Cytology of Carcinogenesis: The Mechanism of Unrestricted Cell Proliferation and of Somatic Cell Mutation

抄録

Both unrestricted cell proliferation and somatic cell mutation of cancer cells of all kinds are, at least in their starting points, intrinsically subjects of cytology and genetics but not of medicine. The explanation of these subjects is practically impossible without an elucidation of the mechanism of mitosis and of the genetic information of genes which control cell proliferation, cell differentiation, and metabolism of tissue cells of organs bearing cancers.
Based on in vivo observations and genetic information on mitosis in eukaryotes, it has been become clear that a spherical metabolic nucleus (a resting nucleus) continuously changes into a spindle-shape mitotic nucleus (a metaphases pindle) in prometaphase. This change of the nucleus is predicted and performed by the spindle formation inducer gene (SFI gene). In the cell division of eukaryotes, karyokinesis always goes ahead of cytokinesis and, cell proliferation and cell differentiation take place antagonistically. Accordingly, prior to entering into cell differentiation, each cell stops its mitosis under the genetic information of the spindle formation repressor gene (SFR gene).
If an epidermic primordial cell of an organ would happen to suffer a deficiency of the SFR gene from any internal or external cause, the cell would aquire a characteristic of unrestricted cell proliferation without cell differentiation and this character would be passed on to the offspring by mitosis. The deficiency of the SFR gene is inferred to be introduced by a recombination error of the gene DNA in chromosomes in the S-phase of dividing tissue cell nuclei. The DNA fractions would appear in and be diffused from the damaged cell nuclei treated with any carcinogens.
The common idea that cancers are composed of embryonal cells is nothing but an old doctrine established upon fixation cytology. Any differentiated tissue cells which can renew themselves by metabolism, always maintain the genes for mitosis and those for cell differentiation in active states. Thus, variously different characters of cancers shown in different organs are nothing but a modified manifestation of phenotypes of genes which characterize each organ. The diversified characteristics of cancers imply, therefore, no evidence of a plurality of causes in carcinogenesis. The author maintains his opinion that the ultimate cause of carcinogenesis is unitary, namely the deficiency of the SFR gene induced in organs treated with carcinogens.
Abnormalities of chromosomes, mitosis, physiology, biochemistry, enzymology, immunological reactions, etc. which appear in young or old cancer cell clumps are modified phenotypes manifested secondarily or thirdly by the genetic information of genes in differentiated tissue cells of organs bearing cancers in a teleonomy responding to their changing circumstances due to cell proliferation and growth.
Extensive research papers on cancers are concentrated mostly on secondary or tertiary changes in cancer cell clumps. These studies may contribute greatly to cancer therapeutics but very little to the elucidation of the intrinsic nature of cancer cells. The descriptions of mitosis in text-books are too old and are in disregard of any principles of modern genetics and of the data on mitosis in living eukaryotic cells.