Abstract
The risk of radiation carcinogenesis is influenced by various factors, including genetic and age factors. The human Apc gene was originally identified as a tumor suppressor gene in both sporadic and hereditary (familial adenomatous polyposis; FAP) colorectal cancers. Recently, missense mutations and promoter hypermethylations of Apc gene have been reported in human breast cancers, suggesting an involvement of Apc mutation in their development. Moreover, FAP model mice with germline Apc mutations have an increased susceptibility to mammary carcinogenesis. To investigate the effect of age at exposure on X ray-induced mammary carcinogenesis in the FAP model ApcMin/+ mice, we examined the mammary tumor development after X irradiation (2 Gy) at various weeks of age. We found that, whereas no tumor was seen in the wild-type littermates, ApcMin/+ mice developed mammary tumors, with significantly higher incidence in those irradiated at 7 and 10 weeks than those irradiated at 5 weeks. Histologically, all tumors were adenoacanthomas. We discuss the possibility that age dependency of the risk of radiation carcinogenesis is modulated by genetic factors. [J Radiat Res 44:397 (2003)]
