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Background: Vonoprazan, a potassium‐competitive acid blocker, is superior to traditional proton pump inhibitor (PPI) in acid suppression and has been approved in the treatment of acid‐related disorders. Accumulating evidence suggest associations between PPI use and gut microbiota, yet the effect of vonoprazan on GI microbiota is obscure. Methods: Transgenic FVB/N insulin‐gastrin (INS‐GAS) mice as a model of gastric cancer (GC) were administered vonoprazan by gavage every other day for 12 weeks. Stomachs were evaluated by histopathology, Ki‐67 proliferation index, and inflammatory cytokines. The mucosal and lumen microbiota from stomach, jejunum, ileum, cecum, and feces were detected using 16S rRNA gene sequencing. Results: Higher incidence of intestinal metaplasia and epithelial proliferation were observed in the vonoprazan group than that in the control mice. Vonoprazan also elevated the gastric expression of proinflammatory cytokines, including TNF‐α, IL‐1β, and IL‐6. Each mice comprised a unique microbiota composition that was consistent across different niches. The structure of GI microbiota changed dramatically after vonoprazan treatment with the stomach being the most disturbed segment. Vonoprazan administration shifted the gut microbiota toward the enrichment of pathogenic Streptococcus, Staphylococcus, Bilophila, and the loss of commensal Prevotella, Bifidobacterium, and Faecalibacterium. Interestingly, compared to the controls, microbial interactions were weaker in the stomach while stronger in the jejunum of the vonoprazan group. Conclusions: Long‐term vonoprazan treatment promoted gastric lesions in male INS‐GAS mice, with the disequilibrium of GI microbiome. The clinical application of vonoprazan needs to be judicious particularly among those with high risk of GC. [ABSTRACT FROM AUTHOR]

The aim of this current study was to identify the prevalence and risk factors of H. pylori infection in the low-risk area of gastric cancer in China, and evaluate the value of different gastric cancer screening methods. An epidemiological study was conducted in Yudu County, Jiangxi, China, and participants were followed up for 6 years. All participants completed a questionnaire, laboratory tests and endoscopy. Patients were divided into H. pylori positive and negative groups, and risk factors for H. pylori infection were identified using multivariate logistic regression analysis. A total of 1962 residents were included, the prevalence of H. pylori infection was 33.8%. Multivariate analysis showed that annual income ≤20,000 yuan (OR: 1.44, 95% CI: 1.18–1.77, p < 0.001), loss of appetite (OR: 1.71, 95% CI: 1.29-2.26, p < 0.001), PG II >37.23 ng/mL (OR: 2.11, 95% CI: 1.50–2.97, p < 0.001), G-17 > 1.5 and ≤5.7 pmol/L (OR: 2.52, 95% CI: 1.93–3.30, p < 0.001), and G-17 > 5.7 pmol/L (OR: 1.96, 95% CI: 1.48–2.60, p < 0.001) were risk factors of H. pylori infection, while alcohol consumption (OR: 0.70, 95% CI: 0.54–0.91, p = 0.006) was a protective factor. According to the new gastric cancer screening method, the prevalence of low-grade intraepithelial neoplasia in the low-risk group, medium-risk group and high-risk group was 4.4%, 7.7% and 12.5% respectively (p < 0.001). In a low-risk area of gastric cancer in China, the infection rate of H. pylori is relatively low. Low income, loss of appetite, high PG II, and high G-17 were risk factors for H. pylori infection, while alcohol consumption was a protective factor. Moreover, the new gastric cancer screening method better predicted low-grade intraepithelial neoplasia than the ABC method and the new ABC method. [ABSTRACT FROM AUTHOR]

Gastrointestinal (GI) cancers, especially gastric cancer and colorectal cancer (CRC), represent a major global health burden. A large population of microorganisms residing in the GI tract regulate physiological processes, such as the immune response, metabolic balance, and homeostasis. Accumulating evidence has revealed the alteration of microbial communities in GI tumorigenesis. Experimental studies in cell lines and animal models showed the functional roles and molecular mechanisms of several bacteria in GI cancers, including Helicobacter pylori in gastric cancer as well as Fusobacterium nucleatum, Escherichia coli, Peptostreptococcus anaerobius , and Bacteroides fragilis in CRC. The transcriptional factor NF-κB plays a crucial role in the host response to microbial infection through orchestrating innate and adaptive immune functions. Moreover, NF-κB activity is linked to GI cancer initiation and development through its induction of chronic inflammation, cellular transformation and proliferation. Here, we provide an overview and discussion of modulation of the NF-κB signaling pathway by microbiota, especially infectious bacteria, in GI tumorigenesis, with a major focus on gastric cancer and CRC. [ABSTRACT FROM AUTHOR]

Background and Aim: China is a country with high prevalence of Helicobacter pylori (H. pylori) infection, which in turn is closely related to the occurrence of gastric cancer. Therefore, the risks of H. pylori infection and gastric cancer are highly overlapping, and the prevention and treatment of H. pylori infection are necessary to prevent gastric cancer. Methods: Based on evidence‐based medicine and the Delphi method, the National Clinical Medical Research Center for Digestive Disease along with the National Early Gastrointestinal Cancer Prevention and Treatment Center Alliance organized dozens of experts in the fields of digestive diseases, H. pylori research, gastric cancer surgery, epidemiology, health economics, and health management to discuss the relationship between H. pylori eradication and prevention and the treatment of gastric cancer. Results: A preliminary consensus on the relationship between H. pylori infection and gastric cancer, H. pylori eradication and gastric cancer prevention, and H. pylori screening and eradication strategy was reached. The consensus further clarified the relationship between H. pylori and gastric cancer and how to formulate future prevention and control strategies for gastric cancer. Conclusions: This consensus could provide guidance on early detection, diagnosis, and treatment of H. pylori to reduce the occurrence of gastric cancer in China. [ABSTRACT FROM AUTHOR]

The Hippo and Wnt signalling pathways play crucial roles in maintaining tissue homeostasis and organ size by orchestrating cell proliferation, differentiation and apoptosis. These pathways have been frequently found to be dysregulated in human cancers. While the canonical signal transduction of Hippo and Wnt has been well studied, emerging evidence shows that these two signalling pathways contribute to and exhibit overlapping functions in gastrointestinal (GI) tumorigenesis. In fact, the core effectors YAP/TAZ in Hippo signalling pathway cooperate with β‐catenin in Wnt signalling pathway to promote GI neoplasia. Here, we provide a brief review to summarize the molecular mechanisms underlying the crosstalk between these two pathways and elucidate their involvement in GI tumorigenesis, particularly focusing on the intestine, stomach and liver. [ABSTRACT FROM AUTHOR]

The development of new nucleotide sequencing techniques and advanced bioinformatics tools has opened the field for studying the diversity and complexity of the gastrointestinal microbiome independent of traditional cultural methods. Owing largely to the gastric acid barrier, the human stomach was long thought to be sterile. The discovery of Helicobacter pylori, the gram-negative bacterium that infects upwards of 50% of the global population, has started a major paradigm shift in our understanding of the stomach as an ecologic niche for bacteria. Recent sequencing analysis of gastric microbiota showed that H. pylori was not alone and the interaction of H. pylori with those microorganisms might play a part in H. pylori-associated diseases such as gastric cancer. In this review, we summarize the available literature about the changes of gastrointestinal microbiota after H. pylori infection in humans and animal models, and discuss the possible underlying mechanisms including the alterations of the gastric environment, the secretion of hormones and the degree of inflammatory response. In general, information regarding the composition and function of gastrointestinal microbiome is still in its infancy, future studies are needed to elucidate whether and to what extent H. pylori infection perturbs the established microbiota. It is assumed that clarifying the role of gastrointestinal communities in H. pylori-associated diseases will provide an opportunity for translational application as a biomarker for the risk of serious H. pylori diseases and perhaps identify specific organisms for therapeutic eradication. [ABSTRACT FROM AUTHOR]