By Lodovico Balducci, Martine Extermann
This quantity highlights study matters particular to geriatric oncology within the box of carcinogenesis and melanoma prevention and therapy, in response to the biologic interactions of melanoma and age. It conveys a sustainable frame of mind approximately melanoma and aging.
Read Online or Download Biological Basis of Geriatric Oncology (Cancer Treatment and Research) PDF
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Extra info for Biological Basis of Geriatric Oncology (Cancer Treatment and Research)
The grade of malignancy is considered to increase with every stage. Various carcinogenic agents (exogenous as well as endogenous) may modulate the process. In addition, some agents act at early stages of carcinogenesis and others at later stages 24. Epidemiological data, analyzed within the framework of a multi-stage model, have helped to estimate the contribution of various factors to the development of cancer. These factors include the time from the start of carcinogenic exposure, and the age of onset of exposure.
These findings are in agreement with data on age-related decrease in cellular DNA repair capacity in skin 44,45 and increasing p53 mutation frequency with advancing age in human normal skin 46 and in basal-cell skin carcinomas 47,48. Post-ultraviolet DNA repair capacity was found to undergo an age-related decline to which corresponded age-related increase in post-ultraviolet mutability in cultured primary skin fibroblasts from normal donors from the first to the tenth decade of life 44. It was suggested that there was the age-related increase in the number of telomerase positive basal cells in the skin 49.
In contrast, the life span of tg/- rats was 7 to 10% longer than -/- rats. It was found that tumors caused earlier death in tg/tg rats; in contrast, tg/- rats had reduced nonneoplastic diseases and a prolonged life span. Immunological analysis revealed a smaller population and lower activity of splenic natural killer cells in homozygous tg/tg rats. These results BIOLOGICAL INTERACTIONS 37 provided evidence that an optimal level of the GH-IGF-1 axis function needs for longevity in mammals. Recently it was shown that the incidence of mutations in insulin regulatory region (IRE) of APO C-III T-455 C directly correlates with longevity in humans.