Abstract
TPA promotion of skin tumors in mice can be modified by application of various prostaglandins or their precursors. The effects depend on the particular prostaglandin used: PGF2alpha enhances promotion, whereas PGE1 consistently inhibits promotion. Time of application of the prostaglandin with respect to TPA determines whether PGE2 enhances or inhibits. Dose-dependent inhibition was observed for arachidonic acid. The prostaglandins alone were unable to elicit tumors in initiated mice.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Animals
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Arachidonic Acid / pharmacology
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Carcinogens / toxicity*
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Cell Transformation, Neoplastic / chemically induced*
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Cocarcinogenesis
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Dinoprost / pharmacology
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Dinoprostone / pharmacology
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Female
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Mice
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Mice, Inbred SENCAR
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Oxytocics / pharmacology
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Papilloma / chemically induced*
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Prostaglandins / pharmacology*
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Skin Neoplasms / chemically induced*
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Tetradecanoylphorbol Acetate / toxicity*
Substances
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Carcinogens
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Oxytocics
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Prostaglandins
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Arachidonic Acid
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Dinoprost
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Dinoprostone
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Tetradecanoylphorbol Acetate