The evidence is accumulating that age is a chronic and progressive inflammation, and the levels of some inflammatory markers, including IL-6, D-dimer, and C-reactive proteins, correlate with life expectancy, risk of disability, sarcopenia, and risk of common geriatric syndromes (10,14,28). The basic question of aging biology is whether chronic inflammation is just a marker of aging or instead is responsible for the manifestations of aging. In other words, is it possible that reversal of chronic inflammation may delay the manifestations of aging, including carcinogenesis? From the cancer standpoint, is it important to ask whether
1. chronic inflammation causes epigenetic changes characteristic both of aging and carcinogenesis;
2. chronic inflammation favors tumor growth and metastases. This effect could, in part, be mediated by immune suppression caused by chronic inflammation; or
3. chronic inflammation is a viable target for chemoprevention, as suggested by studies of COX inhibitors (31).
Other environmental changes that may favor carcinogenesis include immune and proliferative senescence.
This area is poorly known and extremely important for understanding the prognosis of cancer in older individuals. It is not impossible that these effects may also become targets of prevention and treatment. Promising questions are as follows:
1. Is it demonstrable in humans, as it appears to be the case in experimental animals, that the growth of poorly immunogenic tumors is hampered and that of the highly immunogenic ones is enhanced with age? If this is the case, how can one identify highly and poorly immunogenic tumors? Can immune competence be restored, at least to some extent, in older individuals? Is this a viable strategy of cancer prevention and cancer treatment?
2. Does the senescence of the tumor stroma favor tumor growth and metastases?
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