© The Author 2005. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
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COX and cancer
From the Department of Cancer Medicine, Imperial College of Science, Technology & Medicine, London, UK
Address correspondence to Professor J. Waxman, Department of Cancer Medicine, Faculty of Medicine, Imperial College of Science, Technology & Medicine, Hammersmith Campus, Du Cane Road, London W12 0NN. email: j.waxman@ic.ac.uk
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| Introduction |
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The willow tree has been a source of remedies against fever and inflammation since ancient times. Just over a century ago, Hoffman isolated and modified an active compound from the willow tree and offered it for sale as aspirin. Subsequently, a number of similar compounds have been derived, and these have been classified as non-steroidal anti-inflammatory drugs or NSAIDs. These drugs inhibit the enzyme cyclo-oxygenase (COX), which catalyses the conversion of arachidonic acid to prostaglandins (PGs). PGs are important mediators of signal transduction pathways, and are involved in cellular adhesion, growth and differentiation. Aspirin and other NSAIDs are extensively used in cancer patients, primarily for analgesia. However, since the late 1970s, researchers have been interested in whether regular ingestion of aspirin and other NSAIDs can decrease cancer risk. The most persuasive evidence to date relates to colorectal cancer. Is there a role for these drugs in the primary prevention of
| COX enzymes |
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| Anti-tumoural activity of COX-2 inhibition |
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Apoptosis
Angiogenesis
Xenobiotic metabolism
Tumour cell invasiveness
Aromatase modulation
Synergy with other modalities
| COX-2 inhibition in human cancer |
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Epidemiological studies
Randomized trials
COX-2 inhibitors in primary cancer treatment
| Long-term safety of COX inhibition |
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| Conclusions |
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