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Effects of in utero radiation exposure on lymphomagenesis in Mlh1-deficient mice
https://repo.qst.go.jp/records/70746
https://repo.qst.go.jp/records/707462dab975b-65b0-41ff-ae96-4a2265bf91b1
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2012-05-19 | |||||
| タイトル | ||||||
| タイトル | Effects of in utero radiation exposure on lymphomagenesis in Mlh1-deficient mice | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Kakinuma, Shizuko
× Kakinuma, Shizuko× Takimoto, Misaki× Fujimoto, Shinji× Amasaki, Yoshiko× Hirano, Shinobu× Kito, Seiji× Oota, Yuki× Fukushi, Masahiro× Shimada, Yoshiya× 柿沼 志津子× 滝本 美咲× 甘崎 佳子× 坂入 しのぶ× 鬼頭 靖司× 太田 有紀× 島田 義也 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | The Oxford Survey of Childhood Cancers after in utero exposure has demonstrated an increase in childhood lymphoma/leukemia. However, the potential role of fetal exposure in the increase of childhood cancers is still a matter of debate. Environmental and genetic factors, or combined effects of radiation with these factors need to be considered. Moreover, data are insufficient for estimation the cancer risk later in life after in utero exposure. We studied the effect of in utero exposure on lymphoma development using Mlh1-deficient mice, which are genetically prone to lymphoma. A germline mutation in MLH1, one of the DNA mismatch repair (MMR) genes associated with hereditary nonpolyposis colorectal cancer, causes childhood T- and B-cell leukemia, when homozygously defective. The tumors obtained from non-irradiated and in utero irradiated groups were diagnosed either thymic lymphoma or splenic lymphoma based on lymphoma-appearing anatomical site. Microsatellite instability in thymic lymphoma was higher than that in splenic lymphoma. According the cell-surface marker status, splenic lymphomas were further divided into two groups, T-cell origin (TCR+, CD4+ and CD8+) and B-cell origin (IgH+). Mutation analysis of Ikaros, Pax5 and Trp53 revealed that these genes were frequently mutated by one base insertion or deletion at mononucleotide repeat sequences, resulting in a frameshift mutation. Ikaros frameshift mutations were only found in thymic lymphomas, which were characterized TCR+, CD4+ and CD8+, indicating an immature T-cell. Trp53 frameshift mutation was found both T-cell and B-cell splenic lymphomas, the mutations were occurred about 50 % in each lymphoma with a heterozygous status. Pax5 frameshift mutations were found in a part of splenic lymphomas. Radiation exposure increased point mutations in these genes in both thymic and splenic lymphomas. Interestingly, in utero exposure significantly shortened the latency of B-cell origin splenic lymphomas only, but did not affect those of thymic lymphomas and T-cell origin splenic lymphoma. Our data demonstrated that B-cell lymphoma development is accelerated by in utero exposure in Mlh1-deficient mice. Hence, in utero exposure should be paid more attention especially to persons with MMR gene-deficient background. | |||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | International scientific conference on early exposure and childhood cancer | |||||
| 発表年月日 | ||||||
| 日付 | 2012-04-26 | |||||
| 日付タイプ | Issued | |||||
