Abstract
Gastric cancer is one of the most frequent neoplasms and a main cause of death worldwide, especially in China and Japan. Numerous epidemiological, animal and experimental studies support a positive association between chronic Helicobacter pylori (H. pylori) infection and the development of gastric cancer. However, the exact mechanism whereby H. pylori causes gastric carcinogenesis remains unclear. It has been demonstrated that expression of cyclooxygenase-2 (COX-2) is elevated in gastric carcinomas and in their precursor lesions. In this review, we present the latest clinical and experimental evidence showing the role of gastrin and COX-2 in H. pylori-infected patients and their possible association with gastric cancer risk.
Keywords:
Cyclooxygenase-2; Gastric cancer; Gastrin; Helicobacter pylori.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Anti-Bacterial Agents / therapeutic use
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Anticarcinogenic Agents / therapeutic use
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Cell Transformation, Neoplastic / genetics
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Cell Transformation, Neoplastic / metabolism*
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Cell Transformation, Neoplastic / pathology
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Cyclooxygenase 2 / metabolism*
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Cyclooxygenase 2 Inhibitors / therapeutic use
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DNA Methylation
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Epigenesis, Genetic
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Gastrins / metabolism*
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Gene Expression Regulation, Neoplastic
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Helicobacter Infections / complications*
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Helicobacter Infections / drug therapy
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Helicobacter Infections / enzymology
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Helicobacter Infections / microbiology
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Helicobacter pylori / drug effects
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Helicobacter pylori / pathogenicity*
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Humans
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Risk Factors
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Signal Transduction
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Stomach / drug effects
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Stomach / enzymology*
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Stomach / microbiology*
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Stomach / pathology
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Stomach Neoplasms / enzymology
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Stomach Neoplasms / etiology*
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Stomach Neoplasms / genetics
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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-Bacterial Agents
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Anticarcinogenic Agents
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Cyclooxygenase 2 Inhibitors
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Gastrins
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Cyclooxygenase 2