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Selective activation of p53-mediated tumour suppression in high-grade tumours

Author

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  • Melissa R. Junttila

    (University of California San Francisco
    Present addresses: Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 ORE, UK (C.P.M.); Department of Biochemistry, Tennis Court Road, University of Cambridge, Cambridge CB2 1GA, UK (G.I.E.); Department of Molecular Biology, Genentech. Inc. South San Francisco, CA 94080 , USA (M.R.J.).)

  • Anthony N. Karnezis

    (University of California San Francisco)

  • Daniel Garcia

    (University of California San Francisco)

  • Francesc Madriles

    (Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre)

  • Roderik M. Kortlever

    (University of California San Francisco)

  • Fanya Rostker

    (University of California San Francisco)

  • Lamorna Brown Swigart

    (University of California San Francisco)

  • David M. Pham

    (University of California San Francisco)

  • Youngho Seo

    (University of California San Francisco)

  • Gerard I. Evan

    (University of California San Francisco
    Present addresses: Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 ORE, UK (C.P.M.); Department of Biochemistry, Tennis Court Road, University of Cambridge, Cambridge CB2 1GA, UK (G.I.E.); Department of Molecular Biology, Genentech. Inc. South San Francisco, CA 94080 , USA (M.R.J.).)

  • Carla P. Martins

    (University of California San Francisco
    Present addresses: Cancer Research UK Cambridge Research Institute, Li Ka Shing Centre, Robinson Way, Cambridge CB2 ORE, UK (C.P.M.); Department of Biochemistry, Tennis Court Road, University of Cambridge, Cambridge CB2 1GA, UK (G.I.E.); Department of Molecular Biology, Genentech. Inc. South San Francisco, CA 94080 , USA (M.R.J.).)

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

  • Melissa R. Junttila & Anthony N. Karnezis & Daniel Garcia & Francesc Madriles & Roderik M. Kortlever & Fanya Rostker & Lamorna Brown Swigart & David M. Pham & Youngho Seo & Gerard I. Evan & Carla P. M, 2010. "Selective activation of p53-mediated tumour suppression in high-grade tumours," Nature, Nature, vol. 468(7323), pages 567-571, November.
    • Handle: RePEc:nat:nature:v:468:y:2010:i:7323:d:10.1038_nature09526
    DOI: 10.1038/nature09526
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    Cited by:

    1. Jonuelle Acosta & Qinglan Li & Nelson F. Freeburg & Nivitha Murali & Alexandra Indeglia & Grant P. Grothusen & Michelle Cicchini & Hung Mai & Amy C. Gladstein & Keren M. Adler & Katherine R. Doerig & , 2023. "p53 restoration in small cell lung cancer identifies a latent cyclophilin-dependent necrosis mechanism," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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