Fenton reaction‐induced renal carcinogenesis in <i>Mutyh</i>‐deficient mice exhibits less chromosomal aberrations than the rat model

DOI 機関リポジトリ 機関リポジトリ (HANDLE) Web Site Web Site ほか1件をすべて表示 一部だけ表示 被引用文献8件 参考文献42件 オープンアクセス

書誌事項

タイトル別名
  • Fenton reaction-induced renal carcinogenesis in Mutyh-deficient mice exhibits less chromosomal aberrations than the rat model
公開日
2017-11
資源種別
journal article
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.
DOI
  • 10.1111/pin.12598
公開者
Wiley

この論文をさがす

説明

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.

収録刊行物

被引用文献 (8)*注記

もっと見る

参考文献 (42)*注記

もっと見る

関連プロジェクト

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ