Role of Helicobacter pylori in gastric carcinogenesis: The origin of gastric cancers and heterotopic proliferative glands in mongolian gerbils

Masae Tatematsu, Tetsuya Tsukamoto, Tsutomu Mizoshita

研究成果: ジャーナルへの寄稿総説査読

49 被引用数 (Scopus)

抄録

Helicobacter pylori infection is well accepted to be a very important factor for the development of gastric carcinogenesis in the human stomach. In Mongolian gerbils treated with chemical carcinogens, H. pylori infection enhances glandular stomach carcinogenesis, and eradication of infection and results in curtailment of enhancing effects, particularly at early stages of associated inflammation. A high-salt diet exacerbates the effects of H. pylori infection on gastric carcinogenesis, and these two factors act synergistically to promote the development of gastric cancers in this animal model. However, the bacterium exerts the greater effects. Early acquisition significantly increases gastric chemical carcinogenesis in Mongolian gerbils, as compared to later infection. While heterotopic proliferative glands, hyperplastic and dilated glands localized beneath the muscularis mucosae, frequently develop with H. pylori infection alone in this animal model, they obviously regress on eradication, suggesting a relation to severe gastritis, rather than a malignant character. Furthermore, endocrine cells, positive for chromogranin A, are observed in the heterotopic proliferative glands, in contrast to cancerous lesions which lack endocrine elements. In conclusion, H. pylori is not an initiator, but rather a strong promoter of gastric carcinogenesis, whose eradication, together with reduction in salt intake, might effectively prevent gastric cancer development.

本文言語英語
ページ(範囲)97-106
ページ数10
ジャーナルHelicobacter
10
2
DOI
出版ステータス出版済み - 2005
外部発表はい

All Science Journal Classification (ASJC) codes

  • 消化器病学
  • 感染症

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