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© 1993 Oxford University Press

research-article

DNA mutilation of the pepsin 1 gene during rat glandular stomach carcinogensis induced by N-methyl-N'-nitro-N-nitrosoguanidine or catechol

Masae Tatematsu 3, Masao Ichinose 1, Shinko Tsukada 1, Nobuyuki Kakei 1, Satoru Takahashi, Kumiko Ogawa, Masao Hirose, Chie Furihata 2, Kazumasa Miki 1, Kiyoshi Kurokawa 1 and Nobuyuki Ito

First Department of Pathology, Nagoya City University, Medical School 1Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467
1First Department of Internal Medicine, Faculty of Medicine, University of Tokyo Bunkyo-ku, Tokyo 113
2Department of Molecular Oncology, Institute of Medical Science, University of Tokyo Minato-ku, Tokyo 108, Japan

The methylation patterns of the rat pepsinogen 1 (Pg1) gene in preneoplastic and neoplastic stomach lesions induced by genotoxic N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or the non-genotoxic carcinogen catechol were investigated. Male WKY/Ncrj rats were given MNNG in their drinking water (50 mg/l) for 30 weeks or 0.8% catechol throughout the experiment (60 weeks). MNNG induced Pg1 altered pyloric glands (PAPG), adenomatous hyperplasias and well-differentiated adenocarcinomas. Catechol also induced PAPG and adenomatous hyperplasias although cancers did not develop. Adenomatous hyperplasias and adenocarcinomas all considered of gastric type cells resembling surface mucous cells or pyloric gland cells with little or no Pg1 expression. In MNNG-induced stomach cancers generally lacking Pg1, altered Pg1 gene methylation was observed with both CCGG and GCGC sites being methylated more than normal pyloric mucosa. MNNG or catechol-induced adenomatous hyperplasias also demonstrated essentially the same methylation changes in the CCGG, but not in the GCGC sites. In the mucosa containing PAPG in groups treated with MNNG or catechol the methylation patterns of the Pg1 gene were quite similar to those of normal pyloric mucosa, although the CCGG sites tended to demonstrate slightly increased methylation. The results suggest that the altered methylation of the Pg1 gene observed in stomach cancers is acquired early in the carcinogenic process and progressive methylation changes occur with tumor development.


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