![]() ![]() Finally, comparing primary and metastatic prostate cancer identifies a set of genomic markers that may inform risk stratification. We identify a total of 97 SMGs, including 70 not previously implicated in prostate cancer, such as the ubiquitin ligase CU元 and the transcription factor SPEN. We find that the incidence of significantly mutated genes (SMGs) follows a long-tail distribution, with many genes mutated in less than 3% of cases. We identify and validate a new class of E26 transformation-specific (ETS)-fusion-negative tumors defined by mutations in epigenetic regulators, as well as alterations in pathways not previously implicated in prostate cancer, such as the spliceosome pathway. Here we aggregate and uniformly analyze exome sequencing data from 1,013 prostate cancers. However, larger and uniform genomic analysis may identify additional recurrently mutated genes at lower frequencies. genomic characterization of prostate cancer has identified recurrent alterations in genes involved in androgen signaling, DNA repair, and PI3K signaling, among others. 22 Cancer Program, Broad Institute of MIT and Harvard, Cambridge, MA, USA. 21 Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA. 20 Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA. Kravis Center for Molecular Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA. 18 Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.1 Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. ![]() 17 Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.16 Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA. ![]()
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