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Review
E2F1 as a Target: Promoter-Driven Suicide and Small Molecule Modulators
William G. Kaelin, Jr.
volume 2
july/august 2003 supplementPages: S048-S054
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Decreased requirements for mitogens and diminished sensitivity to antiproliferative signals are among the hallmarks of human cancer. These attributes are due, at least partly, to mutations that directly or indirectly compromise the function of the retinoblastoma tumor suppressor protein (pRB), which is a negative regulator of a family of cell-cycle regulatory transcription factors referred to generically as E2F. Activation of E2F target genes is sufficient to induce unscheduled cellular proliferation but, under certain circumstances, can also lead to programmed cell death (apoptosis). This chapter will review the role of E2F in cancer and outline opportunities for the development of anticancer agents based on E2F biology.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.




