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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.