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ETS rearrangements and prostate cancer initiation

Author

Listed:
  • Brett S. Carver

    (Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
    Memorial Sloan-Kettering Cancer Center)

  • Jennifer Tran

    (Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center)

  • Zhenbang Chen

    (Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
    Cancer Genetics Program, Beth Israel Deaconess Medical Center, Harvard Medical School)

  • Arkaitz Carracedo-Perez

    (Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center)

  • Andrea Alimonti

    (Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
    Cancer Genetics Program, Beth Israel Deaconess Medical Center, Harvard Medical School)

  • Caterina Nardella

    (Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
    Cancer Genetics Program, Beth Israel Deaconess Medical Center, Harvard Medical School)

  • Anuradha Gopalan

    (Memorial Sloan-Kettering Cancer Center)

  • Peter T. Scardino

    (Memorial Sloan-Kettering Cancer Center)

  • Carlos Cordon-Cardo

    (Columbia University)

  • William Gerald

    (Memorial Sloan-Kettering Cancer Center)

  • Pier Paolo Pandolfi

    (Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center
    Memorial Sloan-Kettering Cancer Center
    Cancer Genetics Program, Beth Israel Deaconess Medical Center, Harvard Medical School)

Abstract

Arising from: Tomlins et al. Nature 448, 595–599 (2007)10.1038/nature06024 ; Tomlins et al. reply The first recurrent translocation event in prostate cancer has been recently described1; it results in the translocation of an ETS (E26 transformation specific) transcription factor (ERG or ETV1) to the TMPRSS2 promoter region, which contains androgen responsive elements1. The TMPRSS2:ERG genetic rearrangement has been reported to occur in approximately 40% of primary prostate tumours (ETV1 genetic rearrangements occur at a much lower frequency), and it results in the aberrant androgen-regulated expression of ERG1,2,3. Tomlins et al.4 concluded that ETS genetic rearrangements are sufficient to initiate prostate neoplasia. However, here we show that ETS genetic rearrangements may in fact represent progression events rather than initiation events in prostate tumorigenesis. To this end, we demonstrate that the prostate-specific overexpression of ERG does not initiate prostate tumorigenesis.

Suggested Citation

  • Brett S. Carver & Jennifer Tran & Zhenbang Chen & Arkaitz Carracedo-Perez & Andrea Alimonti & Caterina Nardella & Anuradha Gopalan & Peter T. Scardino & Carlos Cordon-Cardo & William Gerald & Pier Pao, 2009. "ETS rearrangements and prostate cancer initiation," Nature, Nature, vol. 457(7231), pages 1-1, February.
    • Handle: RePEc:nat:nature:v:457:y:2009:i:7231:d:10.1038_nature07738
    DOI: 10.1038/nature07738
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