Aging and cancer: the double-edged sword of replicative senescence

Abstract

Normal cells do not divide indefinitely. This trait, termed the finite replicative life span of cells, limits the capacity for cell division by a process termed cellular or replicative senescence. Replicative senescence is thought to be a tumor suppression mechanism and also a contributor to organismic aging. This article reviews what is known about the genetics and molecular biology of cell senescence. It discusses the evidence that replicative senescence suppresses tumorigenesis, at least in young organisms, and that it also contributes to the aging of mitotic tissues. Finally, it puts forth the somewhat unorthodox view that, in older organisms, senescent cells may actually contribute to carcinogenesis.