This article originally appeared on Brownstone Institute and was republished with permission.
Guest post by Dr. Charlotte Kuperwasser
I’m going to touch on a highly controversial subject, one that has become the third rail among cancer biologists and the broader medical community: the possible link between Covid-19 vaccination and cancer. Because my laboratory’s mission is centered on cancer prevention, I cannot in good conscience ignore the elephant in the room.
As my colleague, internationally renowned cancer biologist Dr. Wafik El-Deiry, and I articulated in the September ACIP meeting on Covid vaccines, nearly 50 publications have reported a temporal association between Covid-19 mRNA vaccination and the onset of cancer. Epidemiological studies (one from Italy and one from South Korea) have also described increased cancer incidence among Covid-vaccinated individuals compared to unvaccinated groups (albeit with caveats). These reports are mounting and it’s time we acknowledge that something meaningful may be occurring rather than dismissing them outright; this latter response seems to be the dominant reaction in academia, the media, and by our regulatory agencies.
My goal here is to unpack the science and outline plausible biological mechanisms between the association of Covid mRNA vaccination and cancer that warrant further and urgent investigation. The purpose is not to make claims either way but to frame the issue that must be addressed in hopes that open scientific discussion and more importantly, research funding can be directed towards this urgent and growing area of concern. The current climate has made it impossible for scientists to study this without fear of personal or professional repercussions.
What We Know and Don’t Know
At present, there are no published studies demonstrating a direct causal mechanism by which the mRNA vaccines induce cancer. However, that does not mean such a causal connection doesn’t exist. In fact, there are at least three biologically plausible mechanisms that, in my view, merit rigorous study and evaluation given their known links to causing cancer. I’ve written about these mechanisms before in other contexts, but here I’ll explain how they may apply to the Covid-19 mRNA vaccines.
Mechanism 1: Cellular Transformation Due to Spike Protein Biology
The transformation of a normal cell into a cancer cell involves the disruption of multiple safeguards controlling cell growth, survival, and DNA repair. The Covid mRNA vaccines work by instructing the body’s cells to produce the SARS-CoV-2 spike protein for prolonged periods of time (anywhere from days to weeks, to months, and even years). This foreign spike protein then elicits an immune response.
Laboratory studies have reported that the spike protein, whether it is produced by infection or by vaccination, has biological activities. It interacts with cellular pathways that regulate the cell cycle, tumor suppressor functions, and DNA damage repair pathways and machinery. Therefore, in theory, such interactions of spike protein with these pathways could contribute to cellular transformation—although the same could be said for infection with Covid-19 itself. The difference, however, lies in the duration of spike protein produced after vaccination compared to natural infection. This also raises an important question about whether multiple Covid infections are biologically equivalent to the artificial spike protein produced by the vaccine.
Since the spike protein that is produced by the mRNA can persist for as little as a few days, to weeks, months, and even years after vaccination, it is important to acknowledge whether cancer incidence correlates with spike protein expression (or persistence) in the body, but also whether it is present in tumors. A recent case study showed evidence that spike protein can be found expressed in metastatic breast cancer. Thus, in thinking about the relationship between Covid vaccination and cancer, chronic exposure to an agent with biological activity that disrupts cell cycle and DNA damage response pathways is very important to consider. Outright dismissing this possibility seems negligent. Currently data is insufficient to make any firm conclusions about any of this in a conclusive manner, and in the absence of such data means this mechanism cannot be dismissed outright.
Mechanism 2: Genomic Integration and Dysregulated Gene Expression Due to Residual DNA Contaminants
It is now acknowledged by the manufacturers, the FDA, as well as others, including a lab from the NIH, that residual DNA impurities are present in mRNA vaccines.
While many have argued that the quantities present in the vaccine preparations are too small to pose harm, the facts remain: (1) these fragments exist, (2) they are delivered in a lipid nanoparticle that efficiently allows the DNA to enter cells and the nucleus, and (3) the size of these fragments can readily integrate into the genome—especially when cells are dividing and undergoing natural DNA repair. Since no studies have been conducted demonstrating that the quantity of these impurities is insufficient to transfect cells, and that they do not integrate, it is complete speculation at this time that this cannot and does not happen. Said differently, no studies have yet shown that these impurities are too minimal to enter cells or integrate into DNA.
For the Pfizer vaccine, a subset of the impurities contains DNA sequences that are viral regulatory elements, which by definition influence gene expression. In addition, new findings suggest that the Pfizer vaccine also contains DNA that is methylated, which can stimulate a pathway in cells called cGAS-STING. Therefore, at least in the case of the Pfizer vaccine, these DNA impurities cannot only integrate, but they can potentially have far-reaching effects.
DNA integration events in the wrong genomic context could, in principle, dysregulate gene expression and contribute to cellular transformation, especially if combined with prolonged cGAS-STING pathway activation and SV40 promoter gene regulation.
The bedrock of molecular biology is the ability to use lipid nanoparticles to introduce DNA into cells. An undisputed byproduct of this is that some fraction of the DNA will integrate. And when it integrates, it has the ability to alter gene expression and disrupt gene function. To assume this cannot happen with the DNA impurities in the mRNA vaccines is misleading. We simply do not know the fate of the DNA impurities in the mRNA vaccine products when they come into contact with cells (either in vitro or in vivo). There is no data to assert that this cannot happen, and that it does not happen after vaccination.
Nearly all molecular biologists would agree that delivering DNA in lipid nanoparticles to cells is DNA transfection – pure and simple. Hence, this mechanism (and the effects of SV40 promoter sequence integration as well as transfected methylated DNA) makes it possible, in theory, for the DNA contaminants to initiate or drive cellular transformation in the right context. The open question is how often it occurs, and does it occur. To date, the answer to this is unknown, and as mentioned above, no one is studying whether this occurs and at what frequency. Therefore, we cannot draw any conclusions either in support or against these mechanisms at this time.
Mechanism 3: Immune Dysregulation: The Most Plausible Link
The most plausible mechanism linking vaccination to cancer, especially with respect to the temporal associations, involves the immune system. Several peer-reviewed studies have documented immune alterations following repeated mRNA vaccination, including increased inflammatory cytokines, T-cell exhaustion, elevated IgG4 antibody production, and transient immune suppression.
The immune system serves as a critical gatekeeper against cancer, identifying and eliminating transformed cells before they can progress. It can also act as a potent carcinogen and cancer driver in the form of inflammation, especially when chronic. Hence, if the immune system is temporarily impaired or dysregulated, or excessively reactive, the combination of failed immunosurveillance and chronic inflammation could not only allow preexisting abnormal cells to expand, but in fact promote them towards full neoplastic transformation. This could lead to promoted and even accelerated tumorigenesis, easily observed within the temporal windows that have been described.
Timing and Cancer Development
Most solid tumors require years to develop. Therefore, any cancer that appears within 6–12 months of vaccination (except for certain lymphomas, which can progress from initial malignant transformation within weeks to a few months) is unlikely to result from initiating events caused by the mRNA vaccine through mechanisms 1 or 2.
However, even if the Covid-19 mRNA vaccine is not the initiating factor, there remain plausible scenarios in which pre-existing pre-malignant or occult cancer cells (already genetically unstable and poised for full neoplastic transformation) could be accelerated by unintended effects of the spike protein or by rare DNA-integration events. Moreover, any dormant or microscopic cancer held in check by immune surveillance could, in principle, be unleashed or promoted through immune dysregulation (mechanism 3).
Patterns to Watch
Several studies have documented measurable changes in immune function after repeated mRNA vaccination, including inflammation, autoimmunity, and a form of acquired functional immunodeficiency. These changes have also been documented with long Covid, so it will be important to parse out data trends and patterns between vaccinated versus unvaccinated and also between long-Covid vaccinated versus long-Covid unvaccinated.
Since immunodeficiency is often accompanied by chronic inflammation, both have direct implications for tumor surveillance and tumor permissiveness. Hence, there are signals one might expect to observe based on predictable patterns of cancer observed in other forms of acquired immunodeficiency (eg, HIV or organ-transplant recipients). The mechanisms driving these cancers are well established and broadly recognized among cancer biologists.
Lymphoid Cancers
The first and most immediate observation would be an uptick in lymphoid malignancies, particularly non-Hodgkin lymphomas (NHL), T-cell lymphomas, and aggressive B-cell lymphomas such as Burkitt-like or diffuse large B-cell lymphoma (DLBCL). These cancers are tightly linked to immune control mechanisms and to EBV oncogenesis. Under conditions of immune stress or exhaustion, B cells with latent EBV infection may escape control, undergo clonal expansion, and acquire the additional genomic alterations required for full transformation.
In immunocompromised patients, such lymphomas often appear within months of immune dysfunction. Therefore, similar temporal dynamics following repeated mRNA vaccination, or any sustained immune perturbation, would warrant close epidemiologic scrutiny.
Notably, there has been a disproportionate representation of post-vaccine lymphomas in published case reports, including both newly emergent cases and rapid relapses after remission. Whether these observations represent coincidence, reporting bias, or genuine immune disruption remains unknown. However, the pattern itself is biologically consistent with what we would expect if immunosurveillance fails.
Viral Associated Cancers
The next category of cancers that would be expected to increase would include those with a viral etiology, since their emergence is often due to failed immunosurveillance. These include Kaposi sarcoma, Merkel cell carcinoma, cervical and oropharyngeal cancers (HPV-driven), and hepatocellular carcinoma (HBV/HCV). Such tumors typically arise in the setting of immune suppression, chronic inflammation, or both.
A surge in these cancer types, especially among individuals without classical immunosuppression, could indicate a breakdown in immunoediting where host–virus equilibrium is lost. A lapse in immune control of latent HPV infection could accelerate oncogenic progression within the cervix or oropharynx. Similarly, reduced cytotoxic T-cell activity might allow for subclinical Merkel cell or Kaposi lesions to manifest.
Leukemias and Myelodysplastic Syndromes
Several temporal association studies have reported cases of acute leukemias and myelodysplastic syndromes (MDS) following vaccination. These malignancies are highly sensitive to inflammatory and immune-modulatory environments, but also to environmental exposures that affect DNA integrity. Therefore, it is plausible that a rise in sustained immune activation followed by suppression could accelerate the expansion of pre-leukemic clones already present in aging bone marrow. It is also plausible that DNA impurities present in the mRNA vaccines could preferentially integrate into hematopoietic precursor cells, which are particularly susceptible to genotoxic stress. Integration within vulnerable genomic regions of these cells could, in theory, initiate leukemic transformation.
Although such clonal dynamics might be subtle at the population level, they could become detectable through longitudinal studies, particularly if stratified by age, vaccination history, and markers of immune activation.
Aggressive or Unusual Solid Tumors
Finally, one might expect to see rare or unusually aggressive solid tumors emerging in temporal proximity to mRNA vaccination. These could include high-grade gliomas, pancreatic carcinomas, rapidly proliferating sarcomas, breast cancers, and other solid tumors.
On a population level, the association between cancer with vaccination would likely appear as disproportionate increases in hematologic cancers (lymphomas, leukemias) and virus-associated cancers relative to baseline trends. One might also expect to observe an increase in earlier onset cancers or clusters of rapidly progressing or treatment-resistant cancers within short intervals post-vaccination if chronic inflammation or T-cell exhaustion were the culprit. Dormant, occult, in-situ cancers, or micrometastases might become more active if immunosurveillance is blunted or if inflammatory cytokines alter the stromal microenvironment. These could easily manifest over 12–36 months post-vaccinations.
While none of these patterns would prove causation, such a pattern should not be dismissed as a coincidence either. Other environmental exposures, such as tobacco, asbestos, and endocrine disruptors, have been linked to cancer. The initial warnings were met with skepticism, yet in each of these examples, rigorous study, observation, and experimental research demonstrated their causal relationship. The same principle should apply here. Researchers must be empowered to replicate and expand upon these analyses, free from censorship, personal, or professional retaliation.
Assessing and quantifying these potential mechanisms must become a research priority if we are to make sense of the growing number of reports linking cancer onset to Covid-19 vaccination and to determine whether these associations reflect true causal relationships.
Long-term, population-level studies will be essential to reveal whether certain cancer types, particularly rare or aggressive subtypes, occur more frequently in vaccinated compared to unvaccinated individuals. For this reason, it is imperative for public health that the scientific community and regulatory agencies commit to rigorous, unbiased investigation of these questions.
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