Encyclopedia of Cancer

Living Edition
| Editors: Manfred Schwab

DNA Damage-Induced Apoptosis

Living reference work entry
First Online:
Received:
Accepted:
DOI: https://doi.org/10.1007/978-3-642-27841-9_1673-2
How to cite

Synonyms

DNA damage-triggered death signaling pathways; DNA repair and damage processing

Definition

DNA damage-induced cell death is executed by apoptosis, necrosis, parthanatos, mitotic catastrophe, and overactivated autophagy. From these different forms of cell inactivation, apoptosis is the main route of death following DNA damage. Cells undergo apoptosis upon genotoxic stress via the death receptor and/or the intrinsic mitochondrial pathway. DNA damage-induced apoptosis is thought to be a mechanism protecting against cancer because it eliminates genetically damaged cells. This is most obvious in sunburned skin in which p53 upregulation initiates the apoptotic process in response to light-induced DNA damage.

Characteristics

Summary

Not every type of DNA damage induces apoptosis. Many DNA lesions are tolerated by the cell, some are mutagenic without being toxic and some are more toxic than mutagenic. Apoptosis-inducing lesions are O6-methylguanine, O6-chloroethylguanine, base N-alkyl...

Keywords

Mismatch Repair Nucleotide Excision Repair Ataxia Telangiectasia Mutate Ataxia Telangiectasia Mitotic Catastrophe 
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.
This is a preview of subscription content, log in to check access

References

  1. Kaina B (2003) DNA damage-triggered apoptosis: critical role of DNA repair, double-strand breaks, cell proliferation and signaling. Biochem Pharmacol 66(8):1547–1554CrossRefPubMedGoogle Scholar
  2. Lavin MF et al (2005) ATM signaling and genomic stability in response to DNA damage. Mutat Res 569:123–132CrossRefPubMedGoogle Scholar
  3. Ljungman M, Zhang F (1996) Blockage of RNA polymerase as a possible trigger for UV light-induced apoptosis. Oncogene 13:823–831PubMedGoogle Scholar
  4. Mansouri A et al (2003) Sustained activation of JNK/p38 MAPK pathways in response to cisplatin leads to Fas ligand induction and cell death in ovarian carcinoma cells. J Biol Chem 278(21):19245–19256CrossRefPubMedGoogle Scholar
  5. Roos WP, Kaina B (2006) DNA damage-induced cell death by apoptosis. Trends Mol Med 12:440–450CrossRefPubMedGoogle Scholar
  6. Roos WP, Thomas AD, Kaina B (2016) DNA damage and the balance between survival and death in cancer biology. Nature Rev Cancer, 16 (1): 20–33.CrossRefGoogle Scholar

See Also

  1. (2012) Ataxia Telangiectasia. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 298. doi: 10.1007/978-3-642-16483-5_426Google Scholar
  2. (2012) ATR. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 302. doi: 10.1007/978-3-642-16483-5_443Google Scholar
  3. (2012) Caspase-3. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 675. doi: 10.1007/978-3-642-16483-5_874Google Scholar
  4. (2012) CD95. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 703. doi: 10.1007/978-3-642-16483-5_939Google Scholar
  5. (2012) CHK1. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 817. doi: 10.1007/978-3-642-16483-5_1101Google Scholar
  6. (2012) Cytochrome c. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1043. doi: 10.1007/978-3-642-16483-5_1458Google Scholar
  7. (2012) DNA Double Strand Breaks. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1139. doi: 10.1007/978-3-642-16483-5_1675Google Scholar
  8. (2012) FAS. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1379. doi: 10.1007/978-3-642-16483-5_2121Google Scholar
  9. (2012) G1/S Transition. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1484. doi: 10.1007/978-3-642-16483-5_2291Google Scholar
  10. (2012) Ionizing Radiation. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1907. doi: 10.1007/978-3-642-16483-5_3139Google Scholar
  11. (2012) JUN. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1929. doi: 10.1007/978-3-642-16483-5_3186Google Scholar
  12. (2012) Knock-Out Mouse. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 1957. doi: 10.1007/978-3-642-16483-5_3239Google Scholar
  13. (2012) MRN Complex. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 2382. doi: 10.1007/978-3-642-16483-5_6622Google Scholar
  14. (2012) NBS1. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 2468. doi: 10.1007/978-3-642-16483-5_3984Google Scholar
  15. (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
  16. (2012) Replication. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 3254. doi: 10.1007/978-3-642-16483-5_5031Google Scholar
  17. (2012) Transcription. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 3752. doi: 10.1007/978-3-642-16483-5_5899Google Scholar
  18. (2012) Ultraviolet Light. In: Schwab M (ed) Encyclopedia of Cancer, 3rd edn. Springer Berlin Heidelberg, p 3841. doi: 10.1007/978-3-642-16483-5_6101Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  1. 1.Department of ToxicologyUniversity Medical Center MainzMainzGermany