Senescence and epigenetic dysregulation in cancer

Peter Neumeister, Chris Albanese, Beate Balent, John Greally, Richard G. Pestell

Research output: Contribution to journalShort surveypeer-review

46 Scopus citations


Mammalian cells have a finite proliferative lifespan, at the end of which they are unable to enter S phase in response to mitogenic stimuli. They undergo morphological changes and synthesize an altered repertoire of cell type-specific proteins. This non-proliferative state is termed replicative senescence and is regarded as a major tumor suppressor mechanism. The ability to overcome senescence and obtain a limitless replicative potential is called immortalization, and considered to be one of the prerequisites of cancer formation. While senescence mainly represents a genetically governed process, epigenetic changes in cancer have received increasing attention as an alternative mechanism for mediating gene expression changes in transformed cells. DNA methylation of promoter-containing CpG islands has emerged as an epigenetic mechanism of silencing tumor suppressor genes. New insights are being gained into the mechanisms causing aberrant methylation in cancer and evidence suggests that aging is accompanied by accumulation of cells with aberrant CpG island methylation. Aberrant methylation may contribute to many of the physiological and pathological changes associated with aging including tumor development. Finally, we describe how genes involved in promoting longevity might inhibit pathways promoting tumorigenesis.

Original languageEnglish (US)
Pages (from-to)1475-1490
Number of pages16
JournalInternational Journal of Biochemistry and Cell Biology
Issue number11
StatePublished - Nov 2002


  • Acetylation
  • Aging
  • Cancer
  • Methylation
  • Senescence

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology


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