Prenatal and childhood exposure to carcinogenic factors.
Transplacental carcinogenic effects have been demonstrated for about 60 chemicals in eight animal species and even in the human. Many carcinogens are much more active in the fetus than in the adult animal. The stage specificity of transplacental carcinogenesis is characterized by the possibility of inducing tumors only at certain stages of embryogenesis (at the end of organogenesis and during the whole period of histogenesis). Risk of transplacental carcinogenesis is owing to the passage of carcinogens or their active metabolites into embryonic tissue and the possibility of metabolic activation of substances within the fetus. In this connection, four main pathways can be hypothesized for the carcinogenic effect of a substance on the fetus. Organotropism with transplacental carcinogenesis is determined by genetic predisposition, differentiation, and proliferative activity in the target tissues. For indirect carcinogens the level of metabolizing enzymes is also important. Teratogenesis and carcinogenesis can be either independent processes or pathogenetically related to each other (eg, DES action). Experimental data can readily be applied to the discussion of prophylaxis of prenatal tumors in the human.
D000014:Abnormalities, Drug-Induced; D000022:Abortion, Spontaneous; D000818:Animals; D002273:Carcinogens / Q000633:toxicity*; D002648:Child; D006224:Cricetinae; D004622:Embryo, Mammalian / Q000187:drug effects; D005314:Embryonic and Fetal Development / Q000187:drug effects; D005260:Female; D006801:Humans; D008431:Maternal-Fetal Exchange; D051379:Mice; D009369:Neoplasms / Q000139:chemically induced; D011247:Pregnancy; D051381:Rats; D013045:Species Specificity
D002273:Carcinogens