Gain-of-function p53 mutants co-opt chromatin pathways to drive cancer growth

Jiajun Zhu, Morgan A. Sammons, Greg Donahue, Zhixun Dou, Masoud Vedadi, Matthäus Getlik, Dalia Barsyte-Lovejoy, Rima Al-awar, Bryson W. Katona, Ali Shilatifard, Jing Huang, Xianxin Hua, Cheryl H. Arrowsmith and Shelley L. Berger ()
Additional contact information
Jiajun Zhu: Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania
Morgan A. Sammons: Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania
Greg Donahue: Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania
Zhixun Dou: Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania
Masoud Vedadi: Structural Genomics Consortium, University of Toronto
Matthäus Getlik: Drug Discovery Program, Ontario Institute for Cancer Research
Dalia Barsyte-Lovejoy: Structural Genomics Consortium, University of Toronto
Rima Al-awar: University of Toronto
Bryson W. Katona: Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania
Ali Shilatifard: Feinberg School of Medicine, Northwestern University
Jing Huang: Cancer and Stem Cell Epigenetics, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute
Xianxin Hua: Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania
Cheryl H. Arrowsmith: Structural Genomics Consortium, University of Toronto
Shelley L. Berger: Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania

Nature, 2015, vol. 525, issue 7568, 206-211

Abstract: A ChIP-seq analysis of the DNA-binding properties of mutant gain-of-function p53 protein compared to wild-type p53 reveals the gain-of-function proteins bind to and activate a distinct set of genes including chromatin modifying enzymes such as the histone methyltransferase MLL; small molecular inhibitors of MLL function may represent a new target for cancers with mutant p53.

Date: 2015
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DOI: 10.1038/nature15251

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