期刊
NATURE COMMUNICATIONS
卷 8, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-017-01355-0
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资金
- Francis Crick Institute - Cancer Research UK [FC001202]
- UK Medical Research Council [FC001202]
- Wellcome Trust [FC001202]
- Research Foundation-Flanders (FWO) [G.0687.12N]
- GOA MaNet
- KUL [PFV/10/016 SymBioSys]
- iMinds
- Hercules III PacBio RS
- IWT TBM Haplotyping
- Action [BM1006]
- European Union's Horizon Research and Innovation programme (Marie Sklodowska-Curie) [703594-DECODE]
- Li Ka Shing foundation
- Norwegian Radium Hospital Foundation
- Wellcome Trust
- National Science Foundation [OISE-1129076]
- Gordon and Betty Moore Foundation
- Norwegian Regional Health authorities [2014061]
- Norwegian Cancer Association
- The Francis Crick Institute [10202, 10508] Funding Source: researchfish
Homozygous deletions are rare in cancers and often target tumour suppressor genes. Here, we build a compendium of 2218 primary tumours across 12 human cancer types and systematically screen for homozygous deletions, aiming to identify rare tumour suppressors. Our analysis defines 96 genomic regions recurrently targeted by homozygous deletions. These recurrent homozygous deletions occur either over tumour suppressors or over fragile sites, regions of increased genomic instability. We construct a statistical model that separates fragile sites from regions showing signatures of positive selection for homozygous deletions and identify candidate tumour suppressors within those regions. We find 16 established tumour suppressors and propose 27 candidate tumour suppressors. Several of these genes (including MGMT, RAD17, and USP44) show prior evidence of a tumour suppressive function. Other candidate tumour suppressors, such as MAFTRR, KIAA1551, and IGF2BP2, are novel. Our study demonstrates how rare tumour suppressors can be identified through copy number meta-analysis.
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