Aging and cancer biology

Abstract

The incidence of cancer increases with age in humans and in laboratory animals alike. There are different patterns of age-related distribution of tumors in different organs and tissues. Aging may increase or decrease the susceptibility of various tissues to initiation of carcinogenesis and usually facilitates promotion and progression of carcinogenesis. Aging may predispose to cancer at least by two mechanisms: tissue accumulation of cells in late stages of carcinogenesis and alterations in internal homeostasis, in particular, disturbances in immune and endocrine system. Increased susceptibility to the effects of tumor promoters is found both in aged animals and aged humans, as predicted by the multistage model of carcinogenesis. Aging is associated with number of events at the molecular, cellular/tissue, and systemic/organismal levels that influence carcinogenesis and subsequent cancer growth. The available data on the effects of environmental carcinogens on life span and the aging at different levels of integration are critically analyzed. The exposure to various mutagenic agents, i.e., 5-bromodeoxyuridine, alkylating substances, carcinogenic polycyclic aromatic hydrocarbons, nitroso compounds, and ionizing radiation, decreases the life span of treated animals in direct proportion to dose and was considered as an acceleration of aging. There are significant similarities between normal aging features and effects of environmental carcinogens on DNA, neuroendocrine and immune system, and carbohydrate and lipid metabolism, whereas main difference was observed at cellular level.