Attempt at a systemic outlook on aging and carcinogenesis

Two of the key problems plaguing humanity – aging and carcinogenesis – are inexorably linked. While their nature seems different, their mechanisms have a lot in common. Evidence suggests that aging is the result of spontaneous synthesis and accumulation of improperly folded proteins in cells, leading to a variety of pathologies. As for carcinogenesis, it is tied to genetic mutations – permanent, covalent changes in the DNA. Both processes are random in character; however, unlike mutations, the accumulation of malformed proteins is not genetically determined. Instead, control over this process hinges upon regulating the protein exchange rate – a phenomenon that seems a likely candidate for the basic aging control mechanism. Although mutations themselves may be counteracted in a controlled manner, their effects typically cannot. The mechanisms of aging and carcinogenesis, while functionally different, remain correlated: an aging cell is rendered more susceptible to mutational changes. The rapidly growing body of information regarding aging and carcinogenesis enables a systemic approach to both these phenomena – an approach that is attempted in this review.