<p> <span><span style="font-family:;" "=""><span>Normal cells must become cancer-enabling before anything else occurs, according to latest literature. The goal in this ...<p> <span><span style="font-family:;" "=""><span>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</span><span> </span><span>specific methylation transferase genes were activated in normal human cells in tissue fields</span><span>, </span><span>containing different cell growth stages of the cancerous process. Histology studies, in addition to molecular chemistry for identification of oncogenic mutational change</span></span></span><span><span><span>,</span></span></span><span><span><span> w</span></span></span><span><span><span>ere</span></span></span><span><span><span style="font-family:;" "=""><span> 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<span style="color:#4F4F4F;white-space:normal;background-color:#FFFFFF;">°</span> relative to the cytoskeleton axis, and divided genome reductive to diploid, First Cells, in a perpendicular </span><span>orientation to the surrounding normal cells they had originated from. This unique division system was herein shown to occur at metastasis stage, imply</span><span>ing activity throughout the cancerous evolution. Another study showed 4-chromatid tetraploidy in development to B-cell lymp展开更多
文摘<p> <span><span style="font-family:;" "=""><span>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</span><span> </span><span>specific methylation transferase genes were activated in normal human cells in tissue fields</span><span>, </span><span>containing different cell growth stages of the cancerous process. Histology studies, in addition to molecular chemistry for identification of oncogenic mutational change</span></span></span><span><span><span>,</span></span></span><span><span><span> w</span></span></span><span><span><span>ere</span></span></span><span><span><span style="font-family:;" "=""><span> 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<span style="color:#4F4F4F;white-space:normal;background-color:#FFFFFF;">°</span> relative to the cytoskeleton axis, and divided genome reductive to diploid, First Cells, in a perpendicular </span><span>orientation to the surrounding normal cells they had originated from. This unique division system was herein shown to occur at metastasis stage, imply</span><span>ing activity throughout the cancerous evolution. Another study showed 4-chromatid tetraploidy in development to B-cell lymp
