Uncovering the genetic landscape driving castration-resistant prostate cancer

Timothy J. Martin, Cody J. Peer, William D. Figg*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


Identification of the mechanisms that drive progression of metastatic castration-resistant prostate cancer (CRPC) has fostered interest since early androgen studies in the 1940s. Little knowledge has surfaced about the role mutations play in prostate cancer development. A group at the Michigan Center for Translation Pathology studied exomes of lethal, metastatic CRPC and documented the overall mutation rates. In classifying these mutations, the monoclonal cause of CRPC was recognized. Nine identified genes showed significant mutations. Six of these genes had previously been reported as mutated in prostate cancer. The analysis also found significantly mutated androgen receptor (AR) cofactors and linked proteins, including FOXA1 and MLL2. Another finding concerned an aberration in CHD1. Prostate cancers with deletions or mutations in CHD1 showed a strong correlation with ETS gene family fusion negative prostate cancers (96%). In profiling these exomes, this group provides an original method to identify deletions and mutations that drive CRPC progression.

Original languageEnglish
Pages (from-to)399-400
Number of pages2
JournalCancer Biology and Therapy
Issue number5
StatePublished - May 2013
Externally publishedYes


  • Castration-resistant prostate cancer
  • Genetics
  • Mutations


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