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• W2017932924 abstract "Cancer cells often contain mutations that lead to the loss of retinoblastoma tumor suppressor (Rb) function and the activation of E2F-dependent transcription. As a result, proliferation is deregulated, and sensitivity to apoptotic stimuli is increased. In cell culture studies, the transcription factor E2F1 has been shown to be equally adept at inducing proliferation and apoptosis. Several groups using mouse models have been examining how these E2F1-regulated processes impact the development of cancer. The conclusion from these studies is that E2F1 can function as both oncogene and tumor suppressor gene and that both positive and negative effects on tumorigenesis can be observed whether E2F1 is absent or overexpressed. These findings are discussed in the context of a model in which pathways controlling cell-cycle progression and apoptosis are intimately linked. Mol. Carcinog. 27:151–157, 2000. © 2000 Wiley-Liss, Inc." @default.
• W2017932924 created "2016-06-24" @default.
• W2017932924 creator A5068325660 @default.
• W2017932924 date "2000-03-01" @default.
• W2017932924 modified "2023-10-09" @default.
• W2017932924 title "The paradox ofE2F1: Oncogene and tumor suppressor gene" @default.
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• W2017932924 doi "https://doi.org/10.1002/(sici)1098-2744(200003)27:3<151::aid-mc1>3.0.co;2-c" @default.
• W2017932924 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10708476" @default.
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