Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: intermediate generalizations.
A previous rendition of a mechanism for the induction of embryonic gene activity, derived from the viewpoint of agents capable of such inductions, concluded that a perturbed methylation pattern of DNA and/or chromatin proteins would be an essential feature. A more specific treatment of the mechanism centers on enhancer regions of proto-oncogenes as being the point of modification for any induction of new gene activity. DNA binding type proteins may be involved with deheterochromatization processes after complexing near long terminal repeat segments containing enhancer elements. Chemical carcinogens and steroids would modify the chromatin and directly or indirectly interfere with maintenance DNA methylation. The resulting hypomethylated enhancer and promoter regions would allow for enhancer mechanisms to activate repressed embryonic genes inappropriate to the developmental stage forcing embryonic features to be expressed by differentiating (or differentiated) cells.
Hancock
R L
RL
Canadian Institute of Theoretical Biology, Scott's Bay, Nova Scotia.
D000818:Animals; D002273:Carcinogens / Q000633:toxicity*; D005326:Fetal Proteins / Q000096:biosynthesis* / Q000235:genetics; D005786:Gene Expression Regulation / Q000187:drug effects; D006801:Humans; D008954:Models, Biological; D009857:Oncogenes / Q000187:drug effects; D013256:Steroids / Q000494:pharmacology
D002273:Carcinogens; D005326:Fetal Proteins; D013256:Steroids