| Literature DB >> 15549092 |
Scott W Lowe1, Enrique Cepero, Gerard Evan.
Abstract
Mutations that drive uncontrolled cell-cycle progression are requisite events in tumorigenesis. But evolution has installed in the proliferative programmes of mammalian cells a variety of innate tumour-suppressive mechanisms that trigger apoptosis or senescence, should proliferation become aberrant. These contingent processes rely on a series of sensors and transducers that act in a coordinated network to target the machinery responsible for apoptosis and cell-cycle arrest at different points. Although oncogenic mutations that disable such networks can have profound and varied effects on tumour evolution, they may leave intact latent tumour-suppressive potential that can be harnessed therapeutically.Entities:
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Year: 2004 PMID: 15549092 DOI: 10.1038/nature03098
Source DB: PubMed Journal: Nature ISSN: 0028-0836 Impact factor: 49.962