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p53 that is activated in response to DNA-damaging stress can induce apoptosis or either transient or permanent cell cycle arrests. Apoptosis and permanent cell cycle arrest (senescence) are bona-fide tumor suppressor mechanisms through which p53 inhibits cancer cell survival. In contrast, transient cell cycle arrests induced by p53 can increase survival by allowing cells time to repair their DNA before proceeding with cell division. Mechanisms that control the choice of response to p53 (apoptosis vs arrest) are not fully understood. There is abundant crosstalk between p53 and the IGF-1R/AKT/mTORC1 signaling pathway. Recent studies indicate this crosstalk can determine the choice of response to p53. These findings have clear implications for the potential use of IGF-1R pathway inhibitors against p53 wild-type or p53-null or mutant cancers.

The IGF-1R/AKT pathway determines cell fate in response to p53