Abstract
The Scid mouse is well known to be immunodeficient and also radiosensitive because of point mutation in the DNA-dependent protein kinase catalytic subunits (DNA-PKcs) gene. To analyze the effects of Scid mutation on radiation carcinogenesis, Scid ( Scid homozygote), C.B-17 (wild-type) and their (C.B-17×Scid) F1 hybrid ( Scid heterozygote) were used. These strains of mice were first examined for acute effects, and then irradiated with 1–3 Gy gamma rays for carcinogenesis experiments. Scid mice are extremely susceptible to the induction of thymic lymphomas by ionizing radiation. Molecular analyses demonstrated that mutation of the Ras gene contributed less to the induction of thymic lymphomas, although Notch1 mutation played a role. These results suggest a close relationship between radiosensitivity and the development of thymic lymphomas in Scid mice, and correlation of reduced DNA-PK activity with an increase in the yield of deletions or insertions in oncogene(s) rather than point mutations.
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