A Perfectly Engineered Cancer Machine: How the Spike Protein, via SPED, is a Diabolical Inducer of Cancer

90% of cancers are linked to somatic mutations and environmental factors – the Spike Protein embodies both.

Different faces of inflammation and its role in tumorigenesis 

Let’s take a step back and get back to basics.  

What is Inflammation? 

Inflammation is defined as increased vascular permeability accompanied by an infiltration of ‘inflammatory’ cells, initially polymorphonuclear leucocytes (usually neutrophils) and later macrophages, lymphocytes and plasma cells. 

Misbah, Siraj A.; Spickett, Gavin P.; Dalm, Virgil A. S. H.. Chapel and Haeney's Essentials of Clinical Immunology (p. 30). Wiley. 

What could possibly be a better agent at increasing vascular permeability than the Spike Protein? 

Our study reveals the capacity and mechanism by which SARS-CoV-2 S mediates barrier dysfunction in epithelial and endothelial cells in vitro and vascular leak in vivo, thus suggesting that S alone can mediate barrier dysfunction independently from viral infection. 

SARS-CoV-2 Spike triggers barrier dysfunction and vascular leak via integrins and TGF-β signaling  
https://www.nature.com/articles/s41467-022-34910-5 

And there’s the key! “INDEPENDENTLY FROM VIRAL INFECTION,” 

The Spike Protein is its own “key” that opens its own doors of destruction. 

Now, for part two of the inflammation story: the infiltration of inflammatory cells. 

In conclusion, our study demonstrates that the SARS-CoV-2 spike protein promotes the infiltration of cells expressing inflammatory cytokines, as well as Th2 and Th17 cells, into the skin and lung tissues in a BLM-induced SSc mouse model. 

SARS-CoV-2 spike protein accelerates systemic sclerosis by increasing inflammatory cytokines, Th17 cells, and fibrosis 
https://journal-inflammation.biomedcentral.com/articles/10.1186/s12950-023-00362-x 

For those readers who have followed me from the beginning, this process is part of what I have termed “SPED” for Spike Protein Endothelial Disease. 

In 2019 (!) a paper was published that details the links between inflammation and cancer. The authors make a very powerful statement:  

Only a minority of all cancers are caused by germline mutations, whereas the vast majority (90%) are linked to somatic mutations and environmental factors. 

Inflammation and Cancer 
https://pmc.ncbi.nlm.nih.gov/articles/PMC6704802/ 

Given the recent DELUGE of de novo cancers, I’m quite certain that germline mutations are not the cause... 

The authors then proceed to lay out their case. They note that both Extrinsic and Intrinsic causes exist for cancer-inducing inflammation. I will demonstrate how the Spike Protein mimics cancer-initiating mutations. Therefore, enabling both pathways towards the induction of cancer. I highly recommend that everyone read this superb review. 

Inflammation is often associated with the development and progression of cancer. The cells responsible for cancer-associated inflammation are genetically stable and thus are not subjected to rapid emergence of drug resistance; therefore, the targeting of inflammation represents an attractive strategy both for cancer prevention and for cancer therapy. Tumor-extrinsic inflammation is caused by many factors, including bacterial and viral infections, autoimmune diseases, obesity, tobacco smoking, asbestos exposure, and excessive alcohol consumption, all of which increase cancer risk and stimulate malignant progression. In contrast, cancer-intrinsic or cancer-elicited inflammation can be triggered by cancer-initiating mutations and can contribute to malignant progression through the recruitment and activation of inflammatory cells. Both extrinsic and intrinsic inflammations can result in immunosuppression, thereby providing a preferred background for tumor development. The current review provides a link between inflammation and cancer development. 

Inflammation and Cancer 
https://pmc.ncbi.nlm.nih.gov/articles/PMC6704802/ 

This is the mechanism by which the Spike Protein mimics mutations (damaged DNA) that promote inflammation: 

Nevertheless, previously existing knowledge on the role of cytoplasmatic or circulating self-DNA as a pro-inflammatory damage-associated molecular pattern (DAMP) was largely ignored. Pathologies reported ‘de novo’ for patients infected with Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2 to be outcomes of self-DNA-driven inflammation in fact had been linked earlier to self-DNA in different contexts, e.g., the infection with Human Immunodeficiency Virus (HIV)-1, sterile inflammation, and autoimmune diseases. I highlight particularly how synergies with other DAMPs can render immunogenic properties to normally non-immunogenic extracellular self-DNA, and I discuss the shared features of the gp41 unit of the HIV-1 envelope protein and the SARS-CoV 2 Spike protein that enable HIV-1 and SARS-CoV-2 to interact with cell or nuclear membranes, trigger syncytia formation, inflict damage to their host’s DNA, and trigger inflammation – likely for their own benefit. 

Self-DNA driven inflammation in COVID-19 and after mRNA-based vaccination: lessons for non-COVID-19 pathologies 
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.1259879/full 

Lastly, why do I believe this has all been engineered in a lab? Because of ACE2. I believe these particular (RaTG13-related) coronaviruses were targeted for study because they already had the “built-in” docking ability to connect to every organ via the vasculature. 

Here, we report the expression pattern of ACE2 across > 150 different cell types corresponding to all major human tissues and organs based on stringent immunohistochemical analysis. The results were compared with several datasets both on the mRNA and protein level. ACE2 expression was mainly observed in enterocytes, renal tubules, gallbladder, cardiomyocytes, male reproductive cells, placental trophoblasts, ductal cells, eye, and vasculature. 

The protein expression profile of ACE2 in human tissues 
https://pmc.ncbi.nlm.nih.gov/articles/PMC7383091/