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

E. M. Alexandrova, A. R. Yallowitz, D. Li, S. Xu, R. Schulz, D. A. Proia, G. Lozano, M. Dobbelstein and U. M. Moll ()
Additional contact information
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

Nature, 2015, vol. 523, issue 7560, 352-356

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.

Date: 2015
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DOI: 10.1038/nature14430

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