[The use of mutagenic and transgenic mice for the study of aging mechanisms and age pathology].

Increased interest is emerging for using mouse models to assess the genetics of aging and age-related diseases, cancer including. Despite this demand, relatively little information is available on relations between aging and spontaneous tumor development in transgenic and null mutant mice. Analysis of various transgenic and knockout rodent models which characterized by shortening or extension of the life span gives an unique possibility to evaluate the role of involved in aging genes in mechanisms of carcinogenesis. Only few models represent examples of life span extension. Ames dwarf mutant mice, p66-/- knocked out mice, aMUPA and MGMT, transgenic mice live longer than wild-type strains. The incidence of spontaneous tumors in these mice was usually similar to those in controls, whereas the latent period of tumor development was increased. Practically all models of accelerated aging show the increased tumor incidence and shortening of tumor latency. This phenomenon has been observed both in animals which display phenotype more resemble to the natural aging and in animals showed only partial features of normal aging process. These observations are in agreement with the data on the positive correlation between tumor incidence and the rate of its age-related increase, and the aging rate in a population.