Abstract
Helicobacter pylori infection is an important factor for gastric carcinogenesis in human. In carcinogen-treated Mongolian gerbils, H. pylori infection enhances stomach carcinogenesis, while infection alone induced severe hyperplasia called heterotopic proliferative glands. A high-salt diet or early acquisition of the bacteria exacerbates inflammation and carcinogenesis. Oxygen radical scavengers or anti-inflammatory chemicals as well as eradication of H. pylori are effective to prevent carcinogenesis. H. pylori-associated inflammation induces intestinal metaplasia and intestinalization of stomach cancers independently. It is necessary to control cancer development not only in H. pylori-positive cases but also in H. pylori-negative metaplastic gastritis.
MeSH terms
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Animals
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Anti-Inflammatory Agents / therapeutic use*
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Free Radical Scavengers / therapeutic use*
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Gerbillinae
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Helicobacter Infections / complications
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Helicobacter Infections / drug therapy*
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Helicobacter Infections / immunology
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Helicobacter Infections / pathology
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Helicobacter pylori / immunology*
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Humans
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Metaplasia / etiology
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Metaplasia / immunology
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Metaplasia / microbiology
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Metaplasia / pathology
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Metaplasia / prevention & control
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Mice
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Neoplasms, Experimental / immunology
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Neoplasms, Experimental / microbiology
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Neoplasms, Experimental / pathology
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Neoplasms, Experimental / prevention & control
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Rats
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Stomach Neoplasms* / etiology
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Stomach Neoplasms* / immunology
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Stomach Neoplasms* / microbiology
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Stomach Neoplasms* / pathology
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Stomach Neoplasms* / prevention & control
Substances
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Anti-Inflammatory Agents
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Free Radical Scavengers