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Page 1 od 41 rezultati
Structure and tumor-promoting activity of analogues of anthralin (1,8-dihydroxy-9-anthrone).
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Seventeen analogues of the tumor-promoting agent anthralin were tested for the same biological property by repeated skin application on mouse skin using female ICR/Ha Swiss mice, after a single application of a subcarcinogenic dose of 7,12-dimethylbenz[a]anthracene. Seven of the compounds tested are
Synergistic stimulation of prostaglandin E2 release by epidermal growth factor and a tumor promoter anthralin from primary cultures of mouse epidermal cells.
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The tumor promoter anthralin stimulated prostaglandin E2 (PGE2) and arachidonic acid release from primary cultures of mouse epidermal cells. Epidermal growth factor (EGF) hardly stimulated PGE2 release by itself; however, a combination of anthralin and EGF synergistically stimulated PGE2 release.
Inhibition of anthralin-caused skin tumor promotion and interleukin-1 alpha production by potent immunosuppressant FK506.
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The effect of FK506, a potent immunosuppressive agent, on 7,12-dimethylbenz[alpha]anthracene-initiated and anthralin-promoted skin tumor formation was examined in CD-1 mice. A topical application of 0.1 mumol FK506 to mouse skin 15 min prior to each anthralin treatment markedly inhibited skin tumor
Cocarcinogenic and tumor-promoting capabilities of anthralin.
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Numerous chemicals to which humans are exposed either therapeutically or as a result of living in an industrial environment constitute a potential threat as carcinogens, mutagens, and/or tumor promoters and cocarcinogens. Anthralin, and antipsoriatic agent, acts as a tumor promoter for Balb/c-3T3
Tumor-producing and skin-irritating activity of dithranol (anthralin) and its 10-acyl analogues in SENCAR mice.
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The tumor-producing and skin-irritating activity of the antipsoriatic drug dithranol and its 10-acyl analogues butantrone (10-butyryl dithranol), 10-isobutyryl dithranol and 10-valeryl dithranol were studied in 650 SENCAR mice using a two-stage skin carcinogenesis assay. An initiation with 20
Anthralin (dithranol) in vitro inhibits human monocytes to secrete IL-6, IL-8 and TNF-alpha, but not IL-1.
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Anthralin is a most widely used compound for topical treatment of psoriasis. Whereas numerous studies have ascertained anthralin as a safe and effective drug its mode of action still remains unclear. Previous studies demonstrated dose-dependent inhibition of a number of pro-inflammatory functions in
Effect of tumor-promoting agents on density and morphometric parameters of mouse epidermal Langerhans and Thy-1+ cells.
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Topical application of tumor-promoting agents to the dorsal skin of female SENCAR mice on a twice-weekly basis resulted in a reduction in density per unit area of bone marrow-derived Thy-1+ dendritic cells. Activity was observed for well-established tumor-promoting doses of promoting agents of
Effect of tumor promoters on ultraviolet light-induced mutation and mitotic recombination in Saccharomyces cerevisiae.
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Recently, it has been suggested that mitotic recombination is involved in tumor promotion. On this basis, one might expect tumor promoters to be recombinagenic. D7 is a diploid strain of yeast in which both mutation and mitotic recombination can be measured. We have used this strain to assay the
Further characterization of tumor-promoter-mediated activation of protein kinase C.
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Tumor promoting phorbol esters are able to activate Ca2+-sensitive, phospholipid-dependent protein kinase (protein kinase C) in a reconstituted system. Indol alkaloid teleocidin, a tumor promoter, has been found to be as potent as tumor promoters from the series of phorbol esters and mezerein in
Antioxidants attenuate anthralin-induced skin inflammation in BALB/c mice: role of specific proinflammatory cytokines.
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Anthralin is the most common therapeutic agent among a small number of pro-oxidant, 9-anthrones effective in the topical treatment of psoriasis. However, the usefulness of this drug is diminished by toxic side effects, including skin irritation and inflammation. The activities of anthralin are
Decreased ratio of reduced/oxidized glutathione in mouse epidermal cells treated with tumor promoters.
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Cellular pro-oxidant states appear to play role in the promotion phase, presumably because tumor promoter-treated cells overproduce activated forms of oxygen and/or deficient in their ability to destroy them. Since one of the earliest responses to the potent tumor promoter
Cytokines and signal transduction pathways mediated by anthralin in alopecia areata-affected Dundee experimental balding rats.
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Although many therapeutic modalities have been tested on alopecia areata, patient outcomes have been disappointing. Use of animal models would help to develop more efficient therapies as well as understanding therapeutic mechanisms. We have demonstrated that 0.1% topical anthralin ointment is 100%
Effect of anthralin on cell viability in human prostate adenocarcinoma.
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The study revealed the key role of serine protease hepsin activity in transition of in situ prostate adenocarcinoma into the metastasizing form. Inhibition of hepsin activity suppresses the invasive growth of the tumor. Hepsin is an convenient target for pharmacological agents, so the study of its
Cancer resistance, carcinogenesis and ground substance viscosity.
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Tumor host resistance and promotion are multiple complex simultaneous phenomena. This paper relates only to the effect of ground substance viscosity on tumor host interaction. Tar, anthralin, ultraviolet light, x-ray and arsenic have been widely used to treat inflammatory skin disorders such as
Induction of the polyamine-biosynthetic enzymes in mouse epidermis and their specificity for tumor promotion.
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The induction of ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase in mouse epidermis by various classes of tumor-promoting and nonpromoting compounds has been studied in order to determine the specificity of this response for tumor promotion. The effect of topical applications of a
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