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Abstract
Although the primary cellular targets of many anticancer agents have been identified,
less is known about the processes leading to the selective cell death of cancer cells
or the molecular basis of drug resistance. p53-deficient mouse embryonic fibroblasts
were used to examine systematically the requirement for p53 in cellular sensitivity
and resistance to a diverse group of anticancer agents. These results demonstrate
that an oncogene, specifically the adenovirus E1A gene, can sensitize fibroblasts
to apoptosis induced by ionizing radiation, 5-fluorouracil, etoposide, and adriamycin.
Furthermore, the p53 tumor suppressor is required for efficient execution of the death
program. These data reinforce the notion that the cytotoxic action of many anticancer
agents involves processes subsequent to the interaction between drug and cellular
target and indicate that divergent stimuli can activate a common cell death program.
Consequently, the involvement of p53 in the apoptotic response suggests a mechanism
whereby tumor cells can acquire cross-resistance to anticancer agents.