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- W2314485594 abstract "Recent investigation further defines the role of p53 and of signaling events upstream and downstream of p53 in apoptosis following drug-induced DNA damage. The transcription factors NF-kappaB and AP-1 can be activated, and then directly transactivate FasL in response to chemotherapeutic agents. Death receptors for FasL (Fas) and for TRAIL (DR4, DR5) are emerging as important regulators of drug-induced apoptosis in human cancers, mediated by caspase activation. Apoptosis has been accepted as the predominant mechanism of drug-induced cell death in preclinical experimental models and in clinically sensitive tumors. However, drug-induced cell death can include acute or delayed apoptosis, necrosis, or a delayed mitotic death, and require further delineation for their relative contribution to tumor responses in vivo." @default.
- W2314485594 created "2016-06-24" @default.
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- W2314485594 date "1999-11-01" @default.
- W2314485594 modified "2023-10-12" @default.
- W2314485594 title "Apoptosis and drug response" @default.
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- W2314485594 doi "https://doi.org/10.1097/00001622-199911000-00008" @default.
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