@misc{oai:repo.qst.go.jp:00061235,
 author = {Kodama, Youtarou and Kakinuma, Shizuko and Tokairin, Yutaka and Monobe, Manami and Kojima, Shuji and Shimada, Yoshiya and 小玉 陽太郎 and 柿沼 志津子 and 東海林 裕 and 物部 真奈美 and 島田 義也},
 month = {Nov},
 note = {DNA mismatch repair (MMR) system is one of the important mechanisms to suppress cancer development. MMR deficiency is a cause of hereditary non-polyposis colorectal cancer (HNPCC) as well as mammary, gastric, pancreatic cancers and leukemia. Colon cancers in HNPCC patients and the lymphomas in Msh2-deficient mice have shown frequent frame shift mutations in TgfbrII. It has not yet examined whether MMR deficiency is involved in the susceptibility to radiation carcinogenesis. The aims of the current study are both to elucidate the susceptibility of Mlh1-/- mice to radiation induced tumors and to determine the mutation of TgfbrII in the tumors. Eleven-day- and 10-week-old Mlh1-/- mice were exposed to 2 Gy of X-rays. The mice were sacrificed at moribund and autopsied. Mutation of TgfbrII was analyzed in the DNA from pathological samples after microdissection or fresh samples. Thymic lymphomas (TL) after irradiation at 11-days and 10-weeks developed much earlier than spontaneous ones with the incidence of 87% (13/15) and 87%(13/15), respectively, which was significantly higher than that of spontaneous ones (61%, 11/18). Gastrointestinal tumors (GIT) also developed earlier when irradiated at 10-weeks, but not 11-days, old. The mutation of TgfbrII was not found in any tumors. We conclude that Mlh1 deficiency accelerates radiation-induced TL and GIT development. TgfbrII mutation, however, was not involved in cancer induction of Mlh1-/- mice., 第48回日本放射線影響学会／第1回アジア放射線研究会議},
 title = {Radiation carcinogenesis in Mlh1 knock-out mice},
 year = {2005}
}