Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins. II. Perturbations of post-translational nuclear protein modification.
An hypothesis of carcinogenesis is derived which suggests that carcinogens initially induce derepressions of structional genes of post-translational modifying enzymes. Although the resulting cascade of changes in genic activity would be measureable because of the large number of differentiated cells present in a tissue, only stem cells are vulnerable to the neoplastic array of genic expression by virtue of their repressors being more vulnerable to conformational modification. Furthermore it is derived that there are at least three major classes of repressors and the repressors that are synthesized during embryogenesis are particularly susceptible to derepression mechanisms.
D000818:Animals; D004247:DNA / Q000096:biosynthesis; D005001:Ethionine / Q000494:pharmacology*; D006657:Histones / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D008715:Methionine / Q000494:pharmacology; D009369:Neoplasms / Q000201:enzymology / Q000235:genetics; D010047:Ovalbumin / Q000096:biosynthesis*; D010641:Phenotype; D014176:Protein Biosynthesis / Q000187:drug effects; D051381:Rats; D013489:Suppression, Genetic / Q000187:drug effects; D014158:Transcription, Genetic / Q000187:drug effects; D000509:alpha-Fetoproteins / Q000096:biosynthesis*; D012359:tRNA Methyltransferases / Q000096:biosynthesis*
D006657:Histones; D000509:alpha-Fetoproteins; D010047:Ovalbumin; D004247:DNA; D008715:Methionine; D012359:tRNA Methyltransferases; D005001:Ethionine