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22 July 2008
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ETV1 rearrangements heterogeneous in prostate cancer
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MedWire News: There is a great degree of heterogeneity of Ets variant gene 1 (ETV1) rearrangements in prostate cancer, says an international team of researchers in findings that identified a novel fusion partner for the gene.
Although studies have revealed that ETV1 overexpression occurs in approximately 10% of prostate cancer cases, with several underlying genetic alterations discovered, the clinical significance of alternations in this locus remains unknown.
Jeremy Clark, from the Institute of Cancer Research in Sutton, Surrey, UK, and colleagues used a fluorescence in situ hybridization assay to screen for ETV1 rearrangements in 429 prostate cancer patients diagnosed by transurethral resection, which yielded a total of 945 prostate cancer cores for analysis.
The team reports in the British Journal of Cancer that 5.4% of patients had ETV1 gene rearrangements, one of whom had both ETV1 and V-ets erythroblastosis virus E26 oncogene homolog (avian) (ERG) gene rearrangements. In all, 36% of patients had ERG gene rearrangements.
Comparing the 22 patients with only ETV1 rearrangements and 252 patients with neither ETV1 nor ERG gene rearrangements, the team found that ETV1 rearrangement was significantly associated with Gleason score, baseline prostate-specific antigen, clinical stage, and age, but not with survival.
Just eight (34%) of the ETV1 rearrangements identified were accounted for by the six previously characterized ETV1 translocation partners, with four of these due to fusion to the androgen-repressed gene chromosome 15 open reading frame 21 (C15orf21).
In addition, the androgen-upregulated gene acyl-CoA synthetase long-chain family member 3 was identified as a novel 5'-translocation partner of ETV1 in rapid amplification of 5' complementary DNA ends experiments on RNA extracted from formalin-fixed tissue.
The researchers write: "Our studies report a novel fusion partner for ETV1 and highlight the wide heterogeneity in the range of the ETV1 fusion partners. Interestingly, fusion to the androgen repressed gene C15orf21 was the most common event suggesting the existence of a significant subgroup of cancers that may not respond in a conventional manner to androgen withdrawal therapies."
Br J Cancer 2008; 99: 314-320
http://www.nature.com/bjc/journal/v99/n2/abs/6604472a.html
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