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• W2003350005 abstract "In mouse skin, tumor development promoted by ‘non-genotoxic’ carcinogens is closely related to the wound response. In both cases endogenous factors such as cytokines and eicosanoids released primarily from ‘activated keratinocytes’ play a key role as mediators of inflammation and cellular hyperproliferation. The liberation of interleukin-1a and arachidonic acid from human keratinocytes has been used as an in vitro parameter of irritancy. The results (from experiments with 15 different chemicals) being validated at present in a clinical study indicate a quantitative relationship between irritancy in vivo and mediator release in vitro. In the course of experimental skin carcinogenesis an overproduction of eicosanoids due to a constitutive overexpression of the corresponding enzymes (i.e. PGH synthase-H and 8- and 12-lipoxygenase) is observed. Enzyme inhibitors, for instance nonsteroidal antiinflammatory drugs (NSAIDs), exert a strong tumoristatic effect. Thus, the approach of multistage skin carcinogenesis provides a suitable animal model for a mechanistic evaluation and further improvement of chemopreventive measures such as the inhibition of colorectal tumor development in humans by NSAIDs (‘aspirin effect’)." @default.
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• W2003350005 date "1995-12-01" @default.
• W2003350005 modified "2023-09-23" @default.
• W2003350005 title "Mechanisms in tumor promotion: guidance for risk assessment and cancer chemoprevention" @default.
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• W2003350005 doi "https://doi.org/10.1016/0378-4274(95)03529-x" @default.
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