| Literature DB >> 25125257 |
Julie E Bauman1, Christine H Chung2.
Abstract
Mutations in TP53, encoding the master tumor suppressor p53, have posed a developmental therapeutic dilemma due to inability to target loss of function. Inhibition of WEE1 or CHK1 kinase, negative regulators of the G2-M checkpoint, selectively sensitizes p53-deficient cells to exogenous DNA damage, abrogating G2 arrest and precipitating mitotic catastrophe. ©2014 American Association for Cancer Research.Entities:
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Year: 2014 PMID: 25125257 PMCID: PMC4860818 DOI: 10.1158/1078-0432.CCR-14-0720
Source DB: PubMed Journal: Clin Cancer Res ISSN: 1078-0432 Impact factor: 12.531