Telomere dysfunction and tumour suppression: The senescence connection

Yibin Deng, Suzanne S. Chan, Sandy Chang

Research output: Contribution to journalReview articlepeer-review

279 Scopus citations

Abstract

Long-lived organisms such as humans have evolved several intrinsic tumour suppressor mechanisms to combat the slew of oncogenic somatic mutations that constantly arise in proliferating stem-cell compartments. One of these anticancer barriers is the telomere, a specialized nucleoprotein complex that caps the ends of eukaryotic chromosome. Impaired telomere function activates the canonical DNA damage response pathway that engages p53 to initiate apoptosis or replicative senescence. Here, we discuss how p53-dependent senescence induced by dysfunctional telomeres may be as potent as apoptosis in suppressing tumorigenesis in vivo.

Original languageEnglish (US)
Pages (from-to)450-458
Number of pages9
JournalNature Reviews Cancer
Volume8
Issue number6
DOIs
StatePublished - Jun 2008
Externally publishedYes

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