Promotion of skin tumours by TPA in the progeny of mice exposed pre-natally to DMBA.
Pregnant SHR mice were treated once with 7,12-dimethylbenz[a]anthracene (DMBA) on day 17-19 of gestation, and F1 and F2 descendants received multiple skin applications of 12-O-tetradecanoylphorbol-13-acetate (TPA) twice a week for 24 weeks beginning at 12 weeks of age. Post-natal promoter treatment resulted in a high incidence of skin tumours in F1 and F2 mice (37.3 and 19.7%, respectively), whereas only 6.6% of control animals treated with TPA only developed skin tumours. DMBA was shown previously to be capable of initiating skin carcinogenesis transplacentally; however, our results on the second generation provide suggestive evidence of hereditary transmission of at least part of the initiating action of this carcinogen.
D015127:9,10-Dimethyl-1,2-benzanthracene / Q000633:toxicity*; D000818:Animals; D003433:Crosses, Genetic; D005260:Female; D008297:Male; D008431:Maternal-Fetal Exchange; D051379:Mice; D008815:Mice, Inbred Strains; D011247:Pregnancy; D012878:Skin Neoplasms / Q000139:chemically induced* / Q000473:pathology; D013755:Tetradecanoylphorbol Acetate / Q000633:toxicity*
D015127:9,10-Dimethyl-1,2-benzanthracene; D013755:Tetradecanoylphorbol Acetate