losses, were significantly higher in cases with sarcomatous overgrowth. Frequent gains of chromosomal 12q were noted, often involving cancer-associated genes CDK4 (six cases), MDM2, CPM, YEATS4, DDIT3, GLI1 (five each), HMGA2 and STAT6 (four), without association with sarcomatous overgrowth status. The most frequent losses involved chromosomes 13q (five cases), 9p, 16q and 17q (four cases each) and were almost limited to cases with sarcomatous overgrowth. MDM2 and CDK4 amplification, as well as losses of RB1 (observed in two cases) and CDKN2A/B (one case), was verified by FISH. By immunohistochemistry, all MDM2/CDK4-coamplified cases were confirmed to overexpress both encoded proteins, whereas all four cases with (plus an additional four without) gain of HMGA2 overexpressed the HMGA2 protein. Both cases with RB1 loss were negative for the immunostaining of the encoded protein. Chromothripsis-like copy number profiles involving chromosome 12 or 14 were observed in three fatal cases, all of which harbored sarcomatous overgrowth. With whole chromosome painting and deconvolution fluorescent microscopy, dividing tumor cells in all three cases were shown to have scattered extrachromosomal materials derived from chromosomes involved by chromothripsis, suggesting that this phenomenon may serve as visual evidence for chromothripsis in paraffin tissue. In conclusion, we identified frequent chromosome 12q amplifications, including loci containing potential pharmacological targets. Global chromosomal instability and chromothripsis were more frequent in cases with sarcomatous overgrowth. To our knowledge, this is the first time that evidence of chromothripsis has been demonstrated in paraffin-embedded clinical tissues and in adenosarcomas.		GSE67107			Yes	NA
CTDB0454	Research	26872047	Forero-Castro M, Robledo C, Benito R, Abaigar M, Africa Martin A, Arefi M, Fuster JL, de Las Heras N, Rodriguez JN, Quintero J, Riesco S, Hermosin L, de la Fuente I, Recio I, Ribera J, Labrador J, Alonso JM, Olivier C, Sierra M, Megido M, Corchete-Sanchez LA, Ciudad Pizarro J, Garcia JL, Ribera JM, Hernandez-Rivas JM	Genome-Wide DNA Copy Number Analysis of Acute Lymphoblastic Leukemia Identifies New Genetic Markers Associated with Clinical Outcome	PLoS One	2016 Feb	6	Acute lymphoblastic leukemia	array CGH	Homo sapiens	cth6	NimbleGen CGH 12x135K array				IBSAL, IBMCC, University of Salamanca, CSIC, Cancer Research Center, Salamanca, Spain	Aims: To characterize the presence of additional DNA copy number alterations (CNAs) in children and adults with ALL by whole-genome oligonucleotide array (aCGH) analysis, and to identify their associations with clinical features and outcome. Array-CGH was carried out in 265 newly diagnosed ALLs (142 children and 123 adults). The NimbleGen CGH 12x135K array (Roche) was used to analyze genetic gains and losses. CNAs were analyzed with GISTIC and aCGHweb software. Clinical and biological variables were analyzed. Three of the patients showed chromothripsis (cth6, cth14q and cth15q). CNAs were associated with age, phenotype, genetic subtype and overall survival (OS). In the whole cohort of children, the losses on 14q32.33 (p = 0.019) and 15q13.2 (p = 0.04) were related to shorter OS. In the group of children without good- or poor-risk cytogenetics, the gain on 1p36.11 was a prognostic marker independently associated with shorter OS. In adults, the gains on 19q13.2 (p = 0.001) and Xp21.1 (p = 0.029), and the loss of 17p (p = 0.014) were independent markers of poor prognosis with respect to OS. In summary, CNAs are frequent in ALL and are associated with clinical parameters and survival. Genome-wide DNA copy number analysis allows the identification of genetic markers that predict clinical outcome, suggesting that detection of these genetic lesions will be useful in the management of patients newly diagnosed with ALL	NCBI 36/hg18	GSE75671			Yes	NA
CTDB0455	Research	26872047	Forero-Castro M, Robledo C, Benito R, Abaigar M, Africa Martin A, Arefi M, Fuster JL, de Las Heras N, Rodriguez JN, Quintero J, Riesco S, Hermosin L, de la Fuente I, Recio I, Ribera J, Labrador J, Alonso JM, Olivier C, Sierra M, Megido M, Corchete-Sanchez LA, Ciudad Pizarro J, Garcia JL, Ribera JM, Hernandez-Rivas JM	Genome-Wide DNA Copy Number Analysis of Acute Lymphoblastic Leukemia Identifies New Genetic Markers Associated with Clinical Outcome	PLoS One	2016 Feb	14	Acute lymphoblastic leukemia	array CGH	Homo sapiens	cth14q	NimbleGen CGH 12x135K array				IBSAL, IBMCC, University of Salamanca, CSIC, Cancer Research Center, Salamanca, Spain	Aims: To characterize the presence of additional DNA copy number alterations (CNAs) in children and adults with ALL by whole-genome oligonucleotide array (aCGH) analysis, and to identify their associations with clinical features and outcome. Array-CGH was carried out in 265 newly diagnosed ALLs (142 children and 123 adults). The NimbleGen CGH 12x135K array (Roche) was used to analyze genetic gains and losses. CNAs were analyzed with GISTIC and aCGHweb software. Clinical and biological variables were analyzed. Three of the patients showed chromothripsis (cth6, cth14q and cth15q). CNAs were associated with age, phenotype, genetic subtype and overall survival (OS). In the whole cohort of children, the losses on 14q32.33 (p = 0.019) and 15q13.2 (p = 0.04) were related to shorter OS. In the group of children without good- or poor-risk cytogenetics, the gain on 1p36.11 was a prognostic marker independently associated with shorter OS. In adults, the gains on 19q13.2 (p = 0.001) and Xp21.1 (p = 0.029), and the loss of 17p (p = 0.014) were independent markers of poor prognosis with respect to OS. In summary, CNAs are frequent in ALL and are associated with clinical parameters and survival. Genome-wide DNA copy number analysis allows the identification of genetic markers that predict clinical outcome, suggesting that detection of these genetic lesions will be useful in the management of patients newly diagnosed with ALL	NCBI 36/hg18	GSE75671			Yes	NA
CTDB0456	Research	26872047	Forero-Castro M, Robledo C, Benito R, Abaigar M, Africa Martin A, Arefi M, Fuster JL, de Las Heras N, Rodriguez JN, Quintero J, Riesco S, Hermosin L, de la Fuente I, Recio I, Ribera J, Labrador J, Alonso JM, Olivier C, Sierra M, Megido M, Corchete-Sanchez LA, Ciudad Pizarro J, Garcia JL, Ribera JM, Hernandez-Rivas JM	Genome-Wide DNA Copy Number Analysis of Acute Lymphoblastic Leukemia Identifies New Genetic Markers Associated with Clinical Outcome	PLoS One	2016 Feb	15	Acute lymphoblastic leukemia	array CGH	Homo sapiens	cth15q	NimbleGen CGH 12x135K array				IBSAL, IBMCC, University of Salamanca, CSIC, Cancer Research Center, Salamanca, Spain	Aims: To characterize the presence of additional DNA copy number alterations (CNAs) in children and adults with ALL by whole-genome oligonucleotide array (aCGH) analysis, and to identify their associations with clinical features and outcome. Array-CGH was carried out in 265 newly diagnosed ALLs (142 children and 123 adults). The NimbleGen CGH 12x135K array (Roche) was used to analyze genetic gains and losses. CNAs were analyzed with GISTIC and aCGHweb software. Clinical and biological variables were analyzed. Three of the patients showed chromothripsis (cth6, cth14q and cth15q). CNAs were associated with age, phenotype, genetic subtype and overall survival (OS). In the whole cohort of children, the losses on 14q32.33 (p = 0.019) and 15q13.2 (p = 0.04) were related to shorter OS. In the group of children without good- or poor-risk cytogenetics, the gain on 1p36.11 was a prognostic marker independently associated with shorter OS. In adults, the gains on 19q13.2 (p = 0.001) and Xp21.1 (p = 0.029), and the loss of 17p (p = 0.014) were independent markers of poor prognosis with respect to OS. In summary, CNAs are frequent in ALL and are associated with clinical parameters and survival. Genome-wide DNA copy number analysis allows the identification of genetic markers that predict clinical outcome, suggesting that detection of these genetic lesions will be useful in the management of patients newly diagnosed with ALL	NCBI 36/hg18	GSE75671			Yes	NA
CTDB0457	Research	26871565	Anderson SE, Kamath A, Pilz DT, Morgan SM	A rare example of germ-line chromothripsis resulting in large genomic imbalance	Clin Dysmorphol	2016 Apr	X	Developmental delay and dysmorphism	array CGH	Homo sapiens	26871565_1	Illumina CytoChip ISCA 8x60K (v2.0) platforms	chrX:0-30327448:0;chrX:100179620-155270560:0;chrX:30327449-32339828:-1;chrX:32339829-36826428:0;chrX:36826429-39147743:-1;chrX:39147744-40036425:0;chrX:40036426-48120226:-1;chrX:48120227-49016637:0;chrX:49016638-53458883:-1;chrX:53458884-53459068:0;chrX:53459069-54756791:-1;chrX:54756792-88410915:0;chrX:88410916-89032507:-1;chrX:89032508-90650704:0;chrX:90650705-97810995:-1;chrX:97810996-99852633:0;chrX:99852634-100179619:-1		ATP6AP2;BCOR;BMP15;CACNA1F;CASK;CFP;CLCN5;CYBB;DIAPH2;DMD;FGD1;FOXP3;GK;HSD17B10;HUWE1;IL1RAPL1;IQSEC2;KDM5C;KDM6A;MAOA;NDP;NROB1;NYX;OTC;PHF8;RBM10;RP2;RPGR;SRPX2;SYN1;TSPAN7;UBA1;USP9X;XK;ZNF81	Laboratory Genetics, Institute of Medical Genetics, University Hospital of Wales, Cardiff, UK	Chromothripsis is a recently described 'chromosome catastrophe' phenomenon in which multiple genomic rearrangements are generated in a single catastrophic event. Chromothripsis has most frequently been associated with cancer, but there have also been rare reports of chromothripsis in patients with developmental disorders and congenital anomalies. In contrast to the massive DNA loss that often accompanies chromothripsis in cancer, only minimal DNA loss has been reported in the majority of cases of chromothripsis that have occurred in the germ line. Presumably, this is because in most instances, large genomic losses would be lethal in utero. We report on a female patient with developmental delay and dysmorphism. G-banded chromosome analysis detected a subtle, interstitial deletion of chromosome 13 and a complex rearrangement of one X chromosome. Subsequent array comparative genomic hybridisation studies indicated nine deletions on the X chromosome ranging from 327 kb to 8 Mb in size. A 4.4 Mb deletion on chromosome 13 was also confirmed, compatible with the patient's clinical phenotype. We propose that this is a rare example of constitutional chromothripsis in association with relatively large genomic imbalances and that these have been tolerated in this case as they have occurred in a female on the X chromosome, which has undergone preferential X inactivation.	GRCh37/hg19				No	NA
CTDB0458	Research	26862731	Morishita M, Muramatsu T, Suto Y, Hirai M, Konishi T, Hayashi S, Shigemizu D, Tsunoda T, Moriyama K, Inazawa J	Chromothripsis-like chromosomal rearrangements induced by ionizing radiation using proton microbeam irradiation system	Oncotarget	2016 Mar	2,5,7,20	Irradiated oral squamous cell carcinoma cell line	Next Generation Sequencing	Homo sapiens	LM200-#25	Illumina HiSeq2500	chr2:0-16112058:0;chr2:16112059-16374530:1;chr2:16374531-48874200:0;chr2:48874201-83960470:1;chr2:83960471-243199373:0;chr5:0-60181451:0;chr5:180693129-180915260:0;chr5:60181452-95997250:-1;chr5:95997251-96133484:0;chr5:96133485-180693128:-1;chr7:0-26267810:0;chr7:117737888-127700972:0;chr7:127700973-159119487:-1;chr7:159119488-159138663:0;chr7:26267811-56070567:-1;chr7:56070568-90400491:0;chr7:90400492-91667757:-1;chr7:91667758-93403512:0;chr7:93403513-117737887:-1	hs1:71158954-71158954,hs7:62926589-62926589;hs1:188668262-188668262,hs7:97211292-97211292;hs2:15742427-15742427,hs2:16708647-16708647;hs2:48744071-48744071,hs2:48747466-48747466;hs2:48937460-48937460,hs2:81807493-81807493;hs2:53106376-53106376,hs2:53252067-53252067;hs2:56565085-56565085,hs2:56567839-56567839;hs2:65827048-65827048,hs22:35021325-35021325;hs2:76773545-76773545,hs2:76775446-76775446;hs2:80900266-80900266,hs2:80902393-80902393;hs2:163267921-163267921,hs13:21026190-21026190;hs2:184164179-184164179,hs6:53249177-53249177;hs2:219807376-219807376,hs12:55980975-55980975;hs3:51204229-51204229,hs7:136312283-136312283;hs3:151238360-151238360,hs5:101050301-101050301;hs5:6330715-6330715,hs5:6378446-6378446;hs5:12037575-12037575,hsX:54658517-54658517;hs5:12734098-12734098,hs5:12772396-12772396;hs5:17285317-17285317,hs15:34587946-34587946;hs5:19854136-19854136,hs5:89613574-89613574;hs5:26699124-26699124,hsX:70598444-70598444;hs5:35097012-35097012,hs5:35100018-35100018;hs5:39026838-39026838,hs5:39028538-39028538;hs5:75087709-75087709,hs5:75098716-75098716;hs5:89613939-89613939,hs20:14453979-14453979;hs5:95994648-95994648,hs5:96157386-96157386;hs5:117106928-117106928,hs11:98419831-98419831;hs5:130420471-130420471,hs15:24577473-24577473;hs7:26274040-26274040,hs7:123601514-123601514;hs7:51228105-51228105,hs7:51281767-51281767;hs7:54282791-54282791,hs15:48978914-48978914;hs7:61968855-61968855,hs8:43607720-43607720;hs7:62252943-62252943,hs9:66855983-66855983;hs7:84778168-84778168,hs7:84780433-84780433;hs7:103591420-103591420,hs7:103594627-103594627;hs7:127757865-127757865,hs7:127820843-127820843;hs7:127757919-127757919,hs11:23404608-23404608;hs7:157089773-157089773,hs7:157091014-157091014;hs9:75394745-75394745,hs20:16772828-16772828;hs12:53845486-53845486,hs20:5707706-5707706;hs20:7144623-7144623,hs20:7157143-7157143;hs20:46422302-46422302,hs20:46423898-46423898;hs20:57562332-57562332,hs20:57708381-57708381		Department of Molecular Cytogenetics, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan	Chromothripsis is the massive but highly localized chromosomal rearrangement in response to a one-step catastrophic event, rather than an accumulation of a series of subsequent and random alterations. Chromothripsis occurs commonly in various human cancers and is thought to be associated with increased malignancy and carcinogenesis. However, the causes and consequences of chromothripsis remain unclear. Therefore, to identify the mechanism underlying the generation of chromothripsis, we investigated whether chromothripsis could be artificially induced by ionizing radiation. We first elicited DNA double-strand breaks in an oral squamous cell carcinoma cell line HOC313-P and its highly metastatic subline HOC313-LM, using Single Particle Irradiation system to Cell (SPICE), a focused vertical microbeam system designed to irradiate a spot within the nuclei of adhesive cells, and then established irradiated monoclonal sublines from them, respectively. SNP array analysis detected a number of chromosomal copy number alterations (CNAs) in these sublines, and one HOC313-LM-derived monoclonal subline irradiated with 200 protons by the microbeam displayed multiple CNAs involved locally in chromosome 7. Multi-color FISH showed a complex translocation of chromosome 7 involving chromosomes 11 and 12. Furthermore, whole genome sequencing analysis revealed multiple de novo complex chromosomal rearrangements localized in chromosomes 2, 5, 7, and 20, resembling chromothripsis. These findings suggested that localized ionizing irradiation within the nucleus may induce chromothripsis-like complex chromosomal alterations via local DNA damage in the nucleus.	GRCh37/hg19				No	NA
CTDB0459	Research	26856307	Ernst A, Jones DT, Maass KK, Rode A, Deeg KI, Jebaraj BM, Korshunov A, Hovestadt V, Tainsky MA, Pajtler KW, Bender S, Brabetz S, Grobner S, Kool M, Devens F, Edelmann J, Zhang C, Castelo-Branco P, Tabori U, Malkin D, Rippe K, Stilgenbauer S, Pfister SM, Zapatka M, Lichter P	Telomere dysfunction and chromothripsis	Int J Cancer	2016 Jun	15	Li-Fraumeni syndrome	Next Generation Sequencing	Homo sapiens	LFS MDAH087 p145	Illumina MiSeq				Division of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany	Chromothripsis is a recently discovered form of genomic instability, characterized by tens to hundreds of clustered DNA rearrangements resulting from a single dramatic event. Telomere dysfunction has been suggested to play a role in the initiation of this phenomenon, which occurs in a large number of tumor entities. Here, we show that telomere attrition can indeed lead to catastrophic genomic events, and that telomere patterns differ between cells analyzed before and after such genomic catastrophes. Telomere length and telomere stabilization mechanisms diverge between samples with and without chromothripsis in a given tumor subtype. Longitudinal analyses of the evolution of chromothriptic patterns identify either stable patterns between matched primary and relapsed tumors, or loss of the chromothriptic clone in the relapsed specimen. The absence of additional chromothriptic events occurring between the initial tumor and the relapsed tumor sample points to telomere stabilization after the initial chromothriptic event which prevents further shattering of the genome.	GRCh37/hg19				Yes	NA
CTDB0460	Research	26856307	Ernst A, Jones DT, Maass KK, Rode A, Deeg KI, Jebaraj BM, Korshunov A, Hovestadt V, Tainsky MA, Pajtler KW, Bender S, Brabetz S, Grobner S, Kool M, Devens F, Edelmann J, Zhang C, Castelo-Branco P, Tabori U, Malkin D, Rippe K, Stilgenbauer S, Pfister SM, Zapatka M, Lichter P	Telomere dysfunction and chromothripsis	Int J Cancer	2016 Jun	8	Li-Fraumeni syndrome	Next Generation Sequencing	Homo sapiens	LFS MDAH172 p170	Illumina MiSeq				Division of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany	Chromothripsis is a recently discovered form of genomic instability, characterized by tens to hundreds of clustered DNA rearrangements resulting from a single dramatic event. Telomere dysfunction has been suggested to play a role in the initiation of this phenomenon, which occurs in a large number of tumor entities. Here, we show that telomere attrition can indeed lead to catastrophic genomic events, and that telomere patterns differ between cells analyzed before and after such genomic catastrophes. Telomere length and telomere stabilization mechanisms diverge between samples with and without chromothripsis in a given tumor subtype. Longitudinal analyses of the evolution of chromothriptic patterns identify either stable patterns between matched primary and relapsed tumors, or loss of the chromothriptic clone in the relapsed specimen. The absence of additional chromothriptic events occurring between the initial tumor and the relapsed tumor sample points to telomere stabilization after the initial chromothriptic event which prevents further shattering of the genome.	GRCh37/hg19				Yes	NA
CTDB0461	Research	26856307	Ernst A, Jones DT, Maass KK, Rode A, Deeg KI, Jebaraj BM, Korshunov A, Hovestadt V, Tainsky MA, Pajtler KW, Bender S, Brabetz S, Grobner S, Kool M, Devens F, Edelmann J, Zhang C, Castelo-Branco P, Tabori U, Malkin D, Rippe K, Stilgenbauer S, Pfister SM, Zapatka M, Lichter P	Telomere dysfunction and chromothripsis	Int J Cancer	2016 Jun	1	Li-Fraumeni syndrome	Next Generation Sequencing	Homo sapiens	LFS MDAH174 p84	Illumina MiSeq				Division of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany	Chromothripsis is a recently discovered form of genomic instability, characterized by tens to hundreds of clustered DNA rearrangements resulting from a single dramatic event. Telomere dysfunction has been suggested to play a role in the initiation of this phenomenon, which occurs in a large number of tumor entities. Here, we show that telomere attrition can indeed lead to catastrophic genomic events, and that telomere patterns differ between cells analyzed before and after such genomic catastrophes. Telomere length and telomere stabilization mechanisms diverge between samples with and without chromothripsis in a given tumor subtype. Longitudinal analyses of the evolution of chromothriptic patterns identify either stable patterns between matched primary and relapsed tumors, or loss of the chromothriptic clone in the relapsed specimen. The absence of additional chromothriptic events occurring between the initial tumor and the relapsed tumor sample points to telomere stabilization after the initial chromothriptic event which prevents further shattering of the genome.	GRCh37/hg19				Yes	NA
CTDB0462	Research	26856307	Ernst A, Jones DT, Maass KK, Rode A, Deeg KI, Jebaraj BM, Korshunov A, Hovestadt V, Tainsky MA, Pajtler KW, Bender S, Brabetz S, Grobner S, Kool M, Devens F, Edelmann J, Zhang C, Castelo-Branco P, Tabori U, Malkin D, Rippe K, Stilgenbauer S, Pfister SM, Zapatka M, Lichter P	Telomere dysfunction and chromothripsis	Int J Cancer	2016 Jun	15	Li-Fraumeni syndrome	Next Generation Sequencing	Homo sapiens	LFS MDAH041 p308	Illumina MiSeq				Division of Molecular Genetics, German Cancer Research Center (DKFZ), Heidelberg, Germany	Chromothripsis is a recently discovered form of genomic instability, characterized by tens to hundreds of clustered DNA rearrangements resulting from a single dramatic event. Telomere dysfunction has been suggested to play a role in the initiation of this phenomenon, which occurs in a large number of tumor entities. Here, we show that telomere attrition can indeed lead to catastrophic genomic events, and that telomere patterns differ between cells analyzed before and after such genomic catastrophes. Telomere length and telomere stabilization mechanisms diverge between samples with and without chromothripsis in a given tumor subtype. Longitudinal analyses of the evolution of chromothriptic patterns identify either stable patterns between matched primary and relapsed tumors, or loss of the chromothriptic clone in the relapsed specimen. The absence of additional chromothriptic events occurring between the initial tumor and the relapsed tumor sample points to telomere stabilization after the initial chromothriptic event which prevents further shattering of the genome.	GRCh37/hg19				Yes	NA
CTDB0463	Research	26833333	Cheng C, Zhou Y, Li H, Xiong T, Li S, Bi Y, Kong P, Wang F, Cui H, Li Y, Fang X, Yan T, Li Y, Wang J, Yang B, Zhang L, Jia Z, Song B, Hu X, Yang J, Qiu H, Zhang G, Liu J, Xu E, Shi R, Zhang Y, Liu H, He C, Zhao Z, Qian Y, Rong R, Han Z, Zhang Y, Luo W, Wang J, Peng S, Yang X, Li X, Li L, Fang H, Liu X, Ma L, Chen Y, Guo S, Chen X, Xi Y, Li G, Liang J, Yang X, Guo J, Jia J, Li Q, Cheng X, Zhan Q, Cui Y	Whole-Genome Sequencing Reveals Diverse Models of Structural Variations in Esophageal Squamous Cell Carcinoma	Am J Hum Genet	2016 Feb	3,8,10	Esophageal Squamous Cell Carcinoma	Next Generation Sequencing	Homo sapiens	ESCC-16T		chr10:0-18799686:0;chr10:107295464-107524429:-1;chr10:109152318-109161696:1;chr10:129314910-130150677:1;chr10:131665143-131805976:1;chr10:132021472-132043752:1;chr10:132608501-135534747:0;chr10:18799687-132608500:-1;chr10:36567859-37354034:-1;chr10:59338920-113561260:-1;chr10:64152636-85727158:-1;chr10:77889913-119683337:-1;chr10:86894560-87123885:-1;chr10:91938941-116723370:1;chr10:95986188-96920838:-1;chr10:97665896-97713580:-1;chr10:97716486-100342350:1;chr3:0-16233013:0;chr3:101580883-101630647:-1;chr3:101630648-102491180:0;chr3:102491181-102493196:-1;chr3:102493197-102497507:0;chr3:102497508-102498064:-1;chr3:102498065-113357003:0;chr3:113357004-113431917:-1;chr3:113431918-150469539:0;chr3:150469540-150471823:-1;chr3:150471824-195892079:0;chr3:16233014-16916643:-1;chr3:16916078-18001210:-1;chr3:18001211-25114479:0;chr3:195892080-195892363:1;chr3:195892364-198022430:0;chr3:25114480-25525392:1;chr3:25525393-36590902:0;chr3:36590903-63520366:1;chr3:41141612-63517257:-1;chr3:41428504-63288749:-1;chr3:44029942-44156406:-1;chr3:63510324-64078201:1;chr3:64078202-101580882:0;chr8:0-2511118:0;chr8:113632773-113669250:0;chr8:113669251-141013010:-1;chr8:115564476-115632269:-1;chr8:141013011-143600971:0;chr8:143600972-143601425:1;chr8:143601426-146364022:0;chr8:2511119-100010158:1;chr8:2534604-38155351:-1;chr8:3118861-3134815:-1;chr8:38223598-38541430:1;chr8:38328480-113632772:1;chr8:38556565-47790553:-1;chr8:38570827-38613056:-1;chr8:63003083-109359733:-1;chr8:84025443-113629666:-1;chr8:94392450-97126855:1;chr8:97479690-105063301:1	hs10:18799687-18799687,hs10:132608500-132608500;hs10:64152636-64152636,hs10:85727158-85727158;hs10:77889913-77889913,hs10:119683337-119683337;hs10:86894560-86894560,hs10:87123885-87123885;hs10:95986188-95986188,hs10:96920838-96920838;hs10:97665896-97665896,hs10:97713580-97713580;hs3:101580883-101580883,hs3:101630647-101630647;hs3:113357004-113357004,hs3:113431917-113431917;hs8:2534604-2534604,hs8:38155351-38155351;hs8:63003083-63003083,hs8:109359733-109359733;hs8:84025443-84025443,hs8:113629666-113629666;hs8:115564476-115564476,hs8:115632269-115632269;hs10:107295464-107295464,hs10:107524429-107524429;hs3:41428504-41428504,hs3:63288749-63288749;hs3:44029942-44029942,hs3:44156406-44156406;hs3:102491181-102491181,hs3:102493196-102493196;hs3:102497508-102497508,hs3:102498064-102498064;hs3:150469540-150469540,hs3:150471823-150471823;hs8:3118861-3118861,hs8:3134815-3134815;hs10:22788853-22788853,hs10:25446672-25446672;hs10:31335227-31335227,hs10:127456844-127456844;hs10:51114263-51114263,hs10:107644289-107644289;hs10:56257329-56257329,hs10:58800207-58800207;hs10:57931391-57931391,hs10:59669581-59669581;hs10:70162216-70162216,hs10:85727435-85727435;hs3:93655186-93655186,hs3:93656757-93656757;hs8:38528682-38528682,hs8:38545835-38545835;hs8:50553129-50553129,hs8:60712307-60712307;hs8:38186885-38186885,hs8:100009977-100009977;hs10:38408429-38408429,hs10:38409339-38409339;hs10:54735824-54735824,hs10:54740580-54740580;hs10:63494715-63494715,hs10:65127791-65127791;hs8:38327526-38327526,hs8:38365764-38365764;hs8:70871734-70871734,hs8:80980343-80980343;hs3:16916078-18001210,hs13:97656007-114591288;hs3:41141612-63517257,hs13:75527349-80875718;hs10:36567859-37354034,hs10:111273520-113129551;hs8:38570827-38613056,hs8:2525371-38505175;hs8:113669251-141013010,hs8:62349687-113632785;hs8:38556565-47790553,hs8:2516754-38344139;hs10:59338920-113561260,hs10:86796758-97716318;hs3:16233014-16916643,hs3:16233557-16818503;hs10:22610610-22610610,hs11:49907500-49907500;hs10:128157670-128157670,hs4:129909276-129909276;hs10:128157767-128157767,hs2:179505467-179505467;hs10:128158158-128158158,hs12:40431733-40431733;hs10:128158714-128158714,hs8:65121951-65121951;hs3:57460418-57460418,hs6:32459056-32459056;hs8:93409789-93409789,hsY:23951604-23951604	C10orf107;C10orf90;CLVS1;FGFR1;JMJD1C;LETM2;SLC2A13;TRAPPC9;WHSC1L1	Translational Medicine Research Center, Shanxi Medical University, Taiyuan, Shanxi 030001, China; Key Laboratory of Cellular Physiology, Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi 030001, China; Department of Pathology, the First Hospital, Shanxi Medical University, Taiyuan, Shanxi 030001, China	Comprehensive identification of somatic structural variations (SVs) and understanding their mutational mechanisms in cancer might contribute to understanding biological differences and help to identify new therapeutic targets. Unfortunately, characterization of complex SVs across the whole genome and the mutational mechanisms underlying esophageal squamous cell carcinoma (ESCC) is largely unclear. To define a comprehensive catalog of somatic SVs, affected target genes, and their underlying mechanisms in ESCC, we re-analyzed whole-genome sequencing (WGS) data from 31 ESCCs using Meerkat algorithm to predict somatic SVs and Patchwork to determine copy-number changes. We found deletions and translocations with NHEJ and alt-EJ signature as the dominant SV types, and 16% of deletions were complex deletions. SVs frequently led to disruption of cancer-associated genes (e.g., CDKN2A and NOTCH1) with different mutational mechanisms. Moreover, chromothripsis, kataegis, and breakage-fusion-bridge (BFB) were identified as contributing to locally mis-arranged chromosomes that occurred in 55% of ESCCs. These genomic catastrophes led to amplification of oncogene through chromothripsis-derived double-minute chromosome formation (e.g., FGFR1 and LETM2) or BFB-affected chromosomes (e.g., CCND1, EGFR, ERBB2, MMPs, and MYC), with approximately 30% of ESCCs harboring BFB-derived CCND1 amplification. Furthermore, analyses of copy-number alterations reveal high frequency of whole-genome duplication (WGD) and recurrent focal amplification of CDCA7 that might act as a potential oncogene in ESCC. Our findings reveal molecular defects such as chromothripsis and BFB in malignant transformation of ESCCs and demonstrate diverse models of SVs-derived target genes in ESCCs. These genome-wide SV profiles and their underlying mechanisms provide preventive, diagnostic, and therapeutic implications for ESCCs.	GRCh37/hg19				Yes	TRAPPC9,CLVS1;C10orf107,JMJD1C;C10orf90,SLC2A13
CTDB0464	Research	26689541	Genesio R, Fontana P, Mormile A, Casertano A, Falco M, Conti A, Franzese A, Mozzillo E, Nitsch L, Melis D	Constitutional chromothripsis involving the critical region of 9q21.13 microdeletion syndrome	Mol Cytogenet.	2015 Dec	9	Congenital abnormality	array CGH	Homo sapiens	26689541_1	NimbleGen CGX-6 PKI Array				Department of Molecular Medicine and Medical Biotechnology, Federico II University, Naples, Italy	Background: The chromothripsis is a biological phenomenon, first observed in tumors and then rapidly described in congenital disorders. The principle of the chromothripsis process is the occurrence of a local shattering to pieces and rebuilding of chromosomes in a random order. Congenital chromothripsis rearrangements often involve reciprocal rearrangements on multiple chromosomes and have been described as cause of contiguous gene syndromes. We hypothesize that chromothripsis could be responsible for known 9q21.13 microdeletion syndrome, causing a composite phenotype with additional features. CASE PRESENTATION: The case reported is a 16- years-old female with a complex genomic rearrangement of chromosome 9 including the critical region of 9q21.13 microdeletion syndrome. The patient presents with platelet disorder and thyroid dysfunction in addition to the classical neurobehavioral phenotype of the syndrome. CONCLUSIONS: The presence of multiple rearrangements on the same chromosome 9 and the rebuilding of chromosome in a random order suggested that the rearrangement could origin from an event of chromthripsis. To our knowledge this is the first report of congenital chromothripsis involving chromosome 9. Furthermore this is the only case of 9q21.13 microdeletion syndrome due to chromothripsis.	GRCh37/hg19				No	NA
CTDB0465	Research	26687355	Maciejowski J, Li Y, Bosco N, Campbell PJ, de Lange T	Chromothripsis and Kataegis Induced by Telomere Crisis	Cell	2015 Dec	4,13,X	Retinal pigment epithelial cell line RPE-1	Next Generation Sequencing	Homo sapiens	X-25	Illumina X-ten				Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA	Telomere crisis occurs during tumorigenesis when depletion of the telomere reserve leads to frequent telomere fusions. The resulting dicentric chromosomes have been proposed to drive genome instability. Here, we examine the fate of dicentric human chromosomes in telomere crisis. We observed that dicentric chromosomes invariably persisted through mitosis and developed into 50-200 um chromatin bridges connecting the daughter cells. Before their resolution at 3-20 hr after anaphase, the chromatin bridges induced nuclear envelope rupture in interphase, accumulated the cytoplasmic 3' nuclease TREX1, and developed RPA-coated single stranded (ss) DNA. CRISPR knockouts showed that TREX1 contributed to the generation of the ssDNA and the resolution of the chromatin bridges. Post-crisis clones showed chromothripsis and kataegis, presumably resulting from DNA repair and APOBEC editing of the fragmented chromatin bridge DNA. We propose that chromothripsis in human cancer may arise through TREX1-mediated fragmentation of dicentric chromosomes formed in telomere crisis.	GRCh37/hg19				No	NA
CTDB0466	Research	26687355	Maciejowski J, Li Y, Bosco N, Campbell PJ, de Lange T	Chromothripsis and Kataegis Induced by Telomere Crisis	Cell	2015 Dec	11,18,20	Retinal pigment epithelial cell line RPE-1	Next Generation Sequencing	Homo sapiens	X-29	Illumina X-ten				Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA	Telomere crisis occurs during tumorigenesis when depletion of the telomere reserve leads to frequent telomere fusions. The resulting dicentric chromosomes have been proposed to drive genome instability. Here, we examine the fate of dicentric human chromosomes in telomere crisis. We observed that dicentric chromosomes invariably persisted through mitosis and developed into 50-200 um chromatin bridges connecting the daughter cells. Before their resolution at 3-20 hr after anaphase, the chromatin bridges induced nuclear envelope rupture in interphase, accumulated the cytoplasmic 3' nuclease TREX1, and developed RPA-coated single stranded (ss) DNA. CRISPR knockouts showed that TREX1 contributed to the generation of the ssDNA and the resolution of the chromatin bridges. Post-crisis clones showed chromothripsis and kataegis, presumably resulting from DNA repair and APOBEC editing of the fragmented chromatin bridge DNA. We propose that chromothripsis in human cancer may arise through TREX1-mediated fragmentation of dicentric chromosomes formed in telomere crisis.	GRCh37/hg19				No	NA
CTDB0467	Research	26687355	Maciejowski J, Li Y, Bosco N, Campbell PJ, de Lange T	Chromothripsis and Kataegis Induced by Telomere Crisis	Cell	2015 Dec	8	Retinal pigment epithelial cell line RPE-1	Next Generation Sequencing	Homo sapiens	X-33	Illumina X-ten				Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA	Telomere crisis occurs during tumorigenesis when depletion of the telomere reserve leads to frequent telomere fusions. The resulting dicentric chromosomes have been proposed to drive genome instability. Here, we examine the fate of dicentric human chromosomes in telomere crisis. We observed that dicentric chromosomes invariably persisted through mitosis and developed into 50-200 um chromatin bridges connecting the daughter cells. Before their resolution at 3-20 hr after anaphase, the chromatin bridges induced nuclear envelope rupture in interphase, accumulated the cytoplasmic 3' nuclease TREX1, and developed RPA-coated single stranded (ss) DNA. CRISPR knockouts showed that TREX1 contributed to the generation of the ssDNA and the resolution of the chromatin bridges. Post-crisis clones showed chromothripsis and kataegis, presumably resulting from DNA repair and APOBEC editing of the fragmented chromatin bridge DNA. We propose that chromothripsis in human cancer may arise through TREX1-mediated fragmentation of dicentric chromosomes formed in telomere crisis.	GRCh37/hg19				No	NA
CTDB0468	Research	26687355	Maciejowski J, Li Y, Bosco N, Campbell PJ, de Lange T	Chromothripsis and Kataegis Induced by Telomere Crisis	Cell	2015 Dec	15	Retinal pigment epithelial cell line RPE-1	Next Generation Sequencing	Homo sapiens	X-37	Illumina X-ten				Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA	Telomere crisis occurs during tumorigenesis when depletion of the telomere reserve leads to frequent telomere fusions. The resulting dicentric chromosomes have been proposed to drive genome instability. Here, we examine the fate of dicentric human chromosomes in telomere crisis. We observed that dicentric chromosomes invariably persisted through mitosis and developed into 50-200 um chromatin bridges connecting the daughter cells. Before their resolution at 3-20 hr after anaphase, the chromatin bridges induced nuclear envelope rupture in interphase, accumulated the cytoplasmic 3' nuclease TREX1, and developed RPA-coated single stranded (ss) DNA. CRISPR knockouts showed that TREX1 contributed to the generation of the ssDNA and the resolution of the chromatin bridges. Post-crisis clones showed chromothripsis and kataegis, presumably resulting from DNA repair and APOBEC editing of the fragmented chromatin bridge DNA. We propose that chromothripsis in human cancer may arise through TREX1-mediated fragmentation of dicentric chromosomes formed in telomere crisis.	GRCh37/hg19				No	NA
CTDB0469	Research	26687355	Maciejowski J, Li Y, Bosco N, Campbell PJ, de Lange T	Chromothripsis and Kataegis Induced by Telomere Crisis	Cell	2015 Dec	7,12	Retinal pigment epithelial cell line RPE-1	Next Generation Sequencing	Homo sapiens	24-141	Illumina X-ten				Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA	Telomere crisis occurs during tumorigenesis when depletion of the telomere reserve leads to frequent telomere fusions. The resulting dicentric chromosomes have been proposed to drive genome instability. Here, we examine the fate of dicentric human chromosomes in telomere crisis. We observed that dicentric chromosomes invariably persisted through mitosis and developed into 50-200 um chromatin bridges connecting the daughter cells. Before their resolution at 3-20 hr after anaphase, the chromatin bridges induced nuclear envelope rupture in interphase, accumulated the cytoplasmic 3' nuclease TREX1, and developed RPA-coated single stranded (ss) DNA. CRISPR knockouts showed that TREX1 contributed to the generation of the ssDNA and the resolution of the chromatin bridges. Post-crisis clones showed chromothripsis and kataegis, presumably resulting from DNA repair and APOBEC editing of the fragmented chromatin bridge DNA. We propose that chromothripsis in human cancer may arise through TREX1-mediated fragmentation of dicentric chromosomes formed in telomere crisis.	GRCh37/hg19				No	NA
CTDB0470	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	6	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N407T	Complete Genomics				Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0471	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N783T	Complete Genomics			MYCN	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0472	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N492T	Complete Genomics			TERT	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0473	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N753T	Complete Genomics			TERT	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0474	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	2,5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N732T	Complete Genomics			MYCN;TERT	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0475	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	2,5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N538T	Complete Genomics			MYCN;TERT	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0476	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N752T	Complete Genomics			TERT	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0477	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	8	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N481T	Complete Genomics			MYC	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0478	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	1	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N790T	Complete Genomics				Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0479	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N089T	Complete Genomics			MYCN	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0480	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N106T	Complete Genomics			MYCN	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0481	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N608T	Complete Genomics			MYCN	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0482	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	2,19	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N637T	Complete Genomics			MYCN	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0483	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	2	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N834T	Complete Genomics			MYCN	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0484	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	1	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N814T	Complete Genomics				Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0485	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	7	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N576T	Complete Genomics				Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0486	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	5	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N804T	Complete Genomics				Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0487	Research	26523776	Valentijn LJ, Koster J, Zwijnenburg DA, Hasselt NE, van Sluis P, Volckmann R, van Noesel MM, George RE, Tytgat GA,, Molenaar JJ, Versteeg R	TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors	Nat Genet	2015 Dec	4,12,17	Neuroblastoma	Next Generation Sequencing	Homo sapiens	N770T	Complete Genomics			CDK4	Department of Oncogenomics, Academic Medical Center, Amsterdam, the Netherlands	Whole-genome sequencing detected structural rearrangements of TERT in 17 of 75 high-stage neuroblastomas, with five cases resulting from chromothripsis. Rearrangements were associated with increased TERT expression and targeted regions immediately up- and downstream of TERT, positioning a super-enhancer close to the breakpoints in seven cases. TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.	GRCh37/hg19				Yes	NA
CTDB0488	Research	26439695	Tang MH, Dahlgren M, Brueffer C, Tjitrowirjo T, Winter C, Chen Y, Olsson E, Wang K, Torngren T, Sjostrom M, Grabau D, Bendahl PO, Ryden L, Nimeus E, Saal LH, Borg A, Gruvberger-Saal SK	Remarkable similarities of chromosomal rearrangements between primary human breast cancers and matched distant metastases as revealed by whole-genome sequencing	Oncotarget	2015 Nov	17,19	Breast cancer	Next Generation Sequencing	Homo sapiens	P6	Illumina HiSeq 2000				Division of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden	To better understand and characterize chromosomal structural variation during breast cancer progression, we enumerated chromosomal rearrangements for 11 patients by performing low-coverage whole-genome sequencing of 11 primary breast tumors and their 13 matched distant metastases. The tumor genomes harbored a median of 85 (range 18-404) rearrangements per tumor, with a median of 82 (26-310) in primaries compared to 87 (18-404) in distant metastases. Concordance between paired tumors from the same patient was high with a median of 89% of rearrangements shared (range 61-100%), whereas little overlap was found when comparing all possible pairings of tumors from different patients (median 3%). The tumors exhibited diverse genomic patterns of rearrangements: some carried events distributed throughout the genome while others had events mostly within densely clustered chromothripsis-like foci at a few chromosomal locations. Irrespectively, the patterns were highly conserved between the primary tumor and metastases from the same patient. Rearrangements occurred more frequently in genic areas than expected by chance and among the genes affected there was significant enrichment for cancer-associated genes including disruption of TP53, RB1, PTEN, and ESR1, likely contributing to tumor development. Our findings are most consistent with chromosomal rearrangements being early events in breast cancer progression that remain stable during the development from primary tumor to distant metastasis.	GRCh37/hg19				Yes	NA
CTDB0489	Research	26439695	Tang MH, Dahlgren M, Brueffer C, Tjitrowirjo T, Winter C, Chen Y, Olsson E, Wang K, Torngren T, Sjostrom M, Grabau D, Bendahl PO, Ryden L, Nimeus E, Saal LH, Borg A, Gruvberger-Saal SK	Remarkable similarities of chromosomal rearrangements between primary human breast cancers and matched distant metastases as revealed by whole-genome sequencing	Oncotarget	2015 Nov	16,17	Breast cancer	Next Generation Sequencing	Homo sapiens	P16	Illumina HiSeq 2000				Division of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden	To better understand and characterize chromosomal structural variation during breast cancer progression, we enumerated chromosomal rearrangements for 11 patients by performing low-coverage whole-genome sequencing of 11 primary breast tumors and their 13 matched distant metastases. The tumor genomes harbored a median of 85 (range 18-404) rearrangements per tumor, with a median of 82 (26-310) in primaries compared to 87 (18-404) in distant metastases. Concordance between paired tumors from the same patient was high with a median of 89% of rearrangements shared (range 61-100%), whereas little overlap was found when comparing all possible pairings of tumors from different patients (median 3%). The tumors exhibited diverse genomic patterns of rearrangements: some carried events distributed throughout the genome while others had events mostly within densely clustered chromothripsis-like foci at a few chromosomal locations. Irrespectively, the patterns were highly conserved between the primary tumor and metastases from the same patient. Rearrangements occurred more frequently in genic areas than expected by chance and among the genes affected there was significant enrichment for cancer-associated genes including disruption of TP53, RB1, PTEN, and ESR1, likely contributing to tumor development. Our findings are most consistent with chromosomal rearrangements being early events in breast cancer progression that remain stable during the development from primary tumor to distant metastasis.	GRCh37/hg19				Yes	NA
CTDB0490	Research	26439695	Tang MH, Dahlgren M, Brueffer C, Tjitrowirjo T, Winter C, Chen Y, Olsson E, Wang K, Torngren T, Sjostrom M, Grabau D, Bendahl PO, Ryden L, Nimeus E, Saal LH, Borg A, Gruvberger-Saal SK	Remarkable similarities of chromosomal rearrangements between primary human breast cancers and matched distant metastases as revealed by whole-genome sequencing	Oncotarget	2015 Nov	11	Breast cancer	Next Generation Sequencing	Homo sapiens	P17	Illumina HiSeq 2000				Division of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden	To better understand and characterize chromosomal structural variation during breast cancer progression, we enumerated chromosomal rearrangements for 11 patients by performing low-coverage whole-genome sequencing of 11 primary breast tumors and their 13 matched distant metastases. The tumor genomes harbored a median of 85 (range 18-404) rearrangements per tumor, with a median of 82 (26-310) in primaries compared to 87 (18-404) in distant metastases. Concordance between paired tumors from the same patient was high with a median of 89% of rearrangements shared (range 61-100%), whereas little overlap was found when comparing all possible pairings of tumors from different patients (median 3%). The tumors exhibited diverse genomic patterns of rearrangements: some carried events distributed throughout the genome while others had events mostly within densely clustered chromothripsis-like foci at a few chromosomal locations. Irrespectively, the patterns were highly conserved between the primary tumor and metastases from the same patient. Rearrangements occurred more frequently in genic areas than expected by chance and among the genes affected there was significant enrichment for cancer-associated genes including disruption of TP53, RB1, PTEN, and ESR1, likely contributing to tumor development. Our findings are most consistent with chromosomal rearrangements being early events in breast cancer progression that remain stable during the development from primary tumor to distant metastasis.	GRCh37/hg19				Yes	NA
CTDB0491	Research	26439695	Tang MH, Dahlgren M, Brueffer C, Tjitrowirjo T, Winter C, Chen Y, Olsson E, Wang K, Torngren T, Sjostrom M, Grabau D, Bendahl PO, Ryden L, Nimeus E, Saal LH, Borg A, Gruvberger-Saal SK	Remarkable similarities of chromosomal rearrangements between primary human breast cancers and matched distant metastases as revealed by whole-genome sequencing	Oncotarget	2015 Nov	3	Breast cancer	Next Generation Sequencing	Homo sapiens	P20	Illumina HiSeq 2000				Division of Oncology and Pathology, Department of Clinical Sciences, Lund University, Lund, Sweden	To better understand and characterize chromosomal structural variation during breast cancer progression, we enumerated chromosomal rearrangements for 11 patients by performing low-coverage whole-genome sequencing of 11 primary breast tumors and their 13 matched distant metastases. The tumor genomes harbored a median of 85 (range 18-404) rearrangements per tumor, with a median of 82 (26-310) in primaries compared to 87 (18-404) in distant metastases. Concordance between paired tumors from the same patient was high with a median of 89% of rearrangements shared (range 61-100%), whereas little overlap was found when comparing all possible pairings of tumors from different patients (median 3%). The tumors exhibited diverse genomic patterns of rearrangements: some carried events distributed throughout the genome while others had events mostly within densely clustered chromothripsis-like foci at a few chromosomal locations. Irrespectively, the patterns were highly conserved between the primary tumor and metastases from the same patient. Rearrangements occurred more frequently in genic areas than expected by chance and among the genes affected there was significant enrichment for cancer-associated genes including disruption of TP53, RB1, PTEN, and ESR1, likely contributing to tumor development. Our findings are most consistent with chromosomal rearrangements being early events in breast cancer progression that remain stable during the development from primary tumor to distant metastasis.	GRCh37/hg19				Yes	NA
CTDB0492	Research	26312826	Bertelsen B, Nazaryan-Petersen L, Sun W, Mehrjouy MM, Xie G, Chen W, Hjermind LE, Taschner PE, Tumer Z	A germline chromothripsis event stably segregating in 11 individuals through three generations	Genet Med	2016 May	3	Gilles de la Tourette syndrome	Next Generation Sequencing	Homo sapiens	II-6	Illumina HiSeq2000		hs3:135821271-135827387,hs3:138506677-138509766;hs3:137890352-137896723,hs3:138510303-138516517;hs3:142214220-142218199,hs3:135827724-135833075;hs3:137728817-137735850,hs5:118834950-118841284;hs5:118826179-118833935,hs3:137876903-137889696;hs3:137845421-137852283,hs3:142218739-142223545	A4GNT;ATR;CLDN18;DBR1;DZIP1L;HSD17B4;PPP2R3A	Department of Clinical Genetics, Applied Human Molecular Genetics, Kennedy Center, Copenhagen University Hospital, Glostrup, Denmark	PURPOSE: Parentally transmitted germ-line chromothripsis (G-CTH) has been identified in only a few cases. Most of these rearrangements were stably transmitted, in an unbalanced form, from a healthy mother to her child with congenital abnormalities probably caused by de novo copy-number changes of dosage sensitive genes. We describe a G-CTH transmitted through three generations in 11 healthy carriers. METHODS: Conventional cytogenetic analysis, mate-pair sequencing, and polymerase chain reaction (PCR) were used to identify the chromosome rearrangement and characterize the breakpoints in all three generations. RESULTS: We identified an apparently balanced translocation t(3;5), later shown to be a G-CTH, in all individuals of a three-generation family. The G-CTH stably segregated without occurrence of additional rearrangements; however, several spontaneous abortions were reported, possibly due to unbalanced transmission. Although seven protein-coding genes are interrupted, no clinical features can be definitively attributed to the affected genes. However, it can be speculated that truncation of one of these genes, encoding ataxia-telangiectasia and Rad3-related protein kinase (ATR), a key component of the DNA damage response, may be related to G-CTH formation. CONCLUSION: G-CTH rearrangements are not always associated with abnormal phenotypes and may be misinterpreted as balanced two-way translocations, suggesting that G-CTH is an underdiagnosed phenomenon.Genet Med 18 5, 494-500.	GRCh37/hg19				No	CLDN18,HSD17B4;HSD17B4,DBR1
CTDB0493	Research	29073611	Kato T, Ouchi Y, Inagaki H, Makita Y, Mizuno S, Kajita M, Ikeda T, Takeuchi K, Kurahashi H	Genomic Characterization of Chromosomal Insertions: Insights into the Mechanisms Underlying Chromothripsis	Cytogenet Genome Res.	2017 Oct	4,14	Developmental delay	Next Generation Sequencing	Homo sapiens	case_1	Illumina HiSeq 1500	chr14:0-104549510:0;chr14:104549511-107285437:-1;chr14:107285438-107349540:0;chr4:0-156376845:0;chr4:156376846-169441822:1;chr4:169441823-190659208:0;chr4:190659209-190957473:1;chr4:190957474-191154276:0			Division of Molecular Genetics, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan	Chromosomal insertions are rare structural rearrangements, and the molecular mechanisms underlying their origin are unknown. In this study, we used whole genome sequencing to analyze breakpoints and junction sequences in 4 patients with chromosomal insertions. Our analysis revealed that none of the 4 cases involved a simple insertion mediated by a 3-chromosomal breakage and rejoining events. The inserted fragments consisted of multiple pieces derived from a localized genomic region, which were shuffled and rejoined in a disorderly fashion with variable copy number alterations. The junctions were blunt ended or with short microhomologies or short microinsertions, suggesting the involvement of nonhomologous end-joining. In one case, analysis of the parental origin of the chromosomes using nucleotide variations within the insertion revealed that maternal chromosomal segments were inserted into the paternal chromosome. This patient also carried both maternal alleles, suggesting the presence of zygotic trisomy. These data indicate that chromosomal shattering may occur in association with trisomy rescue in the early postzygotic stage.	GRCh37/hg19				no	NA
CTDB0494	Research	29073611	Kato T, Ouchi Y, Inagaki H, Makita Y, Mizuno S, Kajita M, Ikeda T, Takeuchi K, Kurahashi H	Genomic Characterization of Chromosomal Insertions: Insights into the Mechanisms Underlying Chromothripsis	Cytogenet Genome Res.	2017 Oct	8,10,12	Langer-Giedion syndrome	Next Generation Sequencing	Homo sapiens	case_3	Illumina HiSeq 1500	chr8:0-114340064:0;chr8:114340065-114527620:-1;chr8:114527621-114806299:0;chr8:114806300-114925879:-1;chr8:114925880-115101168:0;chr8:115101169-122616401:-1;chr8:122616402-146364022:0			Division of Molecular Genetics, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan	Chromosomal insertions are rare structural rearrangements, and the molecular mechanisms underlying their origin are unknown. In this study, we used whole genome sequencing to analyze breakpoints and junction sequences in 4 patients with chromosomal insertions. Our analysis revealed that none of the 4 cases involved a simple insertion mediated by a 3-chromosomal breakage and rejoining events. The inserted fragments consisted of multiple pieces derived from a localized genomic region, which were shuffled and rejoined in a disorderly fashion with variable copy number alterations. The junctions were blunt ended or with short microhomologies or short microinsertions, suggesting the involvement of nonhomologous end-joining. In one case, analysis of the parental origin of the chromosomes using nucleotide variations within the insertion revealed that maternal chromosomal segments were inserted into the paternal chromosome. This patient also carried both maternal alleles, suggesting the presence of zygotic trisomy. These data indicate that chromosomal shattering may occur in association with trisomy rescue in the early postzygotic stage.	GRCh37/hg19				no	NA
CTDB0495	Research	29073611	Kato T, Ouchi Y, Inagaki H, Makita Y, Mizuno S, Kajita M, Ikeda T, Takeuchi K, Kurahashi H	Genomic Characterization of Chromosomal Insertions: Insights into the Mechanisms Underlying Chromothripsis	Cytogenet Genome Res.	2017 Oct	7	Recurrent pregnancy loss	Next Generation Sequencing	Homo sapiens	case_4	Illumina HiSeq 1500	chr7:25471046¨C38067611:-1			Division of Molecular Genetics, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan	Chromosomal insertions are rare structural rearrangements, and the molecular mechanisms underlying their origin are unknown. In this study, we used whole genome sequencing to analyze breakpoints and junction sequences in 4 patients with chromosomal insertions. Our analysis revealed that none of the 4 cases involved a simple insertion mediated by a 3-chromosomal breakage and rejoining events. The inserted fragments consisted of multiple pieces derived from a localized genomic region, which were shuffled and rejoined in a disorderly fashion with variable copy number alterations. The junctions were blunt ended or with short microhomologies or short microinsertions, suggesting the involvement of nonhomologous end-joining. In one case, analysis of the parental origin of the chromosomes using nucleotide variations within the insertion revealed that maternal chromosomal segments were inserted into the paternal chromosome. This patient also carried both maternal alleles, suggesting the presence of zygotic trisomy. These data indicate that chromosomal shattering may occur in association with trisomy rescue in the early postzygotic stage.	GRCh37/hg19				no	NA
CTDB0493	Research	29073611	Kato T, Ouchi Y, Inagaki H, Makita Y, Mizuno S, Kajita M, Ikeda T, Takeuchi K, Kurahashi H	Genomic Characterization of Chromosomal Insertions: Insights into the Mechanisms Underlying Chromothripsis	Cytogenet Genome Res.	2017 Oct	4,14	Developmental delay	Next Generation Sequencing	Homo sapiens	case_1	Illumina HiSeq 1500	chr14:0-104549510:0;chr14:104549511-107285437:-1;chr14:107285438-107349540:0;chr4:0-156376845:0;chr4:156376846-169441822:1;chr4:169441823-190659208:0;chr4:190659209-190957473:1;chr4:190957474-191154276:0			Division of Molecular Genetics, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan	Chromosomal insertions are rare structural rearrangements, and the molecular mechanisms underlying their origin are unknown. In this study, we used whole genome sequencing to analyze breakpoints and junction sequences in 4 patients with chromosomal insertions. Our analysis revealed that none of the 4 cases involved a simple insertion mediated by a 3-chromosomal breakage and rejoining events. The inserted fragments consisted of multiple pieces derived from a localized genomic region, which were shuffled and rejoined in a disorderly fashion with variable copy number alterations. The junctions were blunt ended or with short microhomologies or short microinsertions, suggesting the involvement of nonhomologous end-joining. In one case, analysis of the parental origin of the chromosomes using nucleotide variations within the insertion revealed that maternal chromosomal segments were inserted into the paternal chromosome. This patient also carried both maternal alleles, suggesting the presence of zygotic trisomy. These data indicate that chromosomal shattering may occur in association with trisomy rescue in the early postzygotic stage.	GRCh37/hg19				no	NA
CTDB0494	Research	29073611	Kato T, Ouchi Y, Inagaki H, Makita Y, Mizuno S, Kajita M, Ikeda T, Takeuchi K, Kurahashi H	Genomic Characterization of Chromosomal Insertions: Insights into the Mechanisms Underlying Chromothripsis	Cytogenet Genome Res.	2017 Oct	8,10,12	Langer-Giedion syndrome	Next Generation Sequencing	Homo sapiens	case_3	Illumina HiSeq 1500	chr8:0-114340064:0;chr8:114340065-114527620:-1;chr8:114527621-114806299:0;chr8:114806300-114925879:-1;chr8:114925880-115101168:0;chr8:115101169-122616401:-1;chr8:122616402-146364022:0			Division of Molecular Genetics, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan	Chromosomal insertions are rare structural rearrangements, and the molecular mechanisms underlying their origin are unknown. In this study, we used whole genome sequencing to analyze breakpoints and junction sequences in 4 patients with chromosomal insertions. Our analysis revealed that none of the 4 cases involved a simple insertion mediated by a 3-chromosomal breakage and rejoining events. The inserted fragments consisted of multiple pieces derived from a localized genomic region, which were shuffled and rejoined in a disorderly fashion with variable copy number alterations. The junctions were blunt ended or with short microhomologies or short microinsertions, suggesting the involvement of nonhomologous end-joining. In one case, analysis of the parental origin of the chromosomes using nucleotide variations within the insertion revealed that maternal chromosomal segments were inserted into the paternal chromosome. This patient also carried both maternal alleles, suggesting the presence of zygotic trisomy. These data indicate that chromosomal shattering may occur in association with trisomy rescue in the early postzygotic stage.	GRCh37/hg19				no	NA
CTDB0495	Research	29073611	Kato T, Ouchi Y, Inagaki H, Makita Y, Mizuno S, Kajita M, Ikeda T, Takeuchi K, Kurahashi H	Genomic Characterization of Chromosomal Insertions: Insights into the Mechanisms Underlying Chromothripsis	Cytogenet Genome Res.	2017 Oct	7	Recurrent pregnancy loss	Next Generation Sequencing	Homo sapiens	case_4	Illumina HiSeq 1500	chr7:25471046¨C38067611:-1			Division of Molecular Genetics, Institute for Comprehensive Medical Science (ICMS), Fujita Health University, Toyoake, Japan	Chromosomal insertions are rare structural rearrangements, and the molecular mechanisms underlying their origin are unknown. In this study, we used whole genome sequencing to analyze breakpoints and junction sequences in 4 patients with chromosomal insertions. Our analysis revealed that none of the 4 cases involved a simple insertion mediated by a 3-chromosomal breakage and rejoining events. The inserted fragments consisted of multiple pieces derived from a localized genomic region, which were shuffled and rejoined in a disorderly fashion with variable copy number alterations. The junctions were blunt ended or with short microhomologies or short microinsertions, suggesting the involvement of nonhomologous end-joining. In one case, analysis of the parental origin of the chromosomes using nucleotide variations within the insertion revealed that maternal chromosomal segments were inserted into the paternal chromosome. This patient also carried both maternal alleles, suggesting the presence of zygotic trisomy. These data indicate that chromosomal shattering may occur in association with trisomy rescue in the early postzygotic stage.	GRCh37/hg19				no	NA
CTDB0496	Research	28787462	Rozenblum E, Sotelo-Silveira JR, Kim GY, Zhu JY, Lau CC, McNeil N, Korolevich S, Liao H,, Cherry JM, Munroe DJ,, Ried T, Meltzer PS, Kuehl WM, Roschke AV	Novel near-diploid ovarian cancer cell line derived from a highly aneuploid metastatic ovarian tumor	PLoS One	2017 Aug	18	Ovarian cancer	Array CGH	Homo sapiens	OVDM1-P18	Agilent CGH Microarray Kit 244A 				Genetics Branch, CCR, NCI, NIH, Bethesda, Maryland, United States of America	A new ovarian near-diploid cell line, OVDM1, was derived from a highly aneuploid serous ovarian metastatic adenocarcinoma. A metastatic tumor was obtained from a 47-year-old Ashkenazi Jewish patient three years after the first surgery removed the primary tumor, both ovaries, and the remaining reproductive organs. OVDM1 was characterized by cell morphology, genotyping, tumorigenic assay, mycoplasma testing, spectral karyotyping (SKY), and molecular profiling of the whole genome by aCGH and gene expression microarray. Targeted sequencing of a panel of cancer-related genes was also performed. Hierarchical clustering of gene expression data clearly confirmed the ovarian origin of the cell line. OVDM1 has a near-diploid karyotype with a low-level aneuploidy, but samples of the original metastatic tumor were grossly aneuploid. A number of single nucleotide variations (SNVs)/mutations were detected in OVDM1 and the metastatic tumor samples. Some of them were cancer-related according to COSMIC and HGMD databases (no founder mutations in BRCA1 and BRCA2 have been found). A large number of focal copy number alterations (FCNAs) were detected, including homozygous deletions (HDs) targeting WWOX and GATA4. Progression of OVDM1 from early to late passages was accompanied by preservation of the near-diploid status, acquisition of only few additional large chromosomal rearrangements and more than 100 new small FCNAs. Most of newly acquired FCNAs seem to be related to localized but massive DNA fragmentation (chromothripsis-like rearrangements). Newly developed near-diploid OVDM1 cell line offers an opportunity to evaluate tumorigenesis pathways/events in a minor clone of metastatic ovarian adenocarcinoma as well as mechanisms of chromothripsis.	GRCh35/hg17	GSE70264			Yes	NA
CTDB0497	Research	28787462	Rozenblum E, Sotelo-Silveira JR, Kim GY, Zhu JY, Lau CC, McNeil N, Korolevich S, Liao H,, Cherry JM, Munroe DJ,, Ried T, Meltzer PS, Kuehl WM, Roschke AV	Novel near-diploid ovarian cancer cell line derived from a highly aneuploid metastatic ovarian tumor	PLoS One	2017 Aug	18	Ovarian cancer	Array CGH	Homo sapiens	OVDM1-P30	Agilent CGH Microarray Kit 244A 				Genetics Branch, CCR, NCI, NIH, Bethesda, Maryland, United States of America	A new ovarian near-diploid cell line, OVDM1, was derived from a highly aneuploid serous ovarian metastatic adenocarcinoma. A metastatic tumor was obtained from a 47-year-old Ashkenazi Jewish patient three years after the first surgery removed the primary tumor, both ovaries, and the remaining reproductive organs. OVDM1 was characterized by cell morphology, genotyping, tumorigenic assay, mycoplasma testing, spectral karyotyping (SKY), and molecular profiling of the whole genome by aCGH and gene expression microarray. Targeted sequencing of a panel of cancer-related genes was also performed. Hierarchical clustering of gene expression data clearly confirmed the ovarian origin of the cell line. OVDM1 has a near-diploid karyotype with a low-level aneuploidy, but samples of the original metastatic tumor were grossly aneuploid. A number of single nucleotide variations (SNVs)/mutations were detected in OVDM1 and the metastatic tumor samples. Some of them were cancer-related according to COSMIC and HGMD databases (no founder mutations in BRCA1 and BRCA2 have been found). A large number of focal copy number alterations (FCNAs) were detected, including homozygous deletions (HDs) targeting WWOX and GATA4. Progression of OVDM1 from early to late passages was accompanied by preservation of the near-diploid status, acquisition of only few additional large chromosomal rearrangements and more than 100 new small FCNAs. Most of newly acquired FCNAs seem to be related to localized but massive DNA fragmentation (chromothripsis-like rearrangements). Newly developed near-diploid OVDM1 cell line offers an opportunity to evaluate tumorigenesis pathways/events in a minor clone of metastatic ovarian adenocarcinoma as well as mechanisms of chromothripsis.	GRCh35/hg17	GSE70264			Yes	NA
CTDB0498	Research	28643781	Behjati S, Tarpey PS, Haase K, Ye H, Young MD, Alexandrov LB, Farndon SJ, Collord G, Wedge DC, Martincorena I, Cooke SL, Davies H, Mifsud W, Lidgren M, Martin S, Latimer C, Maddison M, Butler AP, Teague JW, Pillay N, Shlien A, McDermott U, Futreal PA, Baumhoer D, Zaikova O, Bjerkehagen B, Myklebost O, Amary MF, Tirabosco R, Van Loo P, Stratton MR, Flanagan AM, Campbell PJ	Recurrent mutation of IGF signalling genes and distinct patterns of genomic rearrangement in osteosarcoma	Nat Commun	2017 Jun	17	Osteosarcoma	Next Generation Sequencing	Homo sapiens	PD13494a	Illumina HiSeq 2000 or 2500	chr17:0-525:0;chr17:10011784-12166176:-1;chr17:12166177-19613356:0;chr17:19613357-19631915:1;chr17:19631916-19637539:0;chr17:19637540-20115602:-1;chr17:20115603-37955801:0;chr17:2212616-6131809:0;chr17:37955802-39154663:-1;chr17:39154664-42027329:0;chr17:42027330-43183420:-1;chr17:43183421-46223221:0;chr17:46223222-47263785:-1;chr17:47263786-49209749:0;chr17:49209750-50524095:-1;chr17:50524096-52760719:0;chr17:526-2212615:-1;chr17:52760720-52869546:-1;chr17:52869547-55256018:0;chr17:55256019-59481373:-1;chr17:59481374-59483607:0;chr17:59483608-59496545:1;chr17:59496546-62072636:0;chr17:6131810-8099683:-1;chr17:62072637-62460996:-1;chr17:62460997-63642962:0;chr17:63642963-64366238:-1;chr17:64366239-66223666:0;chr17:66223667-66224617:1;chr17:66224618-68761858:0;chr17:68761859-70317514:-1;chr17:70317515-72407979:0;chr17:72407980-72852176:-1;chr17:72852177-75211311:0;chr17:75211312-76484046:-1;chr17:76484047-78925648:0;chr17:78925649-79447708:1;chr17:79447709-81195210:0;chr17:8099684-10011783:0	hs17:6002131-6002131,hs17:76512941-76512941;hs17:8195283-8195283,hs17:72278658-72278658;hs17:29435055-29435055,hs17:74696121-74696121;hs17:36621985-36621985,hs17:71799270-71799270;hs17:5031609-5031609,hs17:76995509-76995509;hs17:35727788-35727788,hs17:45352944-45352944;hs17:43371172-43371172,hs17:75207133-75207133;hs17:43489202-43489202,hs17:65411876-65411876;hs17:5998463-5998463,hs17:9262131-9262131;hs17:18219797-18219797,hs17:49243712-49243712;hs17:74465166-74465166,hs17:75204056-75204056;hs17:2397473-2397473,hs17:4445387-4445387;hs17:8938596-8938596,hs17:14020207-14020207;hs17:9050096-9050096,hs17:15953456-15953456;hs17:27066543-27066543,hs17:43149575-43149575;hs17:28070932-28070932,hs17:70760639-70760639;hs17:42947261-42947261,hs17:78036737-78036737;hs17:61370071-61370071,hs17:78039749-78039749;hs17:61325669-61325669,hs17:61459353-61459353;hs17:4983123-4983123,hs17:52980417-52980417;hs2:172724085-172724085,hs3:195029071-195029071;hs17:804709-804709,hs17:2163170-2163170;hs17:8988473-8988473,hs17:73253586-73253586;hs17:9052119-9052119,hs17:15428516-15428516;hs17:9874990-9874990,hs17:29510134-29510134;hs17:20083102-20083102,hs17:58318005-58318005;hs17:28731307-28731307,hs17:45348063-45348063;hs17:29447172-29447172,hs17:35722665-35722665;hs17:47858941-47858941,hs17:65008939-65008939;hs17:53367753-53367753,hs17:70752529-70752529;hs17:18167351-18167351,hs17:53145578-53145578;hs17:80586124-80586124,hs17:80586364-80586364;hs17:8343725-8343725,hs17:74460108-74460108;hs17:28739504-28739504,hs17:46661765-46661765;hs17:32174549-32174549,hs17:38395470-38395470;hs17:37963078-37963078,hs17:65228553-65228553;hs17:41975464-41975464,hs17:74711175-74711175;hs17:64404891-64404891,hs17:74734116-74734116;hs17:10458034-10458034,hs17:15219242-15219242;hs17:12481508-12481508,hs17:54236471-54236471;hs17:19342484-19342484,hs17:61318424-61318424;hs17:48054957-48054957,hs17:77977705-77977705;hs17:20557514-20557514,hs17:70441836-70441836;hs17:213366-213366,hs17:61382185-61382185;hs17:2651786-2651786,hs17:47250503-47250503;hs17:2654683-2654683,hs17:37973149-37973149;hs17:3412684-3412684,hs17:5867556-5867556;hs17:3419397-3419397,hs17:69428796-69428796;hs17:4449301-4449301,hs17:74806307-74806307;hs17:4545103-4545103,hs17:63334128-63334128;hs17:4940003-4940003,hs17:45990041-45990041;hs17:4949555-4949555,hs17:21946524-21946524;hs17:4952722-4952722,hs17:8995722-8995722;hs17:4980804-4980804,hs17:19640408-19640408;hs17:5028887-5028887,hs17:5859942-5859942;hs17:5760414-5760414,hs17:31795439-31795439;hs17:5764284-5764284,hs17:30935774-30935774;hs17:6132082-6132082,hs17:38049947-38049947;hs17:7336765-7336765,hs17:80594070-80594070;hs17:8099144-8099144,hs17:65404591-65404591;hs17:8201222-8201222,hs17:30329612-30329612;hs17:9232609-9232609,hs17:9640543-9640543;hs17:9269079-9269079,hs17:19790308-19790308;hs17:9645548-9645548,hs17:12728401-12728401;hs17:10136254-10136254,hs17:43378581-43378581;hs17:10470646-10470646,hs17:59626090-59626090;hs17:10511141-10511141,hs17:69575490-69575490;hs17:10657269-10657269,hs17:30323555-30323555;hs17:12987253-12987253,hs17:68736750-68736750;hs17:13104044-13104044,hs17:27068734-27068734;hs17:13366466-13366466,hs17:30922429-30922429;hs17:13403688-13403688,hs17:53891308-53891308;hs17:14016159-14016159,hs17:50499779-50499779;hs17:14519253-14519253,hs17:41307584-41307584;hs17:14687573-14687573,hs17:59629864-59629864;hs17:15189386-15189386,hs17:45982995-45982995;hs17:15961861-15961861,hs17:36811372-36811372;hs17:16995699-16995699,hs17:62683699-62683699;hs17:17002085-17002085,hs17:35149274-35149274;hs17:17098436-17098436,hs17:61684068-61684068;hs17:17192477-17192477,hs17:31791266-31791266;hs17:19846885-19846885,hs17:54810414-54810414;hs17:20471132-20471132,hs17:61462655-61462655;hs17:21952665-21952665,hs17:68744390-68744390;hs17:25777357-25777357,hs17:53344443-53344443;hs17:25785621-25785621,hs17:34833782-34833782;hs17:26206324-26206324,hs17:62102202-62102202;hs17:26245115-26245115,hs17:30103219-30103219;hs17:29199843-29199843,hs17:52760250-52760250;hs17:29504661-29504661,hs17:59564527-59564527;hs17:30110281-30110281,hs17:57347628-57347628;hs17:31196775-31196775,hs17:69793211-69793211;hs17:32178137-32178137,hs17:52653092-52653092;hs17:33701470-33701470,hs17:70436529-70436529;hs17:33711513-33711513,hs17:43388491-43388491;hs17:35046492-35046492,hs17:72008682-72008682;hs17:35049752-35049752,hs17:66745042-66745042;hs17:35151098-35151098,hs17:65020701-65020701;hs17:37772427-37772427,hs17:54815883-54815883;hs17:37775218-37775218,hs17:70371926-70371926;hs17:38377377-38377377,hs17:48922509-48922509;hs17:38380961-38380961,hs17:40603225-40603225;hs17:39129076-39129076,hs17:52867836-52867836;hs17:40601243-40601243,hs17:45892256-45892256;hs17:40827446-40827446,hs17:54228538-54228538;hs17:42806100-42806100,hs17:70364365-70364365;hs17:43486990-43486990,hs17:54146357-54146357;hs17:47356970-47356970,hs17:69156847-69156847;hs17:47842215-47842215,hs17:68742884-68742884;hs17:47854660-47854660,hs17:70294048-70294048;hs17:47937280-47937280,hs17:62669191-62669191;hs17:48335601-48335601,hs17:72892245-72892245;hs17:48338211-48338211,hs17:48929124-48929124;hs17:49598550-49598550,hs17:55481747-55481747;hs17:52640943-52640943,hs17:52971990-52971990;hs17:53136541-53136541,hs17:69674410-69674410;hs17:53877102-53877102,hs17:78291131-78291131;hs17:54141218-54141218,hs17:70720309-70720309;hs17:57082084-57082084,hs17:72383364-72383364;hs17:57970286-57970286,hs17:69666723-69666723;hs17:63629123-63629123,hs17:74621483-74621483;hs17:69128320-69128320,hs17:72432695-72432695;hs17:70305771-70305771,hs17:77969891-77969891;hs17:70305771-70305771,hs17:77969891-77969891;hs17:71794422-71794422,hs17:72013973-72013973;hs17:72379360-72379360,hs17:76991206-76991206;hs17:74258515-74258515,hs17:74808848-74808848	TP53;MAP2K4;NF1	Cancer Genome Project, Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK	Osteosarcoma is a primary malignancy of bone that affects children and adults. Here, we present the largest sequencing study of osteosarcoma to date, comprising 112 childhood and adult tumours encompassing all major histological subtypes. A key finding of our study is the identification of mutations in insulin-like growth factor (IGF) signalling genes in 8/112 (7%) of cases. We validate this observation using fluorescence in situ hybridization (FISH) in an additional 87 osteosarcomas, with IGF1 receptor (IGF1R) amplification observed in 14% of tumours. These findings may inform patient selection in future trials of IGF1R inhibitors in osteosarcoma. Analysing patterns of mutation, we identify distinct rearrangement profiles including a process characterized by chromothripsis and amplification. This process operates recurrently at discrete genomic regions and generates driver mutations. It may represent an age-independent mutational mechanism that contributes to the development of osteosarcoma in children and adults alike.	GRCh37/hg19				Yes	NA
CTDB0499	Research	28512242	Kloosterman WP, Coebergh van den Braak RRJ, Pieterse M, van Roosmalen MJ, Sieuwerts AM, Stangl C, Brunekreef R, Lalmahomed ZS, Ooft S, van Galen A, Smid M, Lefebvre A, Zwartkruis F, Martens JWM, Foekens JA, Biermann K, Koudijs MJ, Ijzermans JNM, Voest EE	A Systematic Analysis of Oncogenic Gene Fusions in Primary Colon Cancer	Cancer Res	2017 Jul	X	Colorectal cancer	Next Generation Sequencing	Homo sapiens	A1266	Illumina HiSeq2500 or NextSeq				Department of Genetics, Center for Molecular Medicine, University Medical Center Utrecht, CX Utrecht, the Netherlands	Genomic rearrangements that give rise to oncogenic gene fusions can offer actionable targets for cancer therapy. Here we present a systematic analysis of oncogenic gene fusions among a clinically well-characterized, prospectively collected set of 278 primary colon cancers spanning diverse tumor stages and clinical outcomes. Gene fusions and somatic genetic variations were identified in fresh frozen clinical specimens by Illumina RNA-sequencing, the STAR fusion gene detection pipeline, and GATK RNA-seq variant calling. We considered gene fusions to be pathogenically relevant when recurrent, producing divergent gene expression (outlier analysis), or as functionally important (e.g., kinase fusions). Overall, 2.5% of all specimens were defined as harboring a relevant gene fusion (kinase fusions 1.8%). Novel configurations of BRAF, NTRK3, and RET gene fusions resulting from chromosomal translocations were identified. An R-spondin fusion was found in only one tumor (0.35%), much less than an earlier reported frequency of 10% in colorectal cancers. We also found a novel fusion involving USP9X-ERAS formed by chromothripsis and leading to high expression of ERAS, a constitutively active RAS protein normally expressed only in embryonic stem cells. This USP9X-ERAS fusion appeared highly oncogenic on the basis of its ability to activate AKT signaling. Oncogenic fusions were identified only in lymph node-negative tumors that lacked BRAF or KRAS mutations. In summary, we identified several novel oncogenic gene fusions in colorectal cancer that may drive malignant development and offer new targets for personalized therapy. 	GRCh37/hg19				Yes	USP9X,ERAS
CTDB0500	Research	28260531	Collins RL, Brand H, Redin CE, Hanscom C, Antolik C, Stone MR, Glessner JT, Mason T, Pregno G, Dorrani N, Mandrile G, Giachino D, Perrin D, Walsh C, Cipicchio M, Costello M, Stortchevoi A, An JY, Currall BB, Seabra CM, Ragavendran A, Margolin L, Martinez-Agosto JA, Lucente D, Levy B, Sanders SJ, Wapner RJ, Quintero-Rivera F, Kloosterman W, Talkowski ME	Defining the diverse spectrum of inversions, complex structural variation, and chromothripsis in the morbid human genome	Genome Biol	2017 Mar	1,12,14,15	Autism spectrum disorder	Next Generation Sequencing	Homo sapiens	TL010	Illumina HiSeq 2000 /2500 	chr14:0-77704851:0;chr14:77704852-77739092:-1;chr14:77739093-107349540:0;chr6:0-99267814:0;chr6:102567331-102657383:-1;chr6:102657384-103737414:0;chr6:103737415-103763292:-1;chr6:103763293-116305817:0;chr6:116305818-116423965:-1;chr6:116423966-171115067:0;chr6:99267815-99840246:-1;chr6:99840247-102567330:0		LOC101927314;ASCC3;NT5DC1;LOC643770;NUMB;SLC41A2;ELMSAN1;DLST;RAD51B;ESRRB;COQ3;PNISR;AMD1;LAMA4;RGS6;TMEM63C;POMT2;SV2B;DNAL1;LAMA2;NCOA7;GPHN;FRK;ACOT2;POU3F2;FBXL4;FAXC;NGB	Molecular Neurogenetics Unit and Psychiatric and Neurodevelopmental Genetics Unit, Center for Genomic Medicine, and Department of Neurology, Massachusetts General Hospital, Boston, MA, 02114, USA	BACKGROUND: Structural variation (SV) influences genome organization and contributes to human disease. However, the complete mutational spectrum of SV has not been routinely captured in disease association studies. RESULTS: We sequenced 689 participants with autism spectrum disorder (ASD) and other developmental abnormalities to construct a genome-wide map of large SV. Using long-insert jumping libraries at 105X mean physical coverage and linked-read whole-genome sequencing from 10X Genomics, we document seven major SV classes at ~5 kb SV resolution. Our results encompass 11,735 distinct large SV sites, 38.1% of which are novel and 16.8% of which are balanced or complex. We characterize 16 recurrent subclasses of complex SV (cxSV), revealing that: (1) cxSV are larger and rarer than canonical SV; (2) each genome harbors 14 large cxSV on average; (3) 84.4% of large cxSVs involve inversion; and (4) most large cxSV (93.8%) have not been delineated in previous studies. Rare SVs are more likely to disrupt coding and regulatory non-coding loci, particularly when truncating constrained and disease-associated genes. We also identify multiple cases of catastrophic chromosomal rearrangements known as chromoanagenesis, including somatic chromoanasynthesis, and extreme balanced germline chromothripsis events involving up to 65 breakpoints and 60.6 Mb across four chromosomes, further defining rare categories of extreme cxSV. CONCLUSIONS: These data provide a foundational map of large SV in the morbid human genome and demonstrate a previously underappreciated abundance and diversity of cxSV that should be considered in genomic studies of human disease.	GRCh37/hg19				No	
CTDB0501	Research	28260531	Collins RL, Brand H, Redin CE, Hanscom C, Antolik C, Stone MR, Glessner JT, Mason T, Pregno G, Dorrani N, Mandrile G, Giachino D, Perrin D, Walsh C, Cipicchio M, Costello M, Stortchevoi A, An JY, Currall BB, Seabra CM, Ragavendran A, Margolin L, Martinez-Agosto JA, Lucente D, Levy B, Sanders SJ, Wapner RJ, Quintero-Rivera F, Kloosterman W, Talkowski ME	Defining the diverse spectrum of inversions, complex structural variation, and chromothripsis in the morbid human genome	Genome Biol	2017 Mar	2,7,8,9	Autism spectrum disorder	Next Generation Sequencing	Homo sapiens	UTR22	Illumina HiSeq 2000 /2500 	chr2:0-167032587:0;chr2:167032588-167393745:-1;chr2:167393746-243199373:0		AC0101273;WIPF1;XIRP2;ZNF385B;ACO1;NSMAF;FRMPD1;KIAA1715;TOX;UBAP2;SCN9A;SCN7A;LOC101929680	Molecular Neurogenetics Unit and Psychiatric and Neurodevelopmental Genetics Unit, Center for Genomic Medicine, and Department of Neurology, Massachusetts General Hospital, Boston, MA, 02114, USA	BACKGROUND: Structural variation (SV) influences genome organization and contributes to human disease. However, the complete mutational spectrum of SV has not been routinely captured in disease association studies. RESULTS: We sequenced 689 participants with autism spectrum disorder (ASD) and other developmental abnormalities to construct a genome-wide map of large SV. Using long-insert jumping libraries at 105X mean physical coverage and linked-read whole-genome sequencing from 10X Genomics, we document seven major SV classes at ~5 kb SV resolution. Our results encompass 11,735 distinct large SV sites, 38.1% of which are novel and 16.8% of which are balanced or complex. We characterize 16 recurrent subclasses of complex SV (cxSV), revealing that: (1) cxSV are larger and rarer than canonical SV; (2) each genome harbors 14 large cxSV on average; (3) 84.4% of large cxSVs involve inversion; and (4) most large cxSV (93.8%) have not been delineated in previous studies. Rare SVs are more likely to disrupt coding and regulatory non-coding loci, particularly when truncating constrained and disease-associated genes. We also identify multiple cases of catastrophic chromosomal rearrangements known as chromoanagenesis, including somatic chromoanasynthesis, and extreme balanced germline chromothripsis events involving up to 65 breakpoints and 60.6 Mb across four chromosomes, further defining rare categories of extreme cxSV. CONCLUSIONS: These data provide a foundational map of large SV in the morbid human genome and demonstrate a previously underappreciated abundance and diversity of cxSV that should be considered in genomic studies of human disease.	GRCh37/hg19				No	
CTDB0502	Research	28260531	Collins RL, Brand H, Redin CE, Hanscom C, Antolik C, Stone MR, Glessner JT, Mason T, Pregno G, Dorrani N, Mandrile G, Giachino D, Perrin D, Walsh C, Cipicchio M, Costello M, Stortchevoi A, An JY, Currall BB, Seabra CM, Ragavendran A, Margolin L, Martinez-Agosto JA, Lucente D, Levy B, Sanders SJ, Wapner RJ, Quintero-Rivera F, Kloosterman W, Talkowski ME	Defining the diverse spectrum of inversions, complex structural variation, and chromothripsis in the morbid human genome	Genome Biol	2017 Mar	19	Autism spectrum disorder	Next Generation Sequencing	Homo sapiens	TL009	Illumina HiSeq 2000 /2500 	chr19:0-16868159:0;chr19:16868160-22316097:-1;chr19:22316098-22477874:0;chr19:22477875-23580214:-1;chr19:23580215-29843543:0;chr19:29843544-30967207:-1;chr19:30967208-32841723:0;chr19:32841724-33908877:-1;chr19:33908878-35162171:0;chr19:35162172-35774420:-1;chr19:35774421-38262470:0;chr19:38262471-44025989:-1;chr19:44025990-51937752:0;chr19:51937753-52788019:-1;chr19:52788020-53006099:0;chr19:53006100-56225088:-1;chr19:56225089-58145137:0;chr19:58145138-58410428:1;chr19:58410429-59128983:0		ABHD8;ANKLE1;ANO8;ARMC6;ARRDC2;ATP13A1;B3GNT3;BABAM1;BST2;C19orf60;CCDC124;CERS1;CILP2;COLGALT1;COMP;COPE;CPAMD8;CRLF1;CRTC1;DDA1;DDX49;ELL;F2RL3;FAM129C;FCHO1;FKBP8;GATAD2A;GDF1;GDF15;GMIP;GTPBP3;HAPLN4;HAUS8;HOMER3;IFI30;IL12RB1;INSL3;ISYNA1;JAK3;JUND;KCNN1;KIAA1683;KLHL26;KXD1;LINC00663;LINC00664;LOC641367;LOC729966;LPAR2;LRRC25;LSM4;MAP1S;MAST3;MAU2;MEF2B;MEF2BNB;MEF2BNB-MEF2B;MIR1270-1;MIR1270-2;MIR3188;MIR3189;MPV17L2;MRPL34;MVB12A;MYO9B;NCAN;NDUFA13;NR2C2AP;NR2F6;NXNL1;OCEL1;PBX4;PDE4C;PGLS;PGPEP1;PIK3R2;PLVAP;RAB3A;RFXANK;RPL18A;SIN3B;SLC25A42;SLC27A1;SLC5A5;SNORA68;SSBP4;SUGP1;SUGP2;TM6SF2;TMEM161A;TMEM221;TMEM59L;TSSK6;UBA52;UNC13A;UPF1;USE1;USHBP1;YJEFN3;ZNF100;ZNF101;ZNF14;ZNF208;ZNF253;ZNF257;ZNF429;ZNF43;ZNF430;ZNF431;ZNF486;ZNF493;ZNF506;ZNF626;ZNF682;ZNF708;ZNF714;ZNF737;ZNF738;ZNF826P;ZNF85;ZNF90;ZNF93;IPO5P1;LINC01233;LOC100996349;LOC101929124;LOC101929144;LOC101929164;LOC440518;ZNF492;ZNF724P;ZNF728;ZNF730;ZNF91;ZNF98;ZNF99;C19orf12;CCNE1;PLEKHF1;POP4;URI1;VSTM2B;AC007773.2;ANKRD27;C19orf40;CEBPA;CEBPA-AS1;CEBPG;CEP89;DPY19L3;GPATCH1;LRP3;NUDT19;PDCD5;RGS9BP;RHPN2;SLC7A10;SLC7A9;TDRD12;WDR88;FAM187B;FXYD1;FXYD3;FXYD5;FXYD7;GRAMD1A;HPN;HPN-AS1;LGI4;LINC00904;LOC102723513;LOC400685;LSR;MIR6887;SCN1B;USF2;ZNF181;ZNF30;ZNF302;ZNF599;ZNF792;AC004603.4;AC006129.4;AC016582.2;ACTN4;ADCK4;AKT2;ARHGEF1;ATP1A3;ATP5SL;AXL;B3GNT8;B9D2;BCKDHA;BLVRB;C19orf33;C19orf47;C19orf54;CAPN12;CATSPERG;CCDC97;CCER2;CD177;CD79A;CEACAM1;CEACAM21;CEACAM3;CEACAM4;CEACAM5;CEACAM6;CEACAM7;CEACAM8;CIC;CLC;CNFN;CNTD2;CXCL17;CYP2A13;CYP2A6;CYP2A7;CYP2B6;CYP2B7P;CYP2F1;CYP2G1P;CYP2S1;DEDD2;DLL3;DMRTC2;DPF1;DYRK1B;ECH1;EGLN2;EID2;EID2B;EIF3K;ERF;ERICH4;EXOSC5;FAM98C;FBL;FBXO17;FBXO27;FCGBP;GGN;GMFG;GRIK5;GSK3A;HIPK4;HNRNPL;HNRNPUL1;IFNL1;IFNL2;IFNL3;IFNL4;ITPKC;KCNK6;LEUTX;LGALS13;LGALS14;LGALS16;LGALS17A;LGALS4;LGALS7;LGALS7B;LIPE;LIPE-AS1;LOC100129935;LOC100505622;LOC284344;LOC644554;LRFN1;LTBP4;LYPD3;LYPD4;MAP3K10;MAP4K1;MED29;MEGF8;MIA;MIA-RAB4B;MIR4323;MIR4530;MIR641;MIR6719;MIR6796;MIR6797;MIR8077;MRPS12;NCCRP1;NFKBIB;NUMBL;PAF1;PAFAH1B3;PAK4;PAPL;PCAT19;PHLDB3;PLD3;PLEKHG2;POU2F2;PPP1R14A;PRG1;PRR19;PRX;PSG1;PSG10P;PSG11;PSG2;PSG3;PSG4;PSG5;PSG6;PSG7;PSG8;PSG9;PSMC4;PSMD8;RAB4B;RAB4B-EGLN2;RABAC1;RASGRP4;RINL;RPS16;RPS19;RYR1;SAMD4B;SARS2;SELV;SERTAD1;SERTAD3;SHKBP1;SIPA1L3;SIRT2;SNRPA;SPINT2;SPRED3;SPTBN4;SUPT5H;SYCN;TEX101;TGFB1;TIMM50;TMEM145;TMEM91;TTC9B;WDR87;YIF1B;ZFP36;ZNF526;ZNF546;ZNF574;ZNF780A;ZNF780B;CEACAM18;FLJ30403;FPR1;FPR2;FPR3;HAS1;HCCAT3;LOC101928571;MIR125A;MIR643;MIR6801;MIR99B;MIRLET7E;PPP2R1A;SIGLEC12;SIGLEC14;SIGLEC5;SIGLEC6;SIGLEC8;SPACA6P;SPACA6P-AS;ZNF175;ZNF350;ZNF432;ZNF577;ZNF613;ZNF614;ZNF615;ZNF616;ZNF649;ZNF836;ZNF841;BIRC8;BRSK1;CACNG6;CACNG7;CACNG8;CCDC106;CDC42EP5;CNOT3;COX6B2;DNAAF3;DPRX;EPN1;EPS8L1;ERVV-1;ERVV-2;FAM71E2;FAM90A27P;FCAR;FIZ1;GP6;HSPBP1;IL11;ISOC2;KIR2DL1;KIR2DL3;KIR2DL4;KIR2DS4;KIR3DL1;KIR3DL2;KIR3DL3;KIR3DX1;LAIR1;LAIR2;LENG1;LENG8;LENG9;LILRA1;LILRA2;LILRA3;LILRA4;LILRA5;LILRA6;LILRB1;LILRB2;LILRB3;LILRB4;LILRB5;LILRP2;LOC100287534;LOC101928804;LOC284379;MBOAT7;MIR1283-1;MIR1283-2;MIR1323;MIR371A;MIR371B;MIR372;MIR373;MIR4752;MIR498;MIR512-1;MIR512-2;MIR515-1;MIR515-2;MIR516A1;MIR516A2;MIR516B1;MIR516B2;MIR517A;MIR517B;MIR517C;MIR518A1;MIR518A2;MIR518B;MIR518C;MIR518D;MIR518E;MIR518F;MIR519A1;MIR519A2;MIR519B;MIR519C;MIR519D;MIR519E;MIR520A;MIR520B;MIR520C;MIR520D;MIR520E;MIR520F;MIR520G;MIR520H;MIR521-1;MIR521-2;MIR522;MIR523;MIR524;MIR525;MIR526A1;MIR526A2;MIR526B;MIR527;MIR6802;MIR6803;MIR6804;MIR6805;MIR8061;MIR935;MYADM;NAT14;NCR1;NDUFA3;NLRP12;NLRP2;NLRP7;OSCAR;PPP1R12C;PPP6R1;PRKCG;PRPF31;PTPRH;RDH13;RNU6-35P;RNU6-64P;RPL28;RPS9;SBK2;SBK3;SHISA7;SSC5D;SUV420H2;SYT5;TARM1;TFPT;TMC4;TMEM150B;TMEM190;TMEM238;TMEM86B;TNNI3;TNNT1;TPM3P9;TSEN34;TTYH1;U2AF2;UBE2S;VN1R2;VN1R4;VSTM1;ZNF137P;ZNF160;ZNF28;ZNF320;ZNF321P;ZNF331;ZNF347;ZNF415;ZNF468;ZNF524;ZNF525;ZNF579;ZNF580;ZNF581;ZNF600;ZNF611;ZNF628;ZNF665;ZNF677;ZNF701;ZNF702P;ZNF761;ZNF765;ZNF784;ZNF808;ZNF813;ZNF816;ZNF816-ZNF321P;ZNF818P;ZNF83;ZNF845;ZNF865;FKBP1AP1;ZNF154;ZNF211;ZNF551;ZNF552;ZNF586;ZNF587;ZNF587B;ZNF671;ZNF776;ZNF814;ZSCAN4	Molecular Neurogenetics Unit and Psychiatric and Neurodevelopmental Genetics Unit, Center for Genomic Medicine, and Department of Neurology, Massachusetts General Hospital, Boston, MA, 02114, USA	BACKGROUND: Structural variation (SV) influences genome organization and contributes to human disease. However, the complete mutational spectrum of SV has not been routinely captured in disease association studies. RESULTS: We sequenced 689 participants with autism spectrum disorder (ASD) and other developmental abnormalities to construct a genome-wide map of large SV. Using long-insert jumping libraries at 105X mean physical coverage and linked-read whole-genome sequencing from 10X Genomics, we document seven major SV classes at ~5 kb SV resolution. Our results encompass 11,735 distinct large SV sites, 38.1% of which are novel and 16.8% of which are balanced or complex. We characterize 16 recurrent subclasses of complex SV (cxSV), revealing that: (1) cxSV are larger and rarer than canonical SV; (2) each genome harbors 14 large cxSV on average; (3) 84.4% of large cxSVs involve inversion; and (4) most large cxSV (93.8%) have not been delineated in previous studies. Rare SVs are more likely to disrupt coding and regulatory non-coding loci, particularly when truncating constrained and disease-associated genes. We also identify multiple cases of catastrophic chromosomal rearrangements known as chromoanagenesis, including somatic chromoanasynthesis, and extreme balanced germline chromothripsis events involving up to 65 breakpoints and 60.6 Mb across four chromosomes, further defining rare categories of extreme cxSV. CONCLUSIONS: These data provide a foundational map of large SV in the morbid human genome and demonstrate a previously underappreciated abundance and diversity of cxSV that should be considered in genomic studies of human disease.	GRCh37/hg19				No	
CTDB0503	Research	28201779	Abou-El-Ardat K, Seifert M, Becker K, Eisenreich S, Lehmann M, Hackmann K, Rump A, Meijer G, Carvalho B, Temme A, Schackert G, Schrock E, Krex D, Klink B	Comprehensive molecular characterization of multifocal glioblastoma proves its monoclonal origin and reveals novel insights into clonal evolution and heterogeneity of glioblastomas	Neuro Oncol	2017 Apr	2,12	Glioblastoma	Array CGH	Homo sapiens	patient_2	Agilent SurePrint G3 Human CGH Microarray Kit 2x400K 			MYCN; CDK4; MDM2	Institut fur Klinische Genetik, Medizinische Fakultat Carl Gustav Carus, Technische Universitat Dresden, Dresden, Germany	The evolution of primary glioblastoma (GBM) is poorly understood. Multifocal GBM (ie, multiple synchronous lesions in one patient) could elucidate GBM development. METHODS: We present the first comprehensive study of 12 GBM foci from 6 patients using array-CGH, spectral karyotyping, gene expression arrays, and next-generation sequencing. RESULTS: Multifocal GBMs genetically resemble primary GBMs. Comparing foci from the same patient proved their monoclonal origin. All tumors harbored alterations in the 3 GBM core pathways: RTK/PI3K, p53, and RB regulatory pathways with aberrations of EGFR and CDKN2A/B in all (100%) patients. This unexpected high frequency reflects a distinct genetic signature of multifocal GBMs and might account for their highly malignant and invasive phenotype. Surprisingly, the types of mutations in these genes/pathways were different in tumor foci from the same patients. For example, we found distinct mutations/aberrations in PTEN, TP53, EGFR, and CDKN2A/B, which therefore must have occurred independently and late during tumor development. We also identified chromothripsis as a late event and in tumors with wild-type TP53. Only 2 events were found to be early in all patients: single copy loss of PTEN and TERT promoter point mutations. CONCLUSIONS: Multifocal GBMs develop through parallel genetic evolution. The high frequency of alterations in 3 main pathways suggests that these are essential steps in GBM evolution; however, their late occurrence indicates that they are not founder events but rather subclonal drivers. This might account for the marked genetic heterogeneity seen in primary GBM and therefore has important implications for GBM therapy.	GRCh36/hg18				Yes	
CTDB0504	Research	28201779	Abou-El-Ardat K, Seifert M, Becker K, Eisenreich S, Lehmann M, Hackmann K, Rump A, Meijer G, Carvalho B, Temme A, Schackert G, Schrock E, Krex D, Klink B	Comprehensive molecular characterization of multifocal glioblastoma proves its monoclonal origin and reveals novel insights into clonal evolution and heterogeneity of glioblastomas	Neuro Oncol	2017 Apr	10	Glioblastoma	Array CGH	Homo sapiens	patient_6	Agilent SurePrint G3 Human CGH Microarray Kit 2x400K 				Institut fur Klinische Genetik, Medizinische Fakultat Carl Gustav Carus, Technische Universitat Dresden, Dresden, Germany	The evolution of primary glioblastoma (GBM) is poorly understood. Multifocal GBM (ie, multiple synchronous lesions in one patient) could elucidate GBM development. METHODS: We present the first comprehensive study of 12 GBM foci from 6 patients using array-CGH, spectral karyotyping, gene expression arrays, and next-generation sequencing. RESULTS: Multifocal GBMs genetically resemble primary GBMs. Comparing foci from the same patient proved their monoclonal origin. All tumors harbored alterations in the 3 GBM core pathways: RTK/PI3K, p53, and RB regulatory pathways with aberrations of EGFR and CDKN2A/B in all (100%) patients. This unexpected high frequency reflects a distinct genetic signature of multifocal GBMs and might account for their highly malignant and invasive phenotype. Surprisingly, the types of mutations in these genes/pathways were different in tumor foci from the same patients. For example, we found distinct mutations/aberrations in PTEN, TP53, EGFR, and CDKN2A/B, which therefore must have occurred independently and late during tumor development. We also identified chromothripsis as a late event and in tumors with wild-type TP53. Only 2 events were found to be early in all patients: single copy loss of PTEN and TERT promoter point mutations. CONCLUSIONS: Multifocal GBMs develop through parallel genetic evolution. The high frequency of alterations in 3 main pathways suggests that these are essential steps in GBM evolution; however, their late occurrence indicates that they are not founder events but rather subclonal drivers. This might account for the marked genetic heterogeneity seen in primary GBM and therefore has important implications for GBM therapy.	GRCh36/hg18				Yes	
CTDB0505	Research	28196983	Ratnaparkhe M, Hlevnjak M, Kolb T, Jauch A, Maass KK, Devens F, Rode A, Hovestadt V, Korshunov A, Pastorczak A, Mlynarski W, Sungalee S, Korbel J, Hoell J, Fischer U, Milde T, Kramm C, Nathrath M, Chrzanowska K, Tausch E, Takagi M, Taga T, Constantini S, Loeffen J, Meijerink J, Zielen S, Gohring G, Schlegelberger B, Maass E, Siebert R, Kunz J, Kulozik AE, Worst B, Jones DT, Pfister SM, Zapatka M, Lichter P, Ernst A	Genomic profiling of Acute lymphoblastic leukemia in ataxia telangiectasia patients reveals tight link between ATM mutations and chromothripsis	Leukemia	2017 Oct	14	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	patient_10	Illumina HiSeq X Ten				Division of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany	Recent developments in sequencing technologies led to the discovery of a novel form of genomic instability, termed chromothripsis. This catastrophic genomic event, involved in tumorigenesis, is characterized by tens to hundreds of simultaneously acquired locally clustered rearrangements on one chromosome. We hypothesized that leukemias developing in individuals with Ataxia Telangiectasia, who are born with two mutated copies of the ATM gene, an essential guardian of genome stability, would show a higher prevalence of chromothripsis due to the associated defect in DNA double-strand break repair. Using whole-genome sequencing, fluorescence in situ hybridization and RNA sequencing, we characterized the genomic landscape of Acute Lymphoblastic Leukemia (ALL) arising in patients with Ataxia Telangiectasia. We detected a high frequency of chromothriptic events in these tumors, specifically on acrocentric chromosomes, as compared with tumors from individuals with other types of DNA repair syndromes (27 cases total, 10 with Ataxia Telangiectasia). Our data suggest that the genomic landscape of Ataxia Telangiectasia ALL is clearly distinct from that of sporadic ALL. Mechanistically, short telomeres and compromised DNA damage response in cells of Ataxia Telangiectasia patients may be linked with frequent chromothripsis. Furthermore, we show that ATM loss is associated with increased chromothripsis prevalence in additional tumor entities.	GRCh37/hg19				Yes	
CTDB0506	Research	28196983	Ratnaparkhe M, Hlevnjak M, Kolb T, Jauch A, Maass KK, Devens F, Rode A, Hovestadt V, Korshunov A, Pastorczak A, Mlynarski W, Sungalee S, Korbel J, Hoell J, Fischer U, Milde T, Kramm C, Nathrath M, Chrzanowska K, Tausch E, Takagi M, Taga T, Constantini S, Loeffen J, Meijerink J, Zielen S, Gohring G, Schlegelberger B, Maass E, Siebert R, Kunz J, Kulozik AE, Worst B, Jones DT, Pfister SM, Zapatka M, Lichter P, Ernst A	Genomic profiling of Acute lymphoblastic leukemia in ataxia telangiectasia patients reveals tight link between ATM mutations and chromothripsis	Leukemia	2017 Oct	22	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	patient_11	Illumina HiSeq X Ten				Division of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany	Recent developments in sequencing technologies led to the discovery of a novel form of genomic instability, termed chromothripsis. This catastrophic genomic event, involved in tumorigenesis, is characterized by tens to hundreds of simultaneously acquired locally clustered rearrangements on one chromosome. We hypothesized that leukemias developing in individuals with Ataxia Telangiectasia, who are born with two mutated copies of the ATM gene, an essential guardian of genome stability, would show a higher prevalence of chromothripsis due to the associated defect in DNA double-strand break repair. Using whole-genome sequencing, fluorescence in situ hybridization and RNA sequencing, we characterized the genomic landscape of Acute Lymphoblastic Leukemia (ALL) arising in patients with Ataxia Telangiectasia. We detected a high frequency of chromothriptic events in these tumors, specifically on acrocentric chromosomes, as compared with tumors from individuals with other types of DNA repair syndromes (27 cases total, 10 with Ataxia Telangiectasia). Our data suggest that the genomic landscape of Ataxia Telangiectasia ALL is clearly distinct from that of sporadic ALL. Mechanistically, short telomeres and compromised DNA damage response in cells of Ataxia Telangiectasia patients may be linked with frequent chromothripsis. Furthermore, we show that ATM loss is associated with increased chromothripsis prevalence in additional tumor entities.	GRCh37/hg19				Yes	
CTDB0507	Research	28196983	Ratnaparkhe M, Hlevnjak M, Kolb T, Jauch A, Maass KK, Devens F, Rode A, Hovestadt V, Korshunov A, Pastorczak A, Mlynarski W, Sungalee S, Korbel J, Hoell J, Fischer U, Milde T, Kramm C, Nathrath M, Chrzanowska K, Tausch E, Takagi M, Taga T, Constantini S, Loeffen J, Meijerink J, Zielen S, Gohring G, Schlegelberger B, Maass E, Siebert R, Kunz J, Kulozik AE, Worst B, Jones DT, Pfister SM, Zapatka M, Lichter P, Ernst A	Genomic profiling of Acute lymphoblastic leukemia in ataxia telangiectasia patients reveals tight link between ATM mutations and chromothripsis	Leukemia	2017 Oct	14	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	patient_13	Illumina HiSeq X Ten				Division of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany	Recent developments in sequencing technologies led to the discovery of a novel form of genomic instability, termed chromothripsis. This catastrophic genomic event, involved in tumorigenesis, is characterized by tens to hundreds of simultaneously acquired locally clustered rearrangements on one chromosome. We hypothesized that leukemias developing in individuals with Ataxia Telangiectasia, who are born with two mutated copies of the ATM gene, an essential guardian of genome stability, would show a higher prevalence of chromothripsis due to the associated defect in DNA double-strand break repair. Using whole-genome sequencing, fluorescence in situ hybridization and RNA sequencing, we characterized the genomic landscape of Acute Lymphoblastic Leukemia (ALL) arising in patients with Ataxia Telangiectasia. We detected a high frequency of chromothriptic events in these tumors, specifically on acrocentric chromosomes, as compared with tumors from individuals with other types of DNA repair syndromes (27 cases total, 10 with Ataxia Telangiectasia). Our data suggest that the genomic landscape of Ataxia Telangiectasia ALL is clearly distinct from that of sporadic ALL. Mechanistically, short telomeres and compromised DNA damage response in cells of Ataxia Telangiectasia patients may be linked with frequent chromothripsis. Furthermore, we show that ATM loss is associated with increased chromothripsis prevalence in additional tumor entities.	GRCh37/hg19				Yes	
CTDB0508	Research	28196983	Ratnaparkhe M, Hlevnjak M, Kolb T, Jauch A, Maass KK, Devens F, Rode A, Hovestadt V, Korshunov A, Pastorczak A, Mlynarski W, Sungalee S, Korbel J, Hoell J, Fischer U, Milde T, Kramm C, Nathrath M, Chrzanowska K, Tausch E, Takagi M, Taga T, Constantini S, Loeffen J, Meijerink J, Zielen S, Gohring G, Schlegelberger B, Maass E, Siebert R, Kunz J, Kulozik AE, Worst B, Jones DT, Pfister SM, Zapatka M, Lichter P, Ernst A	Genomic profiling of Acute lymphoblastic leukemia in ataxia telangiectasia patients reveals tight link between ATM mutations and chromothripsis	Leukemia	2017 Oct	21	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	patient_16	Illumina HiSeq X Ten				Division of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany	Recent developments in sequencing technologies led to the discovery of a novel form of genomic instability, termed chromothripsis. This catastrophic genomic event, involved in tumorigenesis, is characterized by tens to hundreds of simultaneously acquired locally clustered rearrangements on one chromosome. We hypothesized that leukemias developing in individuals with Ataxia Telangiectasia, who are born with two mutated copies of the ATM gene, an essential guardian of genome stability, would show a higher prevalence of chromothripsis due to the associated defect in DNA double-strand break repair. Using whole-genome sequencing, fluorescence in situ hybridization and RNA sequencing, we characterized the genomic landscape of Acute Lymphoblastic Leukemia (ALL) arising in patients with Ataxia Telangiectasia. We detected a high frequency of chromothriptic events in these tumors, specifically on acrocentric chromosomes, as compared with tumors from individuals with other types of DNA repair syndromes (27 cases total, 10 with Ataxia Telangiectasia). Our data suggest that the genomic landscape of Ataxia Telangiectasia ALL is clearly distinct from that of sporadic ALL. Mechanistically, short telomeres and compromised DNA damage response in cells of Ataxia Telangiectasia patients may be linked with frequent chromothripsis. Furthermore, we show that ATM loss is associated with increased chromothripsis prevalence in additional tumor entities.	GRCh37/hg19				Yes	
CTDB0509	Research	28196983	Ratnaparkhe M, Hlevnjak M, Kolb T, Jauch A, Maass KK, Devens F, Rode A, Hovestadt V, Korshunov A, Pastorczak A, Mlynarski W, Sungalee S, Korbel J, Hoell J, Fischer U, Milde T, Kramm C, Nathrath M, Chrzanowska K, Tausch E, Takagi M, Taga T, Constantini S, Loeffen J, Meijerink J, Zielen S, Gohring G, Schlegelberger B, Maass E, Siebert R, Kunz J, Kulozik AE, Worst B, Jones DT, Pfister SM, Zapatka M, Lichter P, Ernst A	Genomic profiling of Acute lymphoblastic leukemia in ataxia telangiectasia patients reveals tight link between ATM mutations and chromothripsis	Leukemia	2017 Oct	14	Acute lymphoblastic leukemia	Next Generation Sequencing	Homo sapiens	patient_25	Illumina HiSeq X Ten				Division of Molecular Genetics, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany	Recent developments in sequencing technologies led to the discovery of a novel form of genomic instability, termed chromothripsis. This catastrophic genomic event, involved in tumorigenesis, is characterized by tens to hundreds of simultaneously acquired locally clustered rearrangements on one chromosome. We hypothesized that leukemias developing in individuals with Ataxia Telangiectasia, who are born with two mutated copies of the ATM gene, an essential guardian of genome stability, would show a higher prevalence of chromothripsis due to the associated defect in DNA double-strand break repair. Using whole-genome sequencing, fluorescence in situ hybridization and RNA sequencing, we characterized the genomic landscape of Acute Lymphoblastic Leukemia (ALL) arising in patients with Ataxia Telangiectasia. We detected a high frequency of chromothriptic events in these tumors, specifically on acrocentric chromosomes, as compared with tumors from individuals with other types of DNA repair syndromes (27 cases total, 10 with Ataxia Telangiectasia). Our data suggest that the genomic landscape of Ataxia Telangiectasia ALL is clearly distinct from that of sporadic ALL. Mechanistically, short telomeres and compromised DNA damage response in cells of Ataxia Telangiectasia patients may be linked with frequent chromothripsis. Furthermore, we show that ATM loss is associated with increased chromothripsis prevalence in additional tumor entities.	GRCh37/hg19				Yes	
CTDB0510	Research	28126037	Middelkamp S, van Heesch S, Braat AK, de Ligt J, van Iterson M, Simonis M, van Roosmalen MJ, Kelder MJ, Kruisselbrink E, Hochstenbach R, Verbeek NE, Ippel EF, Adolfs Y, Pasterkamp RJ, Kloosterman WP, Kuijk EW, Cuppen E	Molecular dissection of germline chromothripsis in a developmental context using patient-derived iPS cells	Genome Med	2017 Jan	1,3,7,12	Multiple congenital abnormalities and/or mental retardation	Next Generation Sequencing	Homo sapiens	28085746_patient	Illumina HiSeq 2500			AGR3;AGR2;TSPAN13;BZW2;ANKMY2;LRRC72;SOSTDC1;ISPD;MEOX2;agmo_7e;AGMO;PPM1H;C12orf61;MON2;USP15;FAM19A2;ETV1;DPYD;FOXP1;CNTN3;PDZRN3;EBLN2;PPP4R2;GXYLT2;SHQ1;RYBP;PROK2;GPR27;EIF4E3;foxp1_3b;hdac9_7g;HDAC9;FERD3L;TWIST1;dpyd_1b;PTBP2;RWDD3;TMEM56-RWDD3;TMEM56;ALG14;CNN3;SLC44A3;ROBO2;SRGAP1;TMEM5;DPY19L2;AVPR1A;ZNF717;THSD7A;TMEM106B;VWDE;SCIN;ARL4A;etv1_7d;DGKB;agmo_7d;AHR;SNX13;PRPS1L1;hdac9_7f	Center for Molecular Medicine and Cancer Genomics Netherlands, Division Biomedical Genetics, University Medical Center Utrecht, Universiteitsweg 100, Utrecht, 3584CG, The Netherlands	BACKGROUND: Germline chromothripsis causes complex genomic rearrangements that are likely to affect multiple genes and their regulatory contexts. The contribution of individual rearrangements and affected genes to the phenotypes of patients with complex germline genomic rearrangements is generally unknown. METHODS: To dissect the impact of germline chromothripsis in a relevant developmental context, we performed trio-based RNA expression analysis on blood cells, induced pluripotent stem cells (iPSCs), and iPSC-derived neuronal cells from a patient with de novo germline chromothripsis and both healthy parents. In addition, Hi-C and 4C-seq experiments were performed to determine the effects of the genomic rearrangements on transcription regulation of genes in the proximity of the breakpoint junctions. RESULTS: Sixty-seven genes are located within 1 Mb of the complex chromothripsis rearrangements involving 17 breakpoints on four chromosomes. We find that three of these genes (FOXP1, DPYD, and TWIST1) are both associated with developmental disorders and differentially expressed in the patient. Interestingly, the effect on TWIST1 expression was exclusively detectable in the patient's iPSC-derived neuronal cells, stressing the need for studying developmental disorders in the biologically relevant context. Chromosome conformation capture analyses show that TWIST1 lost genomic interactions with several enhancers due to the chromothripsis event, which likely led to deregulation of TWIST1 expression and contributed to the patient's craniosynostosis phenotype. CONCLUSIONS: We demonstrate that a combination of patient-derived iPSC differentiation and trio-based molecular profiling is a powerful approach to improve the interpretation of pathogenic complex genomic rearrangements. Here we have applied this approach to identify misexpression of TWIST1, FOXP1, and DPYD as key contributors to the complex congenital phenotype resulting from germline chromothripsis rearrangements.	GRCh37/hg19				No	
CTDB0511	Research	28099951	Suzuki E, Shima H, Toki M, Hanew K, Matsubara K, Kurahashi H, Narumi S, Ogata T, Kamimaki T, Fukami M	Complex X-Chromosomal Rearrangements in Two Women with Ovarian Dysfunction: Implications of Chromothripsis/Chromoanasynthesis-Dependent and -Independent Origins of Complex Genomic Alterations	Cytogenet Genome Res	2016	X	Ovarian Dysfunction	Array CGH	Homo sapiens	patient_1	Agilent SurePrint G3 Human Catalog 2x400K			SHOX;POF1B;DIAPH2;PGRMC1	Department of Molecular Endocrinology, National Research Institute for Child Health and Development, Tokyo, Japan	Our current understanding of the phenotypic consequences and the molecular basis of germline complex chromosomal rearrangements remains fragmentary. Here, we report the clinical and molecular characteristics of 2 women with germline complex X-chromosomal rearrangements. Patient 1 presented with nonsyndromic ovarian dysfunction and hyperthyroidism; patient 2 exhibited various Turner syndrome- associated symptoms including ovarian dysfunction, short stature, and autoimmune hypothyroidism. The genomic abnormalities of the patients were characterized by array-based comparative genomic hybridization, high-resolution karyotyping, microsatellite genotyping, X-inactivation analysis, and bisulfite sequencing. Patient 1 carried a rearrangement of unknown parental origin with a 46,X,der(X)(pter->p22.1::p11.23->q24::q21.3->q24::p11.4->pter) karyotype, indicative of a catastrophic chromosomal reconstruction due to chromothripsis/chromoanasynthesis. Patient 2 had a paternally derived isochromosome with a 46,X,der(X)(pter->p22.31::q22.1->q10::q10->q22.1::p22.31->pter) karyotype, which likely resulted from 2 independent, sequential events. Both patients showed completely skewed X inactivation. CpG sites at Xp22.3 were hypermethylated in patient 2. The results indicate that germline complex X-chromosomal rearrangements underlie nonsyndromic ovarian dysfunction and Turner syndrome. Disease-causative mechanisms of these rearrangements likely include aberrant DNA methylation, in addition to X-chromosomal mispairing and haploinsufficiency of genes escaping X inactivation. Notably, our data imply that germline complex X-chromosomal rearrangements are created through both chromothripsis/chromoanasynthesis-dependent and -independent processes.	GRCh37/hg19				No	
CTDB0512	Research	28085746	Koduru PR, Wilson K, Wen J, Garcia R, Patel S, Monaghan SA	Cytogenetic and Cytogenomic Microarray Characterization of Chromothripsis in Chromosome 8 Affecting MOZ/NCOA2 (TIF2), FGFR1, RUNX1T1, and RUNX1 in a Pediatric Acute Myeloid Leukemia	J Pediatr Hematol Oncol	2017 May	8	Acute myeloid leukemia	Array CGH	Homo sapiens	28085746_patient	Unknow			MOZ/NCOA2;FGFR1;RUNX1T1;RUNX1	Department of Pathology, UT Southwestern Medical Center, Dallas, TX	Concurrent perturbations in different driver genes have been reported primarily in lymphoma. In acute myeloid leukemia (AML), cases with concurrent alterations in 2 driver genes are infrequently reported. In contrast to pathogenetic pathways in lymphoma with concurrently perturbed genes, the initial gene alteration in AML arrests maturation and the alteration in the second gene promote self-renewal of the blasts. Here, we report a unique case of infantile leukemia in which chromothripsis in chromosome 8 completely altered the G-band structure and resulted in concurrent changes in MOZ/NCOA2, FGFR1, RUNX1T1, and RUNX1. These multiple-hit abnormalities in AML have not been reported previously.	GRCh37/hg19				Yes	FGFR1,RUNX1; RUNX1T1,RUNX1
CTDB0513	Research	27895713	Gu J, Reynolds A, Fang L, DeGraffenreid C, Sterns K, Patel KP, Medeiros LJ, Lin P, Lu X	Coexistence of iAMP21 and ETV6-RUNX1 fusion in an adolescent with B cell acute lymphoblastic leukemia: literature review of six additional cases	Mol Cytogenet	2016 Nov	21	B cell acute lymphoblastic leukemia	SNParray	Homo sapiens	27895713_patient	Affymetrix CytoScan HD array	chr21:0-15006456:0;chr21:15006457-19142414:1;chr21:19142415-24806258:0;chr21:24806259-27905650:1;chr21:27905651-28498599:0;chr21:28498600-28835696:1;chr21:28835697-29805879:0;chr21:29805880-31211807:1;chr21:31211808-31795183:0;chr21:31795184-41909261:1;chr21:41909262-42364148:0;chr21:42364149-48097372:1;chr21:48097373-48129895:0			School of Health Professions, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd. Unit 0002, Houston, TX 77030 USA	Intrachromosomal amplification of chromosome 21 (iAMP21) results from breakage-fusion-bridge cycles and chromothripsis is a distinct marker of a subgroup of B cell acute lymphoblastic leukemia (B-ALL) cases associated with a poor prognosis. iAMP21 accounts for 2% of pediatric B-ALL and occurs predominantly in older children or adolescents. ETV6-RUNX1 fusion, resulting from t(12;21)(p13;q22), is associated with an excellent outcome in younger children with B-ALL. Coexistence of iAMP21 with ETV6-RUNX1 fusion is extremely rare with limited clinical information available. RESULTS: We report the case of an 18-year old Caucasian man diagnosed with ETV6-RUNX1 fusion positive B-ALL. He was treated with intensive chemotherapy and achieved remission for 6 months before relapse, 15 months after the initial diagnosis. G-band karyotyping and Fluorescence in situ hybridization (FISH) analyses performed on bone marrow revealed complex abnormalities: 41,X,-Y,der(3)t(3;20)(p11.2;q11.2),-4,t(5;22)(q32;q11.2),del(9)(p13),dic(9;17)(p13;p11.2),t(12;21)(p13;q22),der(14)t(14;17)(p11.2;q11.2),der(17;22)(q11.2;q11.2),-20,add(21)(q22),-22[4]/46,XY[15] with an iAMP21 and an ETV6-RUNX1. Additional molecular studies confirmed ETV6-RUNX1 fusion and with a TP53 mutation. High-resolution single nucleotide polymorphism microarray (SNP array) revealed the iAMP21 to be chromothripsis of 21q and subsequent metaphase FISH further delineated complex genomic aberrations. Although the patient received intensive chemotherapy with allogenic stem cell transplant, he died 26 months after initial diagnosis. We searched the literature and identified six cases showing coexisting iAMP21 and ETV6-RUNX1. The median age for these six patients was 10 years (range, 2-18) and males predominated. The median overall survival (OS) was 28 months. CONCLUSIONS: Patients with B-ALL associated with both iAMP21 and ETV6-RUNX1 tend to be older children or adolescents and have a poor prognosis.	GRCh37/hg19				Yes	
CTDB0514	Research	27880765	Gu S, Szafranski P, Akdemir ZC, Yuan B, Cooper ML, Magrina MA, Bacino CA, Lalani SR, Breman AM, Smith JL, Patel A, Song RH, Bi W, Cheung SW, Carvalho CM, Stankiewicz P, Lupski JR	Mechanisms for Complex Chromosomal Insertions	PLoS Genet	2016 Nov	6	Individuals with complex chromosome insertions	Array CGH	Homo sapiens	Cplex5	Agilent 4 x 180K oligonucleotide arrays	chr6:111061823-112340466):1;chr6:143001529-143306155):-1;chr6:151111676-159718163):-1			Department of Molecular & Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America	Chromosomal insertions are genomic rearrangements with a chromosome segment inserted into a non-homologous chromosome or a non-adjacent locus on the same chromosome or the other homologue, constituting ~2% of nonrecurrent copy-number gains. Little is known about the molecular mechanisms of their formation. We identified 16 individuals with complex insertions among 56,000 individuals tested at Baylor Genetics using clinical array comparative genomic hybridization (aCGH) and fluorescence in situ hybridization (FISH). Custom high-density aCGH was performed on 10 individuals with available DNA, and breakpoint junctions were fine-mapped at nucleotide resolution by long-range PCR and DNA sequencing in 6 individuals to glean insights into potential mechanisms of formation. We observed microhomologies and templated insertions at the breakpoint junctions, resembling the breakpoint junction signatures found in complex genomic rearrangements generated by replication-based mechanism(s) with iterative template switches. In addition, we analyzed 5 families with apparently balanced insertion in one parent detected by FISH analysis and found that 3 parents had additional small copy-number variants (CNVs) at one or both sides of the inserting fragments as well as at the inserted sites. We propose that replicative repair can result in interchromosomal complex insertions generated through chromothripsis-like chromoanasynthesis involving two or three chromosomes, and cause a significant fraction of apparently balanced insertions harboring small flanking CNVs.	GRCh37/hg19	GSE89306			Unknow	
CTDB0515	Research	27880765	Gu S, Szafranski P, Akdemir ZC, Yuan B, Cooper ML, Magrina MA, Bacino CA, Lalani SR, Breman AM, Smith JL, Patel A, Song RH, Bi W, Cheung SW, Carvalho CM, Stankiewicz P, Lupski JR	Mechanisms for Complex Chromosomal Insertions	PLoS Genet	2016 Nov	X	Individuals with complex chromosome insertions	Array CGH	Homo sapiens	Cplex6	Agilent 4 x 180K oligonucleotide arrays	chrX:0-153354257:0;chrX:153354258-153505599:1;chrX:153400494-153406246:2;chrX:153505600-155270560:0			Department of Molecular & Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America	Chromosomal insertions are genomic rearrangements with a chromosome segment inserted into a non-homologous chromosome or a non-adjacent locus on the same chromosome or the other homologue, constituting ~2% of nonrecurrent copy-number gains. Little is known about the molecular mechanisms of their formation. We identified 16 individuals with complex insertions among 56,000 individuals tested at Baylor Genetics using clinical array comparative genomic hybridization (aCGH) and fluorescence in situ hybridization (FISH). Custom high-density aCGH was performed on 10 individuals with available DNA, and breakpoint junctions were fine-mapped at nucleotide resolution by long-range PCR and DNA sequencing in 6 individuals to glean insights into potential mechanisms of formation. We observed microhomologies and templated insertions at the breakpoint junctions, resembling the breakpoint junction signatures found in complex genomic rearrangements generated by replication-based mechanism(s) with iterative template switches. In addition, we analyzed 5 families with apparently balanced insertion in one parent detected by FISH analysis and found that 3 parents had additional small copy-number variants (CNVs) at one or both sides of the inserting fragments as well as at the inserted sites. We propose that replicative repair can result in interchromosomal complex insertions generated through chromothripsis-like chromoanasynthesis involving two or three chromosomes, and cause a significant fraction of apparently balanced insertions harboring small flanking CNVs.	GRCh37/hg19	GSE89306			Unknow	
CTDB0516	Research	27880765	Gu S, Szafranski P, Akdemir ZC, Yuan B, Cooper ML, Magrina MA, Bacino CA, Lalani SR, Breman AM, Smith JL, Patel A, Song RH, Bi W, Cheung SW, Carvalho CM, Stankiewicz P, Lupski JR	Mechanisms for Complex Chromosomal Insertions	PLoS Genet	2016 Nov	13,X	Individuals with complex chromosome insertions	Array CGH	Homo sapiens	Cplex11	Agilent 4 x 180K oligonucleotide arrays	chr13:0-111923013:0;chr13:10617231-107784175:2;chr13:109760818-110923670:2;chr13:111923014-113766342:-1;chr13:113766343-115169878:0;chrX:0-79677006:0;chrX:79677007-80247351:1;chrX:80247352-81758343:0;chrX:81758344-84170318:1;chrX:82128724-82575149:2;chrX:84170319-155270560:0			Department of Molecular & Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America	Chromosomal insertions are genomic rearrangements with a chromosome segment inserted into a non-homologous chromosome or a non-adjacent locus on the same chromosome or the other homologue, constituting ~2% of nonrecurrent copy-number gains. Little is known about the molecular mechanisms of their formation. We identified 16 individuals with complex insertions among 56,000 individuals tested at Baylor Genetics using clinical array comparative genomic hybridization (aCGH) and fluorescence in situ hybridization (FISH). Custom high-density aCGH was performed on 10 individuals with available DNA, and breakpoint junctions were fine-mapped at nucleotide resolution by long-range PCR and DNA sequencing in 6 individuals to glean insights into potential mechanisms of formation. We observed microhomologies and templated insertions at the breakpoint junctions, resembling the breakpoint junction signatures found in complex genomic rearrangements generated by replication-based mechanism(s) with iterative template switches. In addition, we analyzed 5 families with apparently balanced insertion in one parent detected by FISH analysis and found that 3 parents had additional small copy-number variants (CNVs) at one or both sides of the inserting fragments as well as at the inserted sites. We propose that replicative repair can result in interchromosomal complex insertions generated through chromothripsis-like chromoanasynthesis involving two or three chromosomes, and cause a significant fraction of apparently balanced insertions harboring small flanking CNVs.	GRCh37/hg19	GSE89306			Unknow	
CTDB0517	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	9	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0003	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0518	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	9,17,18,22	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0005	Illumina HiSeq 2500			CDKN2A; TP53;SMAD4	Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0519	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6,10	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0006	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0520	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	4	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0007	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0521	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	3,14,18,20	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0008	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0522	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	14	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0009	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0523	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6,22	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0010	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0524	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	9,13	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0016	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0525	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	12,17,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0017	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0526	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	19	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0022	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0527	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	17	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0025	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0528	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	17,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0026	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0529	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6,8,12,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Ashpc_0027	Illumina HiSeq 2500			SMAD4;GATA6	Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0530	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	4,7,8,10,12,18,21	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0015	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0531	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	12,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0044	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0532	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0072	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0533	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	9	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0077	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0534	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,14,15,18,20	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0080	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0535	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	4,5,6,8,10,14,15,20,22	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0081	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0536	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	8,13,15,16,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0082	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0537	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	12	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0085	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0538	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	7,11,14,15,16,22	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0101	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0539	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0104	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0540	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	3	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0105	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0541	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	7,12	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0109	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0542	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,3,6,8,17	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0111	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0543	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	10,12,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0132	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0544	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	8,14,18,19	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0145	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0545	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	16	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0162	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0546	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	19	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0170	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0547	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	9,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0171	Illumina HiSeq 2500			CDKN2A;SMAD4	Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0548	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	11	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0174	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0549	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	3,11,13	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0175	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0550	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	3,8,17,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0210	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0551	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6,10,12	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0217	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0552	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	12	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0226	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0553	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0228	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0554	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6,7,8,12,15,18,21	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0230	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0555	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,4,8	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0236	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0556	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	2,5,6,21,X	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0237	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0557	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	13	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0239	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0558	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	18,21	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0240	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0559	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	4,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0261	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0560	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,3,11	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0268	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0561	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	4,14,16,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0274	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0562	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	19,22	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0279	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0563	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6,9,11	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0287	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0564	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	3,4,9,12,18,20	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0290	Illumina HiSeq 2500			KRAS	Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0565	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,6,9,11,12,15,17	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0297	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0566	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	7,12	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0300	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0567	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	14,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0303	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0568	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	2,5,11	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0305	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0569	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0307	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0570	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,5	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0324	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0571	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	3,7,8,11,12,18	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0325	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0572	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	13	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0326	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0573	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0328	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0574	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	9	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0341	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0575	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0345	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0576	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,15	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0347	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0577	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	2,6,11,12,17,18,20,21	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0356	Illumina HiSeq 2500			KRAS	Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0578	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	11,16	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0387	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0579	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	14	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0407	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0580	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6,8	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0410	Illumina HiSeq 2500			c-MYC	Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0581	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	3	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0467	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0582	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	9	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0468	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0583	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	14,21	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0469	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0584	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	6	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0473	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0585	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	4,8,11	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0504	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0586	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,7,21	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0549	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0587	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	1,2,14,19	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	Pcsi_0572	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0588	Research	27732578	Notta F, Chan-Seng-Yue M, Lemire M, Li Y, Wilson GW, Connor AA, Denroche RE, Liang SB, Brown AM, Kim JC, Wang T, Simpson JT, Beck T, Borgida A, Buchner N, Chadwick D, Hafezi-Bakhtiari S, Dick JE, Heisler L, Hollingsworth MA, Ibrahimov E, Jang GH, Johns J, Jorgensen LG, Law C, Ludkovski O, Lungu I, Ng K, Pasternack D, Petersen GM, Shlush LI, Timms L, Tsao MS, Wilson JM, Yung CK, Zogopoulos G, Bartlett JM, Alexandrov LB, Real FX, Cleary SP, Roehrl MH, McPherson JD, Stein LD, Hudson TJ, Campbell PJ, Gallinger S	A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns	Nature	2016 Oct	2,4	Pancreatic cancer	Next Generation Sequencing	Homo sapiens	RAMP_0003	Illumina HiSeq 2500				Ontario Institute for Cancer Research, Toronto, Ontario M5G 0A3, Canada	Ancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently. A shortcoming of this model is that clonally expanded precursor lesions do not always belong to the tumour lineage, indicating that the evolutionary trajectory of the tumour lineage and precursor lesions can be divergent. This prevailing model of tumorigenesis has contributed to the clinical notion that pancreatic cancer evolves slowly and presents at a late stage. However, the propensity for this disease to rapidly metastasize and the inability to improve patient outcomes, despite efforts aimed at early detection, suggest that pancreatic cancer progression is not gradual. Here, using newly developed informatics tools, we tracked changes in DNA copy number and their associated rearrangements in tumour-enriched genomes and found that pancreatic cancer tumorigenesis is neither gradual nor follows the accepted mutation order. Two-thirds of tumours harbour complex rearrangement patterns associated with mitotic errors, consistent with punctuated equilibrium as the principal evolutionary trajectory. In a subset of cases, the consequence of such errors is the simultaneous, rather than sequential, knockout of canonical preneoplastic genetic drivers that are likely to set-off invasive cancer growth. These findings challenge the current progression model of pancreatic cancer and provide insights into the mutational processes that give rise to these aggressive tumours.	GRCh37/hg19				Yes	
CTDB0589	Research	27741277	Abaigar M, Robledo C, Benito R, Ramos F, Diez-Campelo M, Hermosin L, Sanchez-Del-Real J, Alonso JM, Cuello R, Megido M, Rodriguez JN, Martin-Nunez G, Aguilar C, Vargas M, Martin AA, Garcia JL, Kohlmann A, Del Canizo MC, Hernandez-Rivas JM	Chromothripsis Is a Recurrent Genomic Abnormality in High-Risk Myelodysplastic Syndromes	PLoS One	2016 Oct	13	Myelodysplastic syndrome	Array CGH	Homo sapiens	27741277_026	NimbleGen 12x135K Whole-Genome Tiling v3.0 Array	chr13:0-18544844:0;chr13:100224902-102938165:-1;chr13:102938166-103453456:0;chr13:103453457-104094273:-1;chr13:104094274-107995454:0;chr13:107995455-110269932:1;chr13:110269933-110284511:0;chr13:110284512-114302034:-1;chr13:114302035-114142980:0;chr13:18544845-20440119:1;chr13:20440120-20511838:0;chr13:20511839-24763687:1;chr13:24763688-24824898:0;chr13:24824899-25847533:1;chr13:25847534-25849288:0;chr13:25849289-30835598:1;chr13:30835599-31664375:0;chr13:31664376-32572721:-1;chr13:32572722-34556708:0;chr13:34556709-35149194:-1;chr13:35149195-35190755:0;chr13:35190756-35198796:1;chr13:35198797-35287334:0;chr13:35287335-49555063:-1;chr13:49555064-53646644:0;chr13:53646645-56086252:-1;chr13:56086253-59126704:0;chr13:59126705-59531321:-1;chr13:59531322-61887290:0;chr13:61887291-89466951:-1;chr13:89466952-89658313:0;chr13:89658314-93680622:1;chr13:93680623-93699130:0;chr13:93699131-95541444:-1;chr13:95541445-98460263:0;chr13:98460264-98747948:-1;chr13:98747949-100224901:0		LINC00417;ANKRD20A9P;RNU6-55P;RNU6-76P;LINC00408;LINC00442;RNU6-52P;TUBA3C;LOC101928697;ANKRD26P3;LINC00421;TPTE2;MPHOSPH8;PSPC1;ZMYM5;ZMYM2;LINC01072;GJA3;GJB2;GJB6;CRYL1;MIR4499;CRYL1;IFT88;IL17D;N6AMT2;XPO4;LINC00367;LATS2;SAP18;SKA3;MRPL57;LINC01046;MIPEPP3;LINC00539;ZDHHC20;MICU2;RNU6-59P;FGF9;LINC00424;LINC00540;BASP1P1;SGCG;RNU6-58P;SACS;SACS-AS1;LINC00327;TNFRSF19;MIPEP;C1QTNF9B-AS1;C1QTNF9B;ANKRD20A19P;SPATA13;MIR2276;SPATA13-AS1;C1QTNF9;PARP4;TPTE2P6;ATP12A;RNF17;CENPJ;TPTE2P1;PABPC3;AMER2;LINC00463;LINC01053;MTMR6;NUPL1;ATP8A2;RNU6-78P;ATP8A2;SHISA2;RNF6;CDK8;WASF3;GPR12;USP12;USP12-AS1;USP12-AS2;LINC00412;RPL21;SNORD102;SNORA27;RASL11A;GTF3A;MTIF3;RNU6-63P;LNX2;POLR1D;GSX1;PDX1-AS1;PDX1;ATP5EP2;CDX2;URAD;FLT3;PAN3-AS1;PAN3;RNU6-82P;FLT1;POMP;SLC46A3;RNU6-53P;MTUS2;MTUS2-AS1;SLC7A1;UBL3;LINC00297;LINC00572;LINC00544;KATNAL1;RNU6-64P;LINC00426;LINC01058;HMGB1;USPL1;ALOX5AP;LINC00398;RXFP2;EEF1DP3;FRY-AS1;FRY;ZAR1L;BRCA2;N4BP2L1;N4BP2L2;MINOS1P1;N4BP2L2-IT2;LINC00457;NBEA;NBEA;NBEA;MAB21L1;DCLK1;CCDC169-SOHLH2;SOHLH2;CCDC169;RNU6-71P;SPG20;SPG20-AS1;CCNA1;SERTM1;RFXAP;SMAD9;ALG5;EXOSC8;SUPT20H;CSNK1A1L;LINC01048;LINC00547;POSTN;TRPC4;LINC00571;UFM1;LINC00437;LINC00366;FREM2;RNU6-56P;STOML3;PROSER1;NHLRC3;LHFP;COG6;MIR4305;LINC00332;LINC00548;LINC00598;FOXO1;MIR320D1;MRPS31;SLC25A15;TPTE2P5;MIR621;SUGT1P3;ELF1;WBP4;MIR3168;KBTBD6;LOC101929140;KBTBD7;MTRF1;NAA16;RNU6-57P;OR7E37P;RGCC;VWA8;MIR5006;VWA8-AS1;DGKH;AKAP11;TNFSF11;FAM216B;LINC01050;LINC00428;EPSTI1;DNAJC15;LINC00400;ENOX1;ENOX1-AS2;CCDC122;LACC1;LINC00284;SMIM2-AS1;SMIM2;SMIM2-IT1;MIR8079;SERP2;TUSC8;TSC22D1;TSC22D1-AS1;LINC00330;NUFIP1;GPALPP1;LOC101929259;GTF2F2;RNU6-69P;KCTD4;TPT1;SNORA31;TPT1-AS1;SLC25A30;SLC25A30-AS1;COG3;ERICH6B;LINC01055;SPERT;SIAH3;ZC3H13;CPB2-AS1;CPB2;LCP1;LRRC63;LINC00563;KIAA0226L;RNU6-68P;LINC01198;LRCH1;ESD;HTR2A;HTR2A-AS1;LINC00562;SUCLA2;NUDT15;MED4;MED4-AS1;ITM2B;LINC00441;RB1;LPAR6;RCBTB2;LINC00462;CYSLTR2;FNDC3A;MLNR;CDADC1;CAB39L;SETDB2;PHF11;RCBTB1;LINC00458;MIR1297;MIR5007;LINC00358;LINC01075;LINC00448;LINC00376;LINC00395;OR7E156P;RNU6-81P;LOC102723968;MIR548X2;MIR4704;PCDH9;PCDH9-AS2;PCDH9-AS3;PCDH9-AS4;LINC00364;LINC00550;LINC00383;KLHL1;ATXN8OS;LINC00348;DACH1;MZT1;BORA;DIS3;PIBF1;RNU6-79P;KLF5;RNU6-66P;LINC00392;KLF12;LINC00381;LINC00347;CTAGE11P;TBC1D4;COMMD6;UCHL3;LMO7-AS1;LMO7;LMO7DN;LMO7DN-IT1;KCTD12;BTF3P11;IRG1;CLN5;FBXL3;MYCBP2;MYCBP2-AS1;SCEL;SCEL-AS1;SLAIN1;MIR3665;EDNRB-AS1;EDNRB;LINC01069;LINC00446;RNF219-AS1;POU4F1;RNF219;LINC00331;RBM26;RBM26-AS1;NDFIP2-AS1;NDFIP2;LINC01068;LINC01038;LINC00382;LINC01080;SPRY2;LINC00377;LINC00564;RNU6-67P;SLITRK1;LINC00333;LINC00375;LINC00351;RNU6-72P;SLITRK6;MIR4500HG;MIR4500;SLITRK5;LINC00397;LINC00433;LINC00440;LINC00559;MIR622;LIN01049;RNU-75P;LINC00410;LINC00380;LINC00379;MIR17HG;MIR17;MIR18A;MIR19A;MIR20A;MIR19B1;MIR92A1;GPC5;GPC5-AS2;MIR48AS;GPC5-AS1;LIN00363;GPC6;GPC6-AS2;GPC6-AS1;DCT;TGDS;GPR180;LOC101927248;SOX21;SOX21-AS1;LINC00557;ABCC4;CLDN10;CLDN10-AS1;STK24;SLC15A1;PCCA;PCCA-AS1;GGACT;TMTC4;NALCN-AS1;LINC00411;NALCN;ITGBL1;FGF14;MIR2681;MIR4705;FGF14-IT1;FGF14-AS1;FGF14-AS2;TPP2;METTL21C;CCDC168;TEX30;KDELC1;BIVM;BIVM-ERCC5;ERCC5;METTL21EP;LIG4;ABHD13;TNFSF13B;MYO16;MYO16-AS1;LINC00399;LINC00676;IRS2;LINC00396;COL4A1;COL4A1;COL4A2;MIR8073;COL4A2-AS1;RAB20;CARKD;CARS2;ING1;LINC00346;ANKRD10;LINC00431;LINC00368;ARHGEF7;ARHGEF7-AS1;LOC101060553;TEX29;LINC00354;LINC00403;SOX1;LINC01070;LOC101928730;LINC01044;SPACA7;TUBGCP3;ATP11AUN;ATP11A;ATP11A-AS1;MCF2L-AS1;MCF2L;F7;F10;F10-AS1;PROZ;PCID2;CUL4A;MIR8075;LAMP1;GRTP1;GRTP1-AS1;LOC101928841;ADPRHL1;DCUN1D2;TMCO3;TFDP1;ATP4B;GRK1;LINC00552;TMEM255B;GAS6-AS1;GAS6;GAS6-AS2;LINC00452;LINC00565;RASA3;CDC16;MIR548AR;MIR4502;UPF3A	Unidad de Diagnostico Molecular y Celular del Cancer, Centro de Investigacion del Cancer-IBMCC (USAL-CSIC), Salamanca, Spain	comparative genomic hybridization (aCGH) and next-generation sequencing (NGS) in a series of MDS and MDS/myeloproliferative neoplasms (MPN) patients. 301 patients diagnosed with MDS (n = 240) or MDS/MPN (n = 61) were studied at the time of diagnosis. A genome-wide analysis of DNA copy number abnormalities was performed. In addition, a mutational analysis of DNMT3A, TET2, RUNX1, TP53 and BCOR genes was performed by NGS in selected cases. 285 abnormalities were identified in 71 patients (23.6%). Three high-risk MDS cases (1.2%) displayed chromothripsis involving exclusively chromosome 13 and affecting some cancer genes: FLT3, BRCA2 and RB1. All three cases carried TP53 mutations as revealed by NGS. Moreover, in the whole series, the integrative analysis of aCGH and NGS enabled the identification of cryptic recurrent deletions in 2p23.3 (DNMT3A; n = 2.8%), 4q24 (TET2; n = 10%) 17p13 (TP53; n = 8.5%), 21q22 (RUNX1; n = 7%), and Xp11.4 (BCOR; n = 2.8%), while mutations in the non-deleted allele where found only in DNMT3A (n = 1), TET2 (n = 3), and TP53 (n = 4). These cryptic abnormalities were detected mainly in patients with normal (45%) or non-informative (15%) karyotype by conventional cytogenetics, except for those with TP53 deletion and mutation (15%), which had a complex karyotype. In addition to well-known copy number defects, the presence of chromothripsis involving chromosome 13 was a novel recurrent change in high-risk MDS patients. Array CGH analysis revealed the presence of cryptic abnormalities in genomic regions where MDS-related genes, such as TET2, DNMT3A, RUNX1 and BCOR, are located.	GRCh36/hg18	GSE67682			Yes	
CTDB0590	Research	27741277	Abaigar M, Robledo C, Benito R, Ramos F, Diez-Campelo M, Hermosin L, Sanchez-Del-Real J, Alonso JM, Cuello R, Megido M, Rodriguez JN, Martin-Nunez G, Aguilar C, Vargas M, Martin AA, Garcia JL, Kohlmann A, Del Canizo MC, Hernandez-Rivas JM	Chromothripsis Is a Recurrent Genomic Abnormality in High-Risk Myelodysplastic Syndromes	PLoS One	2016 Oct	13	Myelodysplastic syndrome	Array CGH	Homo sapiens	27741277_027	NimbleGen 12x135K Whole-Genome Tiling v3.0 Array	chr13:0-18544844:0;chr13:111268759-114302034:1;chr13:114302035-114142980:0;chr13:18544845-28026673:1;chr13:28026674-28092710:0;chr13:28092711-31753393:1;chr13:31753394-31778817:0;chr13:31778818-31923805:-1;chr13:31923806-31934278:0;chr13:31934279-32178937:1;chr13:32178938-32205508:0;chr13:32205509-34693503:-1;chr13:34693504-34738108:0;chr13:34738109-40773999:1;chr13:40774000-40964446:0;chr13:40964447-41385529:-1;chr13:41385530-41393215:0;chr13:41393216-46380250:1;chr13:46380251-46419481:0;chr13:46419482-51739755:-1;chr13:51739756-95471065:0;chr13:95471066-95645135:1;chr13:95645136-111268758:0		LINC00417;ANKRD20A9P;RNU6-55P;RNU6-76P;LINC00408;LINC00442;RNU6-52P;TUBA3C;LOC101928697;ANKRD26P3;LINC00421;TPTE2;MPHOSPH8;PSPC1;ZMYM5;ZMYM2;LINC01072;GJA3;GJB2;GJB6;CRYL1;MIR4499;IFT88;IL17D;N6AMT2;XPO4;LINC00367;LATS2;SAP18;SKA3;MRPL57;LINC01046;MIPEPP3;LINC00539;ZDHHC20;MICU2;RNU6-59P;FGF9;LINC00424;LINC00540;BASP1P1;SGCG;RNU6-58P;SACS;SACS-AS1;LINC00327;TNFRSF19;MIPEP;C1QTNF9B-AS1;C1QTNF9B;ANKRD20A19P;SPATA13;MIR2276;SPATA13-AS1;C1QTNF9;PARP4;TPTE2P6;ATP12A;RNF17;CENPJ;TPTE2P1;PABPC3;AMER2;LINC00463;LINC01053;MTMR6;NUPL1;ATP8A2;RNU6-78P;SHISA2;RNF6;CDK8;WASF3;GPR12;USP12;USP12-AS1;USP12-AS2;LINC00412;RPL21;SNORD102;SNORA27;RASL11A;GTF3A;MTIF3;RNU6-63P;LNX2;POLR1D;GSX1;PDX1-AS1;PDX1;ATP5EP2;CDX2;URAD;FLT3;FLT3;PAN3-AS1;PAN3;RNU6-82P;FLT1;POMP;SLC46A3;RNU6-53P;MTUS2;MTUS2-AS1;SLC7A1;UBL3;LINC00297;LINC00572;LINC00544;KATNAL1;RNU6-64P;LINC00426;LINC01058;HMGB1;USPL1;ALOX5AP;LINC00398;LINC00545;TEX26-AS1;MEDAG;TEX26;HSPH1;B3GALTL;RXFP2;RXFP2;EEF1DP3;EEF1DP3;FRY-AS1;FRY;FRY;ZAR1L;BRCA2;N4BP2L1;N4BP2L2;MINOS1P1;N4BP2L2-IT2;N4BP2L2;PDS5B;LINC00423;KL;STARD13;STARD13-AS;RFC3;LINC00457;NBEA;MAB21L1;DCLK1;SOHLH2;CCDC169-SOHLH2;CCDC169;RNU6-71P;SPG20;SPG20-AS1;CCNA1;SERTM1;RFXAP;SMAD9;ALG5;EXOSC8;SUPT20H;CSNK1A1L;LINC01048;LINC00547;POSTN;TRPC4;LINC00571;UFM1;LINC00437;LINC00366;FREM2;RNU6-56P;STOML3;PROSER1;NHLRC3;LHFP;COG6;MIR4305;LINC00332;LINC00548;LINC00598;FOXO1;MIR320D1;MRPS31;ELF1;WBP4;MIR3168;KBTBD6;LOC101929140;KBTBD7;MTRF1;NAA16;RNU6-57P;OR7E37P;RGCC;VWA8;MIR5006;VWA8-AS1;DGKH;AKAP11;TNFSF11;FAM216B;LINC01050;LINC00428;EPSTI1;DNAJC15;LINC00400;ENOX1;ENOX1-AS2;CCDC122;LACC1;LINC00284;SMIM2-AS1;SMIM2;SMIM2-IT1;MIR8079;SERP2;TUSC8;TSC22D1;TSC22D1-AS1;LINC00330;NUFIP1;GPALPP1;LOC101929259;GTF2F2;RNU6-69P;KCTD4;TPT1;SNORA31;TPT1-AS1;SLC25A30;SLC25A30-AS1;COG3;ERICH6B;LINC01055;SPERT;SIAH3;ZC3H13;CPB2-AS1;CPB2;LCP1;LRRC63;LINC00563;KIAA0226L;LINC01198;LRCH1;ESD;HTR2A;HTR2A-AS1;LINC00562;SUCLA2;NUDT15;MED4;MED4-AS1;ITM2B;LINC00441;RB1;LPAR6;RCBTB2;LINC00462;CYSLTR2;FNDC3A;MLNR;CDADC1;CAB39L;SETDB2;PHF11;RCBTB1;ARL11;EBPL;KPNA3;CTAGE10P;SPRYD7;DLEU2;MIR3613;TRIM13;KCNRG;MIR16-1;MIR15A;DLEU1;ST13P4;DLEU1-AS1;DLEU7;DLEU7-AS1;RNASEH2B-AS1;RNASEH2B;GUCY1B2;LINC00371;FAM124A;SERPINE3;MIR5693;INTS6;INTS6-AS1;MIR4703;WDFY2;CLDN10;CLDN10-AS1;DZIP1;ARHGEF7;TEX29;LINC00354;LINC00403;SOX1;LINC01070;LOC101928730;LINC01044;SPACA7;TUBGCP3;ATP11AUN;ATP11A;ATP11A-AS1;MCF2L-AS1;MCF2L;F7;F10;F10-AS1;PROZ;PCID2;CUL4A;MIR8075;LAMP1;GRTP1;GRTP1-AS1;LOC101928841;ADPRHL1;DCUN1D2;TMCO3;TFDP1;ATP4B;GRK1;LINC00552;TMEM255B;GAS6-AS1;GAS6;GAS6-AS2;LINC00452;LINC00565;RASA3;CDC16;MIR548AR;MIR4502;UPF3A	Unidad de Diagnostico Molecular y Celular del Cancer, Centro de Investigacion del Cancer-IBMCC (USAL-CSIC), Salamanca, Spain	comparative genomic hybridization (aCGH) and next-generation sequencing (NGS) in a series of MDS and MDS/myeloproliferative neoplasms (MPN) patients. 301 patients diagnosed with MDS (n = 240) or MDS/MPN (n = 61) were studied at the time of diagnosis. A genome-wide analysis of DNA copy number abnormalities was performed. In addition, a mutational analysis of DNMT3A, TET2, RUNX1, TP53 and BCOR genes was performed by NGS in selected cases. 285 abnormalities were identified in 71 patients (23.6%). Three high-risk MDS cases (1.2%) displayed chromothripsis involving exclusively chromosome 13 and affecting some cancer genes: FLT3, BRCA2 and RB1. All three cases carried TP53 mutations as revealed by NGS. Moreover, in the whole series, the integrative analysis of aCGH and NGS enabled the identification of cryptic recurrent deletions in 2p23.3 (DNMT3A; n = 2.8%), 4q24 (TET2; n = 10%) 17p13 (TP53; n = 8.5%), 21q22 (RUNX1; n = 7%), and Xp11.4 (BCOR; n = 2.8%), while mutations in the non-deleted allele where found only in DNMT3A (n = 1), TET2 (n = 3), and TP53 (n = 4). These cryptic abnormalities were detected mainly in patients with normal (45%) or non-informative (15%) karyotype by conventional cytogenetics, except for those with TP53 deletion and mutation (15%), which had a complex karyotype. In addition to well-known copy number defects, the presence of chromothripsis involving chromosome 13 was a novel recurrent change in high-risk MDS patients. Array CGH analysis revealed the presence of cryptic abnormalities in genomic regions where MDS-related genes, such as TET2, DNMT3A, RUNX1 and BCOR, are located.	GRCh36/hg18	GSE67682			Yes	
CTDB0591	Research	27741277	Abaigar M, Robledo C, Benito R, Ramos F, Diez-Campelo M, Hermosin L, Sanchez-Del-Real J, Alonso JM, Cuello R, Megido M, Rodriguez JN, Martin-Nunez G, Aguilar C, Vargas M, Martin AA, Garcia JL, Kohlmann A, Del Canizo MC, Hernandez-Rivas JM	Chromothripsis Is a Recurrent Genomic Abnormality in High-Risk Myelodysplastic Syndromes	PLoS One	2016 Oct	13	Myelodysplastic syndrome	Array CGH	Homo sapiens	27741277_072	NimbleGen 12x135K Whole-Genome Tiling v3.0 Array	chr13:0-20223376:0;chr13:105600013-114142980:0;chr13:20223377-21774751:1;chr13:21774752-26008549:0;chr13:26008550-26823821:-1;chr13:26823822-26843551:0;chr13:26843552-29141245:1;chr13:29141246-29153048:0;chr13:29153049-29574970:-1;chr13:29574971-29598385:0;chr13:29598386-31092176:1;chr13:31092177-31109870:0;chr13:31109871-31349780:-1;chr13:31349781-31421871:0;chr13:31421872-31860544:1;chr13:31860545-31902741:0;chr13:31902742-35957157:-1;chr13:35957158-38324761:0;chr13:38324762-38995506:-1;chr13:38995507-39018272:0;chr13:39018273-42380430:1;chr13:42380431-43688279:0;chr13:43688280-45546500:1;chr13:45546501-45555481:0;chr13:45555482-82820718:-1;chr13:82820719-82942589:0;chr13:82942590-83487314:1;chr13:83487315-83666678:0;chr13:83666679-88672589:-1;chr13:88672590-89658313:0;chr13:89658314-92345411:1;chr13:92345412-92419919:0;chr13:92419920-105600012:-1		GJB6;CRYL1;MIR4499;IFT88;IL17D;N6AMT2;XPO4;LINC00367;LATS2;SAP18;SKA3;MRPL57;LINC01046;MIPEPP3;LINC00539;ZDHHC20;MICU2;RNU6-59P;FGF9;ATP8A2;SHISA2;RNF6;CDK8;WASF3;GPR12;USP12;USP12-AS1;USP12-AS2;LINC00412;RPL21;SNORD102;SNORA27;RASL11A;GTF3A;MTIF3;RNU6-63P;LNX2;POLR1D;GSX1;PDX1-AS1;PDX1;ATP5EP2;CDX2;URAD;FLT3;PAN3-AS1;PAN3;RNU6-82P;FLT1;POMP;SLC46A3;RNU6-53P;MTUS2;MTUS2;MTUS2-AS1;SLC7A1;UBL3;LINC00297;LINC00572;LINC00544;KATNAL1;RNU6-64P;LINC00426;LINC01058;HMGB1;USPL1;ALOX5AP;LINC00398;LINC00545;TEX26-AS1;MEDAG;TEX26;HSPH1;B3GALTL;RXFP2;EEF1DP3;EEF1DP3;FRY-AS1;FRY;ZAR1L;BRCA2;N4BP2L1;N4BP2L2;MINOS1P1;N4BP2L2-IT2;N4BP2L2;PDS5B;LINC00423;KL;STARD13;STARD13-AS;RFC3;LINC00457;NBEA;MAB21L1;DCLK1;UFM1;LIN00437;LINC00366;FREM2;RNU6-56P;STOML3;PROSER1;NHLRC3;LHFP;COG6;MIR4305;LINC00332;LINC00548;LINC00598;FOXO1;MIR320D1;MRPS31;SLC25A15;TPTE2P5;MIR621;SUGT1P3;ELF1;WBP4;MIR3168;KBTBD6;LOC101929140;KBTBD7;MTRF1;NAA16;RNU6-57P;OR7E37P;RGCC;VWA8;MIR5006;VWA8-AS1;DGKH;AKAP11;ENOX1;CCDC122;LACC1;LINC00284;SMIM2-AS1;SMIM2;SMIM2-IT1;MIR8079;SERP2;TUSC8;TSC22D1;TSC22D1-AS1;LINC00330;NUFIP1;GPALPP1;LOC101929259;GTF2F2;RNU6-69P;KCTD4;TPT1;SNORA31;TPT1-AS1;SLC25A30;SLC25A30-AS1;COG3;ERICH6B;ERICH6B;LINC01055;SPERT;SIAH3;ZC3H13;CPB2-AS1;CPB2;LCP1;LRRC63;LINC00563;KIAA0226L;RNU6-68P;LINC01198;LRCH1;ESD;HTR2A;HTR2A-AS1;LINC00562;SUCLA2;NUDT15;MED4;MED4-AS1;ITM2B;LINC00441;RB1;LPAR6;RCBTB2;LINC00462;CYSLTR2;FNDC3A;MLNR;CDADC1;CAB39L;SETDB2;PHF11;RCBTB1;ARL11;EBPL;KPNA3;CTAGE10P;SPRYD7;DLEU2;MIR3613;TRIM13;KCNRG;MIR16-1;MIR15A;DLEU1;ST13P4;DLEU1-AS1;DLEU7;DLEU7-AS1;RNASEH2B-AS1;RNASEH2B;GUCY1B2;LINC00371;FAM124A;SERPINE3;MIR5693;INTS6;INTS6-AS1;MIR4703;WDFY2;DHRS12;LINC00282;CCDC70;ATP7B;ALG11;UTP14C;NEK5;LOC101929657;NEK3;MRPS31P5;LOC103191607;THSD1;VPS36;CKAP2;TPTE2P3;HNRNPA1L2;SUGT1;LECT1;MIR759;PCDH8;OLFM4;LINC01065;LINC00558;LINC00458;MIR1297;MIR5007;PRR20C;PRR20B;PRR20A;PRR20D;PRR20E;PCDH17;LOC101926897;DIAPH3;DIAPH3-AS1;DIAPH3-AS2;LINC00434;TDRD3;LINC00378;MIR3169;PCDH20;LINC00358;LINC01075;LINC00448;LINC00376;LINC00395;OR7E156P;RNU6-81P;LOC102723968;MIR548X2;MIR4704;PCDH9;PCDH9-AS2;PCDH9-AS3;PCDH9-AS4;LINC00364;LINC00550;LINC00383;KLHL1;ATXN8OS;LINC00348;DACH1;MZT1;BORA;DIS3;PIBF1;RNU6-79P;KLF5;RNU6-66P;LINC00392;KLF12;LINC00381;LINC00347;CTAGE11P;TBC1D4;COMMD6;UCHL3;LMO7-AS1;LMO7;LMO7DN;LMO7DN-IT1;KCTD12;BTF3P11;IRG1;CLN5;FBXL3;MYCBP2;MYCBP2-AS1;SCEL;SCEL-AS1;SLAIN1;MIR3665;EDNRB-AS1;EDNRB;LINC01069;LINC00446;RNF219-AS1;POU4F1;RNF219;LINC00331;RBM26;RBM26-AS1;NDFIP2-AS1;NDFIP2;LINC01068;LINC01038;LINC00382;LINC01080;SPRY2;LINC00377;LINC00564;RNU6-67P;SLITRK1;LINC00333;LIN00375;LINC00351;RNU6-72P;SLITRK6;MIR4500HG;MIR4500;SLITRK5;LINC00397;LINC00433;LINC00559;MIR622;LINC01049;RNU6-75P;LINC00410;LINC00380;LINC00379;MIR17HG;MIR17;MIR18A;MIR19A;MIR20A;MIR19B1;MIR92A1;GPC5;GPC5-AS2;GPC5;MIR548AS;GPC5-AS1;LINC00363;GPC6;GPC6-AS2;GPC6-AS1;DCT;TGDS;GPR180;LOC101927248;SOX21;SOX21-AS1;LOC101927284;LINC00557;ABCC4;CLDN10;CLDN10-AS1;DZIP1;DNAJC3;UGGT2;HS6ST3;MIR4501;LINC00359;OXGR1;LINC00456;MBNL2;RAP2A;IPO5;FARP1;RNF113B;MIR3170;STK24;SLC15A1;DOCK9;DOCK9-AS1;RNU6-83P;DOCK9-AS2;UBAC2-AS1;UBAC2;GPR18;GPR183;FKSG29;MIR623;LINC01232;TM9SF2;LINC01039;CLYBL;MIR4306;CLYBL-AS2;CLYBL-AS1;LOC101927437;ZIC5;ZIC2;LINC00554;PCCA;PCCA-AS1;GGACT;TMTC4;NALCN-AS1;LINC00411;NALCN;ITGBL1;FGF14;MIR2681;MIR4705;FGF14-IT1;FGF14-AS1;FGF14-AS2;TPP2;METTL21C;CCDC168;TEX30;KDELC1;BIVM;BIVM-ERCC5;ERCC5;METTL21EP;SLC10A2;LINC01309;DAOA-AS1;DAOA	Unidad de Diagnostico Molecular y Celular del Cancer, Centro de Investigacion del Cancer-IBMCC (USAL-CSIC), Salamanca, Spain	comparative genomic hybridization (aCGH) and next-generation sequencing (NGS) in a series of MDS and MDS/myeloproliferative neoplasms (MPN) patients. 301 patients diagnosed with MDS (n = 240) or MDS/MPN (n = 61) were studied at the time of diagnosis. A genome-wide analysis of DNA copy number abnormalities was performed. In addition, a mutational analysis of DNMT3A, TET2, RUNX1, TP53 and BCOR genes was performed by NGS in selected cases. 285 abnormalities were identified in 71 patients (23.6%). Three high-risk MDS cases (1.2%) displayed chromothripsis involving exclusively chromosome 13 and affecting some cancer genes: FLT3, BRCA2 and RB1. All three cases carried TP53 mutations as revealed by NGS. Moreover, in the whole series, the integrative analysis of aCGH and NGS enabled the identification of cryptic recurrent deletions in 2p23.3 (DNMT3A; n = 2.8%), 4q24 (TET2; n = 10%) 17p13 (TP53; n = 8.5%), 21q22 (RUNX1; n = 7%), and Xp11.4 (BCOR; n = 2.8%), while mutations in the non-deleted allele where found only in DNMT3A (n = 1), TET2 (n = 3), and TP53 (n = 4). These cryptic abnormalities were detected mainly in patients with normal (45%) or non-informative (15%) karyotype by conventional cytogenetics, except for those with TP53 deletion and mutation (15%), which had a complex karyotype. In addition to well-known copy number defects, the presence of chromothripsis involving chromosome 13 was a novel recurrent change in high-risk MDS patients. Array CGH analysis revealed the presence of cryptic abnormalities in genomic regions where MDS-related genes, such as TET2, DNMT3A, RUNX1 and BCOR, are located.	GRCh36/hg18	GSE67682			Yes	
CTDB0592	Research	27560999	Brunner C, Brunner-Herglotz B, Ziegler A, Frech C, Amann G, Ladenstein R, Ambros IM, Ambros PF	Tumor Touch Imprints as Source for Whole Genome Analysis of Neuroblastoma Tumors	PLoS One	2016 Aug	12	Neuroblastoma	SNParray	Homo sapiens	NB19	Cytoscan HD SNP array				Department of Tumor Biology, CCRI, Children's Cancer Research Institute, St. Anna Kinderkrebsforschung, Vienna, Austria	INTRODUCTION: Tumor touch imprints (TTIs) are routinely used for the molecular diagnosis of neuroblastomas by interphase fluorescence in-situ hybridization (I-FISH). However, in order to facilitate a comprehensive, up-to-date molecular diagnosis of neuroblastomas and to identify new markers to refine risk and therapy stratification methods, whole genome approaches are needed. We examined the applicability of an ultra-high density SNP array platform that identifies copy number changes of varying sizes down to a few exons for the detection of genomic changes in tumor DNA extracted from TTIs. MATERIAL AND METHODS: DNAs were extracted from TTIs of 46 neuroblastoma and 4 other pediatric tumors. The DNAs were analyzed on the Cytoscan HD SNP array platform to evaluate numerical and structural genomic aberrations. The quality of the data obtained from TTIs was compared to that from randomly chosen fresh or fresh frozen solid tumors (n = 212) and I-FISH validation was performed. RESULTS: SNP array profiles were obtained from 48 (out of 50) TTI DNAs of which 47 showed genomic aberrations. The high marker density allowed for single gene analysis, e.g. loss of nine exons in the ATRX gene and the visualization of chromothripsis. Data quality was comparable to fresh or fresh frozen tumor SNP profiles. SNP array results were confirmed by I-FISH. CONCLUSION: TTIs are an excellent source for SNP array processing with the advantage of simple handling, distribution and storage of tumor tissue on glass slides. The minimal amount of tumor tissue needed to analyze whole genomes makes TTIs an economic surrogate source in the molecular diagnostic work up of tumor samples.	GRCh37/hg19	GSE79187			Yes	
CTDB0593	Research	27426636	Gullett JC, Znoyko IY, Wolff DJ, Schandl CA	Chromothripsis in Two Patients With Renal Cell Carcinoma: A Case Series	Clin Genitourin Cancer	2017 Feb	7	Clear cell renal cell carcinoma	SNParray	Homo sapiens	27426636_patient1	Infinium HD Human Omni1 BeadChip				Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC	Clinical Practice Points: Chromothripsis has been described as the catastrophic shattering of a chromosomal region with inaccurate genomic reassembly. Although chromothripsis occurs in a number of other epithelial cell tumors, it has only rarely been reported in renal cell carcinoma (RCC). We describe 2 individuals in their sixth decade who presented to our institution with RCC and apparent chromothripsis identified by single nucleotide polymorphism whole genome microarray analysis. This result suggests that chromothripsis might be a more common mechanism leading to the development of RCC than previously known. Detection of chromothripsis in patients with RCC might, in part, dictate the prognosis and, ultimately, guide therapeutic decisions based on the typically poorer outcome and more advanced disease documented in other tumor types A specific treatment regimen for chromothripsisrelated tumors is not currently available. However, it is conceivable that molecularly targeted therapies might one day be used to exploit the underlying etiologies and subsequent effects of chromothripsis, because some of the innumerable cells and/or pathways affected might be more sensitive to particular drugs.	GRCh37/hg19				Yes	
CTDB0594	Research	27426636	Gullett JC, Znoyko IY, Wolff DJ, Schandl CA	Chromothripsis in Two Patients With Renal Cell Carcinoma: A Case Series	Clin Genitourin Cancer	2017 Feb	12	Clear cell renal cell carcinoma	SNParray	Homo sapiens	27426636_patient2	Infinium HD Human Omni1 BeadChip				Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC	Clinical Practice Points: Chromothripsis has been described as the catastrophic shattering of a chromosomal region with inaccurate genomic reassembly. Although chromothripsis occurs in a number of other epithelial cell tumors, it has only rarely been reported in renal cell carcinoma (RCC). We describe 2 individuals in their sixth decade who presented to our institution with RCC and apparent chromothripsis identified by single nucleotide polymorphism whole genome microarray analysis. This result suggests that chromothripsis might be a more common mechanism leading to the development of RCC than previously known. Detection of chromothripsis in patients with RCC might, in part, dictate the prognosis and, ultimately, guide therapeutic decisions based on the typically poorer outcome and more advanced disease documented in other tumor types A specific treatment regimen for chromothripsisrelated tumors is not currently available. However, it is conceivable that molecularly targeted therapies might one day be used to exploit the underlying etiologies and subsequent effects of chromothripsis, because some of the innumerable cells and/or pathways affected might be more sensitive to particular drugs.	GRCh37/hg19				Yes	
CTDB0595	Research	27216161	Del Rey J, Santos M, Gonzalez-Meneses A, Mila M, Fuster C	Heterogeneity of a Constitutional Complex Chromosomal Rearrangement in 2q	Cytogenet Genome Res	2016	2	Congenital abnormality	Array CGH	Homo sapiens	27216161_case					Unitat de Biologia Celx00B7;lular i Genx00E8;tica Mx00E8;dica, Facultat de Medicina, Universitat Autx00F2;noma de Barcelona, Barcelona, Spain	Complex chromosome rearrangements (CCRs) are unusual structural chromosome alterations found in humans, and to date only a few have been characterized molecularly. New mechanisms, such as chromothripsis, have been proposed to explain the presence of the CCRs in cancer cells and in patients with congenital disorders and/or mental retardation. The aim of the present study was the molecular characterization of a constitutional CCR in a girl with multiple congenital disorders and intellectual disability in order to determine the genotype-phenotype relation and to clarify whether the CCR could have been caused by chromosomal catastrophic events. The present CCR was characterized by G-banding, high-resolution CGH, multiplex ligation-dependent probe amplification and subtelomeric  q-FISH analyses. Preliminary results indicate that the de novo CCR is unbalanced showing a  q .  deletion and  q q .  partial trisomy. Our patient shows some of the typical traits and intellectual disability described in patients with  q  deletion and also in carriers of  q q .  partial trisomy; thus, the clinical disorders could be explained by additional effects of both chromosome alterations (deletions and duplications). A posterior, sequential FISH study using BAC probes revealed the unexpected presence of at least   different reorganizations affecting  q q . , suggesting the existence of chromosome instability in this region. The present CCR is the first case described in the literature of heterogeneity of unbalanced CCRs affecting a small region of  q, indicating that the mechanisms involved in constitutional chromosome rearrangement may be more complex than previously thought.	GRCh37/hg19				No	
CTDB0596	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	19	Acute myeloid leukemia	Array CGH	Homo sapiens	case174	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0597	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	11	Acute myeloid leukemia	Array CGH	Homo sapiens	case127	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0598	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	16,17	Acute myeloid leukemia	Array CGH	Homo sapiens	case228	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0599	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	5,6,11	Acute myeloid leukemia	Array CGH	Homo sapiens	case146	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0600	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	7,X	Acute myeloid leukemia	Array CGH	Homo sapiens	case170	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0601	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	3	Acute myeloid leukemia	Array CGH	Homo sapiens	case173	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0602	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	8,9,13,16,19,21	Acute myeloid leukemia	Array CGH	Homo sapiens	case179	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0603	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	3	Acute myeloid leukemia	Array CGH	Homo sapiens	case186	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0604	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	11	Acute myeloid leukemia	Array CGH	Homo sapiens	case226	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0605	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	11,22	Acute myeloid leukemia	Array CGH	Homo sapiens	case206	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes	
CTDB0606	Research	26543079	Kjeldsen E	Oligo-based High-resolution aCGH Analysis Enhances Routine Cytogenetic Diagnostics in Haematological Malignancies	Cancer Genomics Proteomics	2015 Nov-Dec	4,6,11,13	Acute myeloid leukemia	Array CGH	Homo sapiens	case218	4x180K Cancer Cytochip array				HaemoDiagnostic Laboratory, Cancer Cytogenetics Section, Department of Hematology, Aarhus University Hospital, Aarhus, Denmark Eigil	BACKGROUND: The purpose of the present study was to evaluate the detection rate of genomic aberrations in haematological malignancies using oligobased array-CGH (oaCGH) analysis in combination with karyotyping and fluorescence in situ hybridization (FISH) analyses, and its feasibility in a clinical pragmatic approach. MATERIALS AND METHODS: The 4x180K Cancer Cytochip array was applied in 96 patients with various haematological malignancies in a prospective setting and in 41 acute myeloid leukemia (AML) patients retrospectively. RESULTS: Combined use of oaCGH analysis and karyotyping improved the overall detection rate in comparison to karyotyping-alone and vice versa. In cases with normal karyotypes oaCGH analysis detected genomic aberrations in 66% (39/60) of cases. In the group of simple karyotypes oaCGH analysis extended karyotypic findings in 39% (12/31) while oaCGH analysis extended the karyotypic findings in 89% (39/44) of cases with complex karyotypes. In 7% (5/75) of cases oaCGH analysis failed in detecting the observed abnormalities by karyotyping. CONCLUSION: oaCGH analysis is a valuable asset in routine cytogenetics of haematological malignancies.	GRCh36/hg18				Yes