Senescence

Helen Rizos*, Lyndee L. Scurr

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Cellular senescence is a program 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 potently prevent tumour formation in vivo. The precise mechanisms driving senescence are still not completely defined, although the pRb and p53 tumour suppressor pathways are critical effectors. Senescent cells also develop aberrant gene expression profiles and acquire pro-inflammatory behaviour that may contribute to organismal ageing and age-related diseases, including cancer. It is not yet clear whether the pro-ageing actions of senescent cells can be minimised in vivo, but the therapeutic potential of this stress-induced program 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
EditorsA Bosserhoff
Place of PublicationWien
PublisherSpringer, Springer Nature
Pages235-254
Number of pages20
ISBN (Electronic)9783709103715
ISBN (Print)9783709103708
DOIs
Publication statusPublished - 18 May 2011
Externally publishedYes

Keywords

  • ONCOGENE-INDUCED SENESCENCE
  • CELL-CYCLE ARREST
  • MELANOMA SUSCEPTIBILITY GENES
  • HUMAN-DIPLOID FIBROBLASTS
  • HEMATOPOIETIC STEM-CELLS
  • DNA-DAMAGE RESPONSE
  • IN-VIVO
  • TUMOR SUPPRESSION
  • BETA-GALACTOSIDASE
  • C-MYC

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