Journal
NATURE REVIEWS CANCER
Volume 8, Issue 6, Pages 450-458Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrc2393
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Funding
- NCI NIH HHS [1K01CA124461, R01 CA129037] Funding Source: Medline
- NIA NIH HHS [R01 AG028888] Funding Source: Medline
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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.
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