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Cell. 2015 Nov 5;163(4):1011-25. doi: 10.1016/j.cell.2015.10.025.

The Molecular Taxonomy of Primary Prostate Cancer.

Collaborators (312)

Abeshouse A, Ahn J, Akbani R, Ally A, Amin S, Andry CD, Annala M, Aprikian A, Armenia J, Arora A, Auman JT, Balasundaram M, Balu S, Barbieri CE, Bauer T, Benz CC, Bergeron A, Beroukhim R, Berrios M, Bivol A, Bodenheimer T, Boice L, Bootwalla MS, Borges dos Reis R, Boutros PC, Bowen J, Bowlby R, Boyd J, Bradley RK, Breggia A, Brimo F, Bristow CA, Brooks D, Broom BM, Bryce AH, Bubley G, Burks E, Butterfield YS, Button M, Canes D, Carlotti CG, Carlsen R, Carmel M, Carroll PR, Carter SL, Cartun R, Carver BS, Chan JM, Chang MT, Chen Y, Cherniack AD, Chevalier S, Chin L, Cho J, Chu A, Chuah E, Chudamani S, Cibulskis K, Ciriello G, Clarke A, Cooperberg MR, Corcoran NM, Costello AJ, Cowan J, Crain D, Curley E, David K, Demchok JA, Demichelis F, Dhalla N, Dhir R, Doueik A, Drake B, Dvinge H, Dyakova N, Felau I, Ferguson ML, Frazer S, Freedland S, Fu Y, Gabriel SB, Gao J, Gardner J, Gastier-Foster JM, Gehlenborg N, Gerken M, Gerstein MB, Getz G, Godwin AK, Gopalan A, Graefen M, Graim K, Gribbin T, Guin R, Gupta M, Hadjipanayis A, Haider S, Hamel L, Hayes DN, Heiman DI, Hess J, Hoadley KA, Holbrook AH, Holt RA, Holway A, Hovens CM, Hoyle AP, Huang M, Hutter CM, Ittmann M, Iype L, Jefferys SR, Jones CD, Jones SJ, Juhl H, Kahles A, Kane CJ, Kasaian K, Kerger M, Khurana E, Kim J, Klein RJ, Kucherlapati R, Lacombe L, Ladanyi M, Lai PH, Laird PW, Lander ES, Latour M, Lawrence MS, Lau K, LeBien T, Lee D, Lee S, Lehmann KV, Leraas KM, Leshchiner I, Leung R, Libertino JA, Lichtenberg TM, Lin P, Linehan WM, Ling S, Lippman SM, Liu J, Liu W, Lochovsky L, Loda M, Logothetis C, Lolla L, Longacre T, Lu Y, Luo J, Ma Y, Mahadeshwar HS, Mallery D, Mariamidze A, Marra MA, Mayo M, McCall S, McKercher G, Meng S, Mes-Masson AM, Merino MJ, Meyerson M, Mieczkowski PA, Mills GB, Mills Shaw KR, Minner S, Moinzadeh A, Moore RA, Morris S, Morrison C, Mose LE, Mungall AJ, Murray BA, Myers JB, Naresh R, Nelson J, Nelson MA, Nelson PS, Newton Y, Noble MS, Noushmehr H, Nykter M, Pantazi A, Parfenov M, Park PJ, Parker JS, Paulauskis J, Penny R, Perou CM, Piché A, Pihl T, Pinto PA, Prandi D, Protopopov A, Ramirez NC, Rao A, Rathmell WK, Rätsch G, Ren X, Reuter VE, Reynolds SM, Rhie SK, Rieger-Christ K, Roach J, Robertson AG, Robinson B, Rubin MA, Saad F, Sadeghi S, Saksena G, Saller C, Salner A, Sanchez-Vega F, Sander C, Sandusky G, Sauter G, Sboner A, Scardino PT, Scarlata E, Schein JE, Schlomm T, Schmidt LS, Schultz N, Schumacher SE, Seidman J, Neder L, Seth S, Sharp A, Shelton C, Shelton T, Shen H, Shen R, Sherman M, Sheth M, Shi Y, Shih J, Shmulevich I, Simko J, Simon R, Simons JV, Sipahimalani P, Skelly T, Sofia HJ, Soloway MG, Song X, Sorcini A, Sougnez C, Stepa S, Stewart C, Stewart J, Stuart JM, Sullivan TB, Sun C, Sun H, Tam A, Tan D, Tang J, Tarnuzzer R, Tarvin K, Taylor BS, Teebagy P, Tenggara I, Têtu B, Tewari A, Thiessen N, Thompson T, Thorne LB, Tirapelli DP, Tomlins SA, Trevisan FA, Troncoso P, True LD, Tsourlakis MC, Tyekucheva S, Van Allen E, Van Den Berg DJ, Veluvolu U, Verhaak R, Vocke CD, Voet D, Wan Y, Wang Q, Wang W, Wang Z, Weinhold N, Weinstein JN, Weisenberger DJ, Wilkerson MD, Wise L, Witte J, Wu CC, Wu J, Wu Y, Xu AW, Yadav SS, Yang L, Yang L, Yau C, Ye H, Yena P, Zeng T, Zenklusen JC, Zhang H, Zhang J, Zhang J, Zhang W, Zhong Y, Zhu K, Zmuda E.

Abstract

There is substantial heterogeneity among primary prostate cancers, evident in the spectrum of molecular abnormalities and its variable clinical course. As part of The Cancer Genome Atlas (TCGA), we present a comprehensive molecular analysis of 333 primary prostate carcinomas. Our results revealed a molecular taxonomy in which 74% of these tumors fell into one of seven subtypes defined by specific gene fusions (ERG, ETV1/4, and FLI1) or mutations (SPOP, FOXA1, and IDH1). Epigenetic profiles showed substantial heterogeneity, including an IDH1 mutant subset with a methylator phenotype. Androgen receptor (AR) activity varied widely and in a subtype-specific manner, with SPOP and FOXA1 mutant tumors having the highest levels of AR-induced transcripts. 25% of the prostate cancers had a presumed actionable lesion in the PI3K or MAPK signaling pathways, and DNA repair genes were inactivated in 19%. Our analysis reveals molecular heterogeneity among primary prostate cancers, as well as potentially actionable molecular defects.

PMID:
26544944
PMCID:
PMC4695400
DOI:
10.1016/j.cell.2015.10.025
[Indexed for MEDLINE]
Free PMC Article

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