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Improving survival by exploiting tumour dependence on stabilized mutant p53 for treatment

Author

Listed:
  • E. M. Alexandrova

    (Stony Brook University)

  • A. R. Yallowitz

    (Stony Brook University)

  • D. Li

    (Stony Brook University)

  • S. Xu

    (Stony Brook University)

  • R. Schulz

    (Institute of Molecular Oncology, University of Göttingen)

  • D. A. Proia

    (Synta Pharmaceuticals Corp.)

  • G. Lozano

    (University of Texas M. D. Anderson Cancer Center)

  • M. Dobbelstein

    (Institute of Molecular Oncology, University of Göttingen)

  • U. M. Moll

    (Stony Brook University
    Institute of Molecular Oncology, University of Göttingen)

Abstract

Novel hotspot mutant p53 gain-of-function mouse model shows that tumours depend on its sustained expression, and genetic and pharmacological approaches reveal mutant p53 as an actionable cancer drug target.

Suggested Citation

  • E. M. Alexandrova & A. R. Yallowitz & D. Li & S. Xu & R. Schulz & D. A. Proia & G. Lozano & M. Dobbelstein & U. M. Moll, 2015. "Improving survival by exploiting tumour dependence on stabilized mutant p53 for treatment," Nature, Nature, vol. 523(7560), pages 352-356, July.
    • Handle: RePEc:nat:nature:v:523:y:2015:i:7560:d:10.1038_nature14430
    DOI: 10.1038/nature14430
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