The Collapse of Cancer Metastases Hypothesis PRW -- The Announcement of New Study Results, Sergey N. Rumyantsev, Andent Inc.

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The announcement of a new study results -- Sergey N. Rumyantsev, Director of research, Andent Inc. The new view of the origin of cancerous cells provides a framework for understanding the genetic prerequisites for cancer epidemics and its rising incidence in ethnically mixed populations. Testing potential parents for hereditary incongruence together with subsequent preclusion of incongruent genetic admixture could be the most effective way to reduce the incidence of cancer in the human population.

The announcement of new study results -- Sergey N. Rumyantsev Director of research, Andent Inc. For the last 50 years the prevailing paradigm in cancer origin, pathogenesis, prevention and treatment has been based upon the rarely questioned ‘somatic mutation hypothesis’. This hypothesis states that (1) cancer primarily occurs in individuals over 40 years of age from a single somatic cell that has accumulated multiple DNA mutations in genes that control proliferation and the cell cycle, (2) cancer is a disease of the control of cell proliferation that leads to (3) the formation of a maternal tumor and (4) subsequent spread (metastasis) of cancer maternal cells outside the primary site to form daughter tumors in distant locations in the body. The recent cancer epidemic, characterized by the aggressive increase in the prevalence of cancer among human populations, is outside of the scope of the ‘somatic mutation hypothesis’ calling into question the premise of this hypothesis.

According to the conventional paradigm, cancer cells metastasize from a maternal tumor through the bloodstream or the lymphatic system; however, this process has not been proven or fully elucidated. In reality we observe the non-simultaneous appearance of several identical tumors in different parts of a diseased body. The details of the supposed metastasis remain hypothetical and mysterious. The lack of evidence of the metastatic pathway prevents effective interventions for cancer healing and prevention.

In contrast to the hypothesis of mutant maternal tumor and its subsequent metastasis, recent evidence revealed that potentially cancerous cell clones do not appear in a body as a result of specific mutation of a somatic cell. The clone is of innate origin formed by heterozygous interbreeding. This leads to genetic admixture between ethnic groups that have developed in ecologically different environments. As a result, differences may exist in the molecular composition of physiological regulators in these individuals. The clone appears in some persons’ bodies as a result of cross-fertilization of parents with genetically incongruent regulators of cell dividing and tissue growth. That is why the highest incidence of cancer is observed in the ethnically mixed populations.

This heterozygous clone is formed and distributed in the offspring’s body before its birth and exists for many decades within the body in a dormant state. The period of dormancy is terminated according to a specific program of the clone ontogenesis. At this time, the clone demonstrates hereditary immunity against the body’s prevailing regulators of cell reproduction and begins to multiply uncontrollably, thus initiating the cancerous growth.

The new view of the origin of cancerous cells supports the trends of the pandemic spread of the disease. It also forces scientists, clinicians and researchers to consider different perspectives for future investigations and reassess the current means and methods for cancer prevention and healing.
It also forces scientists, clinicians and researchers to consider different perspectives for future investigations and reassess the current means and methods for cancer prevention and healing.

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Sergey N. Rumyantsev
Andent Inc.
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