Functions of hereditary immunity and xenogamy in cancer origin and pandemic spread

The efficacy of means exploited currently for cancer prevention and treatment appeared to be very low. New insights into the origin of the disease are sorely needed. The present article synthesizes the results from integrative reconsideration of actual data on cancer from the viewpoint of recent developments in pathology, epidemiology, immunology, genetics, and evolution. In contrast to the 80 years old hypothesis of somatic mutative origin of carcinogenesis, the revealed set of evidence showed the origin of cancerous clones is based on inherent constitutional incongruence between the regulators of cell physiology and their targets realized in inherent immunity of cancerous cells to normal regulation of cell replication and tissue growth. The incongruence arises out of both genome mutations which led to interethnic differences in the regulator-receptor structures and intercourse between ethnoses, the regulator-receptor evolution of which has been processed to deal with different ecologic conditions. The current pandemic spread of cancer is brought about growing expansion of interethnic xenogamy favored by growing industrialization, urbanization, globalization, and migration. The proposed hypothesis of genome intrusion in the origin of cancer induces new research ideas and proposals for cancer prevention and therapy.

Human cancer is transmitted via genome

Recent discredit of “somatic mutation” hypotheses forced the need of new paradigms about the nature of human cancer. The present article is devoted to further development of one such paradigm: the hypothesis of invasive parasitic nature, origin, evolution, pathogenesis and transmission of human cancer. Development was performed by supplementing and supporting the hypothesis by data which could not be applied before. The supplementation included integrative reconsidering, and reinterpretation of the make-ups, traits and processes existing not only in human cancer but also in animal cancers. Special attention has been focused on xenogamous intrusion of carcinogenic traits in the genome of a host. It was evidenced that human cancer possesses the same set of traits characteristic of transmissible animal cancer. In contrast to animal cancer formed of solitary cell lineage, human cancer consists of a couple of lineages constructed under different genetic regulations and performed different structural and physiological functions. The diversity of cancer composition remains stable over sequential propagation. The subsistence of human cancer regularly includes obligetory rotation alternation of its successive forms including genomic, gametic, zygotic, micro-population and tumorous ones. Human cancer possesses its own biological watch and the ability to gobble its victim, transmit via the intrusion of the genome, perform intercommunications within the tumor components and between the dispersed subunits of cancer.

The Negative Entropy in Organisms;Its Maintenance and Extension

Life has been a mystery for most physicists since the question of Maxwell’s demon. In the present paper, the self-reproduction, which is characteristic of the organism, is shown to be essential in resolving the paradox of Maxwell’s demon. For this purpose, a new thermodynamic quantity of biological activity is introduced to represent the molecular events in an organism recently revealed by molecular biology. This quantity gives a measure that the entropy production arising from the difference between acquired energy and stored energy compensates for the negative entropy of systematizing the organism, and is considered to be proportional to the self-reproducing rate of the organism as the first approximation. The equation of replicator dynamics consisting of self-reproducing rate, death rate and mutation terms contains all known types of evolution of unicellular organisms. When the mutation term is restricted to the point mutation mainly due to the nucleotide base changes in genes, this equation automatically leads to Darwinian evolution that the mutant with the higher increase rate is selected to become prevailing in the population. Throughout this evolution, the nucleotide bases in genes are converged to the special arrangement exhibiting the optimal increase rate of the organism. Moreover, the mutants having experienced gene duplication first decline to the minor members in the population but some of the descendants recover as a new style of organisms by generating new gene(s) from the counterpart of duplicated genes. This evolutionary process to expand the repertoire of genes is mathematically formulated by solving the equation of replicator dynamics up to the higher order of mutation terms. The present theoretical approach can be not only extended to the multicellular diploid eukaryotes but also applied to explain the origin of genes in the self-reproducing proto-cells formed anciently.