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Although Rb and p53 represent two important control points in the senescence network, the proteins connecting oncogenicĪctivity to these tumor suppressors are also critical for an efficient anti-tumor response. 1997), and other tumor suppressors have also been linked to senescence ( Lowe et al. The tumor suppressor pathways controlled by p53 and Rb are necessary for the senescence program ( Serrano et al.
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Senescence response previously characterized during serial passage of primary fibroblasts ( Lowe et al. Oncogenes, such as myc or E1A, trigger a cellĭeath program while oncogenes such as ras, raf, or mek induce a permanent growth-arrest program indistinguishable from the
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Normal cells possess natural defenses against transformation into cancer cells. Intriguingly, bypassing oncogene-induced senescence by inactivation of p53 and Rbĭid not eliminate the accumulation of oncogene-induced DNA damage foci (ODDI), suggesting a mechanism that may limit transformation Or RasV12 accumulated DNA damage foci and activated ATM, ATR, Chk1, and Chk2, indicating that aberrant oncogene activation Cells that senesced in response to ca-STAT5A Knocking down ATM was also effective to bypass E2F1-induced senescenceĪnd in combination with Rb inactivation, inhibited RasV12-induced senescence. With Rb inactivation to suppress STAT5A-induced senescence. Here we report that RNA interference against ATM inhibited p53 accumulation in cells expressing oncogenic STAT5 and cooperated