Mammalian somatic cells in culture display a limited proliferative life span, at the end of which they undergo an irreversible cell cycle arrest known as replicative senescence. Cancer cells display several hallmarks that can be distinguished from those of normal counterparts. These include immortalization or bypass of senescence, evasion of apoptosis and/or antigrowth signals, growth factor independence, enhanced glycolysis, and so forth.

The aging of organisms is characterized by a gradual functional decline of all organ systems. Whether cellular senescence contributes to organismal aging has been controversial.

Overall, senescence is considered an antitumorigenic mechanism for avoiding indefinite cell proliferation when a genetic alteration has occurred. Because cellular senescence is a growth suppressing mechanism, it would seem that the accumulation of senescent cells during aging would result in a decrease in the incidence of cancer; however, it is known that there is an increased incidence of cancer with age. Because incidences of most diseases rise rapidly with age, interventions that delay aging would greatly benefit health. We are particularly interested in:

• Novel approaches of how senescence could be applied to the clinics
• Novel senescence pathways that might influence the development of tumors
• Recent advances in biology and medicine which contribute to increase life-expectancy
• Physiological relevance of senescence and how it contributes to organismal aging
• Pharmacological intervention able to extend life-span in mammals

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