Open Access
Article
Aging and cancer in transgenic and mutant mice
Vladimir N Anisimov1
1
Department of Carcinogenesis and Oncogerontology, N.N. Petrov Research Institute of Oncology, Pesochny-2, St. Petersburg 197758, Russia. aging@mail.ru
DOI: 10.2741/1122 Volume 8 Issue 6, pp.883-902
Published: 01 September 2003
(This article belongs to the Special Issue Bio-demographic effects of genome-proteome interactions)
Abstract

Mutant and genetically modified animal models, which are characterized by shortening or extension of the life span, give a unique possibility to evaluate the role of aging genes in mechanisms of carcinogenesis. Transgenic and null mutant ("knockout") animal models also offer an important opportunity to identify and study both carcinogens and chemopreventive agents. The analysis of the available data on transgenic and mutant mice has shown that only a few models represent examples of life span extension. Ames dwarf mutant mice, p66-/- knockout mice, alpha-MUPA and O6-methylguanine-DNA methyltransferase (MGMT) transgenic mice live longer than wild-type strains. The incidence of spontaneous tumors in these mice was similar to those in controls, whereas the latent period of tumor development was increased. Practically all models of accelerated aging (excepting p53+/m mice) show the increased tumor incidence and shortening of tumor latency. These observations are in agreement with an earlier established positive correlation between tumor incidence and the rate of tumor incidence increase associated with aging and the aging rate in a population. Thus, genetically modified animals are a valuable tool in unraveling mechanisms underlying aging and cancer.

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Vladimir N Anisimov. Aging and cancer in transgenic and mutant mice. Frontiers in Bioscience-Landmark. 2003. 8(6); 883-902.