@misc{oai:repo.qst.go.jp:00069843,
 author = {Kakinuma, Shizuko and Takimoto, Misaki and Kodama, Youtarou and Amasaki, Yoshiko and Nishimura, Mayumi and Shimada, Yoshiya and 柿沼 志津子 and 滝本 美咲 and 小玉 陽太郎 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 an early onset of childhood T- or B-cell leukemia. MMR deficient mice, Mlh1-/- or Msh2-/-, also develop aggressive lymphomas, which are predominantly T-cell origin. We previously showed that spontaneously developed Mlh1-/- 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 age-at-exposure on lymphomgenesis in Mlh1-/- mice. We found that exposure of X-rays to 2 or 10 week-old mice increased the incidence of T-cell lymphomas and shortened its latency. Point mutations of Ikaros in addition to frameshift mutations were generated in radiation-induced lymphomas. In utero exposure, unexpectedly, showed no influence on T-cell lymphomagenesis. But, it accelerated B-cell lymphomagenesis. Molecular analysis is now undertaken., KTCC 2009 International Workshop},
 title = {AGE DEPENDENCY OF LYMPHOMAGENESIS BY RADIATION EXPOSURE IN Mlh1-DEFICIENT MICE},
 year = {2009}
}