COVID-19 Virus Could Be Behind Alarming Rise in Rare Cancers Like Gastrointestinal Stromal Tumors
Nikhil Prasad Fact checked by:Thailand Medical News Team May 05, 2025 2 weeks, 4 days, 23 hours, 43 minutes ago
Medical News: In a disturbing trend that could reshape our understanding of cancer development in the post-pandemic world, a new study is warning of a potential link between COVID-19 and a surprising rise in rare cancers—particularly gastrointestinal stromal tumors (GISTs). The findings come from a collaborative team of researchers from Carolina Blood and Cancer Care Associates, North Carolina Oncology Association, Novant Health, Levine Cancer Institute, and other affiliated institutions, who have observed an unusual cluster of GIST cases following the COVID-19 pandemic.
COVID-19 Virus Could Be Behind Alarming Rise in Rare Cancers Like Gastrointestinal Stromal Tumors
Before the pandemic, rare cancers like GISTs were seldom seen in general clinical settings. But in the aftermath of COVID-19, doctors at a rural community oncology practice noted a dramatic increase in these cases—jumping from a single patient before 2020 to 10 new patients shortly after the pandemic's peak. This
Medical News report highlights their growing concerns about the potential oncogenic (cancer-causing) effects of the SARS-CoV-2 virus and how it may be silently triggering malignancies in vulnerable individuals.
Could COVID-19 Be a Hidden Catalyst for Cancer?
SARS-CoV-2, the virus that causes COVID-19, is already known for its short-term respiratory and systemic complications. But scientists are now paying closer attention to its long-term effects—especially the potential for the virus to spark cellular changes that may lead to cancer. Much like other known cancer-causing viruses such as hepatitis B and C, human papillomavirus (HPV), Epstein-Barr virus (EBV), and human T-cell leukemia virus (HTLV), COVID-19 appears to exploit the immune system and key molecular pathways that could eventually result in tumor formation.
According to the researchers, the virus may disrupt tumor-suppressing genes through its nonstructural proteins, activate inflammatory responses such as the notorious “cytokine storm,” and cause long-term tissue damage in multiple organs. These disruptions may create a biological environment that supports the growth of cancer stem cells.
One key area of concern is how SARS-CoV-2 hijacks the renin-angiotensin system (RAS), a hormone system that regulates blood pressure and fluid balance. The virus attaches itself to ACE2 receptors, interfering with normal physiological processes and triggering inflammation. The resulting immune cascade involves numerous pro-inflammatory molecules—especially interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-alpha (TNF-α)—that not only drive severe illness in acute COVID-19 but may also promote cancerous changes over time.
How Inflammation and Immune Disruption Could Lead to Tumors
The study outlines how COVID-19 disturbs the immune system in a way that mirrors cancer-promoting conditions. Initially, lymphocytes (a type of white blood cell) produce interferon-gamma to fight the virus. Bu
t soon after, these protective cells are suppressed, leading to a condition known as lymphopenia. This opens the door for other immune cells—like neutrophils and macrophages—to dominate. These cells produce vast amounts of IL-6 and other cytokines, which sustain a high state of inflammation long after the virus is gone.
A particularly concerning effect is the formation of neutrophil extracellular traps (NETs), which physically block immune surveillance and reawaken dormant cancer cells. Simultaneously, elevated levels of VEGF and PDGF—two growth factors involved in blood vessel formation—support tumor angiogenesis (the development of new blood vessels to feed tumors).
Meanwhile, IL-6 activates a pathway known as the IL-6 amplifier, which includes the transcription factor STAT3. This signaling cascade has already been implicated in several cancers including pancreatic, breast, head and neck, and cervical cancers. When STAT3 is turned on, it causes the upregulation of genes such as c-myc, pim1, and pim2—proto-oncogenes that can drive cells into uncontrollable division.
The situation is further complicated by TNF-α, another cytokine that activates NF-κB, a protein complex linked to inflammation-induced cancer. NF-κB promotes DNA damage, chromosomal instability, and reduces programmed cell death (apoptosis), allowing damaged cells to survive and mutate.
Case Surge in GISTs Raises Red Flags
Gastrointestinal stromal tumors are rare cancers that originate from the interstitial cells of Cajal—the pacemaker cells that control muscle contractions in the gut. Although GISTs account for just 1–2% of all gastrointestinal malignancies, they can be aggressive and deadly if not caught early.
Worldwide, the incidence of GIST is estimated at 10–15 cases per million people per year. In the United States, that translates to roughly 5,000 new cases annually. Prior to COVID-19, the rural clinic involved in the study reported just one case of GIST. But after the pandemic hit, they recorded 10 new cases, four of which were localized while six had already spread to the liver and other distant organs.
While this small sample size does not confirm a direct causal relationship, it raises serious questions. Are these cancers appearing more frequently because COVID-19 weakened the immune defenses of genetically susceptible individuals? Could the virus be acting as a "second hit" in the development of cancer in people who already carried predisposing mutations?
The Growing Evidence Behind Long COVID and Cancer Risk
Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), affects up to 12% of individuals who had severe illness. These patients often experience lingering symptoms such as fatigue, headaches, brain fog, and cardiovascular issues. But beneath the surface, chronic inflammation appears to be silently affecting their entire body—including potentially setting the stage for cancer.
According to the study authors, high serum levels of IL-6 are already used as biomarkers for disease severity in COVID-19. These same inflammatory mediators have long been associated with autoimmune conditions and cancer development.
The IL-6/STAT3 axis is particularly dangerous because it not only drives inflammation but also enables tumors to grow, spread, and resist treatment.
Meanwhile, TNF-α and IL-1β continue to fan the flames of inflammation by activating protein kinases like HSP-27, which blocks apoptosis—a key mechanism the body uses to eliminate faulty or mutated cells. Elevated HSP-27 has been linked to poor outcomes in several types of cancer.
Together, these cytokines and signaling pathways could be creating the ideal storm for neoplastic transformation in individuals recovering from COVID-19.
Conclusion
The potential oncogenicity of SARS-CoV-2 is a growing area of concern that warrants urgent attention. While current evidence remains largely observational, it highlights a plausible and deeply troubling biological mechanism by which COVID-19 may increase the risk of rare and aggressive cancers. From hijacking the immune system and flooding the body with inflammatory cytokines to interfering with tumor suppressor genes and creating a pro-tumor microenvironment, the virus has the tools needed to potentially ignite cancer development in vulnerable hosts.
Long COVID itself is now recognized as a multi-systemic disorder with far-reaching consequences, affecting millions globally. As we continue to uncover the long-term fallout of this pandemic, tracking cancer trends among COVID survivors—especially rare malignancies—should become a research priority. Governments, public health agencies, and oncologists must be proactive in recognizing these potential risks. Diagnostic tools and treatments must evolve to meet the needs of a world where a ubiquitous virus may have quietly rewritten the rules of cancer development. The time to act is now—through robust surveillance, early detection strategies, and intensified research into the long-term molecular effects of SARS-CoV-2.
The study findings were published as a poster abstract at NCODA but will appear soon in a peer reviewed journal.
https://www.ncoda.org/wp-content/uploads/2025/04/NCODA-2025-Poster-4.pdf
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