{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T11:38:58Z","timestamp":1777894738746,"version":"3.51.4"},"reference-count":21,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2005,2,1]],"date-time":"2005-02-01T00:00:00Z","timestamp":1107216000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Toxicol Pathol"],"published-print":{"date-parts":[[2005,2]]},"abstract":"<jats:p>In the present study, susceptibility of CB6F1 mice carrying the human prototype c-Ha- ras gene (rasH2 mice) and p53 gene knockout mice ( p53 (+\/\u2212) mice) to urethane-induced lung carcinogenesis was compared under the same experimental conditions. Both strains were administered 500 ppm urethane in their drinking water for 3 weeks. At week 26, lung adenocarcinomas and adenomas were observed in 53% and 100% of rasH2 mice, respectively, and lung adenomas were observed in 67% of rasH2 littermate (non-Tg) mice. However, lung tumors were not observed in either p53 (+\/\u2212) or p53 (+\/+) mice. Peliosis hepatis and hepatic hemangiomas were observed in 27% and 67% of p53 (+\/\u2212) mice, but only in 6.7% and 6.7% of the rasH2 animals, respectively. Under the same experimental conditions, BALB\/c mice, the strain of origin of the rasH2 mice, developed lung adenomas at an incidence of 93%, whereas none of the C57BL\/6 original strain for p53 (+\/\u2212) mice developed lung tumors. Peliosis hepatis was observed in 40% of the C57BL\/6 mice, but not in BALB\/c mice; hepatic and splenic hemangiomas were not observed in these animals. These results indicate that organ susceptibility of rasH2 and p53 (+\/\u2212) mice is inherited from their strains of origin, the rasH2 and BALB\/c lines being much more sensitive to the induction of pulmonary carcinogenesis.<\/jats:p>","DOI":"10.1080\/01926230590908231","type":"journal-article","created":{"date-parts":[[2005,1,26]],"date-time":"2005-01-26T11:00:56Z","timestamp":1106737256000},"page":"267-271","source":"Crossref","is-referenced-by-count":8,"title":["Susceptibilities of\n                    <i>p53<\/i>\n                    Knockout and rasH2 Transgenic Mice to Urethane-Induced Lung Carcinogenesis are Inherited from their Original Strains"],"prefix":"10.1177","volume":"33","author":[{"given":"Masakazu","family":"Ozaki","sequence":"first","affiliation":[{"name":"Department of Experimental Pathology and Tumor Biology, Nagoya City University, Graduate School of Medical Sciences, Mizuho-ku, Nagoya 467-8601, Japan"},{"name":"Environmental Health Science Laboratories, Sumitomo Chemical Co. 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