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Effects of antiinflammatory agents on mouse skin tumor promotion, epidermal DNA synthesis, phorbol ester-induced cellular proliferation, and production of plasminogen activator. [Fluocinolone acetonide, fluocinonide, fluclorolone acetonide]

Journal Article · · Cancer Res.; (United States)
OSTI ID:7297947
The antiinflammatory steroids fluocinolone acetonide, fluocinonide, and fluclorolone acetonide were found to be very effective inhibitory agents of mouse skin tumor promotion. These steroids also drastically inhibited epidermal DNA synthesis and epidermal cellular proliferation induced by a phorbal ester tumor promoter. In addition, these compounds were potent inhibitors of plasminogen activator production in tumor cell cultures. The clinically used nonsteroidal antiinflammatory agents oxyphenbutazone, indomethacin, and Seclazone also inhibited tumor promotion but were much less effective. Although these agents are useful against inflammatory disorders in general when given p.o., in our studies they had little effect on inflammation and epidermal cellular proliferation induced by a phorbol ester tumor promoter when given topically. The aforementioned nonsteroidal antiinflammatory agents also had little effect on epidermal DNA synthesis. Oxyphenbutazone and indomethacin were less potent inhibitors of plasminogen activator production in tumor cells than were the antiinflammatory steroids, and Seclazone produced a negligible inhibition. There is, therefore, a general correlation in the potencies of a series of steroidal antiinflammatory agents for inhibition of tumor promotion and their ability to inhibit plasminogen activator production by tumor cell cultures and epidermal DNA synthesis.
Research Organization:
Oak Ridge National Lab., TN
OSTI ID:
7297947
Journal Information:
Cancer Res.; (United States), Journal Name: Cancer Res.; (United States) Vol. 37; ISSN CNREA
Country of Publication:
United States
Language:
English