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Cancer Cell Article Integrative Genomic Profiling of Human Prostate Cancer Barry S. Taylor,1,8 Nikolaus Schultz,1,8 Haley Hieronymus,2,8 Anuradha Gopalan,3 Yonghong Xiao,3 Brett S. Carver,4 Vivek K. Arora,2 Poorvi Kaushik,1 Ethan Cerami,1 Boris Reva,1 Yevgeniy Antipin,1 Nicholas Mitsiades,5 Thomas Landers,2 Igor Dolgalev,2 John E. Major,6 Manda Wilson,6 Nicholas D. Socci,6 Alex E. Lash,6 Adriana Heguy,2 James A. Eastham,4 Howard I. Scher,5 Victor E. Reuter,3 Peter T. Scardino,4 Chris Sander,1 Charles L. Sawyers,2,7,* and William L. Gerald2,3,9 1Program in Computational Biology 2Program in Human Oncology and Pathogenesis (HOPP) 3Department of Pathology 4Department of Urology 5Department of Medicine 6Bioinformatics Core Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10065, USA 7Howard Hughes Medical Institute, Chevy Chase, MD 20815-6789, USA 8These authors contributed equally to this work 9Deceased *Correspondence: sawyersc@ DOI 10.1016/j.ccr.2010.05.026 SUMMARY Annotation of prostate cancer genomes provides a foundation for discoveries that can impact disease under- standing and treatment. Concordant assessment of DNA copy number, mRNA expression, and focused exon resequencing in 218 prostate cancer tumors identified the nuclear receptor coactivator NCOA2 as an onco- gene in 11% of tumors. Additionally, the androgen-driven TMPRSS2-ERG fusion was associated with a previously unrecognized, prostate-specific deletion at chromosome 3p14 that implicates FOXP1, RYBP, and SHQ1 as potential cooperative tumor suppressors. DNA copy-number data from primary tumors revealed that copy-number alterations robustly define clusters of low- and high-risk disease beyond that achieved by Gleason score. The genomic and clinical outcome data from these patients are now made avail- able as a public resource. INTRODUCTION into

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