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Tomlins et al. reply

Author

Listed:
  • Scott A. Tomlins

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Bharathi Laxman

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Saravana M. Dhanasekaran

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Beth E. Helgeson

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Xuhong Cao

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • David S. Morris

    (University of Michigan Medical School)

  • Anjana Menon

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Xiaojun Jing

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Qi Cao

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Bo Han

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Jindan Yu

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Lei Wang

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • James E. Montie

    (University of Michigan Medical School
    Comprehensive Cancer Center, University of Michigan Medical School)

  • Mark A. Rubin

    (Brigham and Women’s Hospital, Harvard Medical School
    Dana-Farber Cancer Institute, Harvard Medical School)

  • Kenneth J. Pienta

    (University of Michigan Medical School
    University of Michigan Medical School)

  • Diane Roulston

    (Michigan Center for Translational Pathology, University of Michigan Medical School)

  • Rajal B. Shah

    (Michigan Center for Translational Pathology, University of Michigan Medical School
    University of Michigan Medical School
    Comprehensive Cancer Center, University of Michigan Medical School)

  • Sooryanarayana Varambally

    (Michigan Center for Translational Pathology, University of Michigan Medical School
    Comprehensive Cancer Center, University of Michigan Medical School)

  • Rohit Mehra

    (Michigan Center for Translational Pathology, University of Michigan Medical School
    Comprehensive Cancer Center, University of Michigan Medical School)

  • Arul M. Chinnaiyan

    (Michigan Center for Translational Pathology, University of Michigan Medical School
    University of Michigan Medical School
    Comprehensive Cancer Center, University of Michigan Medical School)

Abstract

Replying to: Carver, B. S. et al. Nature 457, 10.1038/nature07738 (2009) Carver et al. 1 question our recent report that mice expressing ETV1 under the control of the probasin promoter (ARR2Pb) develop mouse prostatic intraepithelial neoplasia (mPIN)2. They report the generation of transgenic ARR2Pb-ERG mice with no phenotypic differences from control mice. They propose that this demonstrates that ETS genetic rearrangements do not initiate prostate tumorigenesis and use data from human prostate cancer studies to propose that ETS rearrangements are associated with progression from PIN to prostate cancer. Although we and others have shown that ARR2Pb-ETV1 and ARR2Pb-ERG mice develop mPIN, we have consistently proposed that in human prostate cancer development, ETS rearrangements mediate the transition from PIN to cancer.

Suggested Citation

  • Scott A. Tomlins & Bharathi Laxman & Saravana M. Dhanasekaran & Beth E. Helgeson & Xuhong Cao & David S. Morris & Anjana Menon & Xiaojun Jing & Qi Cao & Bo Han & Jindan Yu & Lei Wang & James E. Montie, 2009. "Tomlins et al. reply," Nature, Nature, vol. 457(7231), pages 2-3, February.
    • Handle: RePEc:nat:nature:v:457:y:2009:i:7231:d:10.1038_nature07739
    DOI: 10.1038/nature07739
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