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Comment
. 2013 May;14(5):399-400.
doi: 10.4161/cbt.24426.

Uncovering the genetic landscape driving castration-resistant prostate cancer

Timothy J Martin  1 , Cody J Peer, William D Figg
Affiliations
Comment

Uncovering the genetic landscape driving castration-resistant prostate cancer

Timothy J Martin et al. Cancer Biol Ther. 2013 May.

Abstract

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.

Keywords: castration-resistant prostate cancer; genetics; mutations.

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Comment on

  • The mutational landscape of lethal castration-resistant prostate cancer.
    Grasso CS, Wu YM, Robinson DR, Cao X, Dhanasekaran SM, Khan AP, Quist MJ, Jing X, Lonigro RJ, Brenner JC, Asangani IA, Ateeq B, Chun SY, Siddiqui J, Sam L, Anstett M, Mehra R, Prensner JR, Palanisamy N, Ryslik GA, Vandin F, Raphael BJ, Kunju LP, Rhodes DR, Pienta KJ, Chinnaiyan AM, Tomlins SA. Grasso CS, et al. Nature. 2012 Jul 12;487(7406):239-43. doi: 10.1038/nature11125. Nature. 2012. PMID: 22722839 Free PMC article.

References

    1. Sharifi N, Gulley JL, Dahut WL. Androgen deprivation therapy for prostate cancer. JAMA. 2005;294:238–44. doi: 10.1001/jama.294.2.238. - DOI - PubMed
    1. Shen MM, Abate-Shen C. Molecular genetics of prostate cancer: new prospects for old challenges. Genes Dev. 2010;24:1967–2000. doi: 10.1101/gad.1965810. - DOI - PMC - PubMed
    1. Grasso CS, Wu YM, Robinson DR, Cao X, Dhanasekaran SM, Khan AP, et al. The mutational landscape of lethal castration-resistant prostate cancer. Nature. 2012;487:239–43. doi: 10.1038/nature11125. - DOI - PMC - PubMed
    1. Morin RD, Mendez-Lago M, Mungall AJ, Goya R, Mungall KL, Corbett RD, et al. Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma. Nature. 2011;476:298–303. doi: 10.1038/nature10351. - DOI - PMC - PubMed
    1. Crea F, Sun L, Mai A, Chiang YT, Farrar WL, Danesi R, et al. The emerging role of histone lysine demethylases in prostate cancer. Mol Cancer. 2012;11:52. doi: 10.1186/1476-4598-11-52. - DOI - PMC - PubMed