Author/Authors :
Taylor، نويسنده , , Barry S. and Schultz، نويسنده , , Nikolaus and Hieronymus، نويسنده , , Haley and Gopalan، نويسنده , , Anuradha and Xiao، نويسنده , , Yonghong and Carver، نويسنده , , Brett S. and Arora، نويسنده , , Vivek K. and Kaushik، نويسنده , , Poorvi and Cerami، نويسنده , , Ethan and Reva، نويسنده , , Boris and Antipin، نويسنده , , Yevgeniy and Mitsiades، نويسنده , , Nicholas and Landers، نويسنده , , Thomas and Dolgalev، نويسنده , , Igor and Major، نويسنده , , John E. and Wilson، نويسنده , , Manda and Socci، نويسنده , , Nicholas D. and Lash، نويسنده , , Alex E. and Heguy، نويسنده , , Adriana and Eastham، نويسنده , , James A. and Scher، نويسنده , , Howard I. and Reuter، نويسنده , , Victor E. and Scardino، نويسنده , , Peter T. and Sander، نويسنده , , Chris and Sawyers، نويسنده , , Charles L. and Gerald، نويسنده , , William L.، نويسنده ,
Abstract :
Summary
tion of prostate cancer genomes provides a foundation for discoveries that can impact disease understanding 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 oncogene 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 available as a public resource.
