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The molecular taxonomy of primary prostate cancer

Cell | November 2015

DOI: http://dx.doi.org/10.1016/j.cell.2015.10.025

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, FLI1) or mutations (SPOP,FOXA1,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.

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The data are supported by different organizations. All data marked by [DCC] are DCC-validated archives. All data marked by [Supplementary] were created by the manuscript authors and you should contact the corresponding author for support.

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Mutations and VCF files

NOTE: The PRAD MAF files only contains 332 samples since TCGA-CH-5743-01 did not have any mutations


Reverse Phase Protein Array (RPPA) Expression

RNA Expression from IlluminaGA RNASeq and IlluminaHiseq RNASeq

SNP and Copy Number variation from Affymetrix SNP6 and IlluminaHiSeq Low Pass Whole Genome sequencing

miRNA from Illumina HiSeq 2000

Methylation from Illumina Infinium Human Methylation450

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