期刊
CURRENT OPINION IN GENETICS & DEVELOPMENT
卷 10, 期 1, 页码 39-46出版社
CURRENT BIOLOGY LTD
DOI: 10.1016/S0959-437X(99)00047-7
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资金
- NEI NIH HHS [R01EY11267] Funding Source: Medline
- NICHD NIH HHS [R01HD28317] Funding Source: Medline
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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