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Department of Radiation Oncology [W. B. B., G. T. B], Department of Medicine [N. H., J. E., D. A.], The University of Arizona Health Sciences Center, Tucson, Arizona 85724, and the Hormel Institute, University of Minnesota, Austin, Minnesota 55912 [G. L., Z. D.]
We conducted an in vivo carcinogenesis experiment to determine the efficacy of topical aspirin and sodium salicylate (NAS) in preventing UVB-induced nonmelanoma skin cancer. Hairless SKH-1 mice were randomly divided into eight treatment groups. They were treated topically with either 40 or 10 µmol aspirin or NAS three times weekly before 9 kJ/m2 UVB irradiation. The experiment was carried out over 25 weeks. Both dose levels of NAS significantly inhibited (P < 0.05) the rate of tumor formation when compared with vehicle control. The 40 µmol dose of aspirin significantly inhibited the rate of tumor formation (P < 0.05), whereas the 10 µmol dose had no inhibitory effect when compared with the vehicle control. To investigate the mechanism of this inhibition, we studied UVB-induced thymine dimer formation in the epidermis of the mouse skin. We found that NAS inhibited UVB-induced thymine dimer formation (P = 0.0001), whereas aspirin did not. Therefore, we conclude that NAS prevents UVB-induced tumor growth and formation through a sunscreen effect; whereas, the moderate inhibition of aspirin may be because of a molecular event, such as the inhibition of various UVB signaling pathways.
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