Helen Rizos*, Sebastian Haferkamp, Lyndee L. Scurr

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Cellular senescence is a programme initiated by many stress signals including aberrant activation of oncogenes, DNA damage, oxidative lesions, and telomere attrition. Once engaged, senescence irreversibly limits cellular proliferation and can alter metabolism and suppress tumour formation in vivo. The precise mechanisms driving senescence are still not precisely defined, although the p53-DNA damage response and pRb tumour suppressor pathways are critical effectors. Senescent cells also develop aberrant gene expression profiles and acquire pro-inflammatory behaviour that may contribute to organismal aging and age-related diseases, including cancer. It is not yet clear whether the detrimental properties of senescent cells can be minimised in vivo, but the therapeutic potential of this stress-induced programme may depend on establishing a new equilibrium that favours tumour suppressor activity.

Original languageEnglish
Title of host publicationMelanoma development
Subtitle of host publicationmolecular biology, genetics and clinical application
EditorsAnja K. Bosserhoff
Place of PublicationCham
PublisherSpringer, Springer Nature
Number of pages22
ISBN (Electronic)9783319413198
ISBN (Print)9783319413174
Publication statusPublished - 1 Jan 2017


  • Aging
  • Hayflick limit
  • Heterochromatin formation
  • p53
  • pRb
  • SASP
  • Senescence
  • Telomeres


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