Cancer and aging

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Abstract

The current opinions on mechanisms of age-related increase in malignant tumor incidence in human and animal are reviewed. Aging may increase or decrease the susceptibility of various tissues to initiation of carcinogenesis and usually facilitates promotion and progression of carcinogenesis. Aging may prodispose to cancer by several mechanisms: tissue accumulation of cells in late stages of carcinogenesis; alterations in homeostasis, in particular, alterations in endocrine and immune systems; telomere instability linking aging and increased cancer risk. Some common genetic processes (e. g. telomere dysfunction, changes in p53 and Rb activity and in DNA repair, accumulation of DNA lesions, genomic instability) play a critical role both in carcinogenesis and aging. As it was predicted by multi-stage model of carcinogenesis, the increase in susceptibility to tumor promoters have been observed in elderly humans and animals. In genetically modified mouse model (transgenic, knockout or mutant) characterized by the aging delay the tumorigenesis was usually alleviated in comparison to wild type animals, whereas in the case of models of accelerated aging the acceleration of the tumorigenesis was observed. Strategy for cancer prevention must include not only measures to minimize the exposure to exogenous carcinogenic agents, but also measures to normalize the age-related alterations in internal milieu.

About the authors

V. N. Anisimov

N. N. Petrov Research Institute of Oncology

Author for correspondence.
Email: shabanov@mail.rcom.ru
Russian Federation, Saint Petersburg

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