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Analysis of Changes in DNA Copy Number in Radiation-Induced Thymic Lymphomas of Susceptible C57BL/6, Resistant C3H and Hybrid F1 Mice
https://repo.qst.go.jp/records/45152
https://repo.qst.go.jp/records/451521be871bb-dab0-49db-aaef-0fdb407189bc
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2008-05-07 | |||||
| タイトル | ||||||
| タイトル | Analysis of Changes in DNA Copy Number in Radiation-Induced Thymic Lymphomas of Susceptible C57BL/6, Resistant C3H and Hybrid F1 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_6501 | |||||
| 資源タイプ | journal article | |||||
| 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 |
Takabatake, Takashi
× Takabatake, Takashi× Kakinuma, Shizuko× Hirouchi, Tokuhisa× M., Nakamura Masako× Fujikawa, Katsuyoshi× Nishimura, Mayumi× Oghiso, Yoichi× Shimada, Yoshiya× Tanaka, Kimio× 高畠 貴志× 柿沼 志津子× 西村 まゆみ× 島田 義也× 田中 公夫 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Radiation-induced thymic lymphoma in mice is a useful model for studying both the mechanism of radiation carcinogenesis and genetic susceptibility to tumor development. Using array-comparative genomic hybridization, we analyzed genome-wide changes in DNA copy numbers in radiation-induced thymic lymphomas that had developed in susceptible C57BL/6 and resistant C3H mice and their hybrids, C3B6F1 and B6C3F1 mice. Besides aberrations at known relevant genetic loci including Ikaros and Bcl11b and trisomy of chromosome 15, we identified strain-associated genomic imbalances on chromosomes 5, 10 and 16 and strain-unassociated trisomy of chromosome 14 as frequent aberrations. In addition, biallelic rearrangements at Tcrb were detected more frequently in tumors from C57BL/6 mice than in those from C3H mice, suggesting aberrant V(D)J recombination and a possible link with tumor susceptibility. The frequency and spectrum of these copy-number changes in lymphomas from C3B6F1 and B6C3F1 mice were similar to those in C57BL/6 mice. Furthermore, the loss of heterozygosity analyses of tumors in F1 mice indicated that allelic losses at Ikaros and Bcl11b were caused primarily by multilocus deletions, whereas those at the Cdkn2a/Cdkn2b and Pten loci were due mainly to uniparental disomy. These findings provide important clues to both the mechanisms for accumulation of aberrations during radiation-induced lymphomagenesis and the different susceptibilities of C57BL/6 and C3H mice. | |||||
| 書誌情報 |
Radiation Research 巻 169, 号 4, p. 426-436, 発行日 2008-03 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0033-7587 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1667/rr1180.1 | |||||
