Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs) including cyclooxygenase 2 (COX-2) selective inhibitors, are potential agents for the chemoprevention of gastric cancer. Epidemiological and experimental studies have shown that NSAID use is associated with a reduced risk of gastric cancer although many questions remain unanswered such as the optimal dose and duration of treatment. The possible mechanisms for the suppressor effect of NSAIDs on carcinogenesis are the ability to induce apoptosis in epithelial cells and regulation of angiogenesis. Both COX-dependent and COX-independent pathways have a role in the biological activity of NSAIDs. Knowledge of how NSAIDs prevent neoplastic growth will greatly aid the design of better chemopreventive drugs and novel treatments for gastric cancer.
MeSH terms
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Animals
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use*
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Apoptosis / drug effects
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Apoptosis / physiology
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Cell Transformation, Neoplastic / drug effects
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Cyclooxygenase 2 / genetics
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Cyclooxygenase 2 / physiology
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Cyclooxygenase 2 Inhibitors / pharmacology
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Cyclooxygenase 2 Inhibitors / therapeutic use
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Disease Models, Animal
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Gene Expression Regulation, Enzymologic / physiology
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Helicobacter pylori / physiology
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Humans
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Neovascularization, Pathologic / drug therapy
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Neovascularization, Pathologic / physiopathology
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Stomach Neoplasms / epidemiology
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Stomach Neoplasms / physiopathology*
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Stomach Neoplasms / prevention & control*
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase 2