| Abstrakt: |
Chemically induced epidermal carcinogenesis is usually divided into two stages: initiation, which involves the conversion of epidermal cells into latent neoplastic cells; and promotion, which allows the expression of this neoplastic change. One of the characteristics of promotion is the transformation of the normal epidermis into a hyperplastic epidermis. One of the unanswered questions about epidermal tumor promotion is whether the epidermal hyperplasia that characterizes promoted skin is simply a regenerative epidermal hyperplasia resulting from damage produced by the promoter. The opinion currently held is that the epidermal hyperplasia produced by tumor promoters is not simply a regenerative epidermal hyperplasia and possesses characteristics which a regenerative hyperplasia does not have, enabling it to evolve into an epidermal neoplasm. The purpose of this review is to present recent evidence which strongly suggests that promoter induced hyperplasia is a regenerative hyperplasia. Two principal lines of evidence arc reviewed. The first demonstrates that an epidermal regenerative hyperplasia repeatedly produced by wounding or abrasion can promote epidermal carcinogenesis in the initiated skin of mice. The second line of evidence demonstrates that the epidermal hyperplasia produced by the application of 12-0- tetradecanoyl-phorbol-13-acetate (TPA), the most powerful and widely used promoter of skin carcinogenesis, is preceded by damage to the epidermis. This strongly suggests that the epidermal hyperplasia which ensues is a regenerative hyperplasia. The review concludes that during epidermal tumor promotion there is a chronic regenerative epidermal hyperplasia, and that there is no evidence for any other necessary factors during tumor promotion in appropriately initiated mouse skin. [ABSTRACT FROM AUTHOR] |
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