Ontology highlight
ABSTRACT: Prostate cancer is a prevalent cause of cancer morbidity and mortality in men. In order to characterize the full range of somatic mutations in protein-coding genes that may drive the growth of prostate cancer, we sequenced the exonic regions of genomic and tumor DNA from over 100 patients with high-risk primary prostate cancer. Using hybrid capture and paired end DNA sequencing, we identified mutations in several novel putative prostate cancer genes. We interrogated copy number changes across tumor genomes using high-density SNP arrays, and identified a molecular subtype of cancer characterized by mutation of the ubiquitin ligase subunit SPOP and copy number loss at specific genomic loci.
PROVIDER: phs000447.v1.p1 | EGA |
REPOSITORIES: EGA
Berger Michael F MF Lawrence Michael S MS Demichelis Francesca F Drier Yotam Y Cibulskis Kristian K Sivachenko Andrey Y AY Sboner Andrea A Esgueva Raquel R Pflueger Dorothee D Sougnez Carrie C Onofrio Robert R Carter Scott L SL Park Kyung K Habegger Lukas L Ambrogio Lauren L Fennell Timothy T Parkin Melissa M Saksena Gordon G Voet Douglas D Ramos Alex H AH Pugh Trevor J TJ Wilkinson Jane J Fisher Sheila S Winckler Wendy W Mahan Scott S Ardlie Kristin K Baldwin Jennifer J Simons Jonathan W JW Kitabayashi Naoki N MacDonald Theresa Y TY Kantoff Philip W PW Chin Lynda L Gabriel Stacey B SB Gerstein Mark B MB Golub Todd R TR Meyerson Matthew M Tewari Ashutosh A Lander Eric S ES Getz Gad G Rubin Mark A MA Garraway Levi A LA
Nature 20110201 7333
Prostate cancer is the second most common cause of male cancer deaths in the United States. However, the full range of prostate cancer genomic alterations is incompletely characterized. Here we present the complete sequence of seven primary human prostate cancers and their paired normal counterparts. Several tumours contained complex chains of balanced (that is, 'copy-neutral') rearrangements that occurred within or adjacent to known cancer genes. Rearrangement breakpoints were enriched near ope ...[more]