Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XXIII enhancer theory

Abstract

Embryonic gene enhancers may be controlled by deheterochromatization of genes of trans-acting factors caused by altered methylation states of hypersensitive chromatin. Such specific chromatin sites would have a certain required helical pitch (X-type DNA). Non-core regions surrounding the enhancer motif would allow interactions with specific cell type promoters. Differences in embryonic and adult type genes may be reduced to these enhancer activities and certain trans-acting proteins effecting these genic control elements. Furthermore all spurious embryonic gene activities of neoplasms may also be due to such factors. Even pleotrophic and cascade phenomena in dysdifferentiation processes may be described in terms of enhancer mechanisms. Duplications of enhancer sequences may be fundamental to the potential of hyperactivity by embryonic type genes. Examples of this would be alpha-fetoprotein correlations with enhancer activity and possibly increased nucleolar organizer activity of embryonic cells. The manner by which chemical carcinogens would be involved with enhancer processes would be via “key” mechanisms that have been presented previously.