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==Degradation== Multicellular organisms replace worn-out cells through cell division. In some animals, however, cell division eventually halts. In [[human]]s this occurs, on average, after 52 divisions, known as the [[Hayflick limit]]. The cell is then referred to as [[Senescence|senescent]]. With each division the cells [[telomere]]s, protective sequences of DNA on the end of a [[chromosome]] that prevent degradation of the chromosomal DNA, [[Telomere shortening|shorten]]. This shortening has been correlated to negative effects such as age-related diseases and shortened lifespans in humans.<ref>{{cite journal | vauthors = Jiang H, Schiffer E, Song Z, Wang J, Zürbig P, Thedieck K, Moes S, Bantel H, Saal N, Jantos J, Brecht M, Jenö P, Hall MN, Hager K, Manns MP, Hecker H, Ganser A, Döhner K, Bartke A, Meissner C, Mischak H, Ju Z, Rudolph KL | display-authors = 6 | title = Proteins induced by telomere dysfunction and DNA damage represent biomarkers of human aging and disease | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 105 | issue = 32 | pages = 11299–304 | date = August 2008 | pmid = 18695223 | pmc = 2516278 | doi = 10.1073/pnas.0801457105 | bibcode = 2008PNAS..10511299J | doi-access = free }}</ref><ref>{{cite journal | vauthors = Cawthon RM, Smith KR, O'Brien E, Sivatchenko A, Kerber RA | title = Association between telomere length in blood and mortality in people aged 60 years or older | journal = Lancet | volume = 361 | issue = 9355 | pages = 393–5 | date = February 2003 | pmid = 12573379 | doi = 10.1016/S0140-6736(03)12384-7 | s2cid = 38437955 }}</ref> [[Cancer]] cells, on the other hand, are not thought to degrade in this way, if at all. An [[enzyme]] complex called [[telomerase]], present in large quantities in cancerous cells, rebuilds the telomeres through synthesis of telomeric DNA repeats, allowing division to continue indefinitely.<ref>{{cite journal | vauthors = Jafri MA, Ansari SA, Alqahtani MH, Shay JW | title = Roles of telomeres and telomerase in cancer, and advances in telomerase-targeted therapies | journal = Genome Medicine | volume = 8 | issue = 1 | pages = 69 | date = June 2016 | pmid = 27323951 | pmc = 4915101 | doi = 10.1186/s13073-016-0324-x | doi-access = free }}</ref>
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