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Fenton reaction-induced renal carcinogenesis in Mutyh-deficient mice exhibits less chromosomal aberrations than the rat model
http://hdl.handle.net/2237/27310
http://hdl.handle.net/2237/27310a9622bf8-7214-4b93-8c07-4a6f7a2bf54c
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
deposit_1.pdf ファイル公開日:2018/11/01 (2.2 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2018-01-30 | |||||
| タイトル | ||||||
| タイトル | Fenton reaction-induced renal carcinogenesis in Mutyh-deficient mice exhibits less chromosomal aberrations than the rat model | |||||
| 言語 | en | |||||
| 著者 |
Li, Guang Hua
× Li, Guang Hua× Akatsuka, Shinya× Chew, Shan Hwu× Jiang, Li× Nishiyama, Takahiro× Sakamoto, Akihiko× Takahashi, Takashi× Futakuchi, Mitsuru× Suzuki, Hiromu× Sakumi, Kunihiko× Nakabeppu, Yusaku× Toyokuni, Shinya |
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| アクセス権 | ||||||
| アクセス権 | open access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||
| 権利 | ||||||
| 言語 | en | |||||
| 権利情報 | This is the peer reviewed version of the following article: [Li, G. H., Akatsuka, S., Chew, S. H., Jiang, L., Nishiyama, T., Sakamoto, A., Takahashi, T., Futakuchi, M., Suzuki, H., Sakumi, K., Nakabeppu, Y. and Toyokuni, S.(2017), Fenton reaction-induced renal carcinogenesis in Mutyh-deficient mice exhibits less chromosomal aberrations than the rat model.PATHOLOGY INTERNATIONAL.,67: 564–574. doi:10.1111/pin.12598], which has been published in final form at [http://doi.org/10.1111/pin.12598]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving. | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Oxidative stress including iron excess has been associated with carcinogenesis. The level of 8-oxoguanine, a major oxidatively modified base in DNA, is maintained very low by three distinct enzymes, encoded by OGG1, MUTYH and MTH1. Germline biallelic inactivation of MUTYH represents a familial cancer syndrome called MUTYH-associated polyposis. Here, we used Mutyh-deficient mice to evaluate renal carcinogenesis induced by ferric nitrilotriacetate (Fe-NTA). Although the C57BL/6 background is cancer-resistant, a repeated intraperitoneal administration of Fe-NTA induced a high incidence of renal cell carcinoma (RCC; 26.7%) in Mutyh-deficient mice in comparison to wild-type mice (7.1%). Fe-NTA treatment also induced renal malignant lymphoma, which did not occur without the Fe-NTA treatment in both the genotypes. Renal tumor-free survival after Fe-NTA treatment was marginally different (P = 0.157) between the two genotypes. Array-based comparative genome hybridization analyses revealed, in RCC, the loss of heterozygosity in chromosomes 4 and 12 without p16INK[4]A inactivation; these results were confirmed by a methylation analysis and showed no significant difference between the genotypes. Lymphomas showed a preference for genomic amplifications. Dlk1 inactivation by promoter methylation may be involved in carcinogenesis in both tumors. Fe-NTA-induced murine RCCs revealed significantly less genomic aberrations than those in rats, demonstrating a marked species difference. | |||||
| 言語 | en | |||||
| 出版者 | ||||||
| 出版者 | Wiley | |||||
| 言語 | en | |||||
| 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 | |||||
| 出版タイプ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.1111/pin.12598 | |||||
| ISSN | ||||||
| 収録物識別子タイプ | PISSN | |||||
| 収録物識別子 | 1320-5463 | |||||
| 書誌情報 |
en : PATHOLOGY INTERNATIONAL 巻 67, 号 11, p. 564-574, 発行日 2017-11 |
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| 著者版フラグ | ||||||
| 値 | author | |||||
| URI | ||||||
| 識別子 | http://doi.org/10.1111/pin.12598 | |||||
| 識別子タイプ | DOI | |||||
| URI | ||||||
| 識別子 | http://hdl.handle.net/2237/27310 | |||||
| 識別子タイプ | HDL | |||||
