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Sci. STKE, 30 January 2007 PERSPECTIVESEGFR Signaling Inhibits E2F1-Induced Apoptosis in Vivo: Implications for Cancer TherapyMina and Everard Goodman Faculty of Life Science, Bar Ilan University, Ramat Gan 52900, Israel. Abstract: The retinoblastoma tumor suppressor (RB) restricts cell proliferation by regulating members of the E2F family of transcription factors. In human tumors RB is often inactivated, resulting in aberrant E2F-dependent transcription and uncontrolled proliferation. One of the E2F proteins, E2F1, can also induce apoptosis. The extent of E2F1-induced apoptosis is known to be tissue- and cell-specific, but until now, it has been unclear what variables determine cellular sensitivity to E2F1-induced apoptosis in vivo. A recent study reveals epidermal growth factor receptor (EGFR) signaling to be one such variable, as EGFR signaling cooperates with RB in inhibiting E2F1-induced apoptosis. This finding raises the possibility that therapeutic manipulation of EGFR signaling may specifically trigger the death of cancer cells with inactive RB, thereby enabling "targeted" cancer treatments. *Corresponding author. E-mail, ginsbed{at}mail.biu.ac.il
Citation: D. Ginsberg, EGFR Signaling Inhibits E2F1-Induced Apoptosis in Vivo: Implications for Cancer Therapy. Sci. STKE 2007, pe4 (2007). THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
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Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882