Promotion of epidermal carcinogenesis by repeated damage to mouse skin

TS Argyris - American journal of industrial medicine, 1985 - Wiley Online Library
TS Argyris
American journal of industrial medicine, 1985Wiley Online Library
Chemically induced epidermal carcinogenesis is usually divided into two stages: initiation,
which involves the conversion of some epidermal cells into latent neoplastic cells; and
promotion, which results in tumors. The hallmark of chemical promoters is epidermal
hyperplasia. The hyperplasia caused by a strong promoter, such as 12‐O‐
tetradecanoylphorbol‐13‐acetate (TPA), differs morphologically from that caused by weak
promoters, such as acetic acid and mezerin. The epidermal regeneration that follows …
Abstract
Chemically induced epidermal carcinogenesis is usually divided into two stages: initiation, which involves the conversion of some epidermal cells into latent neoplastic cells; and promotion, which results in tumors. The hallmark of chemical promoters is epidermal hyperplasia. The hyperplasia caused by a strong promoter, such as 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA), differs morphologically from that caused by weak promoters, such as acetic acid and mezerin.
The epidermal regeneration that follows abrasion results in a hyperplastic epidermis that resembles the effects of strong promoters. Repeated mechanical injuries are capable of enhancing papillomas and carcinomas in mouse skin initiated with 7,12‐dimethylben‐zanthracene (DMBA). Thus, a regenerative epidermal hyperplasia appears to be a precondition for tumor promotion.
It is highly probable that many epidermal cells are initiated during the lifetime of man. In the work place, repeated mechanical injury could predispose to epidermal neoplasms.
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