Квазибиологическая модель радиогенной заболеваемости раком

The methods: Linear differential equations were used to formalize contemporary assumptions of self –sustaining tissue cell kinetics under the impact of adverse factors, on the formation and repairing of cell “pre-cancer” defects, on inheritance and retaining such defects in daughter cells which results in malignant neoplasms, on age-dependent impairment of human body’s function to eliminate such cells. The results: The model reproduces the well-known regularities of radiogenic cancer morbidity increase depending on instantaneous radiation exposure age and on attained age: the relative reduction at increased radiation age which the model attributes to age decrease of stem cells, relative reduction at increased time after radiation induced by “sorting out” of cells with “pre-cancer” defects, absolute increase with age proportional to natural cause mortality rate. The relevance of the developed quasi-biological model is displayed via comparison to the ICRP model for radiogenic increase of solid carcinomas’ morbidity after single radiation exposure. The latter model had been developed after Japanese cohort observations. For both genders high goodness-of-fit was achieved between the models at values of Gompertz’ law factor which had been defined for men and women in this cohort via selecting the value of the only free parameter indicating age-dependent exponential retardation of stem cells’ division. The conclusion: The proposed model suggests that the estimation of radiogenic risk inter-population transfer can be done on the basis of the data on age-dependent mortality intensity increase from all natural causes. The model also creates the premises for inter-species transfer of risk following the well-known parameters of cell populations’ kinetics in animal’s organs and tissues and Gompertz’s law parameters. This model is applicable also for analyses of age-dependent changes of background cancer morbidity.