Pfizer Jab Endotoxins will cause more Cancer

Every vial of Pfizer Covid19 Jab contains an undisclosed amount of Endotoxin arising from the E coli Bacteria used in production. Short-term exposure increases Cancer.

Pfizer reports Thousands of Cancers after their Jabs

In April 2022 Pfizer reported Thousands of Cancer cases and deliberately spread the clear Warning Signal by dispersing them under 496 different types under the general heading “Neoplasms benign, malignant and unspecified (incl cysts and polyps)”.¹

By June 2022, there were 3,711 cases under that heading.

Mechanisms of Pfizer Endotoxin Cancer Explosion

Looking for mechanisms of fast emerging Cancers, named by Dr Ryan Cole² “Turbo Cancers” or “Wildfire Cancers” becoming increasingly apparent after Pfizer mRNA jabs, a number of researchers speculated about the mRNA or constituents of the Lipid Nanoparticles contributing.

However I think they have overlooked the Elephant in the room.³

There is extensive literature demonstrating Endotoxin (LPS, LipoPolySaccharides) arising from the E coli Bacteria used in production causes activation and proliferation of Cancer in numerous organs.

As mentioned in previous articles, Pfizer was required to measure the Endotoxin⁴ level in every Lot or Batch that it produced, but has prevented the world from seeing those assays.

Breast Cancer from Endotoxin

An important study⁵ found that short-term Endotoxin exposure upregulated Matrix MetalloProteinase-9 (MMP-9) activity in nontumorigenic mammary epithelial cells of Mouse (SCp2) and Human (HMT-3522 S1; S1) and upregulated inflammatory mediators including Nitric Oxide (NO) and Interleukin 1-β in Tumorigenic Human Breast cells (MDA-MB-231), all in a dose-dependent manner.

Short-term (48 hours to 9 days) Endotoxin exposure also preferentially enhanced the invasion of pretumorigenic S1-connexin 43 knockout (Cx43-KO S1) cells compared to nontumorigenic S1 cells and disrupted lumen formation and apicolateral distribution of β-catenin in 3D cultures of S1 cells.

In summary the Inflammation caused by tiny amounts, at concentrations (0.1–10 µg/ml), Endotoxin drove Cancer activation and growth in those experiments.

Breast Cancer Metastasis caused by Endotoxin

Researchers in China demonstrated that Endotoxin not only initiates Breast Cancer, but enhances Death by Metastasis.⁶

In their Figure 8 they show that normal Human Breast tissue (a) contains little TLR4, the target of Endotoxin, but Endotoxin stimulates increased expression of TLR4 in Lymph Node Breast Cancer tissue (NO) in (b)-(e).

Could the recent push⁷ to lower the age of women to be routinely exposed to X-ray Mammograms be due to the anticipated surge in metastatic Breast Cancer as a result of mRNA jabbing?

Prostate Cancer Metastasis enhanced by Endotoxin

Prostate Cancer is a major killer when it spreads to other organs. Endotoxin increases the metastasis.⁸ Dexamethasone was found to worsen the effect.

Colon Cancer Endotoxin Angiogenesis

As mentioned previously⁹, E coli Endotoxin causes systemic epigenetic inflammation, including increased expression of Interleukin 6 which plays a crucial role in angiogenesis of Colon Cancer.¹⁰ A few more references to Endotoxin and Colon Cancer.¹¹¹²¹³

Ovarian Cancer Endotoxin Angiogenesis

Interleukin 6 generated by Endotoxin causes progression of Ovarian Cancer.¹⁴

Lymphoma caused by Endotoxin

Mantle cell lymphoma (MCL) is an incurable B-cell malignancy with the poorest prognosis among B-cell lymphoma patients.¹⁵

Endotoxin activates MCL and upregulates secretion of cytokines such as interleukin (IL)-6 and IL-10, and vascular endothelial growth factor (VEGF). At the same time Endotoxin inhibits the proliferation and cytolytic activity of T cells, giving the Cancer enhanced evasion from normal immune surveillance.

Lymphoma-associated MyD88 mutants and their isolated Toll/interleukin-1 receptor (TIR) domains hyperactivate NF-κB signaling.¹⁶ Endotoxin (LPS in the Figure) enhances this deadly effect in a dose-dependent manner (Red shaded bars at F).

In the Figure from Avbelj et al, focus on part F which shows the dosing of Endotoxin affecting the various mutants studied. EV = Empty Vector; WT = Wild Type of isolated MyD88.

Endotoxin upregulation of miR-155 causes Lymphoma

In earlier articles I pointed to the Endotoxin upregulation of microRNA miR-155 as the cause of Myocarditis and other Heart Disease¹⁷ and Rapid Liver Failure¹⁸ following Covid19 mRNA jabs.

A 2009 review showed that miR-155 has been associated with numerous types of Cancer, including Lymphoma.¹⁹ It is associated with Thyroid Carcinoma, Breastcancer, Colon cancer, Cervical cancer, and Lung cancer.²⁰

In 2005 it was demonstrated that miR-155 and its gene MIR155HG, formerly known as B-cell Integration Cluster (BIC) are highly expressed in Hodgkin, Primary Mediastinal and Diffuse Large B Cell Lymphomas.²¹

Experiments with transgenic mice showed in 2006 that miR-155 is implicated in initiation and/or progression Acute Lymphoblastic Leukemia and high-grade Lymphoma.²² This resulted in enlarged spleens due to expansion of leukemic
lymphoma cells.

Measurement of miR-155 can be used in detection and diagnosis of Lymphoma.²³

Angioimmunoblastic T-cell Lymphoma (AILT)

Actor Sam Neill recently revealed his chemotherapy treatment against Angioimmunoblastic T-cell Lymphoma has failed, leaving him in a terminal condition.²⁴

I was alerted to the fact that these rare Lymphomas are known to occur quickly after Covid19 injections as covered by revered Substack author ArkMedic.

Philadelphia 2023

To June 2022, Pfizer reported 6 cases of Angioimmunoblastic T-cell Lymphoma after their jabs.

In 2021, Serge Goldman published details of his own case where he suffered Angioimmunoblastic T-cell Lymphoma after his Pfizer “Booster” jab.²⁵

I will build references to this particular cancer, but initial searches reveal that Endotoxins are known to be associated with it as found in the US government Comparative Toxicogenomics Database. Endotoxin and its deadliest fragment Lipid A is listed in references to T-cell Lymphoma and miR-155 is one player in the rapid progression. Click on the image to get a better view.

The oncogene c-Maf is overexpressed in AILT.²⁶

Liver Cancer “Escape” caused by Endotoxin

In 2022, Peng and coworkers showed the role of Endotoxin (LPS) in rapid development of Liver Cancer (HepatoCellular Carcinoma, HCC).²⁷

Here is their graphical abstract:

Peng et al. found that “upregulation of METTL14 by LPS promotes the m6A methylation of MIR155HG, which stabilizes MIR155HG relying on the “reader” protein ELAVL1 (also known as HuR)-dependent pathway. MIR155HG functions as a competing endogenous RNA (ceRNA) to modulate the expression of PD-L1 by miR-223/STAT1 axis.”

The US government Comparative Toxicogenomics Database (CTD) has thousands of references and much curation on Programmed Death-Ligand 1 (PD-L1) also known as Cluster of Differentiation 274 (CD274) or B7 homolog 1 (B7-H1) upregulated by Endotoxin, linked to 1,865 diseases.²⁸ Cancers top the list.

Brain Cancer caused and promoted by Endotoxin

Endotoxin in mRNA jabs will give you Brain Cancer.²⁹ TLR4 interaction with Endotoxin in Glioma CD133+ Cancer Stem Cells induces cell Proliferation, Resistance to Chemotherapy and Evasion from cytotoxic T lymphocyte-induced Cytolysis.³⁰

Conclusion

Endotoxin upregulation of microRNA miR-155 is identified as the primary cause of Cancer induction and Metastasis by Covid19 mRNA jabs.

1. APPENDIX 2.1 Cumulative Number of Case Reports (Serious and Non-Serious, Medically Confirmed and Non Medically-Confirmed) from Post-Marketing Data Sources, Overall, by Sex, Country, Age Groups and in Special Populations and Summary Tabulation by Preferred Term and MedDRA System Organ Class BNT162B2 - ALL Reporting Period: Through 15-APR-2022

2. Biotechbabe 2022. https://gettr.com/user/Biotechbabe Transcript of video by Dr Ryan Cole 14 May 2022. Designed to Cross the Blood-Brain Barrier: Pharma and the FDA knew Lipid Nanoparticles Go Everywhere

3. https://rutzconsulting.com/the-elephant-in-the-room-cancer/

4. Extreme Toxicity of Endotoxins in Pfizer Jabs

5. Farah Yassine, Sabreen F. Fostok, Nataly Naser Al Deen, Rabih S. Talhouk. 2021. Endotoxin Triggers Tumor Initiation Events in Nontumorigenic Breast Epithelial Cells and Enhances Invasion-Related Phenotype in Pretumorigenic and Tumorigenic Breast Epithelial Cells. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8642002/

6. Yang H, et al. 2014. Toll-Like Receptor 4 Prompts Human Breast Cancer Cells Invasiveness via Lipopolysaccharide Stimulation and Is Overexpressed in Patients with Lymph Node Metastasis. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109980

7. Mammograms for women 40 & over?

8. Jain, S et al. 2018. Lipopolysaccharide (LPS) enhances prostate cancer metastasis potentially through NF-κB activation and recurrent dexamethasone administration fails to suppress it in vivo. https://onlinelibrary.wiley.com/doi/abs/10.1002/pros.23722

9. Epigenetics of Endotoxin Poisoning from Pfizer Jabs

10. Nagasaki, T et al. 2013. Interleukin-6 released by colon cancer-associated fibroblasts is critical for tumour angiogenesis: anti-interleukin-6 receptor antibody suppressed angiogenesis and inhibited tumour–stroma interaction. https://www.nature.com/articles/bjc2013748

11. Qi HM, Zhu TM, Wang J. Regulation of immune suppressive cytokines by TLR4 activation in colon cancer cells. Zhonghua Wei Chang Wai KeZa Zhi. 2009;12(4):413–5. https://pubmed.ncbi.nlm.nih.gov/19598032/

12. Tang X, Zhu Y. TLR4 signaling promotes immune escape of human colon cancer cells by inducing immunosuppressive cytokines and apoptosis resistance. https://pubmed.ncbi.nlm.nih.gov/23035361/

13. Cao H. 2023. Bacterial endotoxin lipopolysaccharides regulate gene expression in human colon cancer cells. https://bmcresnotes.biomedcentral.com/articles/10.1186/s13104-023-06506-9

14. Nilsson, MB et al. 2005. Interleukin-6, Secreted by Human Ovarian Carcinoma Cells, Is a Potent Proangiogenic Cytokine. https://aacrjournals.org/cancerres/article/65/23/10794/519037/Interleukin-6-Secreted-by-Human-Ovarian-Carcinoma

15. Wang L, et al. 2013. Toll-Like Receptor-4 Signaling in Mantle Cell Lymphoma: Effects on Tumor Growth and Immune Evasion. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4211879/

16. Avbelj M, et al. 2014. Activation of lymphoma-associated MyD88 mutations via allostery-induced TIR-domain oligomerization. https://ashpublications.org/blood/article/124/26/3896/33661/Activation-of-lymphoma-associated-MyD88-mutations

17.

18.

19. Faraoni I, et al. 2009. miR-155 gene: A typical multifunctional microRNA. https://www.sciencedirect.com/science/article/pii/S0925443909000428

20. https://en.wikipedia.org/wiki/MiR-155

21. Kluiver J, et al. 2005. BIC and miR-155 are highly expressed in Hodgkin, primary mediastinal and diffuse large B cell lymphomas. https://pathsocjournals.onlinelibrary.wiley.com/doi/10.1002/path.1825

22. Costinean S, et al. 2006. Pre-B cell proliferation and lymphoblastic leukemia/high-grade lymphoma in Eμ-miR155 transgenic mice. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1459012/#

23. Eis PS, et al. 2005. Accumulation of miR-155 and BIC RNA in human B cell lymphomas. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC552785/

24. https://www.news.com.au/entertainment/celebrity-life/sam-neill-shares-sad-cancer-update-after-chemotherapy-treatment-fails/news-story/232e7ec993a516b7f28edd302368835f

25. Goldman S, et al. 2021. Rapid Progression of Angioimmunoblastic T Cell Lymphoma Following BNT162b2 mRNA Vaccine Booster Shot: A Case Report. https://www.frontiersin.org/articles/10.3389/fmed.2021.798095/full

26. Murakami YI, et al. 2007. c-Maf expression in angioimmunoblastic T-cell lymphoma. https://journals.lww.com/ajsp/abstract/2007/11000/c_maf_expression_in_angioimmunoblastic_t_cell.9.aspx

27. Peng L, et al. 2022. Lipopolysaccharide facilitates immune escape of hepatocellular carcinoma cells via m6A modification of lncRNA MIR155HG to upregulate PD-L1 expression. https://link.springer.com/article/10.1007/s10565-022-09718-0

28. https://ctdbase.org/detail.go?type=gene&acc=29126&view=disease

29.

30. Che F, et al. TLR4 interaction with LPS in glioma CD133+ cancer stem cells induces cell proliferation, resistance to chemotherapy and evasion from cytotoxic T lymphocyte-induced cytolysis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5581125/