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Recurrent fusion of TMPRSS2 and ETS transcription factor genes in prostate cancer

Scott A Tomlins1, Daniel R Rhodes, Sven Perner

  • 1Department of Pathology, University of Michigan Medical School, 1301 Catherine Street, Ann Arbor, MI 48109-0602, USA.

Science (New York, N.Y.)
|October 29, 2005
PubMed

Insights

Researchers discovered specific gene fusions (TMPRSS2-ERG/ETV1) in prostate cancer, driven by androgen-responsive elements. These rearrangements are common and impact cancer development, offering new diagnostic and therapeutic targets.

Area of Science:

  • Genetics
  • Oncology
  • Bioinformatics

Background:

  • Recurrent chromosomal rearrangements are not well-understood in common carcinomas.
  • Identifying oncogenic aberrations is crucial for understanding cancer development.

Purpose of the Study:

  • To identify candidate oncogenic chromosomal aberrations in prostate cancer using a bioinformatics approach.
  • To characterize recurrent gene fusions involving ETS transcription factors.

Main Methods:

  • Bioinformatics analysis of outlier gene expression.
  • Fluorescence in situ hybridization (FISH) to detect gene rearrangements.
  • Cell line experiments to investigate promoter activity.

Main Results:

  • ERG and ETV1 were identified as outlier ETS transcription factors in prostate cancer.
  • Recurrent gene fusions of TMPRSS2 (5' UTR) to ERG or ETV1 were found.
  • Rearrangements in ERG or ETV1 were present in 23 of 29 prostate cancer samples.
  • Androgen-responsive TMPRSS2 promoter elements mediate ETS overexpression.

Conclusions:

  • TMPRSS2-ERG/ETV1 gene fusions are common in prostate cancer.
  • These rearrangements are driven by androgen-responsive promoters.
  • Findings have implications for carcinoma development, molecular diagnosis, and treatment of prostate cancer.

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