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 &l...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 phenotypic cell-shape changes (spindle, polygonal and roundness cells), each intervened by “total” cell destruction. These three different growth patterns </span><span style="font-family:Verdana;">had morphologies, indistinguishably from today’s cancer diagnostic morphologies. “Mitotic” analyses of beginning growths for the three phenotypes revealed the special rosette figure separations from special 4n and higher ploidy level cells, and also total absence of spindle type mitoses. Tumorigenesis-relevant </span><span style="font-family:Verdana;">was centromere-puffing with premature chromatid separation, and chromatin compaction, a mechanism, that was suggested to protect the genome from damage (text). We suggest that the multi-chromatid polyploid cells with their genome reductive division system, can be a tractable </span><i><span style="font-family:Verdana;">in vitro</span></i><span style="font-family:Verdana;"> model system for therapy information, when repeated from a cell-killing agent, producing virus-free recovery growths. Will it be enacted upon? Not likely with profit-greedy industrial Goliath in the helm of cancer research. But, a not for profit cancer organization, could change this appalling situation.展开更多
文摘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 phenotypic cell-shape changes (spindle, polygonal and roundness cells), each intervened by “total” cell destruction. These three different growth patterns </span><span style="font-family:Verdana;">had morphologies, indistinguishably from today’s cancer diagnostic morphologies. “Mitotic” analyses of beginning growths for the three phenotypes revealed the special rosette figure separations from special 4n and higher ploidy level cells, and also total absence of spindle type mitoses. Tumorigenesis-relevant </span><span style="font-family:Verdana;">was centromere-puffing with premature chromatid separation, and chromatin compaction, a mechanism, that was suggested to protect the genome from damage (text). We suggest that the multi-chromatid polyploid cells with their genome reductive division system, can be a tractable </span><i><span style="font-family:Verdana;">in vitro</span></i><span style="font-family:Verdana;"> model system for therapy information, when repeated from a cell-killing agent, producing virus-free recovery growths. Will it be enacted upon? Not likely with profit-greedy industrial Goliath in the helm of cancer research. But, a not for profit cancer organization, could change this appalling situation.
