Oncology | Bioengineering | Published in Scientific Reports, February 9, 2026
University of Pennsylvania School of Dental Medicine
Cancer drugs are supposed to be sophisticated. Precision molecules, engineered in laboratories, administered through IV lines, targeting tumors at the molecular level. The idea that a piece of chewing gum might belong in the same conversation as cancer therapy sounds, at first, like the setup to a joke.
It is not a joke.
Core finding
A bioengineered chewing gum extract reduced three cancer-linked microbes by up to 93%, and in some cases almost to zero, without harming beneficial oral bacteria.
A research team at the University of Pennsylvania’s School of Dental Medicine, led by biochemist Henry Daniell, has published findings in Scientific Reports showing that extracts from a bioengineered chewing gum can reduce levels of three microbes strongly associated with head and neck cancer by up to 93%, and in some cases to almost zero, without harming the beneficial bacteria that keep the mouth healthy.
To understand why this matters, you need to understand the cancer it targets, the microbes that fuel it, why current treatments fail, and how a bean from Asia became the molecular backbone of a potential new therapy.
The Cancer Nobody Talks About Enough
Head and neck squamous cell carcinoma, universally abbreviated HNSCC in the medical literature, is a group of malignancies that develop in the tissues lining the mouth, throat, larynx, and related structures. It is not a rare disease. With approximately 890,000 new cases and 450,000 deaths annually, HNSCC is the seventh most common cancer diagnosis worldwide, accounting for roughly 4.5% of all cancer diagnoses and deaths globally.
And yet it occupies far less public consciousness than breast cancer, prostate cancer, or lung cancer, despite being significantly more deadly than most people realize.
The five-year survival rate for HNSCC is less than 50%. When the disease is caught at an early stage, outcomes are considerably better. But most cases are not caught early. HNSCC often develops in areas of the mouth and throat that are difficult to visualize, where symptoms like a sore throat, hoarseness, or difficulty swallowing are easy to attribute to something more benign. By the time the diagnosis is confirmed, a large proportion of patients are already at an advanced stage.
“Lip and oral cavity cancer was the seventh leading cancer type in cancer incidence and mortality rate worldwide in adolescents, young adults, and middle-aged adults in 2022,” said Henry Daniell, the senior author of the study.
“Lip and oral cavity cancer was the seventh leading cancer type in cancer incidence and mortality rate worldwide in adolescents, young adults, and middle-aged adults in 2022,” said Henry Daniell, the senior author of the study. The disease is more common in men than women, with a male-to-female ratio of approximately 2:1, and has historically been associated with tobacco and alcohol use. But in recent decades, a new driver has emerged that has fundamentally changed the epidemiology of the disease.
That driver is a virus that most people have heard of for a completely different reason.
HPV: From Cervical Cancer to the Throat
Human papillomavirus, HPV, is best known as the cause of cervical cancer. It is also one of the most common sexually transmitted infections in the world. The majority of sexually active adults will contract HPV at some point in their lives, and in most cases the immune system clears it without any lasting effects.
But in some people, certain high-risk strains of HPV, particularly HPV-16, integrate into the DNA of cells in the mouth and throat and drive those cells toward malignant transformation. One-third of males globally are HPV-positive, and one-fifth have high-risk HPV-16, which is transmitted through oral sex.
The result has been a rising epidemic of HPV-associated oropharyngeal cancer, cancers of the tonsils, base of the tongue, and surrounding tissues, in populations with no history of tobacco or alcohol use. “The global increase in oropharyngeal cancer is linked to HPV infection,” Daniell said.
Why HPV matters here
HPV-related head and neck cancers are rising, especially oropharyngeal cancers of the tonsils, tongue base, and throat.
This is not a minor or gradual trend. In developed nations, HPV-related HNSCC has now surpassed tobacco- and alcohol-related disease as the dominant cause of oropharyngeal cancers. Rates of oropharyngeal squamous cell carcinoma have risen steadily by 2.1% among men and 3.9% among women aged 20 to 44 years. The global rise in this specific cancer type is directly attributable to the spread of high-risk HPV.
There is an approved vaccine for the HPV strains most associated with cancer, and it is highly effective when given before exposure. But hundreds of millions of people worldwide were already infected before the vaccine existed or before they had access to it. For them, preventing infection is no longer an option. The question is what to do once the virus is already there.
The Bacterial Co-conspirators
HPV is not the only microbial threat to survival in HNSCC. Two species of bacteria have emerged from the research literature as particularly damaging in the context of this cancer.
The first is Porphyromonas gingivalis, abbreviated Pg. If you have ever seen a dentist who told you that you had early signs of gum disease, Pg is likely to have been involved. It is one of the primary drivers of periodontitis, and it has been found in elevated levels in the oral cavities and tumor tissues of patients with oral squamous cell carcinoma. Pg has multiple mechanisms by which it promotes tumor development: it evades immune surveillance, triggers chronic inflammation in the tumor microenvironment, and interferes with the apoptotic signals that would normally cause damaged cells to self-destruct.
The second is Fusobacterium nucleatum, abbreviated Fn. Fn is a gram-negative anaerobe that is increasingly recognized as a promoter of multiple cancer types, including colorectal cancer and now HNSCC. Outer-membrane vesicles secreted by Fn are able to induce oral cancer metastasis, activating intracellular autophagy pathways that help cancer cells spread to distant sites.
The microbial problem
HPV, Pg, and Fn are not passive passengers. They can actively worsen cancer progression and survival.
Cell culture studies in the Daniell lab showed 1,000-fold higher Pg and Fn levels in the saliva of HNSCC patients and 100-fold higher levels in oral rinse samples compared to non-cancer control participants. This is not a modest elevation. This is an entirely different microbial landscape in the mouths of cancer patients, one dominated by organisms that actively worsen outcomes.
Higher abundance of oral HPV, Porphyromonas gingivalis, and Fusobacterium nucleatum correlate with worse survival of head and neck squamous cell carcinoma. The connection is not just correlational. The biological mechanisms by which these three organisms fuel cancer progression have been documented in the research literature across multiple studies. They are not innocent bystanders. They are active participants in making this disease harder to survive.
Why Current Treatments Fall Short
HNSCC is typically treated with some combination of surgery, radiation, and chemotherapy. For some patients, immunotherapy drugs called checkpoint inhibitors have been added in recent years.
The problem is that most recently approved cancer drugs have not significantly improved quality-of-life or five-year survival rates, Daniell noted, underscoring the need for better therapies.
Radiation is the most common treatment for HNSCC, and it is effective at killing cancer cells. But it is not precise in the biological sense. Radiation damages whatever is in its path, which in the case of oral and throat cancer means not just tumor cells but the entire oral microbiome: the community of hundreds of bacterial species that live in the mouth and perform essential functions for health. After radiation, radiation therapy both reduces beneficial bacteria and increases disease-causing yeast like Candida albicans, leading to painful oral candidiasis, chronic dryness, difficulty swallowing, and long-term impairment of oral function.
The treatment paradox
Radiation can kill cancer cells, but it can also damage the healthy oral microbiome patients need for recovery.
The irony is complete: the treatment that kills the cancer also destroys the protective microbial ecosystem that would otherwise help the patient recover, replacing it with a different set of pathogens that cause their own suffering.
What is needed is something that targets specifically the harmful microbes linked to cancer progression, leaves the beneficial bacteria alone, and can be delivered easily to the one place in the body where these organisms reside: the mouth.
A Bean From Ancient Medicine
The bioengineered gum begins with an unlikely ingredient: the lablab bean, Lablab purpureus, also known as the hyacinth bean or lablab bean. This is a legume in the Fabaceae family, cultivated across Asia and Africa, and mentioned in the Chinese traditional medicine text Compendium of Materia Medica as having properties of “strengthening the spleen and reducing dampness.”
Inside the lablab bean is a protein called FRIL, which stands for Flt3 Receptor Interacting Lectin. It was first identified because of its ability to sustain hematopoietic progenitor cells, blood-forming stem cells, in laboratory culture by binding to their Flt3 surface receptors. It has also been shown to evoke anti-tumor activity by reducing tumor neoangiogenesis through immunomodulation.
But what makes FRIL relevant to the current study is a completely different property: it is a lectin with broad antiviral activity.
FRIL binds preferentially to complex-type N-glycans and neutralizes viruses that possess complex-type N-glycans on their envelopes. As a homotetramer, FRIL is capable of aggregating influenza particles through multivalent binding and trapping influenza virions in cytoplasmic late endosomes, preventing their nuclear entry.
How FRIL works
FRIL acts like molecular flypaper, binding sugar-coated viral surfaces and trapping viruses before they infect cells.
To translate this: many viruses, including influenza viruses, SARS-CoV-2, herpes simplex, and HPV, are coated on their outer surface with specific sugar structures called complex-type N-glycans. These sugar coatings are not decorative. They are functional components that the virus uses to bind to and enter human cells. FRIL grabs onto these sugar structures with high affinity.
When FRIL binds to the sugar-coated surface of a virus, it does two things. First, it physically blocks the viral surface proteins that the virus uses to dock onto and enter host cells. Second, because FRIL is a homotetramer, meaning it has four identical binding sites, it can grab onto multiple viral particles simultaneously and clump them together into aggregates that cells cannot take up. When formulated into chewing gum, this protein works like flypaper for viruses, trapping them and preventing them from infecting cells or being transmitted to others.
The previous work from Daniell’s lab demonstrated that FRIL-containing bean gum reduced SARS-CoV-2 levels in saliva by over 95% during the COVID pandemic, and was shown to be effective against influenza and herpes simplex virus. The earlier gum also demonstrated remarkable stability: the protein stays active for nearly two years in bean powder and even longer in chewing gum, remaining effective even after 794 days at room temperature.
That shelf-life stability is not a minor technical detail. It is what makes a gum-based therapy practical for real-world use, particularly in lower-income settings where cold storage is not always available.
Engineering the Second Weapon: Protegrin
FRIL handles the virus. But two of the three microbial threats in HNSCC are bacteria, specifically Pg and Fn. And bacteria require a different weapon.
For this the team turned to protegrin-1, a small antimicrobial peptide originally isolated from porcine white blood cells. Protegrin-1 belongs to a class of molecules that the immune system of many animals uses as a first-line defense against bacterial infection. It works by disrupting bacterial cell membranes: inserting itself into the lipid bilayer that surrounds bacteria, creating pores through which the bacterial cell’s contents leak out, killing it rapidly.
Crucially, protegrin-1 has a property that distinguishes it from antibiotics: selectivity based on membrane composition. Bacterial cell membranes have a different lipid composition from human cell membranes, and from the membranes of beneficial bacteria that share the oral environment. This selectivity is what allows protegrin-1 to kill harmful bacteria while leaving other organisms intact.
The engineered upgrade
The gum combines natural FRIL antiviral activity with engineered protegrin-1 antibacterial activity.
To get protegrin-1 into the chewing gum alongside FRIL, the researchers used plant genetic engineering. They introduced the gene encoding protegrin-1 into the chloroplast genome of lablab bean plants. Chloroplasts are the organelles in plant cells responsible for photosynthesis, and their genomes are separate from the main nuclear genome. Expressing foreign proteins in chloroplasts has several advantages: the chloroplast environment produces very high levels of the target protein, the protein is contained within the chloroplast and does not escape into the environment before harvest, and proteins expressed this way tend to be stable when the plant material is dried into a powder.
The result is a bean powder containing both FRIL, from the plant’s natural biology, and protegrin-1, from the engineered chloroplast, that can be incorporated into a standard gum base to produce a chewing gum that releases both active agents into saliva as the gum is chewed.
The Study: Real Patients, Real Samples, Real Numbers
The study published in Scientific Reports in February 2026 was an ex vivo clinical study. “Ex vivo” means outside the living body: the researchers took actual saliva and oral rinse samples from real HNSCC patients and tested the gum extracts against those samples in controlled laboratory conditions. This is an important distinction from cell culture studies using laboratory cell lines, which are less representative of actual patient biology.
The study enrolled 44 patients with head and neck squamous cell carcinoma. Their saliva and oral rinse samples were collected and tested against bean gum extracts under standardized conditions.
The HPV results came first.
HPV ELISA detected viruses in 100% of saliva samples and 75% of oral rinse samples from the 44 HNSCC patients. Every single saliva sample from the cancer patients contained HPV. This confirms what the epidemiological literature has long suggested: in this patient population, HPV is essentially universal.
The numbers
FRIL gum extract reduced HPV by 93% in saliva and 80% in oral rinse samples. Protegrin gum reduced Pg and Fn almost to zero.
When bean gum extracts containing FRIL were applied to these samples, bean-lectin gum reduced HPV levels by 93% in saliva samples and by 80% in oral rinse samples. A 93% reduction from a single exposure to gum extract. Not a pharmaceutical drug. Not an injected therapy. A protein from a bean, delivered through chewing gum, removing more than nine out of ten HPV viral particles from a saliva sample.
Then came the bacterial results. When the bioengineered gum containing protegrin-1 was tested against the bacterial samples, a single dose reduced the levels of Pg and Fn to almost zero without affecting the beneficial bacteria normally found in the mouth.
Almost zero. Not reduced. Not meaningfully lowered. Almost zero. From a single dose.
And the beneficial bacteria, the Streptococcus salivarius, the Lactobacillus species, the Rothia and Veillonella that perform essential functions in the healthy oral ecosystem, were left untouched. The gum was not a broad-spectrum antimicrobial carpet-bombing the entire oral microbiome. It was a precision strike against the specific organisms that promote cancer, while protecting the organisms that protect the patient.
This contrasts sharply with radiation therapy, which both reduces beneficial bacteria and increases disease-causing yeast such as Candida albicans.
What Makes This Different From Antibiotics
It is worth pausing on the selectivity finding, because it addresses one of the most important problems in infectious disease and cancer medicine simultaneously.
Antibiotics are the standard treatment for bacterial infections. But they work by targeting broad biological features shared across many bacterial species: cell wall synthesis, protein synthesis, DNA replication. They kill pathogenic bacteria and beneficial bacteria with relatively equal efficiency. This is why antibiotic use is associated with gut dysbiosis, opportunistic infections, and the rise of resistant organisms.
Why this is different
Instead of wiping out the whole oral microbiome, the gum targets cancer-associated microbes while sparing beneficial bacteria.
Protegrin-1’s mechanism of action, disrupting cell membranes based on their specific lipid composition, appears to produce a different selectivity profile. The harmful oral bacteria associated with HNSCC, Pg and Fn, were nearly eliminated. The commensal oral bacteria that constitute a healthy microbiome were not affected.
If this selectivity holds up in clinical trials, it would represent something genuinely unusual: an antimicrobial therapy that kills cancer-associated bacteria in the mouth without collateral damage to the oral microbiome. That would make it compatible with concurrent cancer treatment in a way that broad-spectrum antibiotics are not.
The Numbers Behind the Need
Beyond the clinical mechanism, there is an economic and accessibility argument embedded in this research that deserves explicit attention.
Cancer therapies are expensive. Not just expensive in the sense that patients feel the financial strain, although they do. Expensive in the sense that entire health systems in lower-income countries cannot afford to stock and administer them. Checkpoint inhibitors for HNSCC cost tens of thousands of dollars per patient per year. Even standard chemotherapy regimens require intravenous administration infrastructure, trained oncology nurses, pharmacies capable of handling cytotoxic drugs.
A bioengineered chewing gum made from a plant protein extracted from lablab beans and a synthetic peptide incorporated into a standard gum base costs a fraction of any pharmaceutical alternative. It requires no refrigeration beyond room temperature for extended periods. It requires no IV line, no trained nurse, no hospital infrastructure. It is chewed for a few minutes and provides a therapeutic dose of active agents directly to the site of disease.
“Our findings support the value of advancing these therapies to clinical trials as adjuvants with current treatments or as prophylaxis to prevent infection and transmission,” Daniell said.
“Our findings support the value of advancing these therapies to clinical trials as adjuvants with current treatments or as prophylaxis to prevent infection and transmission,” Daniell said.
That last phrase matters: “prophylaxis to prevent infection and transmission.” The gum is being proposed not just as an adjunct therapy for patients already diagnosed with HNSCC, but potentially as a preventive intervention for people at high risk: individuals who are HPV-positive, who have elevated levels of Pg or Fn in their oral microbiome, or who have a history of tobacco and alcohol use. If the gum can reduce the microbial burden that drives cancer development before a tumor forms, it could prevent some fraction of HNSCC cases from occurring at all.
What Comes Next
The study published in February 2026 is an ex vivo proof of concept. The results are striking, but the path from ex vivo laboratory findings to approved clinical therapy is long and involves studies the researchers have not yet conducted.
The next required step is a Phase 1 clinical trial in which actual HNSCC patients chew the bioengineered gum and researchers measure what happens to HPV, Pg, and Fn levels in vivo: inside a living person, in the real oral environment, over a sustained period of use. Phase 1 trials are primarily designed to establish safety, not efficacy, but they would also provide early signals about whether the ex vivo results translate to clinical practice.
Phase 2 and Phase 3 trials testing efficacy at scale, comparing outcomes between patients who receive the gum as an adjunct to standard therapy versus those who receive standard therapy alone, would follow if Phase 1 is successful. This is a process measured in years, not months.
Reality check
This is promising ex vivo research, not an approved cancer treatment yet. Human clinical trials are still needed.
There are also scientific questions that the current study cannot answer. Does repeated use of protegrin-1 select for resistance in Pg or Fn? Does the gum maintain efficacy when used daily over weeks and months, or does microbial adaptation reduce its effectiveness over time? Does reducing HPV levels in saliva translate to a meaningful reduction in viral integration into mucosal cells, which is the step that drives malignant transformation?
These are not objections to the research. They are the questions that clinical trials are designed to answer. The current study was designed to ask whether the mechanism works in samples from real patients. It answered yes. The next questions are about what that means for real patients in real clinical practice.
The Bigger Picture: The Oral Microbiome as a Cancer Target
The bioengineered gum research sits within a broader shift in oncology toward understanding the tumor microenvironment and the microbial communities that inhabit it.
For most of the history of cancer medicine, tumors were treated as isolated masses of mutant cells. Surgery removed them. Radiation killed them. Chemotherapy poisoned them. The ecosystem surrounding the tumor, including the bacteria, viruses, immune cells, and stromal tissue that interact with cancer cells, was largely ignored.
That has changed. Research over the past decade has established that the tumor microenvironment, including its microbial components, plays an active role in determining how aggressively a cancer grows, how it responds to treatment, and what the patient’s prognosis will be. The oral microbiome is not external to HNSCC. It is part of the disease.
This reframing opens a category of interventions that conventional oncology has not systematically explored: targeting the microbial drivers of cancer as a complement to targeting the cancer cells themselves. If Pg and Fn are active participants in tumor progression and poor survival, eliminating them is not a peripheral concern. It is a direct therapeutic strategy.
The Daniell lab’s bioengineered gum is the most accessible implementation of this strategy yet proposed for HNSCC. It is designed to be affordable, stable, easy to administer, and precise in its microbial targeting. Whether it fulfills that promise in clinical trials is a question for the next several years of research.
What the current study established is that the mechanism is real, the precision is real, and the magnitude of reduction in harmful microbes is large enough to be clinically meaningful if it holds in living patients.
Final thought
A piece of gum may not be a cancer drug, but it could become a low-cost, microbiome-precise tool in the cancer treatment toolkit.
A piece of gum may not be a cancer drug. But it may become something the cancer drug toolkit does not currently have: a low-cost, high-accessibility, microbiome-precise adjunct therapy that patients in every corner of the world can afford to chew.
References
Primary source:
Daniell H., Wakade G., Singh R., Nair S., Basak S.K., Srivatsan E.S., Bur A.M., Thomas S.M., Wang M.B. “Ex vivo HNSCC clinical studies using saliva and antiviral or antibacterial chewing gums reveal reduction in carcinogenic microbes.” Scientific Reports, February 9, 2026. DOI: 10.1038/s41598-026-39062-w
Supporting sources:
Liu Y.M. et al. “A carbohydrate-binding protein from the edible lablab beans effectively blocks the infections of influenza viruses and SARS-CoV-2.” Cell Reports, 2020. DOI: 10.1016/j.celrep.2020.108016
Daniell H. et al. “Debulking influenza and herpes simplex virus strains by a wide-spectrum anti-viral protein formulated in clinical-grade chewing gum.” Molecular Therapy, 2025. DOI: 10.1016/j.ymthe.2024.10.018
Zanoni D.K. et al. “Epidemiology, Risk Factors, and Prevention of Head and Neck Squamous Cell Carcinoma.” Medical Sciences, 2023. DOI: 10.3390/medsci11030042
Frontiers in Cellular and Infection Microbiology. “Implications of oral dysbiosis and HPV infection in head and neck cancer.” DOI: 10.3389/fcimb.2024.1329057
Penn Today, University of Pennsylvania. “Fighting oral cancer with bioengineered chewing gum.” April 2026. https://penntoday.upenn.edu/news/penn-dental-medicine-fighting-oral-cancer-bioengineered-chewing-gum
EurekAlert. “Fighting oral cancer with bioengineered chewing gum.” April 21, 2026. https://www.eurekalert.org/news-releases/1125336
This work was supported by NIH grant 5-R01-HL 107904-13 awarded to Henry Daniell, the Academic Senate Grant of the David Geffen School of Medicine at UCLA, and the National Cancer Institute Cancer Center Support Grant P30 CA168524.
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