TITLE:
Near-Dead Cells to Special Tetraploidy to First Cells to Cancer Diagnostic Morphology: Unlikely Therapy-Gain from For-Profit Industrial Goliath
AUTHORS:
Kirsten H. Walen
KEYWORDS:
Cytogenetics, Atavistic Activation, 4n-Division-Perpendicularity, Amalgamated Amitotic-Mitosis, Loss of Function Genetics, “Death” Recovery Cells, Driver Mutations, Tumor Parasitic Life
JOURNAL NAME:
Journal of Cancer Therapy,
Vol.11 No.7,
July
22,
2020
ABSTRACT: 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 normal human cells with such converted chromosome structure gave
rise to proliferative, fitness-gained, diploid first cells, which 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 characteristics 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 proliferation. 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 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 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 in vitro 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.