Journal
CURRENT OPINION IN GENETICS & DEVELOPMENT
Volume 10, Issue 1, Pages 39-46Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/S0959-437X(99)00047-7
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Funding
- NEI NIH HHS [R01EY11267] Funding Source: Medline
- NICHD NIH HHS [R01HD28317] Funding Source: Medline
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Progressive telomere shortening occurs with the division of primary human cells and activates tumor suppressor pathways, triggering senescence and inhibiting tumorigenesis. Loss of p53 function, however, allows continued cell division despite increasing telomere dysfunction and entry into telomere crisis. Recent data suggest that the severe chromosomal instability of telomere crisis promotes secondary genetic changes that facilitate carcinogenesis. Reactivation of telomerase stabilizes telomere ends and allows continued tumor growth.
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