StudyType	PubMedID	Author	Title	Journal	PublishDate	Chromosome	Disease	Technology	Species	CaseID	Platform	CNA	Connection	Gene	Affiliation	Abstract	GenomeAssembly	GEO	dbGaP	ENA	IsCancer	FusionGene
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
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
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
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
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
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
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
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
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
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
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
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