The Observed Aggressive Cancers are a SYMPTOM of a DNA Disease Induced by the Spike Protein

Syncytia forming properties of the Spike Protein induces Aneuploidy – a DIRECT cause of Cancers.

Schematic representation of the possible effect of SARS-CoV-2 infection (COVID-19) on the brain in the context of aging-related genome (chromosome) instability. Interactome analysis of SARS-CoV-2 infection has highlighted a number of pathways to be potentially altered by the virus which are listed at the bottom of the figure. 

Shortly before the pandemic, a paper was published which demonstrated that cell fusion is an intermediate to Aneuploidy and chromosomal instability. The significance of this is that it is ONCOGENIC. 

Oncogenesis is considered to result from chromosomal instability, in addition to oncogene and tumor-suppressor alterations. Intermediate to aneuploidy and chromosomal instability, genome doubling is a frequent event in tumor development but the mechanisms driving tetraploidization and its impact remain unexplored. Cell fusion, one of the pathways to tetraploidy, is a physiological process involved in mesenchymal cell differentiation. Besides simple genome doubling, cell fusion results in the merging of two different genomes that can be destabilized upon proliferation. By testing whether cell fusion is involved in mesenchymal oncogenesis, we provide evidence that it induces genomic instability and mediates tumor initiation. After a latency period, the tumor emerges with the cells most suited for its development. Furthermore, hybrid tumor genomes were stabilized after this selection process and were very close to those of human pleomorphic mesenchymal tumors. Thus genome restructuring triggered by cell fusion may account for the chromosomal instability involved in oncogenesis. 

Fusion-mediated chromosomal instability promotes aneuploidy patterns that resemble human tumors 
https://pubmed.ncbi.nlm.nih.gov/31270395/ 

One of the most underestimated and least discussed dangers of the pathogenic Spike Protein of SARS-CoV-2 is its ability to cause an abundance of this very type of cell fusion. The following article warns well. And, yes, it has been implicated with the vaccines. 

While the published reports on COVID-19 discuss large syncytia, as these cells are the most noticeable products of cell fusion due to their size and numerous nuclei (thus often called multinucleated giant cells), they are not the only outcome of cell fusion. Cell fusion can produce binuclear or trinuclear cells, which are often more abundant in experimental systems than large syncytia but could go unnoticed in human tissues. Even if noticed, they may not be attributed to cell fusion because distinguishing them reliably from binuclear cells produced by failed mitosis in human tissues may be difficult or impossible with available tools [58]. 

A syncytium, especially if it has only two or three nuclei, can enter mitosis to produce mononuclear daughter cells. These mitoses are commonly multipolar and thus are prone to producing aneuploid cells with chromosomal aberrations, adding another layer of abnormal features to the offspring of cell fusion [59, 60]. Such abnormalities may be particularly significant to COVID-19 patients with neoplastic lesions because chromosomal aberrations contribute to tumor progression [61, 62], as do epigenetic abnormalities found in the products of cell fusion. 

Cell fusion as a link between the SARS-CoV-2 spike protein, COVID-19 complications, and vaccine side effects 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8664391/ 

This also ties into the neurodegenerative effects of the Spike Protein and SARS-CoV-2. 

Brain-specific genomic variations [including aneuploidy (loss/gain of whole chromosomes) and single gene mutations] are associated with a wide spectrum of late-onset brain diseases (Yurov et al., 2010; Rohrback et al., 2018; Iourov et al., 2021). More importantly, chromosome instability mediates neurodegeneration (Iourov et al., 2009; Rohrback et al., 2018; Yurov et al., 2019). Several molecular pathways have been associated with chromosome instability in the neurodegenerating brain including neuronal cell cycle errors, chromosome missegregation, and cellular senescence (Bajic et al., 2015; Caneus et al., 2018; Martínez-Cué and Rueda, 2020). These processes are intimately linked to aging at molecular, cellular, and tissular levels. For instance, premature aging is associated with increased rates of chromosome and genome instability. Natural aging is associated with accumulation and propagation of somatic genome variations (e.g., aneuploidy) and genome instability. Alterations to genome stability maintenance may cause aging-related brain diseases or early manifestations of late-onset neurodegenerative diseases (Yurov et al., 2010; Andriani et al., 2017; Zhang and Vijg, 2018; Iourov et al., 2021). Additionally, DNA regulation and chromatin organization are able to affect genome stability by altering the expression of genes implicated in the pathways demonstrated in Figure 1. Since SARS-CoV-2 interactions with proteins involved in genome stability maintenance pathways are able to contribute to chromosome/genome instability propagation, the coronavirus infection has the potential to cause neurobehavioral abnormalities, neurodegeneration (e.g., Alzheimer's disease) and premature brain deterioration. 

COVID-19 and Aging-Related Genome (Chromosome) Instability in the Brain: Another Possible Time-Bomb of SARS-CoV-2 Infection 
https://www.frontiersin.org/articles/10.3389/fnagi.2022.786264/full 

I had hypothesized this outcome in April of 2021. However, at the time I had not definitively worked out the mechanism. 

It is most likely SARS-CoV-2 is taking the Rembrandt that is our individually unique genome and, like so many gleefully evil gremlins, moving the paint molecules around one by one, leaving behind a dysfunctioning Jackson Pollack. 

https://x.com/Parsifaler/status/1379283875956936704?s=20 

Indeed, it is possible to graphically demonstrate precisely what these syncytia can do to our genomes. 

Staining chromosomes with different dyes highlights the orderly nature of the normal human karyotype (left), that is, humans have precisely two copies of each chromosome with no leftovers. A bladder cancer cell (right) has extra copies of some chromosomes, a few missing normal chromsomes, and a lot of hybrid or marker chromosomes, which characterize cancer cells. 

And, don’t you see? 

“You start with a chromosomal mutation, that is, aneuploidy perhaps from X-rays or cigarettes or radiation, that destabilizes and eventually changes your karyotype or renders it non-viable,” he said. “The rare viable aneuploidies of cancers are, in effect, the karyotypes of new species.” 

Are cancers newly evolved species? 
https://vcresearch.berkeley.edu/news/are-cancers-newly-evolved-species 

Apart from the field day some may have with the “new species” implications, my point here is far more concrete. We are not dealing with an x-ray, or the sun hitting our skin, when it comes to Spike Protein exposure. In some instances, we have TRILLIONS of these proteins causing aneuploidy.  

We are dealing with a protein that can turn our genome into a Jackson Pollock. We need to rethink. Cancer is not so much a sequela of INFECTION in this instance, as a SYMPTOM of a DNA DISEASE. 

Is it any wonder we are observing rampant aggressive cancers? 

I will continue my work and research therapeutics to deal with this pathogenic property of the Spike Protein. As always, thank you for your continued support. You are the wind beneath my wings.