Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XXI oncogenes interpreted as embryonic genes

Abstract

If oncogenes are interpreted as embryonic genes then the mechanisms for induction of these embryonic genes can be generalized and theoretical considerations can be derived as follows. Agents that induce activity by derepressing embryonic genes can be placed into major groups: i) translocation inducers, ii) non-mutating carcinogenic agents, iii) intercalating DNA groove distorters, and iv) mutating agents. Translocation inducers work via long terminal repeat insertions, antibody promoter region associations, or V-type position effects. Non-mutational agents such as ethionine cause hyporibosylation of nucleosome core histones or hypomethylation of promoter regions of conformation inducer proteins. All of these agents cause deheterochromatizations of facultative heterochromatin. These processes (or by a classical mutation with mutating agents), cause DNA replication to acquire a new abnormal methylationpattern that is held constant by maintenance DNA methylases. The resultant active series of repressed reduntant type embryonic genes, such as subsets of rDNA genes and tRNA methylase genes, including oncogenes, e.g., protein phosphokinases among other required genes, and spurious irrelevant embryonic genes to the process of carcinogenesis. From the above theory is derived the concept that normal sets of redundant genes, e.g., rDNA are normally activated by planar intercalating agents (steroids) that would simply be the limiting subset of the mechanism used to create an anomalous state when extended to the set of embryonically repressed genes that become activated.