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Drugging in the absence of p53

期刊

JOURNAL OF MOLECULAR CELL BIOLOGY
卷 11, 期 3, 页码 255-264

出版社

OXFORD UNIV PRESS
DOI: 10.1093/jmcb/mjz012

关键词

therapeutics; metabolism; DNA damage; replication stress; p53; synthetic lethality

资金

  1. Institute of Molecular and Cell Biology (IMCB), Agency of Science, Technology and Research (A*STAR), Singapore

向作者/读者索取更多资源

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.

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