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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 4173-4175 |
| Number of pages | 3 |
| Journal | Clinical Cancer Research |
| Volume | 20 |
| Issue number | 16 |
| DOIs | |
| State | Published - Aug 15 2014 |
| Externally published | Yes |
ASJC Scopus subject areas
- Oncology
- Cancer Research