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Chemoprevention of gastrointestinal malignancies with nonsteroidal antiinflammatory drugs
In multiple studies, the chronic use of nonsteroidal antiinflammatory drugs (NSAIDs) has been associated with a decreased incidence of several types of gastrointestinal (GI) neoplasia. This effect may be mediated by one of several intracellular mechanisms, some of which involve the inhibition of the...
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Published in: | Cancer 2002-02, Vol.94 (4), p.950-963 |
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Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | In multiple studies, the chronic use of nonsteroidal antiinflammatory drugs (NSAIDs) has been associated with a decreased incidence of several types of gastrointestinal (GI) neoplasia. This effect may be mediated by one of several intracellular mechanisms, some of which involve the inhibition of the cyclooxygenase‐2 (COX‐2) isoenzyme. In multiple studies of colorectal carcinoma, chronic NSAID use has shown a protective effect, with the majority of studies demonstrating a 30–70% risk reduction associated with NSAID use. The effect of NSAIDs on other types of GI neoplasia is less clear, but evidence suggests that chronic NSAID use may diminish the risk of esophageal and gastric carcinomas. Data assessing the effects of NSAIDs on the incidence of pancreatic and hepatic malignancies currently are too sparse and inconsistent to draw any conclusions. The newer COX‐2 specific agents may provide a less GI‐toxic alternative to nonselective NSAIDs as chemoprotective agents. Cancer 2002;94:950–63. © 2002 American Cancer Society.
DOI 10.1002/cncr.10333
The chronic use of nonsteroidal antiinflammatory drugs has been associated with a decreased risk of multiple different gastrointestinal (GI) malignancies. In the current study, the authors review possible mechanisms of chemoprevention, the data assessing the strength and magnitude of any risk reduction for major GI malignancies, and future directions in chemoprevention research. |
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ISSN: | 0008-543X 1097-0142 |
DOI: | 10.1002/cncr.10333 |