Cancer and senescence: is there a biological link?
It is shown that sex- and age-specific death rates from all causes of death other than neoplasms have features that resemble those of corresponding rates for all neoplasms. The same generalization holds in connexion with specific neoplastic and non-neoplastic disorders. In both categories of disease many age-patterns suggest that the rate-governing mechanism for their occurrence is stochastic in character; a rather small number of random events, generally fewer than ten, suffice for their initiation. It is not immediately obvious how a widespread degenerative disorder, sometimes involving an astronomical number of target cells, can be initiated by only a few random events. We infer that all such disorders, together with natural cancers, are autoaggressive in nature. They are initiated by random somatic mutations in comparator stem cells of the central system of growth control. Mutant stem cells propagate forbidden clones of cells that attack target cells at one or multiple sites. (In certain disorders, the presence of an extrinsic precipitator in the host in essential to the propagation of forbidden clones). Autoaggressive attacks have consequences that range from the destruction of target cells to their transformation with invasive proliferation. Senescence can be regarded as the cumulative effect of predominantly late-onset autoaggressive disorders. The relevance of studies of twins to this unified theory is discussed.
D000368:Aged; D000375:Aging; D004198:Disease Susceptibility; D004200:Diseases in Twins; D005246:Feedback; D005260:Female; D006801:Humans; D008297:Male; D009154:Mutation; D009369:Neoplasms / Q000209:etiology*; D012306:Risk; D013234:Stem Cells