Working: Are The Clots We Are Seeing Ocurring Because The Spike Protein Is Turning All It Touches Into Tumor Microenvironment?
Small ‘fibrin clots’ are chiefly found in tumor vasculature and interstitial space.
Platelets are crucial for tumor cell-induced coagulation and contribute to the TME of solid tumors. Increased vessel permeability in the vicinity of a tumor, tumor-induced angiogenic sprouting or vasculogenic mimicry vessels are three ways that allow extravasation of platelets and clotting factors from the blood stream into the interstitial stroma of tumor tissue. After the platelets recognize vWF of the subendothelial basement membrane, or collagen of the desmoplastic TME, platelets become activated.
As the readers of my Substack are now well aware, I have realized that what I thought was an endothelial disease, is actually much more. I believe the Spike Protein of SARS-CoV-2 not only invades and damages the endothelium, but I also believe it induces the Tumore Microenvironment (TME) via its interactions with the endothelium and adjacent tissues.
If we examine the current excess of clotting-related deaths and injuries in this light, we can see a certain connection.
Pancreatic ductal adenocarcinomas (PDACs) are poorly responsive to both chemo- and immunotherapies, mainly because of the presence of highly dense fibrotic stroma and extensive myeloid-derived immune cells, which are known major drivers for an immunosuppressive tumor microenvironment (TME). Another feature of PDACs that may suppress the immune microenvironment is the small ‘fibrin clots’ that are chiefly found in tumor vasculature and interstitial space. PDACs exhibit high levels of fibrinogen and fibrin clots throughout the tumor stroma surrounding the tumor cells.
Abstract C008: Intratumoral fibrin as a novel immunomodulatory factor in pancreatic ductal adenocarcinoma
And, when we look closely at the post-Spike exposure clotting, are we not seeing precisely the following?
However, where do platelets meet cancer cells that grow in a solid mass within epithelial or stromal tissue? How do platelets become part of the TME? The answers lay in the high permeability of blood vessels in the vicinity of a tumor mass (Nagy et al., 2012). This leakiness allows the intravascular platelets and fibrinogen to access the extravascular space, where platelets become activated and fibrinogen is converted to fibrin by coagulation (Figure 2, above). Depending on the type of tumor vessel, there are different ways, how tumor vessels lose their gatekeeper functions and allow extravasation of platelets and coagulation factors (Figure 2; Chouaib et al., 2010; Klein, 2018). First, the tumor mass approaches preexisting vessels due to its volume-demanding growth or by vessel co-option (Kuczynski et al., 2019; Niland and Eble, 2019). Vascular endothelial growth factor (VEGF), especially its isoform VEGF-A, and likely other chemokines from the TME increase the permeability of normal blood vessels and activate endothelial cells (Apte et al., 2019). This may result in increased leukocyte extravasion. Moreover, activation of endothelial cells is accompanied by the loss of antithrombotic surface molecules, such as thrombomodulin and heparin sulfate, from the endothelial cell surface (Klein, 2018). This increases the propensity of intravascular coagulation and thrombosis.
Platelets, Constant and Cooperative Companions of Sessile and Disseminating Tumor Cells, Crucially Contribute to the Tumor Microenvironment
I am going to continue on this path. As we continue to peel back the layers of this onion, the more we understand it. And the better we can combat it.
I cannot thank those who donate and continue to donate enough. My continuing work is the greatest thanks I can give. Blessings in this Holiday Season.
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