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E1A and c-myc are oncogenes that can deregulate the cell cycle and promote transformation under conditions where normal cell-cycle checkpoints are inactivated. In situations where cell-cycle checkpoints are intact, the E1A and c-Myc proteins potently induce apoptosis, a property that is believed to be the end result of a cellular response to uncontrolled growth-promoting signals. p53 is a key regulator of E1A and c-myc-induced apoptosis and, together with the oncoproteins, may transcriptionally activate numerous genes whose products influence, or are themselves, members of the core apoptotic machinery. The upstream signaling events and the ultimate apoptotic pathways activated by E1A and c-Myc are discussed in this review.
Breckenridge et al. (Sat,) studied this question.