Published online Oct 24, 2025. doi: 10.5306/wjco.v16.i10.107877
Revised: May 29, 2025
Accepted: September 22, 2025
Published online: October 24, 2025
Processing time: 208 Days and 8.9 Hours
Gastrointestinal malignancies, particularly pancreatobiliary and gastroesophageal cancers, are associated with poor prognosis due to their frequent late-stage dia
Core Tip: Gastrointestinal malignancies, more specifically pancreatobiliary and gastroesophageal cancers, harbor a bad prognosis mainly because tumors are frequently diagnosed in an advanced stage. Most of the tumors of the digestive tract associate anorexia-cachexia syndrome as well as malnutrition. Inflammation is a key feature of neoplasic proliferation and gut microbiome may have an interplay in inflammation and outcomes of these patients. In this article, we want to address this association and the impact of nutritional strategies in patients with gastrointestinal malignancies.
- Citation: Pacheco-Barcia V, Mariño-Mendez A, Hernandez-Jimenez E, Jimenez-Fonseca P, Muñoz Martín AJ, Custodio-Cabello S, Palka-Kotlowska M, Gonzalez-Diaz I, Cabezon-Gutierrez L. Gut microbiome and nutritional strategies in gastrointestinal cancers: Clinical implications and therapeutic perspectives. World J Clin Oncol 2025; 16(10): 107877
- URL: https://www.wjgnet.com/2218-4333/full/v16/i10/107877.htm
- DOI: https://dx.doi.org/10.5306/wjco.v16.i10.107877
Cancer is considered as a main leading cause of death worldwide[1]. The International Agency for Research on Cancer reported an estimated 20 million new cancer cases and 9.7 million cancer deaths in 2022[2]. The hallmarks of cancer were early described to include fourteen biological capabilities which have essential roles in contributing to tumor complexity[3]. Among these are deregulating cellular metabolism, genome instability, tumor-promoting inflammation, and polymorphic microbiomes, which underscore the growing importance of the gut microbiome and inflammation in tumorigenesis.
In the late 19th century, German pathologist Rudolf Virchow proposed that cancer could arise as a consequence of chronic inflammation triggered by persistent exposure to harmful toxic agents, including infections[4]. Around the same time, pioneering research by Robert Koch and Louis Pasteur led to the identification of bacteria within tumor tissues, suggesting a potential link between bacterial infections and cancer development[4]. The term “human microbiome” refers to the diverse community of microorganisms residing within the human body, along with their collective genetic material[5,6].
There is a growing recognition that the complex ecosystems formed by resident bacteria and fungi - the microbiomes - play a crucial role in both health and disease[7]. This understanding has been significantly advanced by the development of next-generation sequencing and bioinformatics, enabling a detailed characterization of microbial populations. In the context of cancer, mounting evidence suggests that inter-individual variability in microbiome composition can profoundly influence cancer phenotypes[8,9]. Currently, approximately 20% of malignancies worldwide are linked to infections[10], accounting for an estimated 1.2 million cases annually[11]. Research into the microbiome, particularly the role of bacteria in cancer pathogenesis, is evolving rapidly, with more than about 100 trillion bacterial cells representing about 10000 species across the human population identified within the human body to date[12,13].
The microbiome has been implicated in tumor development and progression through various mechanisms, including DNA damage, activation of oncogenic pathways and epithelial cell proliferation[14,15], production of carcinogenic metabolites[16], induction of chronic inflammation[17,18], and suppression of antitumor immunity[14,16]. These insights have expanded the understanding of the intricate interactions between the tumor microenvironment and systemic microbial-immune networks, suggesting a broader and more complex influence than previously recognized[19].
Notably, microbial dysbiosis, an imbalance in microbial composition that disrupts host homeostasis, has been shown to significantly affect therapeutic responses to anticancer treatments[20,21]. This is largely attributed to the microbiome’s capacity to metabolize drugs, modulate inflammation, and influence immune responses within the tumor microenvironment, all of which play a crucial role in treatment efficacy and drug toxicity[22]. The relationship between the microbiome and anticancer therapy responses has been described as bidirectional, with both factors exerting significant effects on each other[20,23]. This has led to the emergence of “pharmacomicrobiomics”, a field dedicated to studying the interaction between drugs and microbial communities[20]. In this context, the role of probiotics and antibiotics, whether used alone or in combination with anticancer agents, is being explored as a strategy to manipulate the microbiome and potentially improve cancer prevention and treatment outcomes[20,24].
Increasing evidence supports the role of bacterial infections in the pathogenesis and progression of various gastrointestinal (GI) malignancies[25,26]. Additionally, substantial data indicate that the microbiome influences tumor responses to anticancer therapies, including conventional chemotherapy and targeted treatments[20,27]. Consequently, the bacterial microbiome represents a promising therapeutic target for the prevention and treatment of GI cancers. Moreover, dietary patterns play a significant role in shaping gut microbiome composition, serving as a key factor in cancer development[28].
This article explores the current understanding of the intricate relationship between the bacterial microbiome and inflammation in GI malignancies. Particular emphasis is placed on its potential as a therapeutic target, with a specific focus on nutritional interventions as a modifiable factor in disease management.
The majority of microorganisms comprising the human microbiome are commensal. The highest microbial diversity is observed in the GI tract, particularly in the cecum and proximal colon. This diversity is shaped by multiple factors, including mode of delivery at birth, infant feeding practices, dietary patterns, lifestyle factors, and host genetics[29]. However, substantial evidence has definitively shown that gut microbiome plays a role in the development of various medical conditions, including inflammatory, hepatic, pancreatic, and respiratory diseases, as well as neurological and dermatological disorders, and cancer[30]. Figure 1 summarizes the most common bacterial species associated with cancers affecting GI tract.
Cancer and the immune system are closely interconnected. Similarly, a robust interaction between gut microbiome and both innate and adaptive immunity has been well-documented. The interplay between bacteria, viruses, parasites, fungi, and mucosal immune cells is regulated by a complex network of cytokines[31].
Germ-free mouse models have demonstrated the critical role of gut microbiome in the development and regulation of various organs and systems, including the immune and endocrine systems, blood, liver, and lungs[32]. Within the intestine, the microbiome maintains epithelial homeostasis and supports the formation of gut-associated lymphoid tissue. Additionally, it promotes the production of epithelial cytokines, which in turn regulate the activity of T and B lymphocytes, macrophages, and polymorphonuclear cells[33,34]. Cytokines like interleukin (IL)-1β, tumor necrosis factor (TNF) α, IL-2, IL-6, IL-15, IL-21, and IL-23 can trigger an inflammatory response, whereas IL-10 and TGF-β exhibit anti-inflammatory properties. The balance between these pro-inflammatory and anti-inflammatory cytokines determines the gut’s inflammatory or homeostatic state[35].
Helicobater pylori (H. pylori) colonization induces chronic inflammation by overexpressing pro-inflammatory cytokines like IL-1β, IL-8, IL-17, and TNF-α, which increases the risk of gastric cancer (GC)[36]. In patients with gastric adenocarcinoma, higher abundances of Lactobacillus, Bifidobacterium, Lactococcus, and Streptococcus have been observed[37]. Lactic acid bacteria (LAB) contribute to DNA damage by producing reactive oxygen species (ROS) and reducing nitrates to nitrites, which drive mutagenesis, proto-oncogene overexpression, angiogenesis, and inhibit apoptosis[37]. LAB also plays a key role in epithelial-mesenchymal transition[38]. Escherichia coli (E. coli) produces colibactin, a compound involved in colorectal carcinoma development[39]. Additionally, Fusobacterium nucleatum (F. nucleatum), E. coli NC101, and Bacteroides fragilis promote colorectal cancer (CRC) by activating the Wnt-β-catenin signaling pathway[40]. Increased abundances of genera like Bacteroides fragilis, Campylobacter, Enterococcus, F. nucleatum, Streptococcus, Prevotella, and Peptostreptococcus, and decreased abundances of Bifidobacterium, Clostridium spp., Lactobacillus, Ruminococcus, and Roseburia have been noted in CRC patients[41].
Pathogen-associated molecular patterns are recognized by pattern recognition receptors, such as toll-like receptors (TLRs) on macrophages and dendritic cells. TLRs initiate immune responses by activating signaling cascades, including the nuclear factor kappa B (NF-κB), mitogen-activated protein kinase (MAPK), and interferon regulatory factor pathways[42]. For instance, TLR3 and TLR4 engage interferon regulatory factor to induce interferon-beta, while others signal through the myeloid differentiation primary response 88 (MyD88)-interleukin-1 receptor-associated kinase axis, triggering MAPK like p38 and c-Jun N-terminal kinase (JNK) that culminate in the transcription of pro-inflammatory genes[42]. Although TLR-mediated signaling is vital for maintaining epithelial integrity and immune homeostasis, aberrant activation can contribute to tumorigenesis[43-47]. Overexpression of TLRs has been observed in various cancers, and studies in MyD88-deficient mice demonstrate reduced tumor development[48], underscoring the oncogenic potential of dysregulated TLR signaling. Additionally, JNK activation downstream of TLRs may intersect with Ras pathways, promoting apoptosis resistance and increased matrix metalloproteinase expression-hallmarks of cancer progression[17,47,49,50].
The connection between TLR signaling, JNK activation, and Ras-driven oncogenesis in CRC is largely based on in vitro evidence using human colon epithelial cell lines. Several studies have shown that activation of TLR4 by bacterial ligands can stimulate the JNK cascade and downstream Ras signaling, resulting in increased expression of pro-survival and proliferative genes[51,52]. However, the relevance of this pathway in vivo remains speculative. Animal models have yielded inconsistent results, with some indicating tumor-promoting effects of TLR overactivation, while others report context-dependent roles for JNK that may be either oncogenic or tumor suppressive depending on isoform specificity and the inflammatory milieu[53,54]. Additionally, the crosstalk between TLR/JNK/Ras pathways and host immune responses, microbiota composition, and epithelial integrity is complex and not yet fully characterized in preclinical systems. Thus, while in vitro data support mechanistic hypotheses, further in vivo studies are required to clarify the functional significance of this signaling axis in colorectal tumorigenesis.
CD8+ cytotoxic T-lymphocytes (CTLs) are crucial for anti-cancer immunity, as they kill malignant cells upon recognizing antigenic peptides[35]. Tumor-specific CTL responses are supported by tumor-associated antigens and the presence of tumor-associated antigen-specific CD8+ T-cells in regressing tumors. In CRC, tumor-infiltrating lymphocytes are primarily CD4+ T cells, producing pro-inflammatory cytokines like induce interferon-γ and IL-17, whereas subsets producing IL-4 may promote oncogenesis[55]. Additionally, natural killer cells at tumor sites in long-surviving patients trigger tumor apoptosis and inhibit proliferation[56].
Cancer cells induce an immunosuppressive microenvironment by producing factors like TGF-β and recruiting regulatory immune cells, such as T-regs, which are inversely correlated with tumor prognosis[57]. T-regs suppress tumor-specific T-lymphocytes by producing IL-10 and TGF-β, consuming IL-2, or expressing CTL-associated protein 4 (CTLA-4). They also inhibit pro-inflammatory CD4+ T-helper (Th) cells and stimulate B cells to produce immunoglobulins. Th17 cells, involved in carcinogenesis by promoting cell proliferation and inhibiting apoptosis, produce cytokines like IL-17 and IL-23, contributing to tumor growth[58-62]. Th17 cells also promote the production of Th1-related cytokines, such as C-X-C motif chemokine ligand (CXCL) 9 and CXCL10, at the tumor site. T-cell exhaustion, a phenomenon where persistent tumor antigen stimulation impairs T-cell function, is a primary mechanism of immune escape, allowing tumors to continue growing despite initial immune responses[63-65]. Figure 2 summarizes how the microbiome promotes carcinogenesis through various mechanisms.
In a healthy state, there is a harmonious balance between the gut microbiome and the immune system at the gut interface[66]. Disruption of this balance leads to a pathological condition called “gut dysbiosis”, which fosters the overgrowth of pathogenic bacteria in the intestinal lumen. Dysbiosis can arise from an inflammatory state: In genetically predisposed individuals, factors such as dietary compounds, toxins, and antibiotics can trigger low-grade inflammation, promoting dysbiosis. For instance, high-calorie and high-fat diets common in Western societies have been linked to worsened gut inflammation in patients with inflammatory bowel disease (IBD)[67]. The following sections will develop and analyze the relationship between various treatments for GI tumors and the nutritional strategies that may influence the microbiome and inflammation.
While growing evidence implicates the gut microbiome in the initiation and progression of cancer through mechanisms such as chronic inflammation, genotoxin production, and immune modulation, this pathogenic potential also opens the door to therapeutic opportunities. Among the most accessible and modifiable factors influencing the gut microbiota is diet. The next section explores how targeted nutritional interventions - particularly those involving dietary fiber and microbiota-accessible carbohydrates - can reshape the gut microbial landscape to potentially prevent carcinogenesis and enhance treatment responses.
Probiotics, defined as live microorganisms that, when consumed in sufficient amounts, confer health advantages to the host, have gained attention for their potential role in CRC prevention and treatment. Their beneficial effects are primarily attributed to three mechanisms: Suppression of pathogenic bacterial colonization, modulation of gut immune responses, and reinforcement of intestinal barrier function[68]. The antimicrobial properties of probiotics against pathogenic bacteria have been well-documented. For example, Bacillus species were shown to prevent intestinal colonization by Staphylococcus aureus by disrupting its quorum sensing communication system[69]. Similarly, Clostridium butyricum suppressed biofilm formation by enterotoxigenic Bacteroides fragilis by regulating key virulence and efflux pump-related genes[70]. Certain Lactobacillus strains have also exhibited protective effects by preventing bacterial adhesion. Lactobacillus fermentum 88 and Lactobacillus plantarum 9 demonstrated strong adherence to human enteric cell line HT29 while simultaneously inhibiting E. coli attachment[71]. Furthermore, pre-administration of Lactobacillus rhamnosus GG in a mouse model of periodontitis provided protection against F. nucleatum and Porphyromonas gingivalis-induced cecal dysbiosis, significantly mitigating intestinal inflammation[72].
Probiotics are recognized for their immunomodulatory functions in the gut, where they play a crucial role in mitigating colonic inflammation. In an azoxymethane and dextran sulfate sodium-induced CRC murine model, Lactobacillus species were found to suppress Wnt/β-catenin signaling, leading to reduced inflammation and tumor growth[73]. Additionally, a specific strain of Lactobacillus rhamnosus demonstrated anti-tumor properties by reducing inflammatory responses and promoting apoptosis, ultimately decreasing tumor incidence[74]. In genetic models of CRC, probiotics have exhibited protective effects. In the APC Min/+ mouse model of colon cancer, Lactobacillus plantarum strain YYC-3 was shown to inhibit tumor formation, likely by downregulating inflammatory cytokine production and limiting inflammatory cell infiltration[75]. Furthermore, the administration of a probiotic mixture containing Lactobacillus acidophilus, L. rhamnosus, and Bifidobacterium bifidum significantly reduced colitis and resulted in a 40% decrease in tumor development compared to the control group[76].
Disruptions in tight junction proteins - such as occludin, claudins, junctional adhesion molecules, and zona occludens (ZO) - can lead to increased intestinal permeability, fostering chronic inflammation and heightening the risk of IBD-associated CRC[77]. Probiotics have been shown to enhance gut barrier integrity, providing a potential preventive mechanism. Notably, E. coli nissle 1917 improved intestinal barrier function by upregulating and redistributing tight junction proteins, including ZO-1, ZO-2, and claudin-14[78]. The beneficial effects of probiotics on gut barrier integrity have also been observed in colitis models. A probiotic formulation containing Bifidobacterium, L. acidophilus, and Enterococcus ameliorated colitis in mice by upregulating occludin and claudin-4 expression[79]. Additionally, in a 1,2-dimethylhydrazine dihydrochloride-induced CRC mouse model, supplementation with L. acidophilus, B. bifidum, and Bifidobacterium infantum strengthened gut mucosal barrier integrity through TLR2 signaling, which was associated with a lower incidence of tumor formation[80].
While some strains of LAB have been reported to generate ROS or contribute to nitrate metabolism under specific conditions, it is important to recognize that most probiotic formulations - particularly those used in clinical and nutritional contexts - employ LAB for their protective effects[81]. For instance, some studies[82-84], highlight the role of LAB in safeguarding the gastric mucosa, modulating inflammation, and attenuating the toxicity of chemotherapy agents. Thus, while emerging data suggest that certain LAB strains may possess pro-carcinogenic potential under select circumstances, the broader evidence base supports their beneficial role in GI health and cancer therapy support. A nuanced interpretation is warranted to avoid overgeneralizing LAB as solely pro-carcinogenic.
Prebiotics, such as inulin, fructo-oligosaccharides (FOS), and galactooligosaccharides are non-digestible carbohydrates that selectively stimulate the proliferation of beneficial anaerobic bacteria within the colon. These fibers bypass digestion in the small intestine and undergo fermentation by colonic microbiome, promoting the growth of beneficial bacterial genera, particularly Bifidobacterium spp.[85]. Elevated levels of Bifidobacterium spp. have been associated with a reduced incidence and progression of tumors[86]. Additionally, inulin and its oligofructose derivatives - characterized by a degree of polymerization ≤ 10 - were observed to decrease the formation of aberrant crypt foci in chemically induced colon carcinogenesis models in mice[87]. Research by Taper et al[88-90] explored the impact of dietary supplementation with 15% inulin or oligofructose on chemotherapy efficacy in experimental animals. Findings demonstrated that these prebiotics significantly enhanced the therapeutic efficacy of six commonly used chemotherapeutic agents, including 5-fluorouracil (5-FU) doxorubicin, vincristine, cyclophosphamide, methotrexate, and cytarabine[90].
Consistent with prior investigations from the same research group, inulin notably amplified the therapeutic response to cyclophosphamide by 47%[88]. Moreover, no detrimental interactions or adverse effects were observed when inulin or oligofructose was administered as an adjuvant therapy, highlighting their potential role in optimizing cancer treatment outcomes[90]. A randomized, double-blind, placebo-controlled trial evaluated the effects of a fiber blend (50% inulin and 50% FOS) on gut microbiome in gynecological cancer patients undergoing radiotherapy[91]. Patients receiving the prebiotic mixture exhibited a quicker restoration of Lactobacillus spp. and Bifidobacterium spp. populations within two weeks after radiotherapy, leading to improved stool consistency compared to the placebo group[91,92]. Diarrhea is a frequent side effect of enteral nutrition, often delaying recovery and prolonging hospital stays, particularly in postoperative GC patients. A study of 120 GC patients, divided into three groups (fiber-free nutrition, fiber-enriched nutrition, and fiber- and probiotic-enriched nutrition), found that hospital stays were shorter in the fiber-supplemented groups, with a significant reduction in diarrhea occurrence compared to the fiber-free group[93].
Recently, a phase II randomized controlled trial was initiated to explore the interactions between gut microbiome and prebiotics in patients with localized anal canal squamous cell carcinoma receiving radiotherapy, aiming to assess their impact on treatment outcomes[94]. Another randomized, double-blind clinical trial examined the effects of prebiotics (FOS, xylooligosaccharides, polydextrose, and resistant dextrin) on gut microbiome and immune function in 140 perioperative CRC patients[95]. In the preoperative phase, prebiotic consumption led to increased levels of Bifidobacterium and Enterococcus, along with a decrease in Bacteroides abundance compared to placebo[95]. Postoperatively, the control group exhibited a rise in Enterococcus, Bacillus, Lactococcus, and Streptococcus, whereas the prebiotic group experienced an increase in non-pathogenic Escherichia-Shigella. Additionally, microbial richness declined from pre- to post-surgery in patients who did not receive prebiotics[95].
Beyond microbiome modulation, prebiotics significantly influenced immune function. In the preoperative phase, serum levels of immunoglobulin (Ig) G, IgM, and transferrin were elevated, while in the postoperative phase, levels of IgG, IgA, suppressor/cytotoxic T cells (CD3+ CD8+), and total B lymphocytes increased compared to controls[95]. Rowland et al[87] examined changes in biological markers following three months of daily FOS supplementation (10 g) in 74 French patients, grouped into those with small colorectal adenomas, large adenomas, or no adenomas. Patients with adenomas exhibited significantly higher butyrate levels after FOS intake, while in patients without adenomas, FOS consumption led to increased levels of cholic acid, chenodeoxycholic acid, total primary bile acids, and ursodeoxycholic acid, as well as decreased fecal lithocholic acid, highlighting its potential role in modulating the colonic environment[96].
Inulin supplementation has been shown to enhance the growth of Bifidobacterium spp. and Akkermansia muciniphila[97,98]. An in vitro study demonstrated that culturing fecal samples with inulin and mucin increased the abundance of microbial species involved in suppressing tumor growth in Rnf5-/- mice[99]. Another study found that inulin consumption supports the enrichment of bacterial taxa associated with anti-tumor immune responses[89]. Remarkably, dietary supplementation with inulin or mucin in C57BL/6 mice triggered anti-tumor immunity, yet mucin alone failed to curb tumor growth in germ-free mice, emphasizing the essential role of gut microbiome in tumor-related immune activation[99]. Preclinical studies suggest that inulin may suppress tumor progression in colon cancer and NRAS-mutant melanoma models. Additionally, it has been found to enhance the effectiveness of mitogen-activated protein kinase inhibitors targeting the MAPK/extracellular signal-regulated kinase pathway, which is frequently dysregulated in melanoma[99]. These findings indicate that dietary interventions using inulin or oligofructose could enhance che
The ketogenic diet (KD) is a high-fat, isocaloric diet that significantly reduces carbohydrate intake, originally designed for the treatment of epilepsy and glucose transporter type 1 deficiency syndrome deficiency syndrome[101]. As a therapeutic approach, KD aims to trigger ketosis, and it has recently emerged as a potential strategy for cancer treatment[102]. Vander Heiden et al[103] found that tumor cells consume glucose at higher rates than surrounding tissue and rely on the aerobic glycolytic pathway to produce lactate. By limiting glucose availability, KD could deprive tumor cells of their primary energy source, potentially inhibiting tumor growth and proliferation. In vitro and in vivo animal models have shown that KD suppresses glycolysis and cancer cell proliferation, leading to promising anti-tumor effects[104,105]. However, the specific role of the gut microbiome in mediating these anti-tumor effects in cancer therapy remains unclear. The influence of the microbiome in such effects has been explored in other conditions like autism and epilepsy[106,107]. For example, in mice with autism spectrum disorder, KD was shown to normalize high levels of Akkermansia muciniphila and promote a higher Firmicutes/Bacteroidetes ratio[107]. In infants with refractory epilepsy, KD not only reduced seizure frequency but also increased the levels of Bacteroides and Prevotella, while decreasing Cronobacter abundance[106]. Although similar microbiome shifts could be beneficial for cancer patients undergoing treatment, this remains an area for further investigation.
Dietary strategies include: (1) Caloric restriction (CR), which entails a reduction in energy intake by 20%-50% without causing malnutrition or depleting essential nutrients; (2) Time-restricted feeding, where eating is confined to a specific 4- to 12-hour window; (3) Intermittent fasting, which alternates between 24-hour fasting periods and 24-hour ad libitum eating phases; and (4) The fasting-mimicking diet, a five-day period of CR with a low-calorie, vegetable-based diet, followed by a return to regular eating patterns once a month[108]. In recent years, there has been a growing body of research exploring the potential of these dietary approaches to delay the onset and progression of cancer, as well as other chronic diseases[109,110]. A key factor in how dietary restrictions may positively impact metabolism and immune function is the gut microbiome. As previously discussed, the microbiome plays an important role in cancer development and therapy response by influencing gut homeostasis, which in turn affects both the gut barrier and immune system. Therefore, dietary restrictions may help restore gut dysbiosis, improving metabolism and immune responses. Specifically, disruptions in gut permeability and the translocation of bacteria to the mucosal layer can trigger immune dysfunction. Immune homeostasis in the intestines is largely regulated by interactions between epithelial cells and dendritic cells[111]. Thus, by modulating the microbiome, these dietary changes could enhance cancer treatment outcomes. However, reliable data confirming these effects are still lacking. Moreover, it is important to note that interventions like fasting may worsen cachexia syndrome, which impacts nearly half of all cancer patients[112]. Future research should focus on determining the most effective timing and approach for these dietary interventions, considering factors such as gut microbiome composition, cancer type, and the individual characteristics of patients.
Dietary fiber serves as a key substrate for gut microbial fermentation, leading to the production of short-chain fatty acids, such as butyrate, which have been shown to exert anti-inflammatory and anticancer properties[113]. High-fiber diets have been associated with increased microbiota diversity and favorable shifts in microbial composition, which may enhance antitumor immunity and improve treatment responses[114].
Spencer et al[115] reported that melanoma patients consuming high-fiber diets had improved progression-free survival while on immune checkpoint inhibitor (ICI) therapy, potentially mediated by a more favorable gut microbiome profile[115]. Additionally, dietary fiber has been shown to increase microbial metabolites that promote mucosal immunity and inhibit tumor growth in preclinical models[116].
However, the interplay between diet, microbiota, and host immune responses is complex and influenced by multiple factors, including baseline microbiome composition and genetic background. Ongoing studies are investigating the optimal dietary patterns and fiber types for therapeutic benefit in different cancer types[117].
Fecal microbiota transplantation (FMT) involves the transfer of fecal material from a healthy donor to the GI tract of a recipient, aiming to restore microbial diversity and function[118]. Initially developed for treating recurrent Clostridioides difficile infection[119], FMT is now being explored as an adjunct in cancer therapy[120]. Preclinical studies and early-phase clinical trials suggest that FMT can modulate the gut microbiome in a way that enhances the efficacy of ICIs, particularly in melanoma and other solid tumors[121].
For instance, Baruch et al[122] demonstrated that FMT from ICI responders could induce clinical responses in melanoma patients previously refractory to anti- programmed death 1 (PD-1) therapy. Similarly, Davar et al[123] showed that microbial reprogramming through FMT could overcome primary resistance to immunotherapy in metastatic melanoma. While these findings are promising, further large-scale trials are needed to validate the safety, donor selection criteria, and long-term outcomes of FMT in oncology settings.
CRC is the third most prevalent cancer in men and the second in women and the predominant histological subtype is adenocarcinoma[2]. CRC is a multifactorial disease and the main etiology remains complex, environmental factors - including smoking, diet, and lifestyle - significantly influencing individual susceptibility and sporadic cases constitute approximately 80% of cases[124]. Some well-known risk factors are: Age, genetic predispositions, familial CRC history, IBD[125-127]. Gut microbiome alterations and microbial infections have shown an association with CRC pathogenesis and treatment response[128,129].
The human gut hosts over 500 bacterial species, with the densest microbial populations residing in the colon[130]. The microbiome primarily comprises obligate anaerobes such as Bacteroides, Eubacterium, Bifidobacterium, Fusobacterium, Peptostreptococcus, and Atopobium, while facultative anaerobes like Enterococci, Lactobacilli, Enterobacteriaceae, and Strep
The F. nucleatum protein Fap2 binds to Gal-GalNAc on CRC cells, facilitating bacterial colonization[135]. F. nucleatum also interacts with E-cadherin via FadA, activating the β-catenin and NF-κB pathways, increasing proinflammatory cytokines (TNF-α, IL-6, IL-8, IL-1β), and promoting immune evasion by binding to TIGIT receptors on natural killer cells and tumor-infiltrating lymphocytes[136,137]. It further enhances CRC progression through TLR4/MyD88 signaling[135,136,138,139].
Research has identified F. nucleatum in CRC primary tumors and liver metastases, while Bacteroides fragilis and E. coli disrupt the colonic mucus barrier. Their toxins cause DNA damage, inflammation, and mutations. E. coli also impairs DNA repair via EspF and increases ROS, contributing to genetic instability in CRC[140-144].
Other bacteria linked to CRC include Peptostreptococcus anaerobius, which increases ROS via TLR2/TLR4, and seven species (B. fragilis, F. nucleatum, Porphyromonas asaccharolytica, Parvimonas micra, Prevotella intermedia, Alistipes finegoldii, Thermanaerovibrio acidaminovorans) associated with lipopolysaccharide (LPS)-induced inflammation and energy biosynthesis pathways. Atopobium parvulum and Actinomyces odontolyticus are enriched in early CRC and may serve as biomarkers[145,146]. Enterotoxigenic B. fragilis (ETBF) drives CRC by inducing IL-17, activating NF-κB, and recruiting myeloid-derived suppressor cells, which suppress CD8+ T-cell activity. ETBF also upregulates matrix metalloproteinase 9 and vascular endothelial growth factor A, further promoting tumor progression via CXCL1 and CXCL2[147,148]. Dysbiosis is linked to colorectal diseases, including IBD, colitis, and CRC[149,150]. Several bacteria contribute to CRC development.
Streptococcus gallolyticus: Streptococcus gallolyticus (S. gallolyticus) is associated with enterococcal endocarditis and cecal carcinoma, with up to 40% of bacteremia cases linked to CRC[151-153]. It promotes tumorigenesis by increasing inflammatory markers and oxidative stress, adhering to colorectal tissues via collagen-binding proteins. Colonoscopic screening is recommended for infected patients[153]. While earlier reports suggested an association rate as high as 80%, more recent analyses indicate a lower prevalence. A retrospective cohort study conducted in the Skane Region of Sweden from 2003 to 2018 found that among patients with S. gallolyticus subsp. Gallolyticus bacteremia, 7% were diagnosed with CRC within 12 months. This study highlighted a strong association between this specific subspecies and CRC, with a standardized incidence ratio of 59.8 compared to the general population[154]. Additionally, a 2022 study from Iran reported that 60% of patients with CRC had S. gallolyticus detected in tumor samples, compared to 29.7% in control subjects without CRC[155].
Bacteroides fragilis: Bacteroides fragilis produces fragilysin, which disrupts E-cadherin, activating oncogenic pathways [β-catenin, cellular MYC (c-MYC), cyclin D1][156-159]. Its tumorigenic effects involve signal transducer and activator of transcription 3 activation and a TH17 immune response, which can be mitigated by IL-17/IL-23 blockade[160].
E. coli (pks-positive strains): E. coli produce colibactin, a genotoxin that induces DNA damage, mutations, and genomic instability, driving CRC development in mouse models[161,162].
F. nucleatum: F. nucleatum is enriched in CRC and correlates with poor survival and metastasis. Its virulence factors, Fap2 and FadA, inhibit immune responses and activate oncogenic signaling (β-catenin, TLR4/NF-κB, miR-21), promoting tumor growth and invasion[136,139,163].
Enterococcus faecalis: Enterococcus faecalis (E. faecalis) generates reactive oxygen/nitrogen species, leading to DNA damage and chromosomal instability. H. pylori may contribute to CRC via hypergastrinemia and cytotoxin-associated gene A (CagA)-mediated oncogenic effects, though its role remains unclear[164,165].
Microbial composition shifts in CRC patients include increased Bacteroides/Prevotella, Fusobacterium, Roseburia, and Faecalibacterium in tumors, with reduced Enterobacteriaceae levels[131,132]. Host-microbiome interactions via fecal microRNAs influence bacterial gene expression, potentially driving CRC progression[166]. Case-control studies show CRC-associated bacteria (F. nucleatum, E. faecalis, S. gallolyticus, ETBF) are enriched in adenomatous polyps, while beneficial bacteria (Lactobacillus, Roseburia, Bifidobacterium) are reduced[167,168]. Emerging research suggests gut microbiome profiling combined with machine learning could serve as a non-invasive CRC screening tool, offering accuracy comparable to colonoscopy[150]. A summarized table of the therapeutic approaches related to the gut microbiome in CRC can be found in Table 1[20,133,140,166,169-184].
| Therapeutic approach | Description | Key findings |
| Bacterial eradication | Targeting CRC-associated bacteria using antimicrobial agents | Colibactin-producing E. coli inhibited by ClbP inhibitors, reducing tumor growth in mice[169] |
| F. nucleatum targeted with metronidazole, lowering bacterial load and tumor proliferation[140] | ||
| Probiotics | Using beneficial bacteria to modulate gut microbiome for CRC prevention and chemotherapy support[20,133,170] | Lactobacillus and Bifidobacterium species reduced preneoplastic lesions in animal models[171,172] |
| VSL3 probiotic mix reduced adenoma formation and chemotherapy side effects[173] | ||
| Human studies show mixed results on probiotics’ protective effects against CRC[174-176] | ||
| FMT | Transplanting healthy microbiome to modify gut composition and potentially prevent CRC[177] | FMT from wild mice improved CRC resistance and inflammation markers in recipient mice[177] |
| Clinical evidence remains limited, requiring further studies[178] | ||
| Microbiome and chemotherapy resistance | Gut bacteria influence drug resistance and efficacy in CRC treatment[166] | F. nucleatum linked to resistance against 5-FU and oxaliplatin via immune signaling[166] |
| Mycoplasma hyorhinis and Gammaproteobacteria impair gemcitabine by enzymatic deactivation[179] | ||
| Ciprofloxacin restored gemcitabine sensitivity[179] | ||
| Antibiotic use may reduce chemotherapy efficacy in some cases[180] | ||
| Microbiome and immunotherapy | Gut bacteria influence immune responses to CRC therapies[27] | Microbiome impact responses to immune checkpoint inhibitors (e.g., Ipilimumab)[181] |
| Antibiotic-treated mice showed reduced immunotherapy effectiveness[181] | ||
| Microbiome and drug toxicity | Bacteria alter drug metabolism, affecting side effects and toxicity | E. coli β-glucuronidase reactivates irinotecan, increasing toxicity[182,183] |
| Irinotecan alters microbiome, increasing inflammatory bacteria (Fusobacteria, Proteobacteria)[182] | ||
| Antibiotic treatment reduced oxaliplatin-induced neuropathy in mice[184] |
Pancreatic cancer is a rapidly progressing and highly fatal disease, with only about 25% of patients surviving beyond one year after diagnosis[185]. Due to late-stage detection in most cases, treatment is often palliative, relying on chemotherapy or radiotherapy rather than surgical intervention. Among the different types, pancreatic ductal adenocarcinoma stands out as the most common and aggressive subtype[186]. Chronic pancreatitis is a well-established risk factor, with incidence rates significantly higher in affected individuals[187]. Studies suggest a strong association between bacterial infections and pancreatic cancer, not necessarily as a direct cause but as contributors to tumor progression, immune modulation, and inflammatory responses[188,189].
A growing body of research has associated H. pylori infection to pancreatic cancer development[190,191]. Initial case-control studies reported a twofold increased risk in infected individuals, with prospective cohort studies confirming a higher susceptibility in male smokers carrying H. pylori antibodies, particularly the CagA-positive strains[192]. Further meta-analyses reinforced these findings, with large cohort studies also establishing a correlation between gastric ulcers (often caused by H. pylori) and pancreatic cancer[193,194].
H. pylori is believed to promote pancreatic diseases through its production of ammonia, lipopolysaccharides, and inflammatory mediators. In vitro experiments demonstrated increased levels of IL-8 and vascular endothelial growth factor (VEGF) in pancreatic cancer cell lines co-cultured with H. pylori, contributing to inflammation and tumor growth[195]. Furthermore, H. pylori LPS has been shown to enhance KRAS mutations—present in over 90% of pancreatic adenocarcinomas - thereby initiating carcinogenesis[196,197]. Additionally, the infection was found to activate signal transducer and activator of transcription 3, a signaling pathway that promotes cancer progression by upregulating anti-apoptotic and pro-proliferative proteins such as B-cell lymphoma-extra large, myeloid cell leukemia 1, survivin, c-MYC, and cyclin D1[198,199]. While a clear causal relationship has yet to be established, further clinical intervention studies using H. pylori eradication therapy may provide insights into its role in pancreatic cancer initiation[200].
Periodontal pathogens have also been implicated in pancreatic cancer risk. Porphyromonas gingivalis (P. gingivalis), a major bacterium associated with periodontitis, has been extensively studied in this context[201,202]. The European Prospective Investigation into Cancer cohort reported that individuals with high P. gingivalis antibody levels had more than double the risk of developing pancreatic cancer[202]. Though the precise mechanisms remain unclear, P. gingivalis’ LPS is believed to stimulate the TLR4 signaling pathway, which plays a key role in pancreatic ductal adenocarcinoma (PDAC) by promoting tumor growth, angiogenesis, invasion, and apoptosis suppression.
Additionally, Fusobacterium species have been detected in 8.8% of pancreatic cancer tissues, with their presence linked to poor prognosis[203-205]. These findings suggest Fusobacterium as a potential negative prognostic biomarker for pancreatic cancer[206]. Recent studies have reported a higher prevalence of F. nucleatum in PDAC than previously estimated indicating a range of approximately 20% to 30%[207-209]. For instance, a 2024 review highlighted that F. nucleatum is present in a significant subset of PDAC tumors, with prevalence rates reaching up to 30% in certain cohorts[209]. This bacterium has been associated with tumor progression and poorer patient outcomes. F. nucleatum can promote PDAC cell proliferation and migration through the induction of cytokines such as granulocyte-macrophage colony-stimulating factor, CXCL1, and IL-8, which act via autocrine and paracrine signaling pathways[208]. Additionally, it can influence the tumor microenvironment by modulating immune responses, potentially contributing to an immunosuppressive milieu that favors tumor growth[208]. These findings underscore the importance of considering F. nucleatum in the context of PDAC pathogenesis and suggest potential avenues for therapeutic intervention targeting the tumor microbiome.
Another emerging bacterial player is Pseudomonas aeruginosa, which has been shown to enhance the expression of the ABCB1 gene, contributing to drug resistance, tumor invasion, and metastasis[210]. Table 2 summarizes recent findings on microbiome-targeted therapies for PDAC[179,189,211,212].
| Therapeutic approach | Description | Key findings |
| Antibiotic therapy | Targeting tumor-associated bacteria to reduce tumor burden and enhance immunotherapy | Pushalkar et al[211] found a 50% tumor burden reduction in PDAC mouse models after oral antibiotic treatment |
| Tumor microenvironment reprogrammed, reducing myeloid-derived suppressor cells and increasing M1 macrophages[211] | ||
| Antibiotics improved PD-1 checkpoint inhibitor response, enhancing T-cell activation and reducing tumor size[211] | ||
| A clinical trial is evaluating antibiotic-pembrolizumab combination in locally advanced PDAC[189] | ||
| Probiotics and PDAC prevention | Investigating probiotics’ role in mitigating PDAC risk factors (e.g., pancreatitis, obesity, diabetes) | Lactobacillus plantarum 299 reduced pancreatic sepsis and surgical need in acute pancreatitis patients[212] |
| Probiotics reduced fibrosis, inflammation, necrosis, ductal damage, and atypical cellular regeneration, potentially lowering PDAC risk | ||
| Microbiome and chemotherapy resistance | Examining bacterial interference with chemotherapy efficacy | Gammaproteobacteria enriched in 76% of PDAC samples, degrading gemcitabine into an inactive form[179] |
| Microbiome-targeted approaches could enhance chemotherapy effectiveness |
GC is a multifactorial disease influenced by environmental, dietary, host-related, genetic, and epigenetic factors[213,214]. H. pylori, designated as a group I carcinogen by the World Health Organization, is a major contributor to GC pa
Chronic H. pylori-induced inflammation, as described in the Correa model[217], promotes gastric epithelial turnover, increasing the probability of mitotic errors and malignant transformation[218,219]. This pathological cascade progresses from atrophic gastritis to intestinal metaplasia (IM), dysplasia, and ultimately gastric adenocarcinoma[218-220]. The inflammatory response involves complex interactions between the bacterial pathogen, gastric acid secretion, immune cells, and reactive oxygen and nitrogen species, leading to oxidative DNA damage and upregulation of pro-inflammatory mediators[221,222]. Elevated expression of cytokines (IL-1β, IL-6, IL-8, and TNF-α) and cyclooxygenase-2 has been implicated in promoting atrophic mucosal alterations and oncogenic intracellular signaling[223,224]. Furthermore, H. pylori infection is associated with epigenetic modifications, including aberrant DNA methylation and gene silencing, affecting key regulatory pathways involved in cell adhesion, proliferation, DNA repair, and immune modulation[223].
Recent high-quality evidence reinforces the protective effect of H. pylori eradication therapy in reducing the risk of GC, particularly when administered before the onset of precancerous changes such as IM or dysplasia. A recent meta-analysis published in Frontiers in Microbiology in 2025 evaluated the impact of H. pylori eradication on GC risk among patients with IM or dysplasia. The study included 16 randomized controlled trials involving 15027 participants. The findings indicated that H. pylori eradication was associated with a 45% reduction in the relative risk (RR) of developing GC compared to no treatment [RR = 0.55; 95% confidence interval (CI): 0.46-0.67; P < 0.001]. Subgroup analyses revealed that eradication therapy significantly lowered GC risk in patients with dysplasia (RR = 0.51; 95%CI: 0.32-0.82; P = 0.005) and IM (RR = 0.61; 95%CI: 0.40-0.93; P = 0.022)[225]. Another recent systematic review and meta-analysis published in Gastroenterology in January 2025 evaluated the impact of H. pylori eradication on GC incidence and mortality[226]. The study included 11 randomized controlled trials and 13 observational studies, encompassing a total of 58828 participants. The findings revealed that H. pylori eradication was associated with a 36% reduction in the RR of developing GC (RR = 0.64; 95%CI: 0.48-0.84) and a 22% reduction in GC mortality (RR = 0.78; 95%CI: 0.62-0.98). These results underscore the potential of H. pylori eradication as a preventive strategy against GC.
In addition to inflammation-driven carcinogenesis, H. pylori exerts direct tumorigenic effects through its virulence factors, particularly CagA and vacuolating cytotoxin A (VacA)[227,228]. CagA disrupts intracellular signaling networks such as the MAPK cascade, NF-κB, phosphoinositide 3-kinase/protein kinase B, and epithelial-mesenchymal transition pathways via oncogenic yes-associated protein activation[228,229]. The cag pathogenicity island has also been implicated in H. pylori-induced carcinogenesis through mutations in tumor suppressor genes such as TP53[230,231]. Meanwhile, VacA facilitates immune evasion by impairing T-cell responses and disrupting epithelial integrity, thereby creating a permissive environment for persistent infection and neoplastic progression[232,233]. Table 3 summarizes recent findings on microbiome-targeted treatment strategies in gastroesophageal cancer[234-244].
| Topic | Findings | Key insights |
| Microbiomes in esophageal cancer treatment | Disrupting microbiome with antibiotics decreases xenograft tumor response to CpG oligonucleotide immunotherapy and platinum-based chemotherapy (e.g., oxaliplatin)[180] | A stable commensal microbiome may enhance cancer therapy effectiveness[180] |
| Similar effects observed in germ-free mice[180,234] | Microbiome regulates myeloid-derived cell functions within the tumor microenvironment[234] | |
| Further clinical research is needed | ||
| H. pylori and GC risk | H. pylori eradication reduces GC risk but does not guarantee complete prevention[235,236] | Other factors contribute to GC beyond H. pylori infection[235] |
| A Colombian clinical trial showed no significant GC incidence difference between treated and untreated individuals over six years, but treated individuals had higher precancerous lesion regression rates[235] | Eradication reduces GC risk by about 44% in asymptomatic, infected individuals[236] | |
| Long-term impact of H. pylori eradication | A 15-year study showed a 39% reduction in precancerous lesions[237] | Protective effects are strongest in non-atrophic/atrophic gastritis patients[239,240] |
| An 8-year study found that atrophic body gastritis reversed in 50% of treated patients[238] | Intestinal metaplasia and dysplasia patients do not experience the same benefit | |
| Meta-analyses confirmed a significant reduction in GC risk post-eradication[239] | Early eradication is crucial as intestinal metaplasia is irreversible | |
| Epigenetic modifications in GC prevention | DNA demethylating agent (5-azadC) suppresses aberrant methylation and reduces GC incidence in animal models[241] | Developing safer DNA demethylating agents could benefit high-risk individuals[223] |
| Clinical use is limited due to high toxicity | ||
| Probiotics and H. pylori eradication | Probiotics inhibit H. pylori in animal studies[242] | Probiotics may play a role in GC prevention[243,244] |
| Clinical trials/meta-analyses show probiotics improve eradication rates, patient compliance, and reduce treatment side effects | Used alongside antibiotics, they enhance treatment efficacy |
Biliary tract cancers include cancers of the bile duct, gallbladder, and ampulla of Vater, with gallbladder cancer (GBC) being the most prevalent[245,246]. While rare in the Western world, GBC is more common in Chile, Central Europe, Thailand, Japan, and parts of India and Pakistan[247,248]. The main risk factors include gallstones, obesity, chronic gallbladder inflammation, genetic predisposition, and environmental factors. Additionally, bacterial infections have been linked to malignant transformation in GBC.
Salmonella enterica serovar Typhi (S. Typhi): Chronic typhoid carriers have a significantly higher risk of GBC, with some studies reporting up to a 167-fold increased risk. However, recent metagenomic studies in South America found other bacteria (e.g., E. coli, F. nucleatum, Enterobacter species) predominant in GBC patients instead of S. Typhi[249-251].
Helicobacter species (H. bilis, H. hepaticus, H. pylori)[11,252]: These bile-resistant bacteria can cause chronic inflammation and gallstone formation, contributing to carcinogenesis. Some studies report a 2-3-fold increased risk of GBC in infected individuals. However, more epidemiological studies are needed to confirm causality.
Mixed bacterial infections: E. coli, Enterobacter, Klebsiella, and E. faecalis have been found in high levels in GBC patients. Given their known role in colon cancer, it is hypothesized they might contribute to GBC through similar mechanisms[253,254].
Gallstones facilitate bacterial colonization, increasing the likelihood of persistent infection. S. Typhi infection triggers oncogenic pathways (protein kinase B/MAPK), leading to mutated p53 and amplified c-MYC - both commonly observed in GBC patients[255,256]. Bacterial glucuronidase enzymes produce carcinogenic metabolites from bile, potentially leading to DNA damage and tumor development[256]. Bacterial enzymes increase secondary bile acids, which are known tumor initiators and promoters in GBC[257].
Hepatocellular carcinoma (HCC), the most common primary liver cancer and a leading cause of cancer-related deaths, is often associated with underlying liver diseases such as cirrhosis, fibrosis, and chronic hepatitis B and C infections[258,259]. Other recognized risk factors include alcoholic liver disease, hemochromatosis, obesity, and non-alcoholic fatty liver disease (NAFLD)[260,261]. While bacterial infections are not traditionally considered a primary cause of HCC, growing evidence suggests that gut and hepatic microbiome may influence its development and progression[262,263]. The liver, though generally sterile, is directly connected to the gut through the hepatic portal system. Disruptions in the gut microbiome can lead to increased intestinal permeability, allowing bacteria and their metabolites - such as lipopolysaccharides - to translocate to the liver[264]. This process contributes to chronic inflammation, immune dysregulation, and liver disease progression[265,266].
Certain bacterial species have been implicated in HCC development. E. coli, Atopobium, Bacteroides, Clostridium, and Desulfovibrio were found enriched in the gut microbiome of HCC patients, correlating with increased LPS levels and disease severity[267]. Additionally, obesity-related alterations in gut microbiome contribute to hepatocarcinogenesis through increased production of secondary bile acids, such as deoxycholic acid, which can activate the mammalian target of rapamycin (mTOR) pathway and promote liver tumorigenesis[268]. In high-fat diet-fed mice, elevated deoxycholic acid levels were associated with a higher incidence of HCC, while antibiotic treatment reduced tumor formation. Helicobacter species, particularly Helicobacter hepaticus and H. pylori, have also been linked to HCC[269,270]. In vivo studies showed that H. hepaticus disrupts enterohepatic homeostasis and activates NF-κB and Wnt signaling pathways, leading to oxidative stress and hepatocyte turnover. Furthermore, H. pylori virulence factors such as VacA and CagA were detected in HCC tissues, and its LPS was found to enhance liver cancer cell growth and migration[271,272].
Beyond the gut-liver axis, alterations in oral microbiome have also been observed in HCC patients[273]. A me
| Topic | Findings | Key insights |
| Antibiotics, probiotics, and GBC | Limited experimental and clinical evidence on their use for GBC prevention or treatment[255] | Salmonella infection may trigger lasting oncogenic changes |
| A study by Scanu et al[255] found that Salmonella-infected mouse embryonic fibroblasts formed tumors even after bacterial eradication with ciprofloxacin | ||
| Salmonella infection activates Akt/MAPK signaling pathways, potentially sustaining carcinogenesis post-eradication[255] | Further research is needed to explore microbiome-targeted GBC therapies | |
| Cholecystectomy remains the most effective preventive measure for chronic typhoid carriers at risk of GBC[251] | ||
| Probiotics and HCC prevention | Probiotic-fermented milk and chlorophyllin reduced tumor incidence in AFB1-induced HCC in rats[276] | Probiotics show potential in reducing HCC risk and progression in animal models |
| VSL3 probiotic formula inhibited chemically induced HCC, reducing LPS levels, tumor size, and tumor count[267] | ||
| Prohep (novel probiotic mix) decreased tumor growth by 40%, enhanced anti-inflammatory responses, promoted T-cell activation, and reduced pro-angiogenic factors in mice[277] | Clinical evidence remains limited, requiring large-scale human trials | |
| Probiotics and aflatoxin exposure | Some studies suggest probiotics reduce aflatoxin exposure and toxic DNA adduct formation, potentially lowering HCC risk[278] | Needs further validation in human studies |
| FMT and liver disease | FMT has shown promise in treating[279]: (1) High-fat diet and alcohol-induced liver injury (animal models)[280]; (2) Severe alcoholic hepatitis (clinical studies)[281]; (3) Chronic hepatitis B[282]; and (4) Advanced liver cirrhosis and hepatic encephalopathy | FMT may help restore gut-liver axis balance[279] |
| Its role in HCC prevention and therapy remains unclear, requiring further clinical trials |
Understanding the distinct microbial signatures and dysbiosis patterns across GI cancers such as colorectal, gastric, and pancreatic cancer highlights the intricate role the gut microbiome plays in tumorigenesis and progression. However, the interplay between the microbiome and cancer extends beyond pathogenesis - it also critically influences how patients respond to treatment. The next section explores how common cancer therapies, including chemotherapy, radiotherapy, and immunotherapy, interact with and are modulated by the gut microbiome, shaping both efficacy and toxicity profiles.
One of the major side effects of irinotecan, a key anti-cancer drug used for metastatic CRC, is severe diarrhea[283]. A study demonstrated that irinotecan chemotherapy alters the intestinal microbiome in tumor-bearing rats, leading to an increased abundance of Clostridium clusters I, XI, and Enterobacteriaceae, particularly following dose-intensive therapy[284]. Similarly, 5-FU, an anti-metabolite used to treat several cancers, including colorectal, breast, and liver, also induces diarrhea as a frequent side effect[283]. An observational study on breast cancer patients receiving 5-FU, epirubicin, and cyclophosphamide found alterations in intestinal permeability and changes in gut peptides such as glucagon-like peptide-2, ghrelin, and epidermal growth factor. Notably, patients who experienced diarrhea had higher intestinal permeability than those who did not[285].
van Vliet et al[286] showed that in pediatric patients with acute myeloid leukemia, chemotherapy combined with anti-microbial prophylaxis caused a reduction in anaerobic bacteria and an increase in potentially pathogenic aerobic enterococci. These gut microbiome disturbances may increase the risk of gram-positive infections. Furthermore, a study on paclitaxel-induced neuropathic pain in C57BL/6 (B6) and 129SvEv (129) mice, which display greater neuropathic sensitivity, revealed significant changes in gut microbiome. In particular, paclitaxel chemotherapy led to a decrease in Akkermansia muciniphila abundance in the B6 microbiome. The reduction of this beneficial bacterium was linked to gut barrier dysfunction, which might increase systemic exposure to bacterial products and metabolites, contributing to systemic inflammation and pain sensitivity[165,287].
Given the close association between gut microbiome and the immune system, immunotherapeutic interventions also exert significant effects on microbial composition and function. In a cohort of HCC patients receiving anti-PD1 therapy, microbial shifts were observed by week 3, with a notable increase in E. coli abundance in non-responders' stool samples, while Lactobacillus, Ruminococcaceae, and Akkermansia muciniphila were enriched in responders’ microbiome[288]. Si
Recent advancements in cancer surgery have highlighted the significant impact of surgical interventions on gut microbiome, especially in patients with GI cancers. A study examining gastrectomy in GC patients assessed its effects on the gut microbiome and metabolome, exploring the association between microbial changes and post-gastrectomy outcomes. The analysis showed substantial shifts in microbial diversity and richness in patients who underwent gastrectomy, likely due to the reconstruction of the GI tract following surgery. These microbial alterations could influence microbial functions, including nutrient transport and organic compound biosynthesis, which may contribute to changes in post-surgical metabolism[294]. Similarly, a study conducted in China investigated the fecal microbiome of GC patients before and after radical distal gastrectomy[295]. Significant changes were observed in the microbial composition during the perioperative period, with variations in the abundances of Akkermansia muciniphila, Escherichia/Shigella, Lactobacillus, and Dialister. Post-surgery, there was an increase in Escherichia/Shigella, Veillonella, and Clostridium XVIII, as well as a decrease in Bacteroides, when compared to healthy controls. These shifts are likely driven by surgical stress and other perioperative factors[295]. Additionally, research has shown that a modified microbiota-accessible carbohydrate diet can positively influence the gut microbiome and clinical symptoms in CRC patients following surgical resection[296].
In CRC surgery, animal studies have shown significant alterations in the gut microbiome following colorectal resection, with a marked reduction in Bacteroidetes and Proteobacteria, such as Enterobacteriaceae and Rhodospirillaceae[297]. Moreover, these microbial changes were associated with altered gene expression patterns, including an increase in IL10 and IL12 and a decrease in TNF expression after surgery[297]. In CRC patients, numerous studies have reported post-surgical changes in the gut microbiome, comparing post-surgery samples to those from preoperative CRC patients and healthy controls. These changes include a decrease in Bacteroides, Bifidobacterium, Clostridium, Prevotella, Klebsiella, Faecalibacterium, and Parabacteroides, while Enterococcus, Pseudomonas, Staphylococcus, Escherichia-Shigella, Enterobacteriaceae, and Streptococcus increased post-surgery[298,299]. In contrast, some studies have shown a decrease in Escherichia-Shigella and an increase in Enterococcus and Parabacteroides[300]. At the phylum level, a reduction in Firmicutes and Bacteroidetes was observed, alongside a decrease in the Firmicutes/Bacteroides ratio and an increase in Proteobacteria[301,302]. These microbial changes are likely a consequence of perioperative antibiotic administration, which can alter the gut microbiome, impair immune function, and disrupt metabolic pathways[303]. The resulting disruption in gut barrier integrity, coupled with surgical stress, may contribute to the development of inflammation and other postoperative complications in cancer patients. Recent evidence underscores the benefits of early enteral nutrition and probiotic supplementation in enhancing postoperative recovery for CRC patients.
Early enteral nutrition: Initiating enteral nutrition within 48 hours post-CRC surgery has been associated with improved GI recovery and nutritional status. A retrospective comparative study involving 227 patients in each group demonstrated that early enteral nutrition led to a shorter time to first postoperative flatus, quicker achievement of nutritional goals, and reduced hospital stay, without increasing postoperative complications[304]. Similarly, a randomized controlled trial reported that patients receiving early oral feeding after colorectal surgery experienced faster return of intestinal movements, earlier defecation, and shorter hospital stays compared to those on a regular diet[305].
Probiotic supplementation: Probiotic use in the perioperative period has been shown to reduce postoperative infections and restore beneficial gut microbiota. A systematic review and meta-analysis of randomized controlled trials found that probiotic supplementation significantly decreased the incidence of diarrhea, surgical site infections, urinary infections, and pulmonary infections in CRC patients undergoing surgery[306].
Furthermore, probiotics have been associated with a reduction in postoperative complications such as ileus, abdominal collections, sepsis, and pneumonia. These benefits are attributed to the modulation of gut microbiota, enhancement of intestinal barrier function, and attenuation of inflammatory responses[307].
Radiotherapy stimulates anti-tumor responses through immune activation[308], and like other cancer treatments, it induces alterations in gut microbiome composition. In an animal study, irradiated mice exhibited luminal and mucosa-associated dysbiosis compared to controls at two post-radiation time points, which was linked to increased expression of TNF-α, IL-1β, and IL-6[71]. Another recent study on irradiated mice revealed an increase in the Alistipes genus and a decrease in Prevotella in the large intestine[309]. In human studies, Mitra et al[310] reported a reduction in gut microbiome diversity in cervical cancer patients following chemoradiation therapy, while a study of gynecological cancer patients receiving pelvic radiotherapy found a decrease in Firmicutes and an increase in Fusobacterium[311]. Though further validation is needed, these findings suggest that radiation-induced changes in gut microbiome could lead to alterations in intestinal mucosa, resulting in inflammation[312].
These observations open the door to novel strategies aimed at modulating the gut microbiome to improve cancer treatment outcomes. One such approach is dietary interventions, known to influence gut microbiome composition and functionality[313]. A 2024 study demonstrated that dietary fiber supplementation not only improved tumor control during radiotherapy[314] but also alleviated intestinal radiation toxicity, highlighting the dual benefits of such interventions in cancer therapy[315]. As a result, research into the effects of nutritional interventions during cancer therapy on gut microbiome and clinical outcomes is on the rise. In the following section, we will examine various nutritional strategies that may help optimize gut microbiome and enhance the efficacy of cancer therapies.
The dynamic interplay between cancer therapies and the gut microbiome underscores the bidirectional nature of this relationship - therapies can disrupt microbial homeostasis, while the microbiota, in turn, modulates treatment efficacy and toxicity. These insights not only deepen our mechanistic understanding but also prompt critical questions about how best to leverage the microbiome to optimize clinical outcomes. The following discussion synthesizes these findings, evaluates emerging therapeutic interventions such as dietary modulation and FMT, and highlights future directions for integrating microbiome science into oncology practice.
In addition to standard chemotherapy, several targeted therapies have become integral to the treatment of GI malignancies, including monoclonal antibodies and antibody-drug conjugates. Emerging evidence suggests that the gut microbiota and local inflammatory milieu may significantly influence the efficacy, resistance, and toxicity of these therapies.
Bevacizumab, an anti-VEGF antibody, inhibits tumor angiogenesis and is widely used in combination regimens for metastatic CRC[316,317] and HCC[318]. A recent study investigated the role of the gut microbiota in modulating treatment response by analyzing pretreatment fecal samples from 37 patients[318]. Participants were classified as responders (n = 28) or non-responders (n = 9). Although overall microbial diversity did not differ significantly between the groups, the relative abundance of Bacteroides stercoris and Parabacteroides merdae was higher in responders. Notably, patients lacking both bacterial species had significantly worse prognoses. These findings suggest that specific gut microbiome may influence the therapeutic efficacy of atezolizumab and bevacizumab in advanced HCC.
While the gut microbiota’s impact on chemotherapy in CRC has been studied, its role in targeted therapy remains less understood. Chen et al[318] evaluated the association between gut microbiota composition and treatment outcomes in 110 patients with metastatic CRC undergoing combined chemotherapy and targeted therapy. Patients were stratified into anti- epidermal growth factor receptor (EGFR) (cetuximab) and anti-VEGF (bevacizumab) subgroups. Higher gut microbial α-diversity was observed in the partial response group and specifically in the bevacizumab partial response subgroup. β-diversity significantly differed between the bevacizumab partial response and progressive disease groups (P = 0.029)[319]. Notably, Klebsiella quasipneumoniae showed the highest fold increase in the progressive disease group, while F. nucleatum was about 32 times more abundant in progressive disease vs partial response patients. Despite higher diversity being associated with better outcomes, the bacterial profiles were heterogeneous, underscoring the need for further microbiome-based investigations, particularly in East Asian populations.
EGFR inhibitors are effective in RAS wild-type metastatic CRC. However, the gut microbiota may modulate EGFR pathway activity through inflammation-related mechanisms[319]. As of now, there is limited research directly linking panitumumab or cetuximab - monoclonal antibodies targeting the EGFR - to specific alterations in the gut microbiota in CRC patients[320]. For instance, dysbiosis-induced IL-17 and TNF-α production can interfere with EGFR inhibition and contribute to resistance. Moreover, cetuximab-induced skin toxicity has been linked to microbial alterations, raising the potential for microbiota-based strategies to mitigate adverse effects. A study by Liu et al[321] investigated the characteristics of the skin microbiome in patients experiencing severe skin toxicities induced by EGFR inhibitors, such as afatinib. The research revealed that patients with systemic drug-related intertriginous and flexural exanthema-like lesions exhibited significant skin microbial dysbiosis, characterized by reduced microbial diversity and an increased abundance of pathogenic bacteria. These findings suggest that alterations in the skin microbiota are associated with EGFR inhibitor-induced skin toxicities, highlighting the potential for microbiota-based strategies to mitigate such adverse effects. A review article by Ghidini et al[322] discusses the impact of tumor sidedness on the efficacy of anti-EGFR agents like panitumumab in metastatic CRC. While the article does not delve deeply into microbiota interactions, it acknowledges that the prognostic role of microbiota in CRC requires further clarification before being integrated into clinical practice.
These findings highlight the bidirectional relationship between the gut microbiota and targeted therapies. Microbial composition may affect drug pharmacokinetics, immune activation, and inflammation, thereby altering clinical outcomes. Integrating microbiome profiling into treatment planning and exploring microbiota-modulating strategies (e.g., pro
Emerging evidence supports the idea that an altered gut microbiome contributes to the initiation and progression of GI cancers[29]. Inflammation, a hallmark of cancer, plays a significant role in promoting tumorigenesis, and the gut microbiome is crucial in modulating the inflammatory processes within the GI tract[29]. The relationship between gut microbiome and chronic inflammation has been well-documented, with studies showing that dysbiosis can enhance inflammation by disrupting gut barrier integrity, leading to the translocation of bacteria and their metabolites to the systemic circulation[29,206]. This can activate immune cells and trigger inflammatory cascades that ultimately contribute to the development of cancer.
For instance, certain microbial species such as F. nucleatum in CRC[163] or H. pylori in GC[216] have been associated with chronic inflammation that drives carcinogenesis. These microorganisms can either directly or indirectly manipulate immune responses in the gut, promoting an environment conducive to tumor growth. In CRC, F. nucleatum has been shown to induce an inflammatory response that favors the progression of tumors through mechanisms like the activation of NF-κB[163] and the production of pro-inflammatory cytokines. While inflammation is a key driver of cancer progression, it is also an essential component of the immune response to tumors[288]. The immune system relies on a controlled inflammatory response to detect and destroy cancer cells. However, chronic inflammation, induced by dysbiosis or other factors, can impair immune surveillance and promote tumorigenesis[291]. Thus, the goal of nutritional interventions is to strike a balance - modulating inflammation to prevent cancer progression while ensuring that the immune system remains active and capable of combating tumor cells[108].
One of the major challenges in leveraging dietary interventions is understanding how they can modulate the gut microbiome to produce beneficial effects without compromising immune function. For example, while probiotics can be effective in reducing inflammation, overuse of certain strains or imbalanced supplementation could potentially exacerbate dysbiosis and impair immune responses[24]. Similarly, while fasting can induce beneficial changes in the gut microbiome, excessive or prolonged fasting could worsen conditions like cachexia or malnutrition, which are common in cancer patients[104].
This article has explored the multifaceted role of the gut microbiome in cancer initiation, progression, and response to therapy, emphasizing not only well-established mechanisms but also emerging therapeutic strategies[123,323,324]. A novel contribution of this review is the integration of cutting-edge evidence on interventions such as FMT[120,123] and high-fiber dietary modulation, which have shown promising potential to reshape oncologic outcomes via microbiome-targeted approaches. Specifically, the discussion of FMT in immune checkpoint blockade-refractory melanoma offers a timely update on how microbial reprogramming may overcome therapeutic resistance[122,123]. Recent phase I clinical trials have demonstrated that FMT from ICI responders can induce partial and complete responses in previously nonresponsive melanoma patients, marking a significant shift toward microbiome-informed personalized medicine[122,123]. These trials also provide preliminary data on safety and feasibility, although larger, controlled studies are needed to establish standardized protocols, including donor selection and long-term follow-up.
Additionally, this article highlights the underappreciated role of dietary interventions in modulating gut microbial communities to promote favorable cancer immunosurveillance[28,104,115]. Evidence from recent studies suggests that increased fiber intake correlates with enhanced progression-free survival in melanoma patients treated with immunotherapy[115]. These findings are supported by preclinical work indicating that microbial-derived short-chain fatty acids, such as butyrate, can enhance antitumor immunity[116]. However, interindividual variability in microbiota composition underscores the need for personalized dietary recommendations and further interventional trials.
Although the existing evidence on the role of the gut microbiome in cancer and the potential of nutritional interventions to modulate inflammation is promising, there are several challenges that need to be addressed. First, the precise mechanisms by which the gut microbiome influences cancer progression and response to treatment remain unclear. Further research is needed to identify the specific microbial species and metabolic pathways involved in cancer-related inflammation and how dietary interventions can target these pathways. Second, the heterogeneity of cancer types and patient populations makes it difficult to generalize findings across different cancers. The effects of dietary strategies may vary depending on the cancer type, stage, and the individual’s microbiome composition. Personalized nutrition, which takes into account the unique gut microbiome and metabolic profile of each patient, could offer a more tailored approach to cancer treatment. Finally, larger clinical trials are needed to validate the findings from preclinical studies and assess the long-term effects of dietary interventions on cancer outcomes. Only through well-designed, rigorous studies can we determine the most effective strategies for using the gut microbiome as a therapeutic target in cancer care.
While there is substantial interest in leveraging the gut microbiome for the prevention and treatment of GI cancers, current findings across studies are not always consistent, highlighting the complexity and nascent stage of this field[236,239,324]. One notable example is the ongoing controversy surrounding H. pylori eradication in GC prevention[239,240]. The role of H. pylori eradication in GC prevention remains an area of ongoing debate, particularly in relation to the histological stage of gastric mucosal damage. A meta-analysis of randomized controlled trials involving 7955 participants[240] demonstrated that H. pylori treatment significantly reduced GC risk overall (RR = 0.64), but the protective effect was notably confined to individuals without advanced mucosal changes - specifically those with non-atrophic or atrophic gastritis. In contrast, patients with IM or dysplasia did not experience a statistically significant reduction in GC risk following eradication, suggesting a “point of no return” beyond which eradication offers limited benefit. These findings were corroborated by a larger systematic review and meta-analysis of 26 studies (52363 subjects), which confirmed a significant reduction in GC risk with H. pylori eradication (pooled RR = 0.56)[239]. Subgroup analysis again emphasized that the benefit was primarily observed in patients without IM or dysplasia. Collectively, these studies highlight the critical importance of early H. pylori detection and treatment, as the chemopreventive benefit appears to diminish once precancerous lesions are established.
Similarly, the clinical applicability of microbiome-targeted strategies, including FMT, remains hampered by unresolved concerns. Although FMT has shown promise in restoring microbial diversity and enhancing immunotherapy response[122], its long-term safety - particularly in cancer patients with immunocompromised states - remains inadequately studied. Additionally, the efficacy and safety profiles of individual probiotic strains differ markedly[325].
While nutritional interventions hold promise in modulating the gut microbiome to improve cancer outcomes, their practical application in clinical settings faces significant challenges. The American Society of Clinical Oncology highlights that the heterogeneity of interventions, patient populations, and cancer stages complicates the translation of evidence into practice, and the benefits of nutritional interventions in advanced cancer and cachexia remain inconsistent and modest at best[326].
Cancer patients, particularly those experiencing cachexia or treatment-induced GI complications, often struggle with dietary compliance due to symptoms like anorexia, nausea, diarrhea, and mucositis[327-329]. These symptoms can limit the tolerance for high-fiber or microbiota-targeted diets, narrowing the therapeutic window for nutritional modulation.
Recent studies highlight these challenges. For instance, a systematic review analyzing appetite and dietary intake endpoints in cancer cachexia clinical trials found considerable variability in assessment methods, underscoring the need for standardized and validated tools to effectively monitor nutritional interventions in this population[330]. Additionally, a randomized controlled trial investigating preoperative immunonutrition in GC patients with cachexia demonstrated that while immunonutrition reduced postoperative infectious complications and improved inflammatory and immune parameters, its implementation requires careful consideration of patient-specific factors and potential GI intolerance[331].
Practical barriers include limited access to registered dietitians, lack of standardized protocols, and patient reluctance or inability to adhere to dietary recommendations due to symptom burden or treatment side effects. Additionally, up to half of patients may pursue unproven or restrictive diets and supplements, increasing the risk of adverse interactions and further nutritional compromise. The American Society of Clinical Oncology recommends referral to a registered dietitian to mitigate these risks and provide individualized support, but acknowledges that such resources are not universally available[326].
For patients with severe GI dysfunction, such as those with nonfunctioning alimentary tracts, parenteral nutrition may be considered, but this approach requires careful patient selection, clear goal-setting, and ongoing evaluation due to its risks, costs, and limited indications1. Multidisciplinary collaboration, early identification of at-risk patients, and patient/caregiver education are essential to optimize feasibility and outcomes in real-world settings[326,332,333].
These findings emphasize the necessity for personalized nutrition approaches that account for individual patient conditions and the integration of dietary planning with oncologic care. Moreover, the development of evidence-based guidelines and the inclusion of dietetic support within multidisciplinary teams are crucial to address the heterogeneity of patient needs and the complexities of clinical practice.
Despite growing interest in the gut microbiome and nutritional strategies for GI tumors, several limitations constrain current research. A major challenge lies in the significant individual variability of the gut microbiome, which is shaped by host genetics, diet, environment, medications, and lifestyle factors[324]. This heterogeneity complicates efforts to identify universal microbial biomarkers or design broadly applicable nutritional interventions. Furthermore, while numerous studies have established associations between specific microbial taxa or dietary components and cancer outcomes[12,293,294,334,335], the underlying molecular mechanisms remain largely unresolved. The complexity of the gut ecosystem, involving dynamic interactions between microbes, host immunity, and metabolic pathways, makes it difficult to establish clear causal relationships.
Methodological inconsistencies also limit the comparability of findings across studies[323,324,335]. Variations in sample collection methods, sequencing technologies, bioinformatics pipelines, and data analysis approaches introduce biases and reduce reproducibility. Moreover, much of the current evidence derives from observational studies or preclinical models[150,288,294], with a scarcity of large-scale, well-controlled clinical trials evaluating microbiome-modulating nutritional interventions in GI cancers. These factors highlight the need for more rigorous and standardized research designs to validate initial findings and support clinical translation.
Despite significant advances in understanding the gut microbiome’s role in GI cancers, critical gaps remain that limit translational progress. First, mechanistic insights into microbiota-nutrition-immunity interactions are uneven across GI cancer types. While CRC has been extensively studied, with clear links between diet-modulated microbial metabolites (e.g., short-chain fatty acids) and immune modulation, other GI cancers such as pancreatic[189] and esophageal cancers[334] remain poorly characterized in this context. Detailed mechanistic studies are needed to elucidate how microbiota-derived signals influence tumor immunity and metabolism in these less-studied cancers.
Second, promising microbiota targets for therapeutic intervention - such as Akkermansia muciniphila and Faecalibacterium prausnitzii - have shown potential in preclinical models for enhancing immunotherapy response and reducing inflammation, yet they lack robust clinical validation[239]. Moreover, FMT trials in GI cancer patients are still limited in scale and often lack standardized protocols, impeding definitive conclusions on efficacy and safety[118,119]. Third, although dietary interventions such as high-fiber diets and microbiota-accessible carbohydrates show promise in modulating the gut ecosystem, the heterogeneity in patient responses and challenges in adherence highlight the need for personalized nutritional strategies guided by microbiome profiling[113].
Addressing these gaps will require multidisciplinary efforts integrating microbiology, immunology, nutrition science, and clinical oncology, alongside longitudinal and interventional clinical trials to translate mechanistic insights into effective therapies. Finally, fostering interdisciplinary collaboration among microbiologists, oncologists, nutritionists, and computational biologists will be essential to translate laboratory discoveries into clinical practice. Collectively, these efforts will pave the way for integrating microbiome-informed nutritional strategies into precision oncology for GI tumors.
In conclusion, the interplay between the gut microbiome, inflammation, and cancer development is a complex and evolving area of research. Nutritional strategies that modulate the gut microbiome hold significant potential in enhancing cancer therapy and improving patient outcomes. Probiotics, prebiotics, CR, and fasting-mimicking diets are all promising approaches to managing gut inflammation and promoting a healthy microbiome. However, further research is required to fully understand the mechanisms underlying these effects and to identify the most effective and personalized approaches for cancer patients. By leveraging the gut microbiome’s role in inflammation, we may uncover new avenues for improving cancer treatment efficacy and overall patient quality of life.
In summary, the gut microbiome represents a highly dynamic and therapeutically targetable axis in cancer care. By synthesizing recent advances in FMT and diet-based modulation, this review offers a translational perspective that bridges mechanistic microbiome science with actionable clinical strategies. Future directions should prioritize randomized controlled trials, multi-omics integration, and microbiome-informed precision nutrition to fully realize the promise of microbiome-based interventions in oncology.
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