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
类别
资金
- Institute of Molecular and Cell Biology (IMCB), Agency of Science, Technology and Research (A*STAR), Singapore
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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