IS THE SPIKE PROTEIN INDUCING “PANCREATIC CANCER” WITHOUT THE TUMOR? IN PANCREATIC CANCER, ONLY 5% OF CELLS ARE TUMOR CELLS, THE REST ARE THE MICROENVIRONMENT

Hypercoagulability, De Novo Diabetes and Microvascular Ablation

While researching the hypercoagulability induced by the Spike Protein and its destruction of the microvasculature, I discovered some parallels that gave me pause. If we look at the procoagulant effects of Pancreatic Cancer, they precisely mimic the procoagulant effects of the Spike Protein.

Pancreatic cancer is characterised by high tumoural expression of tissue factor, activation of leukocytes with the release of neutrophil extracellular traps, the dissemination of tumour-derived microvesicles that promote hypercoagulability and increased platelet activation. Furthermore, other coagulation pathways probably contribute to these processes, such as those that involve heparanase, podoplanin and hypofibrinolysis.

The relationship between pancreatic cancer and hypercoagulability: a comprehensive review on epidemiological and biological issues
https://www.nature.com/articles/s41416-019-0510-x

As I mentioned, microvascular destruction, I have long believed, is being caused by the Spike Protein. Very interestingly, Pancreatic Cancer ABLATES the microvasculature!

How Pancreatic ductal adenocarcinoma (PDAC) tumors become hypovascular is poorly understood. We describe an organotypic PDAC-on-a-chip culture model that emulates vascular invasion and tumor–blood vessel interactions to better understand PDAC-vascular interactions. The model features a 3D matrix containing juxtaposed PDAC and perfusable endothelial lumens. PDAC cells invaded through intervening matrix, into vessel lumen, and ablated the endothelial cells, leaving behind tumor-filled luminal structures. Endothelial ablation was also observed in in vivo PDAC models.

A biomimetic pancreatic cancer on-chip reveals endothelial ablation via ALK7 signaling
https://www.science.org/doi/10.1126/sciadv.aav6789?cookieSet=1

To further the hypothesis that the Spike Protein is inducing the phenotype of Pancreatic Cancer, we can also look at the prevalence of de novo onset Diabetes after SARS-CoV-2 infection.

There are increasing evidence that coronavirus disease-19 (COVID-19) can lead to development of denovo diabetes mellitus (DM) (new onset DM). It has also been observed during last 21 months that there is a bidirectional relationship between COVID-19 and DM.

Denovo Diabetes Mellitus among Patients of COVID-19
https://www.hilarispublisher.com/open-access/denovo-diabetes-mellitus-among-patients-of-covid19-84012.html#

What concerns me is that Pancreatic Cancer also causes this very same phenomenon.

It is possible that new-onset diabetes associated with pancreatic cancer is due to a combination of beta cell dysfunction and an increased insulin resistance,

Pancreatic Cancer Presenting as New-Onset Diabetes
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3986008/#

What makes Pancreatic Cancer so lethal, is that it TRANSFORMS normal Pancreatic cells into non-functioning Squamous cells (a kind of skin cell). This is done by activating ZBED2.

ZBED2 confuses the pancreas cell about its own identity. It displaces another transcription factor that is required for the pancreas cell to perform its normal functions as a pancreas cell. ZBED2 turns pancreas cells into squamous cells–a type of cell found in the skin. Patients with the worst outcomes have the highest levels of squamous cells in their tumors.

WHY PANCREATIC DUCTAL ADENOCARCINOMA IS SO LETHAL
https://psscra.org/2020/05/21/why-pancreatic-ductal-adenocarcinoma-is-so-lethal/

This very same transcription factor has been found to be activated in COVID.

Transcripts encoding for transcription factors zinc finger BED-type-containing 2 (ZBED2) and zinc finger and BTB domain-containing protein 32 (ZBTB32) were enriched in TFH cells in cluster 5 and were also expressed at significantly higher levels in hospitalized COVID-19 patients.

Imbalance of Regulatory and Cytotoxic SARS-CoV-2-Reactive CD4+ T Cells in COVID-19
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7534589/

Desmoplasia is the growth of FIBROUS tissue. It is 90% of the Pancreatic Cancer microenvironment, and it allows for the development of cancer and the spread of existing cancer.

The Spike Protein interacts with integrins which activate TGF-B.

Over expressing TGF‐β1 in vivo results in progressive pulmonary fibrosis and TGF‐β increases expression of the TGF‐β activating integrin αvβ6. This upregulation of TGFβ through αvβ6 may suppress alveolar macrophage mediated type I interferon responses and thereby increase the chance of a persistent viral infection. The SARS‐CoV‐2 spike protein contains an RGD integrin‐binding domain close to the ACE2 binding region, which could potentially facilitate binding to RGD‐binding integrins, which includes several TGF‐β ‐activating integrins.

COVID‐19 and pulmonary fibrosis: A potential role for lung epithelial cells and fibroblasts
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8237078/

And, indeed, this can induce Pancreatic Cancer.

The transfer of a single growth factor, TGF-beta1, conveys the ability to induce a fibroblast response similar to that seen in desmoplasia in human pancreatic adenocarcinoma.

Transforming growth factor-beta1 induces desmoplasia in an experimental model of human pancreatic carcinoma
https://pubmed.ncbi.nlm.nih.gov/11212248/

As you can see, I am extremely concerned that everything we have observed all focuses in on creating something I observed well over a year ago. The Spike Protein induces “Cancer Without Tumors.” Except this may be only prelude, as the Tumor Microenvironment precedes tumorigenesis.

Please watch this excellent video explaining much of what is discussed here.

Microenvironment of tumours key to cancer's progression