Journal
NATURE GENETICS
Volume 50, Issue 5, Pages 682-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41588-018-0086-z
Keywords
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Categories
Funding
- Cancer Research UK [C5047/A14835/A22530/A17528, C309/A11566, C368/A6743, A368/A7990, C14303/A17197]
- Dallaglio Foundation (CR-UK Prostate Cancer ICGC Project and Pan Prostate Cancer Group)
- PC-UK/Movember
- NIHR
- Royal Marsden NHS Foundation Trust
- Cancer Research UK
- National Cancer Research Institute (National Institute of Health Research (NIHR)) [G0500966/75466]
- Li Ka Shing Foundation
- Academy of Finland
- Cancer Society of Finland
- NIHR Cambridge Biomedical Research Centre
- Core Facilities at the Cancer Research UK Cambridge Institute
- Orchid and Cancer Research UK
- Orchid
- NIHR Oxford Biomedical Research Centre (Molecular Diagnostics Theme/Multimodal Pathology sub-theme)
- Bob Champion Cancer Trust
- Masonic Charitable Foundation
- King Family
- Stephen Hargrave Trust
- CRUK [C35696/A23187]
- Cancer Foundation Finland sr [130073, 170104, 150069] Funding Source: researchfish
- Cancer Research UK [11566, 21777, 14835, 22530, 22744, 22897, 19556, 15007, 26718, 17528] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0509-10242, NF-SI-0513-10121, NF-SI-0510-10096, CL-2014-14-004, CL-2008-22-001] Funding Source: researchfish
- The Francis Crick Institute [10202] Funding Source: researchfish
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Prostate cancer represents a substantial clinical challenge because it is difficult to predict outcome and advanced disease is often fatal. We sequenced the whole genomes of 112 primary and metastatic prostate cancer samples. From joint analysis of these cancers with those from previous studies (930 cancers in total), we found evidence for 22 previously unidentified putative driver genes harboring coding mutations, as well as evidence for NEAT1 and FOXA1 acting as drivers through noncoding mutations. Through the temporal dissection of aberrations, we identified driver mutations specifically associated with steps in the progression of prostate cancer, establishing, for example, loss of CHD1 and BRCA2 as early events in cancer development of ETS fusion-negative cancers. Computational chemogenomic (canSAR) analysis of prostate cancer mutations identified 11 targets of approved drugs, 7 targets of investigational drugs, and 62 targets of compounds that may be active and should be considered candidates for future clinical trials.
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