The findings, published in Nature Communications, suggest that rectal mucus sampling is a minimally invasive, effective approach for detecting colorectal cancer and other bowel diseases.

Colorectal cancer involves genetic mutations, changes in chemical tags on the DNA molecule, and alterations in the gut microbiota. These factors can sometimes be detected in tumors, blood, or stool, but it’s unclear whether rectal mucus could serve as a reliable source of disease information.

Andrew Tock at Origin Sciences in Cambridge, United Kingdom, and his colleagues set out to test a device that collects rectal mucus to see if it could help detect colorectal cancer and precancerous lesions.

Combined approach

The researchers analyzed samples from 800 people suspected of colorectal cancer and found that genes such as APC, BRAF, and TP53 were most frequently mutated in those with cancer. The amount of detectable mutations was strongest in cancers located near the rectum, where the sample was collected, than in tumors farther away. 

Many colorectal cancer-related genes were located in DNA regions that had extra chemical tags called methyl groups, especially near key regulatory regions. This “hypermethylation” was most common in rectum cancers. 

The team also identified 36 bacterial species—particularly Hungatella hathewayi and Intestinimonas butyriciproducens—associated with colorectal cancer. Other bacteria, such as Porphyromonas asaccharolytica and Clostridium scindens, also showed associations with cancer. 

Cancer biomarker

Next, the researchers combined the three types of biological data—gene mutations, chemical tags on the DNA, and gut microbiota profiles—obtained from rectal mucus to create a “biomarker” of colorectal cancer. Key mutated genes, hypermethylated DNA regions, and certain bacteria such as Hungatella hathewayi could distinguish cancer cases from healthy controls. 

Precancerous lesions fell between controls and cancers, reflecting their potential to progress to malignancy, and rectal cancers were easier to detect than tumors farther away. 

Larger studies are needed to confirm how well this mucus-based method performs in real-world clinical settings, the authors say. However, they add, “we demonstrate the clinical utility of rectal mucus sampling combined with hologenomic analysis as a translatable prospective tool for diagnostic application.”

The findings, published in Cell Reports Medicine, suggest that disruptions in oral microbial balance may partly explain how poor oral health contributes to esophageal cancer.

Scientists have known that the oral microbiota may play a role in esophageal cancer, as imbalances can trigger inflammation and other changes that contribute to cancer. However, more human studies are needed to understand how oral microbes influence cancer risk.

To examine how oral health and the oral microbiota interact in cancer risk, researcher led by Peipei Gao at Fudan University in Shanghai, China, analyzed saliva samples from 206 people with newly diagnosed esophageal cancer and 206 healthy controls.

Poor oral health

The researchers found that poor oral health—such as losing teeth after age 20, having many missing or filled teeth, not using dentures, and brushing teeth infrequently—was linked to a higher risk of esophageal cancer. 

People with esophageal cancer had less diverse and less rich microbial communities in their mouths compared to healthy individuals. About 60 microbial species differed between the two groups, with harmful bacteria linked to gum disease, including Prevotella, Treponema, and Porphyromonas, being more common in people with esophageal cancer, while beneficial microbes such as Neisseria were reduced.

In people with esophageal cancer, the team also found changes in the metabolic activity of oral microbes, including altered amino acid, carbohydrate, and energy metabolism. 

Targeted interventions 

Some microbes, including Campylobacter rectus and Eubacterium brachy, could explain a significant portion of the link between poor oral health and esophageal cancer. Low levels of Streptococcus mitis, a common bacterium in the mouth, increased the risk of esophageal cancer in people with poor oral health, while higher levels appeared to mitigate it, the researchers also found. 

S. mitis produced short-chain fatty acids and other compounds that suppress harmful bacteria. The microbe also survives the acidic environment of the esophagus and stomach, where they may interact with tissues to influence cancer risk, the authors say.

The findings, they add, “highlight the promise of precision-targeted microbial interventions to improve oral health for [esophageal cancer] prevention and management.”

The findings, published in Immunity, suggest that diet and gut microbes can shape immune cell function and improve responses to anti-cancer therapy.

CD8+ T cells are key immune cells that help detect and kill cancer cells, but constant stimulation can cause “T cell exhaustion,” weakening their function. Scientists have known that certain bacteria and their metabolites can boost immunity and improve responses to anti-cancer therapy. 

However, how exactly these microbial signals influence CD8+ T cell activity in cancer remains unclear. Annabell Bachem at the University of Melbourne in Australia and her colleagues set out to investigate how the gut microbiota and its metabolites influence the ability of CD8+ T cells to fight melanoma.

Resisting exhaustion

SCFAs, which are produced by gut bacteria when digesting dietary fiber, were suspected to play a role in regulating CD8+ T cells. In mouse models of melanoma, the researchers found that higher SCFA production was associated with better tumor control. 

Feeding mice a high-fiber diet slowed tumor growth and increased gut bacteria capable of producing SCFAs, such as Akkermansia muciniphila and Bifidobacterium species. The diet also promoted a population of CD8+ T cells that resisted exhaustion and maintained strong anti-tumor activity.

When CD8+ T cells were treated with butyrate in lab dishes before being transferred into mice with melanoma, the cells survived for longer and killed cancer cells more efficiently than cells that were not treated with butyrate. 

Anti-tumor immunity 

The researchers also examined CD8+ T cells from people with melanoma who were undergoing immunotherapy. They found that microbiotas that were predicted to produce higher butyrate levels were linked to better responses to immunotherapy.

The results suggest that increasing butyrate production through dietary interventions can strengthen CD8+ T cells and improve anti-tumor immunity. However, more research is needed to investigate whether these findings can be translated into strategies for cancer treatment.

“Our study points to the preservation of stem-like tumor-specific CD8+ T cells as a critical factor in mediating the clinically highly relevant relationship between the microbiota and cancer immunity and underscores that the microbial context in which the activation of tumor-specific CD8+ T cells occurs has a profound influence on their subsequent functions,” the authors say.

Despite a significant decrease in cancer mortality, PC remains a therapeutic challenge for incidence and mortality. Indeed, early detection screenings are not available at the moment. On the other hand, differentially expressed gut microbes have been proposed as stool biomarkers. The results so far are, however, sparce and controversial. The aim of this study was to expand the current understanding of PC gut microbiota taking into account the population differences and to contribute to the development of an early screening method. Here the major findings.

Alpha diversity in PC gut microbiota

• Finnish and Iranian PDAC patients showed significantly lower alpha diversity than healthy controls. Indeed, Shannon entropy, Chao 1 index, and phylogenetic diversity were significantly reduced in PDAC patients.
• No significant impact of age, alcohol consumption, biliary stenting, neoadjuvant treatment, sex, or smoking on microbial diversity were found in the Finnish cohort. However, obese Finns had significantly lower species richness than normal weight individuals of the same group.
• Smoking and age significantly impacted alpha diversity in the Iranian cohort.
• Shannon entropy and Chao 1 index were significantly lower in smokers than nonsmokers.

Microbial community composition in PC patients and healthy controls

• 16,343 OTUs were identified and assigned to 15 phyla, 26 classes, 110 families, and 348 genera.
• The Finnish PDAC gut microbiota showed the following composition: 41% Firmicutes, 40% Bacteroidota, 8% Proteobacteria, 5% Verrucomicrobiota, 3% Actinobacteriota, 1% Fusobacteriota. There was a difference for the healthy Finnish with 50% Firmicutes, 34% Bacteroidota, 5% Proteobacteria, 4% Verrucomicrobiota, and Fusobacteriota, but higher Actinobacteriota.
• Iranian PDAC gut microbiota showed: 48% Firmicutes, 25% Bacteroidota, 15% Proteobacteria, 6% Actinobacteriota, 5% Verrucomicrobiota.
• Top ten genera in Finnish PDAC patients were: Bacteroides, Alistipes, Faecalibacterium, Akkermansia, Parabacteroides, Bifidobacterium, Escherichia-Shigella, Roseburia, Ruminococcus, and Subdoligranulum.
• Patients and controls within and between cohorts showed significant differences in microbial community composition.
• There were no significant differences between treated and untreated patients or those with and without biliary stents in the Finnish cohort.
• There were significant differences in the Iranian cohort between age groups, sexes, and smoking habits.

PC gut microbiota in the Finnish and Iranian cohorts

After a general comparison, the researchers compared the microbiota composition at phylum, family and genus level.

Phylum-level Differences

• PDAC patients in both Finnish and Iranian cohorts showed greater abundances of Fusobacteriota and Synergistota.
• Iranian PDAC patients had higher abundances of Verrucomicrobiota and Proteobacteria and a lower abundance of Elusimicrobiota while Finnish patients had a greater abundance of Campylobacterota than their respective healthy controls.

Family-level Differences

• 26 families differed between patients and controls in the Finnish cohort, 23 in the Iranian cohort.
• Families with higher abundance in PDAC patients included Entererococcaceae, Fusobacteriaceae, and Enterobacteriaceae.
• In detail, Finnish PDAC patients presented with higher abundances of Yersiniaceae, Hafniaceae, and Campylobacteraceae while Iranian PDAC patients showed higher levels of Lactobacillaceae, Akkermansiaceae, and Streptococcaceae compared with their respective healthy controls.

Genus-level Differences

• 78 taxa differentially abundant between patients and controls were detected in the Finnish, 67 in the Iranian cohort
• The most abundant genera in PDAC in both populations included Enterococcus, Sellimonas, Veillonella, Klebsiella, Hungatella, Eisenbergiella, Fusobacterium, Enterobacter, Flavonifractor, and Coprobacillus.
• Genera with lower abundance common to both populations were Asteroleplasma, Clostridia UCG-014, and Butyricicoccaceae UCG-009.

Overall, the two populations showed several differences. In particular:
• Iranian patients presented significantly greater abundances of Thermoplasmatota, Synergistota, Proteobacteria, Actinobacteriota, and Firmicutes then Finnish PDACs
• Finnish PDAC patients showed significant enrichment of the phyla Campylobacteriota, Cyanobacteria, and Bacteroidota.
• In terms of biomarkers, both populations of PDAC samples were enriched in Klebsiella and Hungatella and depleted of Agathobacter, Anaerostipes, and Clostridia. Finnish PDAC samples were enriched in Christensenellales, Rhodospirillales, Enterobacter, Enterococcus, Citrobacter, Campylobacter, and Oscillospira and depleted in Prevotella_9, Butyrivibrio, Butyricicoccus, Lachnospira, and Romboutsia. Iranian PDAC samples instead showed higher presence of Subdoligranulum, Streptococcus, Lactobacillus, Limosilactobacillus, Klauyvera, and Pantotea with a depletion of Faecalibacterium, Bifidobacterium, Dialister, Blautia, Roseburia, Parasutterella, and Ruminococcus.

Functions of PC gut microbes and pathway analysis

Applying KEGG term analysis, 6417 functions remained after filtering.

• Significant differences were observed between the Finnish and the Iranian PC patients in microbial functions.
• Only 40 of the 500 most distinctive predicted microbial functions overlapped between populations.
• Top four differing predicted functions in PDAC patients versus healthy controls – i.e. Clumping factor B, accessory secretory protein Asp3, and ATP-binding cassette subfamily C.
• The Finnish cohort showed high depletion of predicted functions including rsbT antagonist protein RsbS, serine/threonine-protein kinase RsbT, and rsbT coantagonist protein RsbR; membrane-bound hydrogenase subunit alpha in Iranian patients.
• Pathway analysis revealed enriched peptidoglycan biosynthesis, galactose metabolism, lysine biosynthesis, and furfural degradation pathways.

Statistical analyses and machine learning models were then applied to validate the predictions showing great results (AUC of 0.85 at phylum level).

To conclude, “We observed consistent trends in PC-related microbial diversity and community composition in our two populations—Finnish and Iranian—with profoundly different environments and lifestyles.” This suggests how the gut microbiota plays a crucial role in the development of PC, with increased pathogenic microbes and depletion of protective ones. This unique microbial profile could be used for noninvasive early PC screening, but further research is needed to explore integrating probiotics with conventional drugs.

The findings, published in Med, suggest that changes in gut microbes, especially Akkermansia, could predict treatment success in people with lung cancer.

Current treatments for non-small cell lung cancer combine chemoradiotherapy with consolidative immunotherapy, which boosts the immune system to attack cancer cells. However, treatment outcomes vary and are often accompanied by serious side effects, such as lung inflammation.

Akkermansia and other gut bacteria have been linked to how people respond to immunotherapy in advanced lung cancer, but it remained unclear whether changes during chemoradiotherapy and combined treatments could also affect outcomes. 

So, researchers led by Linfang Wu at the Chinese Academy of Medical Sciences and Peking Union Medical College in Beijing, China, analyzed the gut microbiota of dozens of people with advanced lung cancer undergoing chemoradiotherapy combined with immunotherapy.

Microbial diversity 

Cancer patients who survived longer without cancer progression had higher gut diversity—a measure of the number and variety of bacterial species. Those whose levels of Akkermansia increased during treatment were more likely to experience longer survival and better clinical outcomes.

Akkermansia is known to influence the immune system by helping activate specific immune cells that attack tumor cells. The micrboe can also interfere with metabolic pathways that cancer cells rely on for growth. 

People with severe treatment-related lung toxicity had less diverse gut microbiotas and higher levels of bacteria linked to infection and inflammation. In contrast, those with milder toxicity showed slight increases in Akkermansia and other beneficial bacteria, the researchers found.

Predicting survival 

Akkermansia bacteria were not only more abundant in people with longer survival but also interacted more actively with other gut bacteria, forming complex microbial networks. This suggests that the structure of the gut microbiota is as important as its diversity. 

For example, people whose gut bacteria were more interconnected showed better progression-free survival, even when microbial diversity decreased during treatment. The findings indicate that the gut microbiota adapts during therapy and that these adaptations may influence how the body responds to anti-cancer therapy, the researchers say.“[Akkermansia], a symbiotic gut bacterium and promising probiotic, may be a potential biomarker to predict the survival of patients with lung cancer undergoing [chemoradiotherapy] and [immune checkpoint inhibitors] therapy,” they say.

The findings, published in Cancer Cell, suggest that targeting gut bacteria or butyrate could be a promising therapy for glioma.

Previous studies have shown that gut bacteria can influence tumor growth through compounds such as short-chain fatty acids (SCFAs), which affect brain immune cells. But it’s unclear which gut bacteria and metabolites influence glioma growth, how they affect brain immune cells, and whether targeting them could help treat the disease.

Researchers led by Ming-Liang Chen at the Institute of Pathology and Southwest Cancer Centre in Chongqing, China, investigated how the gut microbiota and its metabolites might influence glioma progression, and whether a high-fat, low-carbohydrate diet, known as a ketogenic diet, could have anti-tumor effects.

Tumor-inhibiting state

Compared to healthy individuals, people with glioma had fewer bacteria that produce SCFAs, especially Roseburia faecis, which declined further as tumors became more aggressive. This decrease was linked to lower levels of the SCFA butyrate in both stool and blood. Glioma patients with higher levels of R. faecis and butyrate also tended to live longer, the researchers found.

In mouse models of glioma, disrupting gut bacteria with antibiotics or raising mice without microbes made brain tumors grow faster and reduced the animals’ survival. When gut bacteria from healthy people were transplanted into mice with glioma, or when R. faecis was given to them, tumor growth slowed, and survival improved. 

Further experiments revealed that R. faecis produces butyrate, which influences brain immune cells called microglia, shifting them to a tumor-inhibiting state.

Glioma therapy

Feeding mice a ketogenic diet also slowed glioma growth, the team found. These benefits were linked to changes in gut bacteria, including increased levels of Akkermansia muciniphila and Ruminococcus faecis. Removing gut bacteria reduced the benefits of the ketogenic diet, while giving mice butyrate or butyrate-producing bacteria restored them. 

The ketogenic diet raised butyrate levels in the gut, blood, and tumors, and this effect depended on a gut protein called MUCIN-2. Removing MUCIN-2 reduced butyrate levels and the diet’s benefits, the researchers found.

Although more research is needed to determine if these findings apply to humans, the authors say, “our results open a new avenue of research regarding the mechanism of the gut microbiota and [ketogenic diet]-mediated protective effect against glioma, indicating that targeting the gut microbiota especially by [ketogenic diet] or supplementing with [butyrate] could serve as a potentially effective strategy for glioma therapy.”

The findings, published in Cell Reports Medicine, suggest that targeting the intratumoral microbiota could become a new strategy to boost cancer immunotherapy.

Scientists have known that both gut and tumor-residing bacteria can influence treatment success, with recent studies suggesting that probiotics or microbiota-based interventions increase ICI effectiveness. However, more research is needed to fully understand these effects.

Researchers led by Junhong Chen at Central South University in Changsha, China, profiled the intratumoral microbiota and its relationship with treatment response in people with cancer who were receiving ICIs.

Microbial ‘modules’

The team collected data from six cancer types, including melanoma, lung, and gastric cancers, and used a computational approach to separate microbial from human genetic material. 

Certain groups of bacteria, such as Proteobacteria, Actinobacteria, Firmicutes, and Bacteroidetes, dominated the tumor microbiota, but the composition varied by cancer type and even between people with the same type of cancer. In melanoma, the microbial profiles of people who responded to ICIs were different from those of people who didn’t, the researchers found.

By organizing microbes into “modules” based on how they co-occur, the team found that certain modules in melanoma and gastric cancer were associated with better treatment responses and longer survival, while a module in esophageal cancer was linked to poorer outcomes. Within these modules, specific bacterial species—including Burkholderia, Sphingomonas, and Ligilactobacillus—were associated with these effects as well as with key signals linked to antitumor immunity.

Combination therapy

A computational analysis of the data identified three promising bacteria—Burkholderia cepacia, Paenibacillus megaterium, and Corynebacterium kroppenstedtii—that were linked to better treatment responses in melanoma patients.

Experiments in mice then showed that injecting these bacteria into tumors boosted the effectiveness of ICI therapy by stimulating the activity of certain immune cells. The treatment was safe and had no harmful effects on the animals. Similar beneficial effects were seen in mice engineered to have a human-like immune system, confirming that these bacteria can improve ICI therapy by activating antitumor immunity. 

“Our findings highlight the essential role of the intratumoral microbiome in the clinical effectiveness differences of ICIs, suggesting its potential in future ICIs combination therapy,” the authors say.

The findings, published in Cell, suggest that the gut microbiota plays a key role in the cancer-fighting benefits of exercise, highlighting formate as a potential target to boost cancer treatment.

Previous studies have found that exercise changes the gut microbiota, and other factors such as diet, probiotics, and antibiotics also affect cancer risk by altering gut bacteria. However, it’s unclear whether the way exercise changes the microbiota directly contributes to its cancer-fighting effects.

Catherine Phelps at the University of Pittsburgh School of Medicine in Pennsylvania and her colleagues investigated how exercise influences cancer by analyzing changes in the mice gut microbiota and their effect on antitumor immunity.

Exercise benefits

The researchers created a controlled treadmill exercise routine and then tested how well this exercise program helped fight melanoma tumors in healthy mice that were kept in a clean environment free from certain pathogens. They found that regular exercise reduced tumor growth and helped mice live longer. 

Exercise boosted the activity of specific immune cells called CD8 T cells, which attack tumors, but didn’t increase the number of these cells overall. Exercise also changed the types of bacteria present in the animals’ guts. 

When gut bacteria from mice that exercised were transferred to other mice, those animals also showed slower tumor growth and stronger immune responses. But when gut bacteria were removed with antibiotics, exercise no longer helped control tumor growth. The team also found that certain microbial metabolites, in particular a molecule called formate, was increased by exercise. Higher formate levels were linked to stronger immune responses against the tumor and slower tumor growth. 

Promising target

Giving mice formate helped slow tumor growth and boosted the immune system’s ability to fight cancer. This compound activates a key immune pathway in CD8 T cells, boosting their ability to fight tumors, the researchers found. 

By analyzing data from multiple studies in humans, the team also identified specific bacterial groups that increase formate production in people who respond well to anti-cancer treatment, similar to changes seen in mice that exercised. When gut bacteria from human donors with high formate levels were transferred to mice, those mice showed stronger immune responses and better tumor suppression compared to mice receiving gut bacteria from human donors with low formate levels. 

“Our findings […] identify formate as a promising metabolic target for improving cancer immunotherapy,” the authors say. The work, the add, could inform the development of therapeutic approaches that combine exercise and microbial metabolites to evaluate the antitumor efficacy of formate and similar molecules in people with cancer.

The findings, published in Cell Reports, suggest that gut microbes can be targeted to improve brain tumor treatment. 

Glioblastoma is difficult to treat because it doesn’t attract enough T cells that can kill the tumor, and many of these cells get stuck in the bone marrow instead of reaching the brain. Gut bacteria are known to influence cancer treatment in other parts of the body, but their role in brain tumors is not well understood.

Researchers led by Hyeon Cheol Kim at the Korea Advanced Institute of Science and Technology in Daejeon, Republic of Korea, explored how gut bacteria and the amino acid tryptophan affect the immune system’s ability to fight brain tumors such as glioblastoma.

Improved survival

In mice with glioblastoma, the gut microbiota composition changed as the tumor progressed, showing fewer beneficial bacteria and more harmful ones. Mice with normal gut bacteria lived longer than those without, and only gut bacteria from healthy, tumor-free mice improved survival when transplanted into other mice. 

The researchers also found that the levels of tryptophan dropped during tumor growth. Feeding tryptophan to mice restored a healthy gut microbiota, boosted the animals’ immune response, reduced tumor size, and improved survival. 

Tryptophan improved survival by increasing the activity of CD8 T cells, which can kill tumor cells. The improved survival disappeared when these T cells were removed, the researchers found. 

Boosting treatment 

Tryptophan also helped T cells move more freely through the body, preventing them from getting trapped in the bone marrow. However, germ-free mice didn’t improve with tryptophan alone but did when they received gut bacteria from tryptophan-treated mice. 

A specific microbe, Duncaniella dubosii, was especially important, as its levels dropped during tumor growth but increased with tryptophan supplementation. Combining tryptophan and D. dubosii with immunotherapy further boosted survival. 
The findings suggest that maintaining a healthy gut microbiota, through diet or dietary supplements, may support brain cancer treatment, the authors say. What’s more, they add, “the investigated dietary intervention and the utilization of D. dubosii in this study offer potential considerations for the treatment of brain tumor patients or lifestyle modifications.”

The findings, published in mBio, suggest that targeting the gut microbiota could help predict, prevent or reduce chemotherapy-related toxicity.

Capecitabine (CAP) is a common chemotherapy drug used to treat colorectal cancer. In the body, CAP is converted to a cancer-fighting compound called 5-fluorouracil, which works by stopping cancer cells from making DNA and RNA. However, only about 40% of people who take CAP see good results, and up to 57% have to reduce or stop treatment due to side effects. 

Studies in mice have shown that gut bacteria can affect CAP’s efficacy and its side effects, so Lars Hillege at Maastricht University in the Netherland and his colleagues set out to investigate how gut bacteria influence the effects of CAP in 56 people with colorectal cancer.

Protective effect

The researchers found that, after three treatment cycles, certain bacterial species—including Clostridiales—increased, while others such as Actinomycetaceae decreased. More than 250 biological pathways were altered, especially those related to the production of menaquinol, a form of vitamin K2 produced by Escherichia bacteria. 

Further analyses showed that certain gut bacteria can protect themselves from the harmful side effects of chemotherapy drugs by producing vitamin K2. People with higher levels of vitamin K2-producing bacteria in their gut microbiotas were less likely to experience nerve pain—a common chemotherapy side effect, when compared to those with lower levels of these bacteria. 

Lab and animal tests confirmed that vitamin K2 could reduce nerve damage caused by chemotherapy without causing other toxic effects. These results suggest that gut bacteria, as well as the compounds they produce, may play a protective role during cancer treatment, the researchers say.

Treatment results

By focusing on specific microbial genes, the team trained machine-learning models to predict which patients were more likely to experience toxic effects and thus needed dose adjustments. 

The models showed moderate accuracy when tested on a group of people with colorectal cancer. Certain gut bacterial genes were linked to fewer dose adjustments and lower risk of side effects, while lower levels of vitamin K2-producing bacteria were associated with a higher risk of nerve pain, the researchers found.

“These results suggest that treatment-associated increases in bacterial vitamin production protect both bacteria and host cells from drug toxicity,” the authors say. This finding, they add, opens chances for new treatments and highlights the importance of understanding how diet and gut bacteria’s production of nutrients such as vitamin K2 affect cancer treatment.