Abstract: |
Annotation 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. © 2010 Elsevier Inc. |
Keywords: |
signal transduction; adult; controlled study; human tissue; aged; aged, 80 and over; middle aged; primary tumor; unclassified drug; gene cluster; animals; mice; metastasis; microrna; gene expression profiling; nuclear protein; tumor markers, biological; relapse; transcription factor; tumor cells, cultured; prostate cancer; prostatic neoplasms; oligonucleotide array sequence analysis; prostatectomy; cancer cell; oncogene proteins, fusion; neoplasm metastasis; transplantation, heterologous; binding protein; androgen receptor; gene dosage; chromosome deletion; comparative genomic hybridization; chromosome 3p; genome, human; chromosomes, human, pair 3; protein shq; ring yy1 and binding protein; transcription factor foxp1
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