The concept of gene transfer-misrepair mechanism of radiation carcinogenesis may challenge the linear extrapolation model of risk estimation for low radiation doses.

The recent demonstration that transformation of cultured cells can be induced by exposure to DNA fragments prepared from normal mouse tissues provides experimental support to the gene transfer-misrepair hypothesis of radiation carcinogenesis. Employing various assumptions with regard to the generation of oncogenic DNA fragments and of cells which are susceptible to incorporate these fragments into their genome, it is predicted that the proposed mechanism implies a non-linear extrapolation model for the calculation of cancer risks caused by very low doses of ionizing radiation of low LET. It also follows from this hypothesis that X- and gamma-radiation delivered at an extremely low dose rate will be less carcinogenic than at high dose rate, in particular where low total doses are concerned. Several aspects of the hypothesis can be verified experimentally by the use of in vitro cultured cell systems.