期刊
TRENDS IN MOLECULAR MEDICINE
卷 17, 期 2, 页码 88-96出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2010.10.009
关键词
-
资金
- Komen Foundation
Defects in p53 function, which occur frequently in human cancers due to mutations in TP53 or disruptions in the p53 regulatory pathway, render cells dependent on CHK1 (Checkpoint Kinase 1) to activate cell cycle checkpoints. In the presence of DNA damage or replication stress, inhibition of CHK1 leads to mitotic catastrophe and cell death in p53-deficient tumors while sparing p53-proficient cells. CHK1 inhibitors sensitize tumors to a variety of DNA-damaging agents or antimetabolites in preclinical models and are being evaluated in early phase clinical trials. In this review, we summarize recent advances and controversies in the development and application of CHK1 inhibitors as cancer therapeutics.
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