Abstract
Carcinogenesis results from the long-term accumulation of genetic and epigenetic aberrations at the molecular level, which are under constant selection pressure for growth advantage. Recognizing that cancer is the result of this long-term, multi-step process provides opportunities for molecularly targeted cancer prevention. Ideally, chemopreventive agents should be low in toxicity, morbidity, and cost. Several individual agents and agent combinations are currently under evaluation in the U.S. National Cancer Institute s (NCI) chemoprevention agent development program. Nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit cyclooxygenase (COX) -1 and -2 are among the most promising classes of agents for targeted molecular prevention.
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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Anti-Inflammatory Agents, Non-Steroidal / toxicity
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Anticarcinogenic Agents / pharmacology*
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Anticarcinogenic Agents / therapeutic use
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Anticarcinogenic Agents / toxicity
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Chemoprevention
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Clinical Trials as Topic
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Cyclooxygenase 1
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Cyclooxygenase 2
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors / pharmacology*
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Cyclooxygenase Inhibitors / therapeutic use
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Cyclooxygenase Inhibitors / toxicity
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Humans
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Isoenzymes / antagonists & inhibitors
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Isoenzymes / biosynthesis
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Membrane Proteins
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Neoplasms / metabolism
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Neoplasms / prevention & control*
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Prostaglandin-Endoperoxide Synthases / biosynthesis
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Treatment Outcome
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Anticarcinogenic Agents
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Cyclooxygenase 2 Inhibitors
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Cyclooxygenase Inhibitors
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Isoenzymes
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Membrane Proteins
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Cyclooxygenase 1
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Cyclooxygenase 2
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PTGS1 protein, human
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases