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Stage-specific sensitivity to p53 restoration during lung cancer progression

Author

Listed:
  • David M. Feldser

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Kamena K. Kostova

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Monte M. Winslow

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Sarah E. Taylor

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Chris Cashman

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Charles A. Whittaker

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Francisco J. Sanchez-Rivera

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Rebecca Resnick

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Roderick Bronson

    (Tufts University, and Harvard Medical School, 77 Avenue Louis Pasteur)

  • Michael T. Hemann

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

  • Tyler Jacks

    (Koch Institute for Integrative Cancer Research, and Howard Hughes Medical Institute, Massachusetts Institute of Technology)

Abstract

Limits to antitumour effect of p53 restoration Inactivation of the p53 tumour-suppressor pathway is a common feature of human cancers, prompting suggestions that restoring p53 function in established tumours might be an effective therapy. However, two papers in this week's Nature highlight a practical limitation of p53-directed cancer therapeutics. They show in a K-Ras-driven lung-cancer model that p53-mediated tumour suppression is engaged only at a late stage of tumour progression, when the K-Ras oncogenic signal reaches a threshold that is sufficient to activate the ARF-p53 pathway. This means that p53 re-expression fails to restrict the early stages of tumorigenesis, although it does induce regression of more aggressive tumours.

Suggested Citation

  • David M. Feldser & Kamena K. Kostova & Monte M. Winslow & Sarah E. Taylor & Chris Cashman & Charles A. Whittaker & Francisco J. Sanchez-Rivera & Rebecca Resnick & Roderick Bronson & Michael T. Hemann , 2010. "Stage-specific sensitivity to p53 restoration during lung cancer progression," Nature, Nature, vol. 468(7323), pages 572-575, November.
    • Handle: RePEc:nat:nature:v:468:y:2010:i:7323:d:10.1038_nature09535
    DOI: 10.1038/nature09535
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