The genomic complexity of primary human prostate cancer

Michael F. Berger, Michael S. Lawrence, Francesca Demichelis, Yotam Drier, Kristian Cibulskis, Andrey Y. Sivachenko, Andrea Sboner, Raquel Esgueva, Dorothee Pflueger, Carrie Sougnez, Robert Onofrio, Scott L. Carter, Kyung Park, Lukas Habegger, Lauren Ambrogio, Timothy Fennell, Melissa Parkin, Gordon Saksena, Douglas Voet, Alex H. Ramos, Trevor J. Pugh, Jane Wilkinson, Sheila Fisher, Wendy Winckler, Scott Mahan, Kristin Ardlie, Jennifer Baldwin, Jonathan W. Simons, Naoki Kitabayashi, Theresa Y. MacDonald, Philip W. Kantoff, Lynda Chin, Stacey B. Gabriel, Mark B. Gerstein, Todd R. Golub, Matthew Meyerson, Ashutosh Tewari, Eric S. Lander, Gad Getz, Mark A. Rubin () and Levi A. Garraway ()
Additional contact information
Michael F. Berger: The Broad Institute of Harvard and MIT
Michael S. Lawrence: The Broad Institute of Harvard and MIT
Francesca Demichelis: Weill Cornell Medical College
Yotam Drier: Weizmann Institute of Science
Kristian Cibulskis: The Broad Institute of Harvard and MIT
Andrey Y. Sivachenko: The Broad Institute of Harvard and MIT
Andrea Sboner: Yale University
Raquel Esgueva: Weill Cornell Medical College
Dorothee Pflueger: Weill Cornell Medical College
Carrie Sougnez: The Broad Institute of Harvard and MIT
Robert Onofrio: The Broad Institute of Harvard and MIT
Scott L. Carter: The Broad Institute of Harvard and MIT
Kyung Park: Weill Cornell Medical College
Lukas Habegger: Program in Computational Biology and Bioinformatics, Yale University
Lauren Ambrogio: The Broad Institute of Harvard and MIT
Timothy Fennell: The Broad Institute of Harvard and MIT
Melissa Parkin: The Broad Institute of Harvard and MIT
Gordon Saksena: The Broad Institute of Harvard and MIT
Douglas Voet: The Broad Institute of Harvard and MIT
Alex H. Ramos: The Broad Institute of Harvard and MIT
Trevor J. Pugh: The Broad Institute of Harvard and MIT
Jane Wilkinson: The Broad Institute of Harvard and MIT
Sheila Fisher: The Broad Institute of Harvard and MIT
Wendy Winckler: The Broad Institute of Harvard and MIT
Scott Mahan: The Broad Institute of Harvard and MIT
Kristin Ardlie: The Broad Institute of Harvard and MIT
Jennifer Baldwin: The Broad Institute of Harvard and MIT
Jonathan W. Simons: The Prostate Cancer Foundation
Naoki Kitabayashi: Weill Cornell Medical College
Theresa Y. MacDonald: Weill Cornell Medical College
Philip W. Kantoff: Harvard Medical School
Lynda Chin: The Broad Institute of Harvard and MIT
Stacey B. Gabriel: The Broad Institute of Harvard and MIT
Mark B. Gerstein: Yale University
Todd R. Golub: The Broad Institute of Harvard and MIT
Matthew Meyerson: The Broad Institute of Harvard and MIT
Ashutosh Tewari: Institute of Prostate Cancer and Lefrak Center of Robotic Surgery, Weill Cornell Medical College and New York Presbyterian Hospitals
Eric S. Lander: The Broad Institute of Harvard and MIT
Gad Getz: The Broad Institute of Harvard and MIT
Mark A. Rubin: Weill Cornell Medical College
Levi A. Garraway: The Broad Institute of Harvard and MIT

Nature, 2011, vol. 470, issue 7333, 214-220

Abstract: Abstract 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 open chromatin, androgen receptor and ERG DNA binding sites in the setting of the ETS gene fusion TMPRSS2–ERG, but inversely correlated with these regions in tumours lacking ETS fusions. This observation suggests a link between chromatin or transcriptional regulation and the genesis of genomic aberrations. Three tumours contained rearrangements that disrupted CADM2, and four harboured events disrupting either PTEN (unbalanced events), a prostate tumour suppressor, or MAGI2 (balanced events), a PTEN interacting protein not previously implicated in prostate tumorigenesis. Thus, genomic rearrangements may arise from transcriptional or chromatin aberrancies and engage prostate tumorigenic mechanisms.

Date: 2011
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DOI: 10.1038/nature09744

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