NSAIDs Protect Against Skin Cancer

Craig A. Elmets, MD


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In This Article

Abstract and Introduction


Compared with never-users, ever-users had reduced risk for SCCs, malignant melanomas, and certain BCCs.


Experimental models have shown procarcinogenic effects of cyclooxygenase (COX) enzymes, which promote inflammation, facilitate invasion through the basement membrane zone, suppress host antitumor defense mechanisms, inhibit tumor cell apoptosis, and stimulate angiogenesis. Nonsteroidal anti-inflammatory drugs (NSAIDs) block COX activity. These authors examined the association between NSAID use and risk for squamous cell carcinoma (SCC), basal cell carcinoma (BCC), and malignant melanoma (MM) in patients with histologically verified cases recorded in the Danish cancer registry between 1991 and 2008. Patients with human immunodeficiency virus infection, organ transplants, or previous cancer diagnoses were excluded.

Overall, NSAID users had a reduction in SCC and MM, but not BCC, compared with those who had never taken NSAIDs. Reduction in risk was associated with duration of NSAID use and dose size. Among long-term, high-dose NSAID users, the risk reduction was 46% for MM, 35% for SCC, and 17% for BCC. The reduced risk for SCC and melanoma was irrespective of anatomic site, but only BCCs sited elsewhere than the head and neck were influenced by NSAID use. Both aspirin and nonselective NSAIDs effectively protected against SCC and MM; newer COX-2 inhibitors were associated with reductions in SCC but not MM. High-dose, long-term use of acetaminophen was associated with a reduced risk for MM and for BCCs other than on the head and neck.


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