Abstract

To explore whether the development of the specific tumor type in experimental animal model for the study of radiation-induced carcinogenesis is caused by genetic predisposition, such as species or strain, or irradiation method, and also to find out the role of cellular oncogenes in radiation-induced carcinogenesis, an experimental study was made using female CBA mice. After total 450 cGy of whole-body irradiation with 3 fractionations at weekly intervals, histopathologic changes and expression of cellular oncogenes were examined with thymus and bone marrow serially till postirradiation 150 days in 18 female CBA mice. Simultaneously unirradiated 12 mice were studied as a control. The results are as follows. 1) Thymic lymphoma/leukemia did not develop in CBA mice with the fractionated whole-body irradiation which has been known to be an effective method af inducing thymic lymphorna/leukemia in C57BL mice. Increment of blasts in bone marrow, which suggests the development of myeloid leukemia, was observed in 33%(2/6) of irradiated mice elapsed 150 days after irradiation. These findings suggest that the development of the specific tumor type in experimental animal is not related to irradiation method but to genetic predisposition, such as differences in species or strain. 2) The expressian of two cellular oncogenes, c-fps and c-myc, as a parameter of chemical changes were examined at thymus serially till postirradiation 150 days. No abnormal expression of c-fps or c-myc was observed as with the findings of histopathology. 3) In the examination of two cellular oncogenes in bone marrow, there was no change in c-myc, but there was strong expression of c-fps in one of mice elapsed 150days after irradiation. The expression of c-fps at preleukemic state suggests that the chemical changes develop before the appearance of malignancy as a phenotype. This result is very meaningful in that specific oncogenes might play a role in radiation-induced carcinogenesis.

• Keywords: Radiation. Genet.ic predisposition, Carcinogenesis, Cellular oncogenes.