机构地区:[1]CROMOS, Richmond, CA, USA
出 处:《Journal of Cancer Therapy》2020年第7期410-432,共23页癌症治疗(英文)
摘 要:The objective in this experimental article is to gain evidential proof of near-dead cells, (sick-cells in relapse tumor) responding with recovery growth from special 4n, multi-chromatid chromosomes. Note, near-dead </span><i><span style="font-family:Verdana;">normal human cells</span></i><span style="font-family:Verdana;"> with such converted chromosome structure gave rise to proliferative, fitness-gained, diploid </span><i><span style="font-family:Verdana;">first cells</span></i><span style="font-family:Verdana;">,</span><i> </i><span style="font-family:Verdana;">which</span><i> </i><span style="font-family:Verdana;">further gave rise to three different cell shape changed, recovery growth patterns. Previously, two cell shape changes had been recovered from same type normal human cells, transiently exposed to amino acid glutamine deficient growth medium with recovery growths also associated with presence of the special 4n cells. The 4n cell-division had been concluded to be a meiotic-like two-step division system to the fitness-gained diploid cells in numerous experiments. The main characteristi</span><span style="font-family:Verdana;">cs of this division system, was firstly whole genomes without polar oriented bent centromeres moving apart followed by much rarer simple fission division to two or three diploid cells, selectable for first cell proliferatio</span><span style="font-family:Verdana;">n. In general these 4n cells showed metaphase type rosette figures moving apart not in the normal spindle associated mitotic shape with centromeres polar-pointing with sloping arms. This sequence of events induced by glutamine-deficiency, was earlier shown to cause DNA breakage in metabolic studies however, the near-death condition was only assumed from normal fibro-blastic cell-sheet shrinkage. This was rectified by an RNA virus (Coxakie-B3), which virology known is a highly cell killing virus (4+ CPE on their scale). This virus replicates only in replicating cells, which led to recovery growths with progressive phenotypThe objective in this experimental article is to gain evidential proof of near-dead cells, (sick-cells in relapse tumor) responding with recovery growth from special 4n, multi-chromatid chromosomes. Note, near-dead </span><i><span style="font-family:Verdana;">normal human cells</span></i><span style="font-family:Verdana;"> with such converted chromosome structure gave rise to proliferative, fitness-gained, diploid </span><i><span style="font-family:Verdana;">first cells</span></i><span style="font-family:Verdana;">,</span><i> </i><span style="font-family:Verdana;">which</span><i> </i><span style="font-family:Verdana;">further gave rise to three different cell shape changed, recovery growth patterns. Previously, two cell shape changes had been recovered from same type normal human cells, transiently exposed to amino acid glutamine deficient growth medium with recovery growths also associated with presence of the special 4n cells. The 4n cell-division had been concluded to be a meiotic-like two-step division system to the fitness-gained diploid cells in numerous experiments. The main characteristi</span><span style="font-family:Verdana;">cs of this division system, was firstly whole genomes without polar oriented bent centromeres moving apart followed by much rarer simple fission division to two or three diploid cells, selectable for first cell proliferatio</span><span style="font-family:Verdana;">n. In general these 4n cells showed metaphase type rosette figures moving apart not in the normal spindle associated mitotic shape with centromeres polar-pointing with sloping arms. This sequence of events induced by glutamine-deficiency, was earlier shown to cause DNA breakage in metabolic studies however, the near-death condition was only assumed from normal fibro-blastic cell-sheet shrinkage. This was rectified by an RNA virus (Coxakie-B3), which virology known is a highly cell killing virus (4+ CPE on their scale). This virus replicates only in replicating cells, which led to recovery growths with progressive phenotyp
关 键 词:CYTOGENETICS Atavistic Activation 4n-Division-Perpendicularity Amalgamated Amitotic-Mitosis Loss of Function Genetics “Death” Recovery Cells Driver Mutations Tumor Parasitic Life
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