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dc.contributor.authorLander, Eric S.
dc.contributor.authorBarbieri, Christopher E.
dc.contributor.authorBaca, Sylvan C.
dc.contributor.authorLawrence, Michael S.
dc.contributor.authorDemichelis, Francesca
dc.contributor.authorBlattner, Mirjam
dc.contributor.authorTheurillat, Jean-Philippe
dc.contributor.authorWhite, Thomas A.
dc.contributor.authorStojanov, Petar
dc.contributor.authorVan Allen, Eliezer
dc.contributor.authorStransky, Nicolas
dc.contributor.authorNickerson, Elizabeth
dc.contributor.authorChae, Sung-Suk
dc.contributor.authorBoysen, Gunther
dc.contributor.authorAuclair, Daniel
dc.contributor.authorOnofrio, Robert
dc.contributor.authorPark, Kyung
dc.contributor.authorKitabayashi, Naoki
dc.contributor.authorMacDonald, Theresa Y.
dc.contributor.authorSheikh, Karen
dc.date.accessioned2014-02-03T20:16:49Z
dc.date.available2014-02-03T20:16:49Z
dc.date.issued2012-05
dc.date.submitted2011-12
dc.identifier.issn1061-4036
dc.identifier.issn1546-1718
dc.identifier.urihttp://hdl.handle.net/1721.1/84658
dc.description.abstractProstate cancer is the second most common cancer in men worldwide and causes over 250,000 deaths each year. Overtreatment of indolent disease also results in significant morbidity. Common genetic alterations in prostate cancer include losses of NKX3.1 (8p21) and PTEN (10q23), gains of AR (the androgen receptor gene) and fusion of ETS family transcription factor genes with androgen-responsive promoters. Recurrent somatic base-pair substitutions are believed to be less contributory in prostate tumorigenesis but have not been systematically analyzed in large cohorts. Here, we sequenced the exomes of 112 prostate tumor and normal tissue pairs. New recurrent mutations were identified in multiple genes, including MED12 and FOXA1. SPOP was the most frequently mutated gene, with mutations involving the SPOP substrate-binding cleft in 6–15% of tumors across multiple independent cohorts. Prostate cancers with mutant SPOP lacked ETS family gene rearrangements and showed a distinct pattern of genomic alterations. Thus, SPOP mutations may define a new molecular subtype of prostate cancer.en_US
dc.description.sponsorshipNational Human Genome Research Institute (U.S.) (Large Scale Sequencing Program Grant U54 HG003067)en_US
dc.language.isoen_US
dc.publisherNature Publishing Groupen_US
dc.relation.isversionofhttp://dx.doi.org/10.1038/ng.2279en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alike 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourcePMCen_US
dc.titleExome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate canceren_US
dc.typeArticleen_US
dc.identifier.citationBarbieri, Christopher E, Sylvan C Baca, Michael S Lawrence, Francesca Demichelis, Mirjam Blattner, Jean-Philippe Theurillat, Thomas A White, et al. “Exome sequencing identifies recurrent SPOP, FOXA1 and MED12 mutations in prostate cancer.” Nature Genetics 44, no. 6 (May 20, 2012): 685-689.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biologyen_US
dc.contributor.mitauthorLander, Eric S.en_US
dc.relation.journalNature Geneticsen_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsBarbieri, Christopher E; Baca, Sylvan C; Lawrence, Michael S; Demichelis, Francesca; Blattner, Mirjam; Theurillat, Jean-Philippe; White, Thomas A; Stojanov, Petar; Van Allen, Eliezer; Stransky, Nicolas; Nickerson, Elizabeth; Chae, Sung-Suk; Boysen, Gunther; Auclair, Daniel; Onofrio, Robert C; Park, Kyung; Kitabayashi, Naoki; MacDonald, Theresa Y; Sheikh, Karen; Vuong, Terry; Guiducci, Candace; Cibulskis, Kristian; Sivachenko, Andrey; Carter, Scott L; Saksena, Gordon; Voet, Douglas; Hussain, Wasay M; Ramos, Alex H; Winckler, Wendy; Redman, Michelle C; Ardlie, Kristin; Tewari, Ashutosh K; Mosquera, Juan Miguel; Rupp, Niels; Wild, Peter J; Moch, Holger; Morrissey, Colm; Nelson, Peter S; Kantoff, Philip W; Gabriel, Stacey B; Golub, Todd R; Meyerson, Matthew; Lander, Eric S; Getz, Gad; Rubin, Mark A; Garraway, Levi Aen_US
mit.licenseOPEN_ACCESS_POLICYen_US


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