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DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome.[1][2] A weakened capacity for DNA repair is a risk factor for the development of cancer.[3] DNA is constantly modified in cells, by internal metabolic by-products, and by external ionizing radiation, ultraviolet light, and medicines, resulting in spontaneous DNA damage involving tens of thousands of individual molecular lesions per cell per day.[4][5] DNA modifications can also be programmed.[5]
Molecular lesions can cause structural damage to the DNA molecule, and can alter or eliminate the cell's ability for transcription and gene expression. Other lesions may induce potentially harmful mutations in the cell's genome, which affect the survival of its daughter cells following mitosis. Consequently, DNA repair as part of the DNA damage response (DDR) is constantly active. When normal repair processes fail, including apoptosis, irreparable DNA damage may occur, that may be a risk factor for cancer.[3]
The degree of DNA repair change made within a cell depends on various factors, including the cell type, the age of the cell, and the extracellular environment. A cell that has accumulated a large amount of DNA damage or can no longer effectively repair its DNA may enter one of three possible states:
- an irreversible state of dormancy, known as senescence
- apoptosis a form of programmed cell death[6][7]
- unregulated division, which can lead to the formation of a tumor that is cancerous
The DNA repair ability of a cell is vital to the integrity of its genome and thus to the normal functionality of that organism. Many genes that were initially shown to influence life span have turned out to be involved in DNA damage repair and protection.[8]
The 2015 Nobel Prize in Chemistry was awarded to Tomas Lindahl, Paul Modrich, and Aziz Sancar for their work on the molecular mechanisms of DNA repair processes.[9][10]
- ^ "Nature Reviews Series: DNA damage". Nature Reviews Molecular Cell Biology. 5 July 2017. Retrieved 7 November 2018.
- ^ Alberts B, Hopkin K, Johnson A, Morgan D, Raff M, Roberts K, et al. (2019). Essential cell biology (Fifth ed.). New York London: W. W. Norton & Company. p. 266. ISBN 9780393680393.
- ^ a b Minten EV, Yu DS (May 2019). "DNA Repair: Translation to the Clinic". Clinical Oncology (Royal College of Radiologists (Great Britain)). 31 (5): 303–310. doi:10.1016/j.clon.2019.02.007. PMC 6450773. PMID 30876709.
- ^ Lodish H, Berk A, Matsudaira P, Kaiser CA, Krieger M, Scott MP, et al. (2004). Molecular Cell Biology (5th ed.). WH Freeman. p. 963. ISBN 978-0-7167-4366-8. OCLC 53798180.
- ^ a b Oksenych V, Kainov DE (January 2021). "DNA Damage Response". Biomolecules. 11 (1): 123. doi:10.3390/biom11010123. PMC 7832852. PMID 33477863.
- ^ Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P (2002). "Programmed Cell Death (Apoptosis)". Molecular Biology of the Cell. 4th edition. Garland Science. Retrieved 12 April 2025.
- ^ "Apoptosis". www.genome.gov. Retrieved 12 April 2025.
- ^ Browner WS, Kahn AJ, Ziv E, Reiner AP, Oshima J, Cawthon RM, et al. (December 2004). "The genetics of human longevity". The American Journal of Medicine. 117 (11): 851–60. CiteSeerX 10.1.1.556.6874. doi:10.1016/j.amjmed.2004.06.033. PMID 15589490.
- ^ Broad WJ (7 October 2015). "Nobel Prize in Chemistry Awarded to Tomas Lindahl, Paul Modrich and Aziz Sancar for DNA Studies". The New York Times. Retrieved 7 October 2015.
- ^ Staff (7 October 2015). "The Nobel Prize in Chemistry 2015 – DNA repair – providing chemical stability for life" (PDF). Nobel Prize. Retrieved 7 October 2015.
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