Normal primary cells proliferate in culture for a limited number of population doublings before undergoing terminal growth arrest and acquiring a senescence phenotype. This finite life is correlated with the age of the organism and with the life expectancy of the species from which the cells were obtained; so the older the age, the shorter the lifespan, the less the cells can double the population.
Senescent cells are characterized by irreversible G1 growth arrest involving repression of the genes that lead to cell cycle progression and upregulation of cell cycle inhibitors such as p16INK4a, p53 and its transcriptional target, p21CIP1. Senescent cells are resistant to mitogen-induced proliferation and adopt a characteristic flattened morphology. Research on the pathways that positively regulate senescence and the ways in which cells prevent senescence is therefore essential to understanding carcinogenesis. Normal cells have several mechanisms in place to protect against uncontrolled proliferation and tumorigenesis.
Senescent cells show common biochemical markers such as expression of β-galactosidase (SA-β-Gal) activity associated with acid senescence. While senescence has been characterized primarily in cultured cells, there is also evidence that this occurs in vivo. Cells expressing senescence markers such as SA-β-Gal have been identified in normal tissues.

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