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Prostate cancer: gene fusions

Nature Reviews Urology volume 7, page 473 (2010)Cite this article

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Two studies, published in Nature Genetics and Nature Medicine, have shed further light on the role of recurrent gene rearrangements in human prostate cancer, indentifying a new mechanism of recombinogenesis in common gene fusions, and a potential molecular target for therapy in a subset of tumors with novel rearrangements.

In the first study, Michael Haffner and colleagues identify topoisomerase II beta (TOP2B) as a mediator of DNA double-strand breaks (DSBs) in the formation of TMPRSS2–ERG fusions—the most common gene fusion in human prostate cancer. The researchers initially hypothesized that the activity of TOP2B (which catalyzes the formation of transient DSBs, and is required for efficient induction of transcription after estrogen-receptor stimulation) would result in TOP2B-mediated DSBs after androgen stimulation of prostate cells. “However,” says Vasan Yegnasubramanian, the corresponding author, “our investigations took some surprising turns.”

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ORIGINAL RESEARCH PAPERS

  1. Haffner, M. C. et al. Androgen-induced TOP2B-mediated double-strand breaks and prostate cancer gene rearrangements. Nat. Genet. 42, 668–675 (2010)

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Palanisamy, N. et al. Rearrangements of the RAF kinase pathway in prostate cancer, gastric cancer and melanoma. Nat. Med. 16, 793–798 (2010)

    Article  CAS  PubMed  PubMed Central  Google Scholar 

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Authors
  1. Nick Groves-Kirkby
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Groves-Kirkby, N. Prostate cancer: gene fusions. Nat Rev Urol 7, 473 (2010). https://doi.org/10.1038/nrurol.2010.125

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  • DOI: https://doi.org/10.1038/nrurol.2010.125

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