A New Paper by Tanriverdi, et al. Supports My 2022 Finding that the Spike Protein Induces a Lethal Cancer Phenotype

Spike Proteins, like cancer cells, can be seen as an “invasive species” which generate a pro-tumorigenic microenvironment. No wonder cancer surges.

Release of toxic swamp gas. (Left) A byproduct of decomposition by anaerobic fermentation is methane gas that bubbles to the surface as swamp gas. When near a sufficient ignition source, accumulation of this gas can lead to smoldering underground fires in peat fields or explosions in coal mines (“firedamp”). (Right) The release of lysed cell products of necrotic cells combined with the pro-inflammatory cytokines secreted from the cancer cells produce the equivalent of swamp gas. At high and persistent levels, the release of this “swamp gas” from multiple metastatic sites leads to cytokine-mediated smoldering (e.g. cachexia or bone pain) or acute (e.g. thrombosis) lethal syndromes, the cause of death in the many of patients. 

I wrote a post on February 1^st of 2022 discussing my observation that the Spike Protein induces a lethal cancer phenotype by creating a tumorigenic microenvironment which parallels that of cancer cells. 

The Spike Protein and the Cancer Swamp 
https://wmcresearch.org/the-spike-protein-and-the-cancer-swamp/ 

Cancer cells become “ecosystem engineers” by tearing apart cellular structure and generating a pro-tumorigenic microenvironment. This is done through a combination of MMPs, cytokine and chemokine production. 

With the advantageous phenotypic traits of an invasive species, tumor cells rapidly become ecosystem engineers by dismantling the host species community structure leading to the destruction of the native ecosystem and by generating a pro-tumorigenic microenvironment. Tumor cells alter the host ecosystem through both allogenic and autogenic means. As allogenic engineers, the cells physically alter the native habitat by secreting factors to destroy the extracellular matrix (production of MMPs), to recruit pro-tumorigenic macrophages (production of cytokines and chemokines including IL-6, TNFα, etc.), and to induce angiogenesis (production of VEGF) [3, 4, 32–34]. Simultaneously, autogenic engineering occurs as the tumor physically grows in size: tumor cells exhaust local sinks of energy and oxygen and increase litter concentration, ultimately overwhelming native feedback mechanisms. 

Ecology meets cancer biology: the cancer swamp promotes the lethal cancer phenotype 
https://www.oncotarget.com/article/3430/text/ 

And this is precisely what the Spike Protein does. It induces sudden increases in MMPs and cytokines due to its bonding with ACE2. 

A very thin alveolocapillary membrane allows oxygen and CO2 to diffuse through the cells. During the first level of infection, the viral spike binds to the ACE2 receptor on the host cell surface. This bond leads to the incapacity of regulating ANG-II which provokes a sudden increase of the inflammatory response. This increase induces the activation of a large scale of cells including cytokines, and MMPs [37,38,39]. The sudden activation of these endopeptidases induces matrix disequilibrium and this phenomenon leads in turn to the collapse of matrix. 

SARS-CoV-2 and pathological matrix remodeling mediators 
https://link.springer.com/article/10.1007/s00011-021-01487-6 

The paper published last week confirms this finding. Please note the use of the term “environment.” This is how the Spike Protein induces cancer. It creates the environment that active cancer creates. Clearly, latent cancers can be “turbified” and new turbo cancers induced. 

COVID-19 causes a disruption in the immune system’s normal functioning, leading to an overproduction of pro-inflammatory cytokines. This immune dysregulation can result in an environment conducive to tumor growth. The prolonged presence of inflammatory cytokines such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β can cause oxidative stress and DNA damage, key factors in carcinogenesis [6-10]. The implications of these findings are profound, given the widespread and ongoing nature of the COVID-19 pandemic. The inflammatory response triggered by SARS-CoV-2 not only affects the acute phase of the disease but also has potential long-term effects on survivors’ health, particularly in terms of cancer risk. The cytokine storm associated with severe COVID-19 can lead to significant immune dysregulation, creating an environment that fosters carcinogenesis. Additional studies support these findings. For instance, Yin et al. reported that COVID-19 patients exhibited elevated levels of pro-inflammatory cytokines even months after recovery, suggesting a prolonged inflammatory state [11]. Their study found a 35% increase in IL-6 and a 28% increase in TNF-α levels three months post-recovery. Similarly, Zhang et al. observed that long-term COVID-19 survivors had higher levels of oxidative stress markers, which correlated with increased cancer risk factors [12]. Their longitudinal study showed a 40% increase in oxidative stress markers and a 22% increase in DNA damage markers in COVID-19 survivors over a year. 

COVID-19 and Carcinogenesis: Exploring the Hidden Links 
https://www.cureus.com/articles/289494-covid-19-and-carcinogenesis-exploring-the-hidden-links#!/ 

I recommend reading the entire above referenced paper. It is a work of superb scholarship. One of my next steps will be investigating therapeutics which may ameliorate and/or inhibit the upregulation of MMPs and expression of cytokines, in particular IL-6 and TNF-a.  

As always, thank you for your readership, dialogue and support.