Tying together the elements of an IgG4-based hypothesis for mRNA-transfection induced "Turbo" cancers

The clue to watch and listen for is, "after the booster".

I was moved write this piece after hearing Professor of medicine at St. Georges University in London and practicing oncologist Angus Dalgleish describe in a video linked at bottom, starting at around 3:30, how eight of his patients with previously well controlled melanoma had “relapsed following the booster vaccine”. He later emphasizes that these relapses are “really quite aggressive”. Professor Dalgleish is recognizing a pattern. If you read enough case studies depicting aggressive cancers that appear in close proximity to mRNA transfections, you will begin to see a pattern too; many of them emerge after the booster. Why would this be?

The story lies in the realm of Immunoglobulin Antibodies, shorthand IgG. The Vaccinators have made a big deal about IgG’s because these are the immune markers their mRNA hammer creates. Viewing our immune system function in such a one-dimensional way as part of the overall Covid-19 narrative has been aptly described by PhD Biologist JJ Couey as a form of “immuno-mythology”. What no lab did before Irrgang, et al. at least in public view, was to perform the extra analysis necessary to bin these spike-induced IgG antibodies into one of the four possible classes; IgG1, IgG2, IgG3, and IgG4. Irrgang and team found that, contrary to expectations, IgG4-type antibodies, which actually mute rather than direct the T-cell response, were becoming detectable after second shot, and blooming dramatically after the third.

Many of us refused the mRNA transfections on the basis of unknown long term consequences. The IgG4 data is an irrefutable receipt that our fears were rational and well grounded. The Vaccinators hubris in wielding this pseudo-uridylated, unnaturally long-lived mRNA antigenic hammer into our complex, delicately balanced immune systems is now naked if you have eyes to see.

I want to make clear that I am not saying everyone who got a booster is going to get cancer. The case being made is that after the booster there is a period, potentially long lasting, whereby the normal cancer-fighting function of our immune system will be heavily muted. If you had a pre-existing, or incipient but undiagnosed cancer when you get the booster, this could be bad mojo indeed. In writing this article, my main focus is on the creation of a single page, printable, data-based roadmap to the hypothesis that can be handed to friends, family, or even one’s doctor.

I will cite three scientific papers to draw out this hypothesis. I am not the first to make these connections - I stand on the shoulders of many other independent researchers. At the same time, I was one of the first to really grasp the importance of the Irrgang paper when it came out as a preprint in July of 2022. At that time I had prodded the excellent Brian Mowrey to look at the finding, and he was one of the first to provide commentary;

Tolerance Cometh: IgG4 After Multiple-mRNA Doses

Across the slew of recent articles that published in the wake of the December, peer-reviewed version of Irrgang was this by Dr. Paul Oosterhuis, that included this statement; “This paper may be one of the most important in the history of Covid.” I agree.

Too much Tolerance can be a bad thing.

Without further ado, here is the IgG4 turbo cancer hypothesis told in data, on one page. We can see not just the evidence of IgG4, but the secondary, and expected effect of decreased T-cell responses in the 3-4X vaccinated as compared to those with only two doses. Finally, mechanistic proof that IgG4 can suppress the normal immune response to cancer, regardless of what antigen those (usually rare) IgG4 antibodies were originally induced by.

Here is the UK doctors interview video that includes testimony by Dr. Angus Dalgleish; https://www.bitchute.com/video/XmONuEssro9I/

The emergence of IgG4 is one of several possible mechanisms underlying the increase in cancers being seen. The other most prominent mechanistic hypothesis relates to potential dis-regulation of p53 gene DNA-repair;

https://childrenshealthdefense.org/defender/covid-boosters-increase-cancer-young-adults-cola/

“Jiang and Mei, quite logically and reasonably, cautioned that the mRNA spike protein would likely have the same effect as the viral spike protein on p53 and therefore cause cancer. …

“[The] Jiang and Mei paper was retracted due to spurious ‘expressions of concern’ (EOC) about the methods of the study despite them being standard practice. …

“Well, despite the retraction, the spike protein circulating in large quantities, in the direct vicinity of the cell nucleus, for elongated periods of time, still has the potential to induce cancer in those cells (ovary, pancreas, breast, prostate, lymph nodes).

“These cancers can take years to develop and so it’s possible that we don’t see much of a safety signal for 5 or 10 years.”

As suggested above, p53-driven cancer is likely something that will play out longer term. When considering the IgG4 hypothesis linking aggressive cancers to the mRNA transfections, always remember to look for the phrase, “after the booster” like below;

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8656165/

Title: Rapid Progression of Angioimmunoblastic T Cell Lymphoma Following BNT162b2 mRNA Vaccine Booster Shot: A Case Report

Before closing, let’s look more deeply at the Wang, et at. paper that teaches how IgG4 antibodies caused by ANY antigen can shut down the tumor specific immune response being initiated by other IgG’s;

https://jitc.bmj.com/content/8/2/e000661

Title: An immune evasion mechanism with IgG4 playing an essential role in cancer and implication for immunotherapy

Results: In a cohort of patients with esophageal cancer we found that IgG4-containing B lymphocytes and IgG4 concentration were significantly increased in cancer tissue and IgG4 concentrations increased in serum of patients with cancer. Both were positively related to increased cancer malignancy and poor prognoses, that is, more IgG4 appeared to associate with more aggressive cancer growth. We further found that IgG4, regardless of its antigen specificity, inhibited the classic immune reactions of antibody-dependent cell-mediated cytotoxicity, antibody-dependent cellular phagocytosis and complement-dependent cytotoxicity against cancer cells in vitro, and these effects were obtained through its Fc fragment reacting to the Fc fragments of cancer-specific IgG1 that has been bound to cancer antigens. We also found that IgG4 competed with IgG1 in reacting to Fc receptors of immune effector cells. Therefore, locally increased IgG4 in cancer microenvironment should inhibit antibody-mediated anticancer responses and help cancer to evade local immune attack and indirectly promote cancer growth. This hypothesis was verified in three different immune potent mouse models. We found that local application of IgG4 significantly accelerated growth of inoculated breast and colorectal cancers and carcinogen-induced skin papilloma. We also tested the antibody drug for cancer immunotherapy nivolumab, which was IgG4 in nature with a stabilizing S228P mutation, and found that it significantly promoted cancer growth in mice. This may provide an explanation to the newly appeared hyperprogressive disease sometimes associated with cancer immunotherapy.

I am herein suggesting that the last sentence above be modified to say, “This may provide an explanation to the newly appeared hyperprogressive cancer sometimes associated with lipid nanoparticle vectored mRNA transfections.”