Aging is not a disease; it causes a decrease in the physiological functions of cells, tissues, and organs. Aging has been considered as one of the biggest risk factors for the development of various diseases such as cancer, type-2 diabetes, obesity, atherosclerotic cardiovascular diseases, and neurodegeneration. Numerous studies have shown that lifespan can be extended in mice by genetic, dietary, and pharmacological interventions. A few prolongevity interventions currently being studied include: the drug rapamycin, that has been found to inhibit mTOR expression and exhibit anticancer properties; reduced caloric intake, a broadly acting dietary intervention for preventing carcinogenesis, and ultimately extending lifespan; and more recently, another promising strategy being studied is crowded litter placement in mice starting from a very young age. We hypothesize that the aforementioned interventions will delay the effects of aging, through enhanced DNA base excision repair activity, which will lead to tumorigenesis prevention
