@misc{oai:repo.qst.go.jp:00071165,
 author = {Kakinuma, Shizuko and Hirano, Shinobu and Fujimoto, Shinji and Takimoto, Misaki and Amasaki, Yoshiko and Nishimura, Mayumi and Shimada, Yoshiya and 柿沼 志津子 and 坂入 しのぶ and 滝本 美咲 and 甘崎 佳子 and 西村 まゆみ and 島田 義也},
 month = {Jun},
 note = {Deficiencies in DNA mismatch repair (MMR) result in replication errors that cause frameshift mutations and/or point mutations within key tumor suppressor genes or oncogenes. Homozygous germline mutations of MMR genes, such as MLH1, MSH2 and PMS2, are manifested by early onset childhood T- or B-cell leukemia. Mlh1-/- mice develop aggressive thymic lymphomas. We previously showed that spontaneously developed Mlh1-/- thymic lymphomas harbored frequent frameshift mutations in Ikaros, a master transcription factor of lymphoid lineage commitment and differentiation. In this study, we examined the effect of fetal radiation exposure on lymphomgenesis in Mlh1-/- mice. Exposure to radiation after birth increased the incidence of thymic lymphomas and shortened their latency. Point mutations and frameshift mutation in Ikaros were generated in radiation-induced lymphomas. In utero radiation exposure, unexpectedly, resulted in no effect on thymic lymphomagenesis, but accelerated splenic lymphomagenesis. Analysis of TCRa and b rearrangement revealed that a half of splenic lymphomas and all lymphomas expressing TCR expressed the Va14−Ja18 rearrangement paired with either Vb-8, -7 or -2, which is specific for invariant natural killer T cell. Mechanisms of lymphomagenesis of iNKT cells are remained to be studied., 6th International Workshop of Kyoto T Cell Conference (KTCC2013)},
 title = {Splenic lymphomas of Mlh1-deficient mice induced by in utero irradiation are derived from invariant natural killer T cell.},
 year = {2013}
}