CHEK1 and cancer: p53 elicits its actions via transcription-dependent and transcription-independent mechanisms.3,4 We have shown that a functional p53 signaling pathway is necessary to sensitize cancer cells to DNA-damaging chemotherapeutic agents, such as CDDP.3,5–11 p53 is activated in response to genomic insults by the DNA damage sensors ataxia talengiectasia mutated protein (ATM) and ataxia talengiectasia and Rad3-related protein (ATR) and their downstream effectors checkpoint kinases 1 and 2 (Chk1 and Chk2).