Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins. V. The steroids.
Since the induction of neoplastic cells by steroids has been well documented, an attempt is made to formulate a mechanism for explaining the resultant embryonic features of such tumour cells. Special emphasis is given to estrogen receptor complexes and their effect on chromatin proteins. Specifically a mechanism is presented for estradiol-17-beta and its ability to alter the gene expression (derepression) of mammary gland epithelial cells. In this model we explore the possible effects of small differences in receptor or repressor proteins associated with estrogens to translate quantitative steroid administration into qualitative cellular responses.
D000818:Animals; D006224:Cricetinae; D004622:Embryo, Mammalian / Q000502:physiology; D004958:Estradiol / Q000502:physiology; D005796:Genes; D006168:Guinea Pigs; D008325:Mammary Neoplasms, Experimental / Q000139:chemically induced; D051379:Mice; D008954:Models, Biological; D009369:Neoplasms / Q000139:chemically induced*; D009698:Nucleoproteins / Q000096:biosynthesis*; D011817:Rabbits; D051381:Rats; D011960:Receptors, Estrogen / Q000502:physiology; D013256:Steroids / Q000009:adverse effects / Q000494:pharmacology*
D009698:Nucleoproteins; D011960:Receptors, Estrogen; D013256:Steroids; D004958:Estradiol