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Stimulatory role of transforming growth factors in multistage skin carcinogenesis: Possible explanation for the tumor‐inducing effect of wounding in initiated nmri mouse skin
Author(s) -
Förstenberger Gerhard,
Rogers Michael,
Schnapke Ruben,
Bauer Georg,
Höufler Petra,
Marks Friedrich
Publication year - 1989
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910430531
Subject(s) - carcinogenesis , transforming growth factor , endogeny , in vivo , cancer research , epidermal growth factor , stimulus (psychology) , wound healing , biology , chemistry , endocrinology , immunology , cell culture , medicine , cancer , psychology , microbiology and biotechnology , genetics , psychotherapist
Mechanical wounding provides a convertogenic (“stage 1 tumor‐promoting”) stimulus in initiated NMRI mouse skin, indicating that this stage of carcinogenesis can be entirely controlled by endogenous factors. A search for such factors led to the finding that both platelet‐derived Epstein‐Barrvirus‐inducing factor (EIF), alias human TGFβ 1 and porcine TGFβ, exhibited—upon intracutaneous injection—convertogenic efficacy in initiated NMRI‐mouse skin in vivo provided that their injection was combined with a single topical application of the non‐convertogenic tumor promoter 12‐O‐retinolyphorbol‐13‐acetate (RPA). Since TGFβ inhibits epidermal cell proliferation, the RPA treatment is thought to provide a mitogenic stimulus required for conversion. The RPA treatment can be replaced by intracutaneous injection of transforming growth factor α (TGFα). These results indicate that the stage of conversion consists of two components, one of which is related to mitogenesis (RPA or TGFα), the other to a still unknown activity exhibited by TGFβ‐like factors. Thus, endogeneous factors with the quality of “wound hormones” may be involved in multistage skin carcinogenesis. This finding could explain the convertogenic effect of skin wounding.