Apr 1, 1997

The biology of replicative senescence

European Journal of Cancer : Official Journal for European Organization for Research and Treatment of Cancer (EORTC) [and] European Association for Cancer Research (EACR)
J Campisi

Abstract

Most cells cannot divide indefinitely due to a process termed cellular or replicative senescence. Replicative senescence appears to be a fundamental feature of somatic cells, with the exception of most tumour cells and possibly certain stem cells. How do cells sense the number of divisions they have completed? Although it has not yet been critically tested, the telomere shortening hypothesis is currently perhaps the best explanation for a cell division 'counting' mechanism. Why do cells irreversibly cease proliferation after completing a finite number of divisions? It is now known that replicative senescence alters the expression of a few crucial growth-regulatory genes. It is not known how these changes in growth-regulatory gene expression are related to telomere shortening in higher eukaryotes. However, lower eukaryotes have provided several plausible mechanisms. Finally, what are the physiological consequences of replicative senescence? Several lines of evidence suggest that, at least in human cells, replicative senescence is a powerful tumour suppressive mechanism. There is also indirect evidence that replicative senescence contributes to ageing. Taken together, current findings suggest that, at least in mammals, replicativ...Continue Reading

  • References46
  • Citations217

References

Mentioned in this Paper

Tumor Cells, Uncertain Whether Benign or Malignant
Cell Aging
Telomere Shortening
Metastasis Suppressor Genes
Cell Division
Neoplasms
Tumor Lysis Syndrome
Senility
Genes, Regulator
Cell Division Phases

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