This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lowe, N. J. Articles by Chalet, M. Search for Related Content PubMed PubMed Citation Articles by Lowe, N. J. Articles by Chalet, M.

Inhibition of Ultraviolet-B Epidermal Ornitithine Decarboxylase Induction and Skin Carcinogenesis in Hairless Mice by Topical Indomethacin and Triamcinolone Acetonide¹

Division of Dermatology, Department of Medicine, UCLA Medical School, Los Angeles, California 90024 [N. J. L., M. J. C., J. B.], and Dermatology and Dermatopathology Service, UCLA-Veterans Administration-Wadsworth Dermatology Program, Los Angeles, California 90024 [M. C.]

Modulation of ultraviolet-B (UVB) skin carcinogenesis by topical treatment with two antiinflammatory drugs expected to have different mechanisms of action has been studied in the hairless mouse. Indomethacin is a nonsteroidal antiinflammatory agent which may act by inhibiting prostaglandin biosynthesis. Triamcinolone acetonide is a steroidal antiinflammatory agent. Both of these drugs inhibited the induction of epidermal ornithine decarboxylase by UVB when applied topically in an accetone vehicle. A UVB skin tumor study was designed. Groups of mice were irradiated daily with UVB for 20 days, each mouse receiving a total of 17.1 kJ UVB per sq m. Group 1 was treated with acetone immediately after each irradiation; Group 2 received 700 nmol indomethacin in acetone immediately after each irradiation; Group 3 received 14.4 nmol triamcinolone acetonide in acetone immediately after each irradiation. Mice were killed after 52 weeks, and the tumors were excised and examined histologically. Both topical indomethacin and topical triamcinolone accetonide were effective in reducing the incidence and size of the skin tumors induced by UVB. This evidence supports the hypothesis that the induction of ornithine decarboxylase may be a critical component of UVB skin carcinogenesis and that inhibition of ornithine decarboxylase induction can be used as a screen for agents which will inhibit UVB skin carcinogenesis.

¹ Supported by NIH Grant CA 25970 and by grants from the Dermatology Research Foundation of Southern California.

² To whom requests for reprints should be addressed.

Received 4/27/82. Accepted 7/ 1/82.

This article has been cited by other articles:

				I. F. Orengo, J. Gerguis, R. Phillips, A. Guevara, A. T. Lewis, and H. S. Black Celecoxib, a Cyclooxygenase 2 Inhibitor as a Potential Chemopreventive to UV-Induced Skin Cancer: A Study in the Hairless Mouse Model Arch Dermatol, June 1, 2002; 138(6): 751 - 755. [Abstract] [Full Text] [PDF]