Abstract: AbstractCellular senescence is broadly defined as the physiological program of terminal growth arrest. Cellular senescence could be triggered by short chromosome telomeres, activated oncogenes, and cell stress and mediated by the p53 and p16/pRB tumor suppressor pathways. Treatment-induced senescence, which has both similarities with, and differences from, replicative senescence of normal cells, was shown to be one of the key determinants of tumor response to therapy in vitro and in vivo. Elucidation of the genes and regulatory mechanisms that determine different aspects of tumor senescence makes it possible to design new therapeutic approaches to improving the efficacy and to decreasing the side effects of cancer therapy. The elucidation of the biological aspects of tumor cell senescence offers plausible approaches to the development of novel therapeutic strategies to stop the growth of tumor cells.

Key words: Cellular senescence, p53, p16/pRB,, Tumor cell