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Drugging in the absence of p53
Obed Akwasi Aning1 and Chit Fang Cheok 1,2,3,*
1 Institute of Molecular and Cell Biology, A*STAR, Singapore
2 Department of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
3 Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, Singapore
*Correspondence to:Chit Fang Cheok, E-mail: cheokcf@imcb.a-star.edu.sg
J Mol Cell Biol, Volume 11, Issue 3, March 2019, Pages 255-264  https://doi.org/10.1093/jmcb/mjz012
Keyword: therapeutics, metabolism, DNA damage, replication stress, p53, synthetic lethality
Inactivation of the p53 gene is a key driver of tumorigenesis in various cancer cohorts and types. The quest for a successful p53-based therapy that holds the promise of treating more than half of the cancer population has culminated in extensive knowledge about the role and function of p53 and led to new proposed innovative strategies against p53-defective cancers. We will discuss some of these latest studies with a focus on metabolic regulation and DNA damage response and also highlight novel functions of p53 in these pathways that may provide a contemporary rationale for targeting p53 loss in tumors.