Abstract
We developed a mathematical model of carcinogenesis with the genomic instability hypothesis, a feature characterized by destabilization of the genome is induced in irradiated cells permanently or semipermanently, leading to an increase of cancer risk at cancer age of the exposed individuals. This model also takes into consideration the “ induction of cell death,” which is another important effect of radiation on cells. It is assumed in this model that the effect of radiation exposure on “cell killing” may occur in all stages of carcinogenic process. Using the resulting model, we can explain not only paradoxical reltionship between low mutation rate and high cancer incidence but also the well known empirical evidence from the cohort study on atomic-bomb survivors in Hiroshima-Nagasaki that the excess relative risk of solid cancer incidence for exposed individuals has been almost constant irrespective of the number of years after exposure.
