Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XIV. Mutational and non-mutational mechanisms as subsets of a more general mechanism. Part C. A defined cancer mutation.
The results of applying a mechanism of ethionine-induced embryonic gene derepressions to explain similar features found in hereditary tyrosinemia have been extended to a well defined cancer mutation. In all three cases, the described mechanism is compatible with the explanation for the etiology of embryonic like phenotypic expressions in cells and potentially for the carcinogenic process. The essence of the formulated process for a human bladder carcinoma mutation in the ras gene for a protein phosphokinase states that a specific proto-oncogene is mutated to an oncogene by various known processes. The protein phosphokinase that has an altered specificity resulting in anomalous phosphorylation of important regulating proteins by a non-mutation mechanism, i.e. by ethionine, would produce the same effect in a hypomethylated state of deoxyribonucleic acid causing an embryonic type protein phosphokinase gene to become activated. These embryonic oncogenes are supersensitive to methylation control mechanisms--thus the link between non-mutation and mutation type mechanisms.
D002273:Carcinogens / Q000633:toxicity*; D002471:Cell Transformation, Neoplastic; D004622:Embryo, Mammalian / Q000502:physiology; D006801:Humans; D008716:Methionine Adenosyltransferase / Q000235:genetics; D009154:Mutation; D009369:Neoplasms / Q000235:genetics*; D009857:Oncogenes; D011494:Protein Kinases / Q000235:genetics; D000090063:Proto-Oncogene Mas
D002273:Carcinogens; C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D008716:Methionine Adenosyltransferase; D011494:Protein Kinases