An integrative hypothesis linking cancer, diabetes and atherosclerosis: the role of mutations and epigenetic changes.
It appears that the disease states of cancer, altherosclerosis and diabetes might share a common etiology. These chronic diseases appear to be multi-staged in their progression, with genetic, nutritional, psycho-social, environmental and viral factors influencing their appearance. We offered a hypothesis (a "mutation theory of disease"), stating that these diseases can be described by initiation and promotion phases; initiation being the result of the production of mutated cells after unrepaired damaged DNA is replicated; promotion being the selective proliferation of the initiated cells to form clones of mutated cells. It was further postulated that promotion affects cell proliferation by altering a membrane-Ca++ regulatory system. Depending on the nature of the mutation in the clone of cells, specific disease states would result. The roles of radiations, chemicals, viruses, genes, nutrition and psycho-social stress were related to either the initiation (mutation production) or the promotion (cell proliferation) phase of these diseases.
D001161:Arteriosclerosis / Q000209:etiology*; D002999:Clone Cells / Q000502:physiology; D003920:Diabetes Mellitus / Q000209:etiology*; D004777:Environment; D006801:Humans; D009153:Mutagens; D009154:Mutation; D009369:Neoplasms / Q000209:etiology* / Q000235:genetics; D009747:Nutritional Physiological Phenomena
D009153:Mutagens