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TMPRSS2-ETS fusion prostate cancer: biological and clinical implications

Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA

Correspondence to:
Dr Mark A Rubin, Department of Pathology and Laboratory Medicine, 1300 York Ave, Room C410-A, New York, NY 10021, USA; rubinma@med.cornell.edu

Accepted 17 March 2007

Keywords: erg; gene fusion; prognosis; prostate cancer; tmprss2

The first 150 words of the full text of this article appear below.

The fusion of TMPRSS2 with ETS genes was recently reported by Tomlins et al¹ as the first recurrent genomic alteration in prostate cancer and has been now confirmed by multiple independent groups. The ETS-related gene (ERG) is the most common fusion partner for the androgen regulated gene TMPRSS2. Both genes are located within 3 Mb on chromosome 21 and the most common mechanism for fusion is through an interstitial deletion. ETV1 and ETV4, other members of the ETS family, have been detected in only a minority of cases.^2–4 The underlying biology of TMPRSS2-ERG fusion prostate cancer is poorly understood. However, emerging data shows that TMPRSS2-ERG fusion is a frequent and early event in prostate cancer pathogenesis, with distinct biology and a more aggressive phenotype. In this issue, Rajput et al show the association between TMPRSS2-ERG fusion and more aggressive prostate cancer based on an . . . [Full text of this article]

Relevant Article

Frequency of the TMPRSS2:ERG gene fusion is increased in moderate to poorly differentiated prostate cancers

Ashish B Rajput, Melinda A Miller, Alessandro De Luca, Niki Boyd, Sam Leung, Antonio Hurtado-Coll, Ladan Fazli, Edward C Jones, Jodie B Palmer, Martin E Gleave, Michael E Cox, and David G Huntsman
J. Clin. Pathol. 2007 60: 1238-1243. [Abstract] [Full Text] [PDF]

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