TMPRSS2-ETS fusion prostate cancer: biological and clinical implications
- Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA
- Dr Mark A Rubin, Department of Pathology and Laboratory Medicine, 1300 York Ave, Room C410-A, New York, NY 10021, USA; rubinma{at}med.cornell.edu
- Accepted 17 March 2007
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 association with tumour grade.5
TMPRSS2-ERG fusion is a frequent event in prostate cancer; however, the proportion of cases that harbour the gene fusion is still unclear. Prostate specific antigen (PSA) screened hospital based cohort studies detect a frequency of TMPRSS2-ERG fusion, ranging between 40% and 78%.3 6 Well characterised prostatectomy series show frequencies around …
