MUTATION-METABOLIC MODEL OF CANCER DEVELOPMENT AND TUMOR PROGRESSION

  • 1 January 1976
    • journal article
    • research article
    • Vol. 22  (8) , 3-16
Abstract
The given data indicate the presence of a negative correlation between metabolic indices (a decrease of the tolerance to glucose, increase of the blood level of free fatty acids, insulin, cholesterol, triglycerides, cortisol, etc.) and the indices of cellular immunity, which is determined by the number of rosette-forming cells and blast transformation reaction to PHA [phytohemagglutinin] and skin tests. Administration of an antidiabetic drug phenformin (phenetylbiguanide), apart from the improvement of metabolic pattern, results in the restoration of cell-mediated immunity indices. These findings provide a basis for stating the phenomenon of metabolic immunodepression. Metabolic immunodepression may prevent immunological surveillance, which normally is realized through signals provided by cells subjected to somatic mutation. The given metabolic conditions (hypercholesterolemia, hyperinsulinemia, enhanced utilization of free fatty acids) promote the division of somatic cells. The same metabolic shifts which increase the pull of proliferating cells and, accordingly, increase the possibility of mutation development, also cause metabolic immunodepression. These opposite metabolic influences on somatic cells and T[thymus]-dependent lymphocytes cause the development of the syndrome of cancrophilia. The syndrome of cancrophilia normally arises at pregnancy, in intensive growth of the organism in childhood, accelerated development, stress and normal aging. Many carcinogens cause decreased glucose tolerance, increased blood insulin levels and elevation of the threshold of sensitivity of the hypothalamus to feedback suppression. This phenomenon is based on decreased catecholamine levels in the hypothalamus in aging, stress and the action of some carcinogens. The carcrophilia syndrome provides the conditions for cancer development and tumor progression. The tumor itself produces the metabolic shifts typical of cancrophilia. In the light of the mutation-metabolic model of cancer development, it is possible to consider the fundamental factors which increase or hinder carcinogenesis in humans, rats and humpback salmon.

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