Vladimir N. Anisimov, MD

Disclosures

Cancer Control. 2007;14(1):23-31. 

In This Article

Abstract and Introduction

Abstract

Background: The incidence of cancer increases with age in both humans and laboratory animals. A clear understanding of the causes of the age-related increase in cancer incidence is needed to develop a strategy for primary cancer prevention.
Methods: We summarized the data available in the literature and our own experience in hormonal metabolic shifts in organisms and disturbances at tissue and cellular levels observed in natural aging and in different types of carcinogenesis in vivo.
Results: There are incongruent 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 by at least two mechanisms: tissue accumulation of cells in late stages of carcinogenesis and alterations in internal homeostasis, in particular, alterations in immune and endocrine system. Increased susceptibility to the effects of tumor promoters is found in both aged animals and aged humans, as predicted by the multistage model of carcinogenesis.
Conclusions: Aging is associated with a number of events at the molecular, cellular and physiologic levels that influence carcinogenesis and subsequent cancer growth. A clearer understanding of these events will help in predicting and treating cancer more effectively.

It is well documented that the incidence of malignant tumors increases progressively with age, in both animals and humans.[1,2,3,4,5,6] Three major hypotheses have been proposed to explain the association of cancer and age. The first hypothesis holds that this association is a consequence of the duration of carcinogenesis. In other words, the high prevalence of cancer in older individuals simply reflects a more prolonged exposure to carcinogens.[7] The second hypothesis proposes that age-related progressive changes in the internal milieu of the organism may provide an increasingly favorable environment for the induction of new neoplasms and the growth of already existent but latent malignant cells.[1,2,8,9,10,11] These mechanisms may also include proliferative senescence, as the senescent cells lose their ability to undergo apoptosis and produce some factors that stimulate epithelial cells with oncogenic mutations.[12] The third hypothesis, which practically joins these two hypotheses, proposes that the cancer-prone phenotype of older humans might reflect the combined effects of cumulative mutational load, increased epigenetic gene silencing, telomere dysfunction, and altered stromal milieu.[13] The elucidation of the causes of the age-related increase in cancer incidence may be the key to a strategy for primary cancer prevention.

Aging is associated with a number of events at the molecular, cellular, and physiologic levels that influence carcinogenesis and subsequent cancer growth.[5,8]

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