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It has long been thought that the carcinogenic effect of radiation is due to the induction of oncogenic mutations, which means that a fraction of the irradiated individuals will be affected in a dose-dependent manner. This dogma was recently challenged because it was found that the model does not properly explain the life shortening effect of radiation which is seen as a parallel shift of mouse survival curves toward younger ages following an exposure to radiation. Specifically, according to the mutation induction theory, an irradiated mouse or human population evolves into two subpopulations with different mean lifespans, which would lead to a wider distribution of individual lifespans, and hence to a shallower slope in the survival curve, which is not what is observed. Instead, the parallel shift indicates that a large fraction of the irradiated mice are affected (but there are exceptions). Thus, it was thought important to pursue how the excess risk for cancer develops following an exposure to radiation. In the present study, cancer mortality data from mice and atomic-bomb survivors is presented to understand the increasing patterns of cancer risks. In both species, it was found that cancer mortality starts to increase earlier in the exposed group. The results are consistent with the notion that in many irradiated organs (but not all) radiation-induced tissue damage can lead to the development of an altered microenvironment (most probably inflammation), which is favorable to the growth of spontaneously arising tumor cells and can lead to an earlier onset of the diseases or to an apparently increased risk of cancer.

Radiation-induced increases in cancer mortality result from an earlier onset of the disease in mice and atomic bomb survivors