We see 5 alternative explanations that may cause a decline in cancer rates at the oldest ages.[...]
First, as we age, increasing arteriosclerosis limits local angiogenesis, perhaps sufficiently impeding the growth of tumors.
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Second, it has been hypothesized that age-dependent remodeling of the immune system is responsible.
46 With increasing age, more cluster of differentiation 4 (CD4) and cluster of differentiation 8 (CD8) cells have natural killer characteristics and secrete cytokines that could contribute to the suppression of tumorigenesis.
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Third, it may not be possible to explain the decline in cancer incidence through 1 or 2 biologic processes. Instead, many processes may contribute substantially, and no 1 process can account for the majority of the effect.
Fourth, there could be strongly varying exposures to carcinogens with age. In the case of the Armitage-Doll multistage theory, the probability of the final stage transition might fall dramatically above age 70 because of decreased exposure to carcinogens. However, that fall would have to be at least a factor of 4.
Fifth, decreased proliferative potential of cells at the oldest ages could make tumorigenesis slower and less likely.
23 The beta model, fit to our results, is consistent with the hypothesis that more cells become senescent as we age, largely losing the ability to divide further and, with it, the option of producing a tumor.
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