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Cancer Suppression at Old Age

Jefferson Laboratories, Department of Physics, Harvard University, Cambridge, Massachusetts

Requests for reprints: Francesco Pompei, Department of Physics, Harvard University, Oxford Street, Cambridge, MA 02138. Phone: 617-495-3387; Fax: 617-495-0416; E-mail: fpompei{at}post.harvard.edu.

Key Words: multistage • anticarcinogen • senescence • age-specific cancer incidence • longevity

Increased age is regularly linked with heightened cancer risk, but recent research suggests a flattening around age 80. We report that, independent of cancer site or time period, most incidence rates decrease in the more elderly and drop to or toward zero near the ceiling of human life span. For all major organ sites, male and female, we use 1979 to 2003 Surveillance, Epidemiology, and End Results registry records (8–26% of the U.S. population) to construct three sequential cross-sections at 10-year intervals, totaling 129 sets of age-specific cancer data. To compute incidence rates, we estimate older populations at risk with census counts and NIH life tables. This article provides both a minimal and a more comprehensive extension of Surveillance, Epidemiology, and End Results cancer rates to those above 85. Almost all cancers peak at age 80. Generally, it seems that centenarians are asymptomatic or untargeted by cancers. We suggest that the best available justification for this pattern of incidence is a link between increased senescence and decreased proliferative potential among cancers. Then, thus far, as senescence may be a carcinogen, it might also be considered an anticarcinogen in the elderly. We model rising and falling incidence rates with a β curve obtained by appending a linearly decreasing factor to the well-known Armitage-Doll multistage model of cancer. Taken at face value, the β model implies that medical, diet, or lifestyle interventions restricting carcinogenesis ought to be examined for possible effects on longevity. [Cancer Res 2008;68(11):4465–78]