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- Publisher
- Springer Journals
- Copyright
- Copyright © 2007 by Nature Publishing Group
- Subject
- Life Sciences; Life Sciences, general; Cell Biology; Cancer Research; Developmental Biology; Stem Cells; Biochemistry, general
- ISSN
- 1471-0072
- eISSN
- 1471-0080
- DOI
- 10.1038/nrm2233
- Publisher site
- See Article on Publisher Site
Abstract
Cellular senescence is a multifaceted process that arrests the proliferation of cells that are at risk of neoplastic transformation. Many stimuli elicit a senescence response. These include dysfunctional telomeres, DNA damage, the expression of certain oncogenes, perturbations to chromatin organization and strong mitogenic signals. Two powerful tumour suppressor pathways, controlled by the p53 and retinoblastoma (pRB) proteins, are important for establishing and maintaining the senescence growth arrest. These pathways respond to somewhat different stimuli but interact and cooperate to control the senescence response. There is now substantial evidence that cellular senescence is a barrier to malignant tumorigenesis in vivo. In mammalian organisms, cells that express markers of senescence have been shown to accumulate with age and at sites of certain age-related pathologies. There is also mounting evidence that cellular senescence contributes to ageing. Although this evidence is still mainly circumstantial, it suggests that the senescence response might be an example of evolutionary antagonistic pleiotropy.
Journal
Nature Reviews Molecular Cell Biology – Springer Journals
Published: Sep 1, 2007