Abstract
Cellular senescence is an important defense against uncontrolled cellular replication and is a critical tumor suppressor mechanism. Although initially described as an in vitro phenomenon, in recent years, several lines of evidence have indicated that senescence also occurs in vivo. Disparate cellular stresses can provoke senescence including telomere shortening, activation of certain oncogenes, oxidative stress and stalled replication forks. These stresses are best known to engage the p16INK4a-RB and ARF-p53 pathways to effect growth arrest and prevent neoplasia. Among these, ‘oncogene-induced senescence’ (OIS) is particularly known for the prevention of melanoma, resulting from the expression of mutant B-RAF or N-RAS in this disease.
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