@article{oai:repo.qst.go.jp:00045296,
 author = {Yoshida, Mitsuaki and Nakata, Akifumi and Akiyma, Miho and Kakinuma, Shizuko and Sado, Toshihiko and Nishimura, Mayumi and Shimada, Yoshiya and 吉田 光明 and 中田 章史 and 穐山 美穂 and 柿沼 志津子 and 西村 まゆみ and 島田 義也},
 issue = {1},
 journal = {Cancer Genetics and Cytogenetics},
 month = {Nov},
 note = {Loss of heterozygosity (LOH) plays an important role in leukemogenesis via inactivation of tumor suppressor genes.  Recent studies have demonstrated that mouse thymic lymphomas (TLs), a suitable model for the mechanistic study on human acute lymphoblastic leukemia, show frequent LOH on chromosomes 4 (p15/p16), 11 (Ikaros), 12 (Bcl11b), 19 (Pten) and X.  Little data, however, are available for the mechanism of LOH, yet.  In this study, we re-evaluated chromosome abnormality and loss of heterozygosity in 26 TL induced by X-rays in C57BL/6 (B6), C3H and F1 (B6 x C3H) mice, using quinacrine-Hoechst double staining method and chromosome painting technique. Chromosomally abnormal cells were present in 25 TLs examined (25/26, 96%).  Most frequent abnormality was trisomy or partial trisomy of chromosome 15 (16/26, 62%), being consistent with previous studies. Structural abnormalities of chromosome 11 with interstitial deletion of proximal region and chromosome 12 with translocation with deletion of distal region were newly identified in 7 (27%) and 12 (46%) cases, respectively.  These results indicate that the distinct mechanism contributes to LOH of each tumor suppressor gene on different chromosomal location.},
 pages = {1--10},
 title = {Distinct structural abnormalities of chromosomes 11 and 12 associated with loss of heterozygosity in X-ray-induced mouse thymic lymphomas.},
 volume = {179},
 year = {2007}
}