TITLE:
Epigenetic Enabled Normal Human Cells, Lead to First Cell’s Unique Division System, Driving Tumorigenesis Evolution
AUTHORS:
Kirsten H. Walen
KEYWORDS:
Mitotic Slippage, DNA Damage, Repair Process, 4-Chromatid Chromosomes, Diplochromosome Tetraploidy, 90°-4n Nucleus Turn, G1-Phase-Diploid Cell Arrest, Time Reduced Cell Cycle, Fitness Increase
JOURNAL NAME:
Journal of Cancer Therapy,
Vol.13 No.1,
January
25,
2022
ABSTRACT: Normal
cells must become cancer-enabling before anything else occurs, according to
latest literature. The goal in this mini-review is to demonstrate special
tetraploidy in the enabling process. This we have shown from genomic damage,
DDR (DNA Damage Response) activity with skip of mitosis leading to diploid G2
cells at the G1 border in need of chromatin repair for continued cell cycling
to the special tetraploid division system. In several studies specific methylation transferase
genes were activated in normal human cells in tissue fields, containing different cell growth
stages of the cancerous process. Histology studies, in addition to molecular
chemistry for identification of oncogenic mutational change, were a welcome change (see below). In a study on melanoma origin, DDR also
showed arrested diploid cells regaining cycling from methylation transferase
activity with causation of 2n melanocytes transforming to 4n melanoblasts,
giving rise to epigenetic tumorigenesis enabled First Cells. Such First Cells
were from Barrett’s esophagus shown to have inherited the unique division
system from 4n diplochromosomal cells, first described in mouse ascites cancer
cells (below). We discovered that the large nucleus prior to chromosomal
division turned 90° relative to the cytoskeleton axis, and divided genome
reductive to diploid, First Cells, in a perpendicular orientation to the surrounding normal cells they had originated from.
This unique division system was herein shown to occur at metastasis stage,
implying activity throughout the cancerous evolution. Another study
showed 4-chromatid tetraploidy in development to B-cell lymphoma, and that such
cancer cells also proliferated with participation of this unusual division
system. Such participation has long been known from Bloom’s inherited syndrome
with repair chiasmas between the four chromatids, also an in vitro observation by us. Our cytogenetic approach also revealed
that they believed mitotic division in cancer cells is wrong because such cell divisions
were found to be from an adaptation between amitosis and mitosis, called amitotic-mitosis.
Amitosis means division without centrosomes, which has long been known from
oral cancer cells, in that MOTCs (microtubule organizing center) were lacking centrioles. This observation calls for
re-introduction of karyotype and cell division studies in cancer cell proliferation.
It has high probability of contributing novel approaches to cancer control from
screening of drugs against the amitotic-mitotic division apparatus.