| First Author | Johnson DG | Year | 2000 |
| Journal | Mol Carcinog | Volume | 27 |
| Issue | 3 | Pages | 151-7 |
| PubMed ID | 10708476 | Mgi Jnum | J:61215 |
| Mgi Id | MGI:1354575 | Doi | 10.1002/(sici)1098-2744(200003)27:3<151::aid-mc1>3.0.co;2-c |
| Citation | Johnson DG (2000) The paradox of E2F1: oncogene and tumor suppressor gene. Mol Carcinog 27(3):151-7 |
| abstractText | 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. Copyright 2000 Wiley-Liss, Inc. |
