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Gastric cancer (GC) is a major global health burden, and chronic atrophic gastritis (CAG), a key precancerous lesion in the Correa cascade, is critical in its pathogenesis. As a Ca² -dependent actin-regulating protein, scinderin (SCIN) has been implicated in tumor progression across multiple malignancies, including gastric cancer. This study investigated SCIN expression dynamics during CAG-to-GC progression, its association with the tumor immune microenvironment (TIME) and clinical prognosis, and validated its role via integrated bioinformatics and experiments. Transcriptomic data from TCGA and GEO were analyzed using R. WGCNA and ceRNA networks identified SCIN as the core RNA and its interacting miRNAs/lncRNAs. GSVA, GSEA, immune infiltration, and checkpoint analyses explored SCIN's immunological relevance. Prognostic value was assessed via Cox models and ROC curves. SCIN expression was validated in 28 human gastric tissues by RT-qPCR and Western blotting. Functional assays (CCK-8, Transwell, flow cytometry) investigated its role in GC cells. SCIN expression significantly increased along normal mucosa→CAG→GC, with high diagnostic performance (AUC). Elevated SCIN correlated with poor survival and served as an independent prognostic factor. It was involved in immune-related pathways, modulated the TIME, and correlated with immune checkpoint markers. SCIN knockdown inhibited GC cell migration, enhanced apoptosis, and altered cell cycle. This study is the first to identify SCIN as a key molecular driver in the CAG-to-GC transition. SCIN represents a robust prognostic biomarker and a potential target for immunotherapeutic intervention in GC.

Gastric adenocarcinoma carries a poor prognosis, in part due to the late stage of diagnosis. Risk factors include Helicobacter pylori infection, family history of gastric cancer—in particular, hereditary diffuse gastric cancer and pernicious anaemia. The stages in the progression to cancer include chronic gastritis, gastric atrophy (GA), gastric intestinal metaplasia (GIM) and dysplasia. The key to early detection of cancer and improved survival is to non-invasively identify those at risk before endoscopy. However, although biomarkers may help in the detection of patients with chronic atrophic gastritis, there is insufficient evidence to support their use for population screening. High-quality endoscopy with full mucosal visualisation is an important part of improving early detection. Image-enhanced endoscopy combined with biopsy sampling for histopathology is the best approach to detect and accurately risk-stratify GA and GIM. Biopsies following the Sydney protocol from the antrum, incisura, lesser and greater curvature allow both diagnostic confirmation and risk stratification for progression to cancer. Ideally biopsies should be directed to areas of GA or GIM visualised by high-quality endoscopy. There is insufficient evidence to support screening in a low-risk population (undergoing routine diagnostic oesophagogastroduodenoscopy) such as the UK, but endoscopic surveillance every 3 years should be offered to patients with extensive GA or GIM. Endoscopic mucosal resection or endoscopic submucosal dissection of visible gastric dysplasia and early cancer has been shown to be efficacious with a high success rate and low rate of recurrence, providing that specific quality criteria are met.

According to a systematic review [11], estimates of the prevalence of CAG worldwide were 23.9% and 27.0% in the general population and in individual groups, respectively, using serology, and 33.4% in the general population, and 31.6 % in selected groups based on biopsies. According to the manufacturer's instructions, a PGI <30 pg / L was taken as a positive marker of gastric atrophy; for inflammation of the coolant, the amount of PGII was considered above 22 pg / l; a PGI to PGII ratio (PGI / PGII) less than 2.5 was considered positive for atrophy. [...]analysis of the obtained data showed that the content of pepsinogens and their ratio significantly decreased in patients with atrophy of the coolant in comparison with those without atrophy (Table 3). Since the degree of atrophy was assessed by the indicators of pepsinogens, with a pronounced degree of atrophy, the PGI was 8.7 ± 0.1 pg / l and the PGI / PGII was 1.1 ± 0.1, respectively; with moderate atrophy 16.6 ± 0.9 pg / l and 1.6 ± 0.1; with mild atrophy 27.2 ± 1.5 and 2.3 ± 0.2, respectively. [...]we can say that the risk factor for both severe atrophic gastritis of the gastric corpus and of a mild and moderate degree was age over 55 years.

Jatrorrhizine (JATR), a natural isoquinoline alkaloid from Coptidis Rhizoma , exhibits various pharmacological activities, including antibacterial, anti-inflammatory, and antitumor effects. While JATR is known to treat chronic gastritis, its therapeutic potential for chronic atrophic gastritis (CAG) and its underlying mechanisms are not fully understood. This study induced CAG in rats using N -Methyl- N ′-nitro- N -nitrosoguanidine (MNNG) for 12 weeks through free drinking and force-feeding. Serological metabolomics identified 23 core targets of JATR related to CAG improvement. Reverse transcription-quantitative polymerase chain reaction and western blotting confirmed the involvement of these targets. Molecular docking revealed interactions between JATR and IL-1β and Caspase-3. JATR significantly alleviated gastric inflammation and atrophy, with Kyoto Encyclopedia of Genes and Genomes analysis showing enrichment in the “Nod-like receptor-related pyroptosis pathway”. JATR also enhanced GES-1 cell proliferation and reduced MNNG-induced cell damage. Additionally, JATR downregulated pyroptosis-related (Gasdermin D, NLRP3, Caspase-1) and apoptosis-related (Bcl-2, Bax, Caspase-3) markers. These findings suggest that JATR may ameliorate MNNG-induced CAG by inhibiting the activation of the Nod-like receptor-related pyroptosis pathway, supporting its potential as a therapeutic intervention for CAG.

Background Chronic atrophic gastritis (CAG) is related to the body’s microbial and metabolic systems. Combined studies of microbiome and metabolomics can clarify the mechanisms of disease occurrence and progression. We used 16S rRNA sequencing, metagenomics sequencing and metabolomics sequencing to depict the landscapes of bacterium and metabolites, construct correlation networks of different bacterium and metabolites describe potential pathogenic mechanisms of chronic atrophic gastritis. Methods The gastric juices of 30 non-atrophic gastritis (NAG) patients and 30 CAG patients were collected. Gastric microflora was analyzed by 16S rRNA sequencing and metagenomics sequencing. Gastric metabolites were analyzed by LC–MS analysis. Different bioinformatics methods were used to analyze the data of microbiome and metabolome, and to analyze the relationship between them. Results In atrophic gastritis, bacteria diversity decreased. The genera with a mean decrease in Gini greater than 1.5 included peptostreptococcus, fusobacterium, prevotella, sphingomonas and bacteroides . KEGG pathway included renal cell carcinoma, proximal tubule bicarbonate reclamation, citrate cycle and aldosterone synthesis and secretion with significant enrichment of differential metabolites. Peptostreptococcus , fusobacterium, prevotella and sphingomonas were in pivot positions of the correlation network of differential metabolites and differential bacterium. Viral carcinogenesis, glycine serine and threonine metabolism, RNA polymerase, galactose metabolism and retinol metabolism were enriched in chronic atrophic gastritis based on the metagenomic sequencing data. Conclusion Peptostreptococcus, fusobacterium, prevotella, sphingomonas and bacteroides were the essential features that distinguish atrophic gastritis from non-atrophic gastritis, and caused disease by altering various metabolic pathways. Viral carcinogenesis, glycine serine and threonine metabolism, RNA polymerase, galactose metabolism and retinol metabolism may be related to the occurrence and progression of CAG.

Background Previous literature has explored the relationship between chronic atrophic gastritis (CAG) and isolated cancers within the upper gastrointestinal cancers; However, an integrative synthesis across the totality of upper gastrointestinal cancers was conspicuously absent. The research objective was to assess the relationship between CAG and the risk of incident upper gastrointestinal cancers, specifically including gastric cancer, oesophageal cancer, and oesophagogastric junction cancer. Methods Rigorous systematic searches were conducted across three major databases, namely PubMed, Embase and Web of Science, encompassing the timeline from database inception until August 10, 2023. We extracted the necessary odds ratio (OR) and their corresponding 95% confidence interval (CI) for subsequent meta-analysis. Statistical analyses were conducted using Stata 17.0 software. Results This meta-analysis included a total of 23 articles encompassing 5858 patients diagnosed with upper gastrointestinal cancers. CAG resulted in a statistically significant 4.12-fold elevated risk of incident gastric cancer (OR = 4.12, 95% CI 3.20–5.30). Likewise, CAG was linked to a 2.08-fold increased risk of incident oesophageal cancer (OR = 2.08, 95%CI 1.60–2.72). Intriguingly, a specific correlation was found between CAG and the risk of incident oesophageal squamous cell carcinoma (OR = 2.29, 95%CI 1.77–2.95), while no significant association was detected for oesophageal adenocarcinoma (OR = 0.62, 95%CI 0.17–2.26). Moreover, CAG was correlated with a 2.77-fold heightened risk of oesophagogastric junction cancer (OR = 2.77, 95%CI 2.21–3.46). Notably, for the same type of upper gastrointestinal cancer, it was observed that diagnosing CAG through histological methods was linked to a 33–77% higher risk of developing cancer compared to diagnosing CAG through serological methods. Conclusion This meta-analysis indicated a two- to fourfold increased risk of gastric cancer, oesophageal cancer, and oesophagogastric junction cancer in patients with CAG. Importantly, for the same upper gastrointestinal cancer, the risk of incident cancer was higher when CAG was diagnosed histologically compared to serological diagnosis. Further rigorous study designs are required to explore the impact of CAG diagnosed through both diagnostic methods on the risk of upper gastrointestinal cancers.

The present study aimed to explore the underlying mechanism of bile reflux-inducing chronic atrophic gastritis (CAG) with colonic mucosal lesion. The rat model of CAG with colonic mucosal lesion was induced by free-drinking 20 mmol/L sodium deoxycholate to simulate bile reflux and 2% cold sodium salicylate for 12 weeks. In comparison to the control group, the model rats had increased abundances of Bacteroidetes and Firmicutes but had decreased abundances of Proteobacteria and Fusobacterium . Several gut bacteria with bile acids transformation ability were enriched in the model group, such as Blautia , Phascolarctobacter , and Enterococcus . The cytotoxic deoxycholic acid and lithocholic acid were significantly increased in the model group. Transcriptome analysis of colonic tissues presented that the down-regulated genes enriched in T cell receptor signaling pathway, antigen processing and presentation, Th17 cell differentiation, Th1 and Th2 cell differentiation, and intestinal immune network for IgA production in the model group. These results suggest that bile reflux-inducing CAG with colonic mucosal lesion accompanied by gut dysbacteriosis, mucosal immunocompromise, and increased gene expressions related to repair of intestinal mucosal injury.

Chronic atrophic gastritis (CAG), affecting approximately 20-30% in high-risk populations, contributes to significant morbidity and mortality due to its progression to gastric cancer. Despite two decades of research into its pathogenesis, the vast body of literature has not yet been systematically mapped. A comprehensive bibliometric analysis mapping the field's evolution, collaborative networks, and knowledge gaps remains lacking. Therefore, we conduct a 20-year bibliometric analysis (2005-2024) of research on the mechanism of CAG to identify seminal works, emerging themes, evaluate global collaboration networks, and highlight translational challenges and opportunities. Data were retrieved from the Web of Science Core Collection (WoSCC) spanning from January 1, 2005, to December 31, 2024. Bibliometric analysis was performed using CiteSpace and VOSviewer to analyze publication trends, influential authors and institutions, keyword clusters, and citation bursts. A total of 954 papers were identified, with China leading in publication output (41.51%), followed by the USA (15.20%). The USA demonstrated high centrality in international collaboration. Key journals included WORLD J GASTROENTERO and GASTROENTEROLOGY. Prolific authors such as Liu Yuetao and co-cited authors like CORREA P were identified. Keyword analysis revealed \"Helicobacter pylori\" as the most prominent term, with clusters focusing on traditional Chinese medicine, macrophage biology, and gastric intestinal metaplasia. The study highlights the significant research output and collaboration in CAG, emphasizing the importance of interdisciplinary approaches and international partnerships. Future research should focus on integrating traditional knowledge with modern mechanistic studies and addressing emerging themes such as microbiome dysbiosis and precision medicine.

Chronic atrophic gastritis (CAG) is a precancerous lesion characterised by gastric mucosal atrophy and inflammation. Identifying key molecular mechanisms and potential therapeutic targets is essential to improve patient outcomes. Key modules and differentially expressed genes (DEGs) were recognised in the GSE153224 dataset using weighted gene co‐expression network analysis (WGCNA) and examination of differential expression. IGFBP7 was identified as a hub gene by protein–protein interaction (PPI) network and expression validation. CAG patients’ blood parameters and gastric mucosal health status were evaluated before and after the treatment of vitamin C (VC). In addition, we investigated the effects of VC and N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) on GES‐1 cells, including cell viability, apoptosis and the expression of inflammatory and angiogenic markers. WGCNA identified that the blue module was significantly associated with CAG with a correlation coefficient 0.924. Among 93 overlapping genes, IGFBP7 was notably underexpressed and selected as a hub gene. ROC analysis confirmed the high diagnostic performance of IGFBP7. CAG patients treated with VC showed significant improvement in blood parameters and improved gastric mucosal health. In vitro, VC increased cell viability, reduced cytotoxicity and apoptosis and lowered COX‐2 and apoptosis‐related protein expression in MNNG‐treated GES‐1 cells. Knockdown of IGFBP7 further influenced these effects. MNNG upregulated HIF‐1α/VEGF signalling proteins, which VC attenuated. Combined VC and IGFBP7 knockdown showed potential protective effects. This study highlights the regulatory role of VC and IGFBP7 in CAG and demonstrates their potential as therapeutic targets for improving gastric mucosal health and mitigating inflammation.

Background and aims: The development of atrophic chronic gastritis (ACG) is multifactorial, involving environment as well as host responses to Helicobacter pylori infection. The aim of this study was to determine factors involved in ACG in a European dyspeptic population. Methods: Data concerning sociodemographics, social behaviour, biological aspects, diet, and virulence factors of H pylori strains were collected in a cross sectional study from 19 European centres in 14 countries. Dyspeptic H pylori positive patients with ACG or non-ACG (NACG) at histology were included. Anti-CagA antibodies were evaluated by two immunoblot tests and anti-VacA antibodies by one. Logistic regression models were constructed, and estimated odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated from the coefficients. Results: Of the 451 patients included in the study, 267 were analysed: 202 had NACG and 65 ACG. Mean age was 44.4 years and 63% were women. Risk factors for atrophy identified by multivariate analysis were: age over 60 years (OR 4.14, 95% CI 1.79–9.58), coffee consumption (OR 2.35, 95% CI 1.07–5.16), sedative consumption (OR 2.17, 95% CI 1.04–4.52), and harbouring anti-CagA and anti-VacA antibodies simultaneously (OR 3.09, 95% CI 1.26–7.56), while the odds were significantly reduced for those with an anxiety score of 6 or more (OR 0.45, 95% CI 0.21–0.99). Conclusion: The simultaneous presence of anti-CagA and anti-VacA antibodies enhanced the risk of ACG in European dyspeptic patients. Failure to discern diet and family history as risk factors for ACG may suggest that diet is homogeneous in Europe and that most of the risk factors for ACG identified so far are identical to risk factors for H pylori infection.