A critical role for telomeres in suppressing and facilitating carcinogenesis

Curr Opin Genet Dev. 2000 Feb;10(1):39-46. doi: 10.1016/s0959-437x(99)00047-7.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Catalytic Domain
  • Cell Division / physiology
  • Cellular Senescence / physiology
  • DNA-Binding Proteins
  • Humans
  • Mice
  • Neoplasms / genetics*
  • Neoplasms / pathology
  • RNA*
  • Telomerase / metabolism
  • Telomere / physiology*


  • DNA-Binding Proteins
  • telomerase RNA
  • RNA
  • Telomerase