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Primary cells suppress oncogene-dependent apoptosis


Oncogenes that promote cell-cycle progression also sensitize cells to agents that induce apoptosis. Sensitization is thought to be caused by the induction of proapoptotic factors. Alternatively, sensitization may require the inactivation of inhibitors that ordinarily provide protection against cell death. Here we show that the adenoviral oncogene E1A sensitizes cells to an anti-cancer drug by at least two pathways. One establishes a link between the drug and pro-apoptotic factors, but is not sufficient for sensitization without the second pathway, which suppresses inhibitors of apoptosis.

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Figure 1: IODA is constitutively present in normal cells and prevents oncogene-dependent apoptosis.
Figure 2: E1A allows etoposide-induced translocation of Bax to mitochondria.


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We thank J. Rodriguez for IMR90myc cells, and G. Hannon, M. Hastings, D. Helfman, A. Krainer and members of the Lazebnik laboratory for critical reading of the manuscript. This work was supported by National Institutes of Health grant no. CA13106-25, a Seraph Foundation grant to Y.L., and a Roche Research Foundation fellowship to D.M.D.

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Correspondence to Yuri A. Lazebnik.

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Duelli, D., Lazebnik, Y. Primary cells suppress oncogene-dependent apoptosis. Nat Cell Biol 2, 859–862 (2000).

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