Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

Senescence and Immortalization

Living reference work entry
DOI: https://doi.org/10.1007/978-3-642-27841-9_5238-2

Definition

Senescence is the permanent exit of a cell from the cell division cycle, accompanied by morphological and biochemical changes characteristic of aging.

Immortalization is the ability of cell populations to undergo an unlimited number of cell divisions.

Characteristics

Senescence

Normal mammalian somatic cells can proliferate only a limited number of times in vitro, and the maximum number is often referred to as the “Hayflick limit.” When this limit is reached, the cells undergo various morphological and biochemical changes suggestive of aging, so the process is referred to as senescence. Senescent cells can remain metabolically active for a long period of time, even though they have permanently exited from the cell cycle. Typically, they secrete inflammatory factors. Senescence is thus distinct from cell death (including apoptosis, necrosis and autophagy). It is also distinct from terminal differentiation, where cells also exit permanently from the cell cycle but undergo...

Keywords

Dyskeratosis Congenita Hayflick Limit Telomere Maintenance Mechanism Normal Human Somatic Cell Heterogeneous Telomere Length 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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References

  1. Blackburn EH, Greider CW, Szostak JW (2006) Telomeres and telomerase: the path from maize, Tetrahymena and yeast to human cancer and aging. Nat Med 12:1133–1138.CrossRefPubMedGoogle Scholar
  2. Campisi J (2013) Aging, cellular senescence, and cancer. Annu Rev Physiol 75:685–705.CrossRefPubMedPubMedCentralGoogle Scholar
  3. Pickett HA, Reddel RR (2015) Molecular mechanisms of activity and derepression of alternative lengthening of telomeres. Nat Struct Molec Biol 22:875–80.CrossRefGoogle Scholar
  4. Reddel RR (2000) The role of senescence and immortalization in carcinogenesis. Carcinogenesis 21:477–484CrossRefPubMedGoogle Scholar
  5. Reddel RR (2014) Telomere maintenance mechanisms in cancer: clinical implications. Curr Pharm Des 20:6361–6374.CrossRefPubMedPubMedCentralGoogle Scholar

See Also

  1. (2012) Alternative Lengthening of Telomeres. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 148. doi:10.1007/978-3-642-16483-5_210Google Scholar
  2. (2012) End Replication Problem. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1221. doi:10.1007/978-3-642-16483-5_1867Google Scholar
  3. (2012) P16INK4A. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 2739. doi:10.1007/978-3-642-16483-5_4575Google Scholar
  4. (2012) P53. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 2747. doi:10.1007/978-3-642-16483-5_4331Google Scholar
  5. (2012) PML Nuclear Bodies. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 2931. doi:10.1007/978-3-642-16483-5_4644Google Scholar
  6. (2012) RB1. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 3189. doi:10.1007/978-3-642-16483-5_4964Google Scholar
  7. (2012) Telomere. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 3637. doi:10.1007/978-3-642-16483-5_5716Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Children’s Medical Research Institute, The University of SydneyWestmeadAustralia