{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T17:20:07Z","timestamp":1761844807677,"version":"3.37.3"},"reference-count":42,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2017,10,13]],"date-time":"2017-10-13T00:00:00Z","timestamp":1507852800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001691","name":"Japan Society for the Promotion of Science","doi-asserted-by":"publisher","award":["JP16K15257","JP24108008","JP17H04064","JP2221S0001","JP22221004","JP15H04298"],"award-info":[{"award-number":["JP16K15257","JP24108008","JP17H04064","JP2221S0001","JP22221004","JP15H04298"]}],"id":[{"id":"10.13039\/501100001691","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pathology International"],"published-print":{"date-parts":[[2017,11]]},"abstract":"<jats:sec><jats:label\/><jats:p>Oxidative stress including iron excess has been associated with carcinogenesis. The level of 8\u2010oxoguanine, a major oxidatively modified base in DNA, is maintained very low by three distinct enzymes, encoded by <jats:italic>OGG1<\/jats:italic>, <jats:italic>MUTYH<\/jats:italic> and <jats:italic>MTH1<\/jats:italic>. Germline biallelic inactivation of <jats:italic>MUTYH<\/jats:italic> represents a familial cancer syndrome called MUTYH\u2010associated polyposis. Here, we used <jats:italic>Mutyh<\/jats:italic>\u2010deficient mice to evaluate renal carcinogenesis induced by ferric nitrilotriacetate (Fe\u2010NTA). Although the <jats:italic>C57BL\/6<\/jats:italic> background is cancer\u2010resistant, a repeated intraperitoneal administration of Fe\u2010NTA induced a high incidence of renal cell carcinoma (RCC; 26.7%) in <jats:italic>Mutyh<\/jats:italic>\u2010deficient mice in comparison to wild\u2010type mice (7.1%). Fe\u2010NTA treatment also induced renal malignant lymphoma, which did not occur without the Fe\u2010NTA treatment in both the genotypes. Renal tumor\u2010free survival after Fe\u2010NTA treatment was marginally different (<jats:italic>P<\/jats:italic>\u2009=\u20090.157) between the two genotypes. Array\u2010based comparative genome hybridization analyses revealed, in RCC, the loss of heterozygosity in chromosomes 4 and 12 without <jats:italic>p16<jats:sup>INK<\/jats:sup><\/jats:italic><jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#pin12598-bib-0004\"\/><jats:sup><jats:italic>A<\/jats:italic><\/jats:sup> inactivation; these results were confirmed by a methylation analysis and showed no significant difference between the genotypes. Lymphomas showed a preference for genomic amplifications. <jats:italic>Dlk1<\/jats:italic> inactivation by promoter methylation may be involved in carcinogenesis in both tumors. Fe\u2010NTA\u2010induced murine RCCs revealed significantly less genomic aberrations than those in rats, demonstrating a marked species difference.<\/jats:p><\/jats:sec>","DOI":"10.1111\/pin.12598","type":"journal-article","created":{"date-parts":[[2017,10,13]],"date-time":"2017-10-13T08:36:39Z","timestamp":1507883799000},"page":"564-574","source":"Crossref","is-referenced-by-count":13,"title":["Fenton reaction\u2010induced renal carcinogenesis in <i>Mutyh<\/i>\u2010deficient mice exhibits less chromosomal aberrations than the rat model"],"prefix":"10.1111","volume":"67","author":[{"given":"Guang Hua","family":"Li","sequence":"first","affiliation":[{"name":"Department of Pathology and Biological Responses Nagoya University Graduate School of Medicine Nagoya 466\u20108550 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shinya","family":"Akatsuka","sequence":"additional","affiliation":[{"name":"Department of Pathology and Biological Responses Nagoya University Graduate School of Medicine Nagoya 466\u20108550 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Shan Hwu","family":"Chew","sequence":"additional","affiliation":[{"name":"Department of Pathology and Biological Responses Nagoya University Graduate School of Medicine Nagoya 466\u20108550 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Li","family":"Jiang","sequence":"additional","affiliation":[{"name":"Department of Pathology and Biological Responses Nagoya University Graduate School of Medicine Nagoya 466\u20108550 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takahiro","family":"Nishiyama","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology Nagoya University Graduate School of Medicine Nagoya 466\u20108550 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Akihiko","family":"Sakamoto","sequence":"additional","affiliation":[{"name":"Department of Hematology and Oncology Nagoya University Graduate School of Medicine Nagoya 466\u20108550 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Takashi","family":"Takahashi","sequence":"additional","affiliation":[{"name":"Division of Molecular Carcinogenesis Center for Neurological Diseases and Cancer Nagoya University Graduate School of Medicine Nagoya 466\u20108550 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mitsuru","family":"Futakuchi","sequence":"additional","affiliation":[{"name":"Department of Molecular Toxicology Nagoya City University Graduate School of Medical Sciences Nagoya 467\u20108601 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hiromu","family":"Suzuki","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology Sapporo Medical University School of Medicine Sapporo 060\u20108556 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University of Sydney NSW 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