This study was performed to investigate the prevalence of gastric epithelial neoplasm of fundic-gland mucosa lineage (GEN-FGML) and time-course changes in endoscopic findings in affected subjects who underwent an esophagogastroduodenoscopy (EGD) examination as part of an annual checkup.

A total of 39,292 EGD examinations (25,228 men, 14,034 women; mean age: 53.6 years) were performed between April 2016 and March 2024. The prevalence of GEN-FGML was analyzed, and time-course changes noted in endoscopic findings of diagnosed tumors were investigated by comparison with previous endoscopic images.

During the study period, we identified 19 patients with 20 GEN-FGML diagnosed based on endoscopic and histological results, with a prevalence of 0.048%. Prevalence was not different between Helicobacter pylori-uninfected and -eradicated cases (0.050% and 0.051%, respectively). Endoscopy findings of 16 of these tumors for which time-course changes could be investigated (median observation period: 8.5 years) showed that 15 were unchanged in size in comparison with previous EGD findings, while one showed enlargement. In addition, three lesions diagnosed after H. pylori eradication were unchanged in size compared to before eradication.

The prevalence of GEN-FGML by screening EGD was 0.048%, with prevalence not different between H. pylori-uninfected and -eradicated subjects. Enlargement over time was not observed in almost all cases, and H. pylori infection status was considered not to influence changes in tumor size.

Atrophic gastritis (AG) is characterized by atrophy of gastric glands-in particular, oxyntic glands-in the setting of chronic inflammation; it is often autoimmune. The diagnosis is confirmed by immunohistochemistry (IHC) for gastrin (to confirm biopsy site), and pathologists often use IHC for neuroendocrine markers to evaluate for enterochromaffin-like cell hyperplasia (ECL-H). The utility of neuroendocrine staining is unclear, and we undertook this study to determine whether ECL pattern provided any additional information in cases of Helicobacter-negative AG.

We reviewed clinicopathologic findings in 184 cases from 184 patients with histologic AG and no evidence of Helicobacter infection. Using neuroendocrine IHC markers, cases were divided into 3 groups: Group 1 showed complete ECL-H (both qualitative and quantitative criteria met), group 2 showed focal ECL-H (qualitative but not quantitative criteria met), and group 3 showed no ECL-H (neither criteria met).

Group 1 patients were more likely to have positive autoantibody serologies (73%, P = .0007 vs group 2) and higher mean gastrin levels (700 pg/mL, P = .017 vs group 3), and only these patients developed gastric neuroendocrine tumors. Group 2 patients were more likely to take proton pump inhibitors (64%, P = .0002 vs group 1). Group 3 patients were more likely to be male (70%, P = .008 vs group 1) and to have microcytic anemia (44%, P = .022 vs group 2) and less likely to have intestinal metaplasia (50%, P = .044 vs group 1).

Stratification based on degree of ECL-H is not necessary for diagnosis of AG but does lead to statistically significant clinical and pathologic differences among groups.

Gastric cancer (GC) represents a significant global health burden due to its high morbidity and mortality. Specific behaviors of GC sub-types, distinct dissemination patterns, and associated risk-factors remain poorly understood. This editorial highlights several key prognostic factors, including pathological staging and vascular invasion, that impact GC. It examines a recent study's investigation of differential metastatic lymph nodes distribution and survival in upper and lower GC sub-types, focusing on histological characterization, pathophysiology, usage of neoadjuvant chemotherapy, and additional predictive determinants. We assess the statistical robustness and clinical applicability of the findings, underscoring the importance of treating GC as a heterogeneous disease and emphasizing how tailored surgical approaches informed by lymph node distribution can optimize tumor detection while minimizing unnecessary interventions. The study's large cohort, multi-center design, and strict inclusion criteria strengthen its validity in guiding surgical planning and risk-stratification. However, integrating genetic and molecular data is critical for refining models and broadening applicability. Additionally, recurrence-metrics and infection-related factors, such as Helicobacter pylori and Epstein-Barr virus, absent in the original study, remain vital for directing future research. By bridging metastatic patterns with prospective methodologies and inclusion of diverse populations, this editorial provides a framework for advancing early detection and personalized GC care.

Helicobacter pylori is a type of bacteria that infects the stomach lining and can cause various gastrointestinal disorders, such as dyspepsia, gastritis and peptic ulcers. Dyspepsia is a common symptom among patients seeking medical care, and Helicobacter pylori infection is one of the most common causes of dyspepsia.

This study aimed to determine the prevalence and factors associated with Helicobacter pylori infection among patients attending Temeke Regional Referral Hospital (RRH) in Dar es Salaam, Tanzania.

A hospital-based cross-sectional study involving dyspeptic patients was conducted between May and June 2023. A Standardized data collection tool was used to collect socio-demographic characteristics and other information such as level of income and source of water. Helicobacter pylori antigen was detected using a stool Helicobacter pylori antigen rapid test according to the manufacturer's instructions. Data analysis was done using STATA 15 computer software.

The study revealed that the prevalence of Helicobacter pylori infection among dyspeptic patients was 43.77%. Also, male sex, occasional hand washing habits and participants who were not sure whether they used treated water for drinking were the factors that were strongly associated with positive Helicobacter pylori infection.

Preventive measures and eradication of Helicobacter pylori infection should be considered worthy by public health authorities. More studies have to be emphasized to check the relationship between sex and Helicobacter pylori infection.

Colonization of the human stomach with cag pathogenicity island (PAI)-positive Helicobacter pylori strains is associated with increased gastric cancer risk compared to colonization with cag PAI-negative strains. To evaluate the contributions of the Cag type IV secretion system (T4SS) and CagA (a secreted bacterial oncoprotein) to gastric molecular alterations relevant for carcinogenesis, we infected Mongolian gerbils with a Cag T4SS-positive wild-type (WT) H. pylori strain, one of two Cag T4SS mutant strains (∆cagT or ∆cagY), or a ∆cagA mutant for 12 weeks. Histologic staining revealed a biphasic distribution of gastric inflammation severity in WT-infected animals and minimal inflammation in animals infected with mutant strains. Atrophic gastritis (a premalignant condition), dysplasia, and gastric adenocarcinoma were only detected in WT-infected animals with high inflammation scores. Transcriptional profiling, liquid chromatography-tandem mass spectrometry analysis of micro-extracted tryptic peptides, and imaging mass spectrometry revealed more than a thousand molecular alterations in gastric tissues from WT-infected animals with high inflammation scores compared to uninfected tissues and few alterations in tissues from other groups of infected animals. Proteins with altered abundance in animals with severe Cag T4SS-induced inflammation mapped to multiple pathways, including the complement/coagulation cascade and proteasome pathway. Proteins exhibiting markedly increased abundance in tissues from H. pylori-infected animals with severe inflammation included calprotectin components, proteins involved in proteasome activation, polymeric immunoglobulin receptor (PIGR), interferon-inducible guanylate-binding protein (GBP2), lactoferrin, lysozyme, superoxide dismutase, and eosinophil peroxidase. These results demonstrate key roles for CagA and Cag T4SS activity in promoting gastric mucosal inflammation, transcriptional alterations, and proteomic alterations relevant to gastric carcinogenesis.IMPORTANCEHelicobacter pylori colonizes the stomachs of about half of humans worldwide, and its presence is the primary risk factor for the development of stomach cancer. H. pylori strains isolated from humans can be broadly classified into two groups based on whether they contain a chromosomal cag pathogenicity island, which encodes a secreted effector protein (CagA) and components of a type IV secretion system (T4SS). In experiments using a Mongolian gerbil model, we found that severe gastric inflammation and gastric transcriptional and proteomic alterations related to gastric cancer development were detected only in animals infected with a wild-type H. pylori strain containing CagA and an intact Cag T4SS. Mutant strains lacking CagA or Cag T4SS activity successfully colonized the stomach without inducing detectable pathologic host responses. These findings illustrate two different patterns of H. pylori-host interaction.

This study aimed to construct and validate diagnostic models for the Operative Link on Gastritis Assessment (OLGA) and Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM) staging systems using three different methodologies based on magnifying endoscopy with narrow-band imaging (ME-NBI) features, to evaluate model performance, and to analyse risk factors for high-risk OLGA/OLGIM stages.

We enrolled 356 patients who underwent white-light endoscopy and ME-NBI at the Department of Gastroenterology, Dongzhimen Hospital, Beijing University of Chinese Medicine, between January 2022 and September 2023. Clinical data were recorded. Chi-square or Fisher's exact tests were used to analyse differences in endoscopic features between OLGA/OLGIM stages. Variables showing statistical significance underwent collinearity diagnosis before model inclusion. We constructed predictive models using Bayesian stepwise discrimination, random forest, and XGBoost algorithms. Receiver operating characteristic (ROC) curves were plotted using Python 3.12.4. Model accuracy, area under the ROC curve (AUC), sensitivity, and specificity were calculated for comprehensive validation.

All three models demonstrated excellent diagnostic performance, with random forest and XGBoost models showing marginally superior accuracy, AUC values, and sensitivity compared with the Bayesian stepwise discrimination model. For OLGA staging, the AUC values were 0.928, 0.958, and 0.966, with accuracies of 0.854, 0.902, and 0.918 for Bayesian, random forest, and XGBoost models, respectively. For OLGIM staging, the corresponding AUC values were 0.924, 0.975, and 0.979, with accuracies of 0.910, 0.938, and 0.927. Risk factors for high-risk OLGA included lesion location (subcardial and lower body greater curvature), intestinal metaplasia patches, lesion size, demarcation line (DL), and margin regularity of micro-capillary demarcation line (MCDL). Risk factors for high-risk OLGIM included Helicobacter pylori infection status, mucosal condition, lesion location (lesser curvature and lower body greater curvature), erosion, lesion size, DL, vessel and epithelial classification (VEC), white globe appearance (WGA), and MCDL margin regularity.

All three models demonstrated robust accuracy and predictive capability, confirming that conventional white-light endoscopy combined with ME-NBI features provides valuable diagnostic reference for clinical risk assessment of precancerous gastric lesions.

Guidelines recommend endoscopic surveillance for gastric cancer without therapeutic intervention every 3 years in patients with high-risk gastric intestinal metaplasia (GIM). This study aimed to evaluate the efficacy of radiofrequency ablation (RFA) in eradicating high-risk GIM.

This randomized self-control trial was conducted between June 2020 and February 2023. Patients with histology-verified high-risk GIM were enrolled. The endoscopist performed a biopsy on both the left and right sides of the stomach (five each) by targeting the suspected GIM area where available; otherwise, a random biopsy was taken. Patients were randomized to receive a unilateral RFA on either the left or right side. A repeated RFA on the assigned side was performed every 2-3 months for a total of two to three times. The primary outcome was complete resolution of GIM at 1 year after RFA.

Forty-six patients with a mean age of 66 ± 8 years were analyzed. The complete resolution rate of overall GIM lesions after RFA was significantly higher (49/142; 34/5%) than that in the observation group (29/127; 22.8%, RR = 0.84, 0.73-0.98, p = 0.03). For the subgroup analysis, the complete resolution rate after RFA revealed a significantly higher value than observation only in the incomplete GIM group (24/87; 27.6% vs. 11/82; 13.4%, RR = 0.83, 0.71-0.97, p = 0.02). The percentage of patients with extensive GIM regression after RFA (15/25; 60%) was higher than in the observation group (9/25; 36%) but did not meet statistical significance (RR = 0.62, 0.35-1.09, p = 0.09).

In high-risk GIM, RFA can significantly eradicate incomplete GIM when compared with observation alone.

Since it is difficult for expert endoscopists to diagnose early gastric cancer in post-eradication status, it may be critical to evaluate the stratification of high-risk groups using the advance of gastric atrophy or intestinal metaplasia. We tried to determine whether the combination of endoscopic artificial intelligence (AI) diagnosis for the evaluation of gastric atrophy could be a useful tool in both pre- and post-eradication status.

270 Helicobacter pylori-positive outpatients (Study I) were enrolled and Study II was planned to compare patients (n = 72) with pre-eradication therapy with post-eradication therapy. Assessment of endoscopic appearance was evaluated by the Kyoto classification and Kimura-Takemoto classification. The trained neural network generated a continuous number between 0 and 1 for gastric atrophy.

There were significant associations between the severity of gastric atrophy determined by AI endoscopic diagnosis and not having a regular arrangement of collecting venules in angle, visibility of vascular pattern, and mucus using Kyoto classification in H. pylori-positive gastritis. There were significant differences (p = 0.037 and p = 0.014) in the severity of gastric atrophy between the high-risk group and low-risk group based on the combination of Kimura-Takemoto classification and endoscopic AI diagnosis in pre- and post-eradication status. The area under the curve values of the severity of gastric atrophy (0.674) determined by the combination of Kimura-Takemoto classification and gastric atrophy determined by AI diagnosis was higher than that determined by Kimura-Takemoto classification alone in post-eradication status.

A combination of gastric atrophy determined by AI endoscopic diagnosis and Kimura-Takemoto classification may be a useful tool for the prediction of high-risk groups in post-eradication status.

Laser endoscopy has a linked color imaging (LCI) mode which has been reported to be superior to white light imaging (WLI) in detecting early gastric cancer (EGC). In this study, we retrospectively investigated the characteristics of superficial gastric neoplasms detected not by WLI but by LCI.

From April 2018 to May 2023, EGC or gastric adenoma identified by EGD was observed using LCI after WLI. The size, location, macroscopic type, color, skill level of the endoscopists, and treatment were examined for lesions detected by WLI (WLI group) and lesions detected not by WLI but by LCI (LCI group).

Eighty-eight lesions of EGCs were differentiated adenocarcinomas, 13 undifferentiated adenocarcinomas, and 28 gastric adenomas. There were 117 lesions (90.7%) in the WLI group and 12 (9.2%) in the LCI group. The mean diameter was 22.9 mm in the WLI group and 9.3 mm in the LCI group, with the latter being significantly smaller (p = 0.003). The numbers of protruding, depressed, and flat lesions were 58, 59, and 0 in the WLI group, and 7, 4, and 1 in the LCI group, respectively, indicating that more protruding lesions were detected in the LCI group (p = 0.005). After multivariate analysis, there was a significant difference in diameter only in the LCI group compared to the WLI group (odds ratio, 0.834; 95% CI, 0.728-0.956).

LCI is more useful than WLI for detecting smaller superficial gastric neoplasms.

Gastric premalignant conditions (GPMC) are common and include atrophic gastritis, gastric intestinal metaplasia, dysplasia, and certain gastric epithelial polyps. GPMC have an increased risk of progression to gastric adenocarcinoma. Gastric cancer (GC) in the United States represents an important cancer disparity because incidence rates are 2- to 13-fold greater in non-White individuals, particularly early-generation immigrants from regions of high GC incidence. The US 5-year survival rate for GC is 36%, which falls short of global standards and is driven by the fact that only a small percentage of GC in the US is diagnosed in the early, curable stage. This document represents the first iteration of American College of Gastroenterology guidelines on this topic and encompasses endoscopic surveillance for high-risk patients with GPMC, the performance of high-quality endoscopy and image-enhanced endoscopy for diagnosis and surveillance, GPMC histology criteria and reporting, endoscopic treatment of dysplasia, the role of Helicobacter pylori eradication, general risk reduction measures, and the management of autoimmune gastritis and gastric epithelial polyps. There is insufficient evidence to make a recommendation on upper endoscopic screening for GC/GPMC detection in US populations deemed high-risk for GC. Surveillance endoscopy is recommended for individuals at high risk for GPMC progression, as defined by endoscopic, histologic, and demographic factors, typically every 3 years, but an individualized interval may be warranted. H. pylori testing, treatment, and eradication confirmation are recommended in all individuals with GPMC. Extensive high-quality data from US populations regarding GPMC management are lacking, but continue to accrue, and the quality of evidence for the recommendations presented herein should be interpreted with this dynamic context in mind. The GPMC research and education agendas are broad and include high-quality prospective studies evaluating opportunistic endoscopic screening for GC/GPMC, refined delineation of what constitutes "high-risk" populations, development of novel biomarkers, alignment of best practices, implementation of training programs for improved GPMC/GC detection, and evaluation of the impact of these interventions on GC incidence and mortality in the US.

Plasmablastic lymphoma (PBL) is a rare B-cell lymphoma. Reports on primary gastric PBL are limited, and its endoscopic features remain poorly understood. We report a case of gastric PBL with multiple polypoid lesions in an immunocompetent individual. A 72-year-old man presented with upper abdominal discomfort. Esophagogastroduodenoscopy (EGD) revealed multiple raised lesions of variable sizes in the stomach, prompting a tumor biopsy. Based on histopathological findings, diffuse large B-cell lymphoma was suspected. Rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy was administered. After six cycles of R-CHOP therapy, EGD showed a partial reduction of the gastric tumor, and a biopsy was performed on the remaining tumor. Histopathology was re-examined, and immunohistochemical analysis revealed that the tumor cells were plasmablastic and strongly positive for both CD38 and CD138. The cells showed cytoplasmic immunoglobulin lambda light-chain restriction, indicating PBL. Furthermore, gastric differentiated adenocarcinoma was incidentally detected in some biopsy samples. Finally, a total gastrectomy was performed, and the postoperative course was uneventful. The patient is currently alive, 15 months after the initial diagnosis. This case reveals an endoscopic feature of gastric PBL and suggests the rare possibility that gastric PBL may coexist with adenocarcinoma.

The online version contains supplementary material available at 10.1007/s13691-025-00751-4.

Recently, the incidence of Helicobacter pylori-uninfected gastric cancers, such as gastric epithelial neoplasm of fundic-gland mucosa lineage (GEN-FGML), has increased with the widespread use of eradication therapy. Because the detection and endoscopic diagnosis of GEN-FGML are difficult, an effective observation method in screening endoscopy is required. We investigated whether texture and color enhancement imaging (TXI) improved the visibility of GEN-FGML compared with white light imaging (WLI).

In this single-center prospective clinical study, 50 GEN-FGML lesions (35 patients) treated at our hospital between October 2020 and June 2023 were analyzed. The endoscopic images of GEN-FGML obtained using WLI, TXI mode 1 (TXI-1), TXI mode 2 (TXI-2), and narrow-band imaging were compared by 10 endoscopists. We analyzed the visibility score and inter-rater reliability (intraclass correlation coefficient and conducted an objective evaluation based on L* a* b* color values and the color difference (ΔE*) in the CIE LAB color space system.

Histologically, GEN-FGML was classified as gastric adenocarcinoma of fundic-gland type (n = 45) and gastric adenocarcinoma of fundic-gland mucosa type (n = 5). The total visibility score for all endoscopists was significantly higher for TXI than for WLI (p < 0.01); and for TXI-1 than for TXI-2 (p < 0.01). The intraclass correlation coefficients for TXI-1 and TXI-2 were "almost perfect" and "substantial," respectively, for all endoscopists. ΔE* was significantly higher for TXI than for WLI (p < 0.01).

TXI improved the visibility of GEN-FGML for all endoscopists compared with WLI when evaluated subjectively and objectively.

Metronidazole (MNZ) is widely used to treat Helicobacter pylori infection worldwide. However, due to excessive and repeated use, resistance rates have exceeded 90% in some regions. The mechanisms of MNZ resistance have been extensively studied, and RdxA has been identified as the primary enzyme responsible for MNZ activation. Mutations in RdxA, particularly termination mutations, can lead to high-level MNZ resistance.

We identified a strain, ICDC15003s, which harbored RdxA termination mutation but remained highly susceptible to MNZ. To explore this phenomenon, we conducted comparative genomic and transcriptomic analyses to define RdxA-independent mechanisms of MNZ metabolism.

We found missense mutations in genes such as yfkO, acxB, alr1, glk, and cobB. Additionally, the expression of multiple genes, including TonB-dependent receptor and mod, significantly changed in resistant strains. Notably, the sequences and expression levels of known nitroreductases like FrxA and FdxB remained unchanged after induction of MNZ resistance, suggesting they were not responsible for MNZ sensitivity in ICDC15003s. Instead, transcriptional alterations were observed in genes encoding NADH-quinone oxidoreductase subunit (M, J, H and K), suggesting a potential compensatory mechanism for the loss of RdxA activity. We proposed that NADH-quinone oxidoreductase might serve as an RdxA-independent mechanism for MNZ metabolism and resistance through regulation of its expression levels. This discovery could provide new strategies to address MNZ resistance and aid in developing nitroimidazole antibiotics.

Recent work has demonstrated that cancer-specific microbial communities often colonize tumor tissues. However, untangling low-biomass signals from environmental contamination makes this research technically challenging. We utilize pseudomyxoma peritonei (PMP), a cancer characterized by the spread of mucus-secreting cells throughout the peritoneal cavity, to develop a robust workflow for identifying reproducible tumor microbiomes. Typically originating from the rupture of an appendiceal tumor into the peritoneal cavity, metastasized tumors have been previously shown to harbor a core set of microbes. However, that work did not control for the potential contamination of these low microbial biomass samples. We expand upon these prior findings by characterizing the microbiome of 70 additional PMP tumors and six normal peritoneal control tissues along with appropriate laboratory controls. Additionally, DNA from a subset of 25 tissues was extracted and sequenced at an independent laboratory. We found evidence of reproducible microbial signatures between the replicates of six different PMP tumors that include a set of core taxa that may be introduced from surgical contamination, as well as patient-specific taxa that are also commonly implicated in colorectal cancer. In addition, preoperative chemotherapy treatment was found to reduce tumor microbiome diversity. Our findings demonstrate how independent sample replication can be a powerful approach to investigate low-biomass microbial communities associated with tumor tissues that will improve low microbial biomass research.IMPORTANCERecent work has demonstrated that microbial communities colonize over 30 different types of tumor tissues. The origin of these communities and their possible involvement in carcinogenesis or cancer treatment outcomes remains an unclear, yet important area of research. A current major challenge in characterizing low-biomass, tumor-associated microbiomes is the introduction of environmental contamination during collection, handling, DNA extraction, PCR, and sequencing. Here, we provide a framework for replicating low-biomass tumor microbiome samples to help identify tumors with robust microbial signals and low background contamination. Using this replication approach, we show that pseudomyxoma peritonei (PMP) tumors host reproducible microbial communities, including organisms that have previously been associated with colorectal cancer. Incorporating sample replication into future tumor microbiome studies is a promising approach that will help identify robust signals and increase reproducibility in the field.

The Operative Link on Gastritis Assessment (OLGA) and Operative Link on Gastric Intestinal Metaplasia Assessment (OLGIM) are established classification systems used to evaluate atrophic gastritis and intestinal metaplasia, respectively.

We evaluated the association of OLGA and OLGIM scores and the risk of gastric cancer (GC) in only prospective cohort studies.

Systematic review and meta-analysis.

We systematically searched four databases for prospective cohorts that evaluated the use of OLGA and OLGIM staging systems in predicting the risk of GC. We primarily compared OLGA/OLGIM III-IV versus OLGA/OLGIM 0-II categories and GC events. Pooled risk ratios (RR) and absolute risk differences with their 95% confidence intervals (CIs) were calculated.

Eight studies were included (n = 12,526). The mean age of the patients ranged from 48.2 to 64.9 years. OLGA III-IV and OLGIM III-IV were associated with the development of GC in comparison to their 0-II categories (RR 32.31, 95% CI 9.14-114.21 and RR 12.38, 95% CI 5.75-26.65, respectively). OLGA III-IV and OLGIM III-IV were associated with an increase in the absolute risk of GC of 4% and 5%, respectively. The risk remained significant if we only included countries with high incidence of GC, and was greater if we excluded one study that included mostly patients with autoimmune gastritis. OLGA II and OLGIM II were associated with higher risk of high-grade dysplasia (HGD) and GC in comparison with OLGA 0-I and OLGIM 0-I, respectively.

Higher stages in OLGA and OLGIM systems are associated with a significantly increased risk of developing HGD and GC, validating these scoring systems for the assessment of GC risk and the design of endoscopic surveillance programs.

CRD42024565771.

A significant association between increased age and an increased risk of metachronous gastric cancer (MGC) following curative endoscopic submucosal dissection (ESD) has previously been reported.

To determine risk factors for the metachronous occurrence of early gastric cancer (EGC) in elderly individuals.

This retrospective cohort study comprised 653 elderly patients (aged ≥ 65 years) who underwent curative ESD for EGC between January 2014 and June 2020 at Nanjing Drum Tower Hospital. Comprehensive analyses were conducted to compare lifestyle habits, comorbidities, and Helicobacter pylori (H. pylori) infections as potential indicators.

During a median follow-up of 38 months, 46 patients (7.0%, 20.46/1000 person-years) developed MGC in the elderly cohort. The cumulative incidences of MGC at 2, 3, and 5 years were 3.3%, 5.3%, and 11.5%, respectively. In multivariate Cox regression analyses, the independent risk factors for MGC included metabolic dysfunction-associated steatotic liver disease (MASLD) [hazard ratio (HR) = 2.44, 95% confidence interval (CI): 1.15-5.17], persistent H. pylori infection (HR = 10.38, 95%CI: 3.36-32.07), severe mucosal atrophy (HR = 2.71, 95%CI: 1.45-5.08), and pathological differentiation of EGC (well/moderately differentiated vs poorly differentiated: HR = 10.18, 95%CI: 1.30-79.65). Based on these risk factors, a risk stratification system was developed to categorize individuals into low (0-1 point), intermediate (2-3 points), and high (4-8 points) risk categories for MGC, with cumulative incidence rates of 12.3%, 21.6%, and 45%, respectively.

Among elderly individuals, MASLD, persistent H. pylori infection, severe mucosal atrophy, and well/moderately differentiated EGC were associated with an increased risk of MGC. Elderly patients are recommended to adopt healthy lifestyle practices, and undergo regular endoscopic screening and H. pylori testing after curative ESD for EGC.

Observational studies suggest that Helicobacter pylori (H. pylori) is associated with an increased risk of gastric cancer, yet the effect of H. pylori eradication on gastric cancer risk in patients with intestinal metaplasia (IM) or dysplasia remains controversial. The purpose of this study was to summarize the evidence from randomized controlled trials (RCTs) investigating H. pylori eradication on gastric cancer risk in patients with IM or dysplasia to determine the evidence base.

PubMed, Embase, Cochrane Library, Web of science and China National Knowledge Internet database were searched for RCTs published through May 2024 in adults with IM or dysplasia comparing the risk of gastric cancer following H. pylori eradication versus no eradication therapy. Relative risk (RR) with its 95% confidence interval (CI) using random-effects model were employed for the effect estimate. Sensitivity, meta-regression, and subgroup analyses were also calculated.

Sixteen RCTs involving 15,027 patients with IM or dysplasia met the inclusion criteria. In a pooled analysis, H. pylori eradication resulted in a 45% reduction in RR for gastric cancer risk relative to no eradication (RR: 0.55; 95% CI: 0.46-0.67; p < 0.001). H. pylori eradication significantly reduced the risk of gastric cancer 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). Further, if the study conducted in countries other than those in Asia, sample size <500, percentage of male <50.0%, follow-up duration <5.0 years, and low study quality, then there was no significant association between H. pylori eradication and a decreased risk of gastric cancer.

H. pylori eradication is protective against gastric cancer in patients with IM or dysplasia.

INPLASY202530010, https://inplasy.com/.

Gastric cancer, a significant global health concern, arises from a complex interplay of genetic and environmental factors. Helicobacter pylori (H. pylori) infection is a major risk factor that can be mitigated through eradication strategies. Epstein-Barr virus (EBV) infection causes a distinct subtype of gastric cancer called EBV-associated gastric cancer. The gastric microbiome, a dynamic ecosystem, is also involved in carcinogenesis, particularly dysbiosis and specific bacterial species such as Streptococcus anginosus. Long-term use of proton pump inhibitors and potassium-competitive acid blockers also increases the risk of gastric cancer, whereas non-steroidal anti-inflammatory drugs including aspirin may have a protective effect. Smoking significantly increases the risk, and cessation can reduce it. Dietary factors such as high intake of salt, processed meats, and red meat may increase the risk, whereas a diet rich in fruits and vegetables may be protective. Extracellular vesicles, which are small membrane-bound structures released by cells, modulate the tumor microenvironment and may serve as biomarkers for risk stratification and as therapeutic targets in gastric cancer. This review highlights the multifaceted etiology of gastric cancer and its risk factors and emphasizes the importance of a multi-pronged approach to prevention including H. pylori eradication and modification of lifestyle factors, as well as the potential of microbiome-based and EV-based interventions. Further research is needed to refine risk stratification and to develop personalized prevention strategies.

Atrophic gastritis-the end stage of chronic gastritis-is an asymptomatic disease due to Helicobacter pylori infection causing decreased vitamin B12 and folate absorption, which may lead to severe haematological and neuropsychological disorders including Alzheimer's disease. The diagnosis requires endoscopy and biopsies from symptomatic patients, explaining why its true prevalence in the population is not well-known.

We aimed to evaluate the prevalence of various stages of chronic gastritis in an autopsy series most closely representing the general population.

Gastric mucosa samples were collected prospectively from out-of-hospital deaths included in the Tampere Sudden Death Study (n = 70, mean age 63, age range 22-91 years). Antrum and corpus samples were stained with a H. pylori antibody and staged histopathologically.

Chronic gastritis with or without atrophic changes was detected in 40% of the cases. The proportion of healthy mucosa decreased age-dependently from 71.4% among individuals aged <50 years to 43.5% among the oldest individuals (>70 years), and that of chronic non-atrophic gastritis from 21.4% to 8.7%. In contrast, the prevalence of atrophic gastritis was 27.1% and increased in the age groups from 7.1% to 47.8% (P = .019) among the oldest individuals, showing a strong association (P < .0001) with H. pylori immunopositivity.

Atrophic gastritis is a common feature of the ageing stomach, which is observed in every second individual aged 70+ years, showing a strong association with H. pylori immunopositivity. Atrophic gastritis may be a more common risk factor in old age for diseases associated with low serum B12 and folate levels than has been previously known.

Endoscopy is widely used to diagnose gastric cancer and has a high diagnostic performance, but it must be performed by a physician, which limits the number of people who can be diagnosed. In contrast, gastric X-rays can be taken by radiographers, thus allowing a much larger number of patients to undergo imaging. However, the diagnosis of X-ray images relies heavily on the expertise and experience of physicians, and few machine learning methods have been developed to assist in this process. We propose a novel and practical gastric cancer diagnostic support system for gastric X-ray images that will enable more people to be screened. The system is based on a general deep learning-based object detection model and incorporates two novel techniques: refined probabilistic stomach image augmentation (R-sGAIA) and hard boundary box training (HBBT). R-sGAIA enhances the probabilistic gastric fold region and provides more learning patterns for cancer detection models. HBBT is an efficient training method that improves model performance by allowing the use of unannotated negative (i.e., healthy control) samples, which are typically unusable in conventional detection models. The proposed system achieved a sensitivity (SE) for gastric cancer of 90.2%, higher than that of an expert (85.5%). Under these conditions, two out of five candidate boxes identified by the system were cancerous (precision = 42.5%), with an image processing speed of 0.51 s per image. The system also outperformed methods using the same object detection model and state-of-the-art data augmentation by showing a 5.9-point improvement in the F1 score. In summary, this system efficiently identifies areas for radiologists to examine within a practical time frame, thus significantly reducing their workload.

Helicobacter pylori infection is a significant contributing factor of gastric cancer. Metachronous neoplasms also pose a risk. The mechanism underlying the impact of H. pylori eradication on preventing metachronous gastric cancer is unclear. This study aimed to investigate immunity changes in gastric mucosa after H. pylori eradication and to identify mechanisms preventing metachronous recurrence.

Patients diagnosed with gastric neoplasm and H. pylori infection, who underwent endoscopic resection, were included. Thirty-six cases of metachronous neoplasms occurring after eradication (metachronous group) were compared to 36 controls matched for age, sex, atrophy, and metaplasia (control group). Histological features and immunohistochemical staining for T-cell (CD3, CD4, and CD8) and immune exhaustion (forkhead/winged helix transcription factor and programmed cell death-ligand 1) markers in the non-tumor-bearing mucosa were evaluated.

In histologic features, glandular atrophy and intestinal metaplasia in the gastric mucosa significantly improved following H. pylori eradication in the control group (p < 0.001, 0.008), whereas they did not improve in the metachronous group (p = 0.449, 0.609). CD8 and CD8/CD3 ratios increased in the control group (p < 0.001, 0.04), but did not show differences in the metachronous group (p = 0.057, 0.245). The CD4/CD3 ratio and programmed cell death-ligand 1/CD4 expression significantly decreased after H. pylori eradication in the control group (p = 0.003, 0.042), but not in the metachronous group (p = 0.54, 0.55).

This observational study suggests that H. pylori eradication may prevent the recurrence of gastric neoplasia by improving histological inflammation and overcoming immune exhaustion.

Microbial communities inhabiting various body sites play critical roles in the initiation, progression, and treatment of cancer. The gut microbiota, a highly diverse microbial ecosystem, interacts with immune cells to modulate inflammation and immune surveillance, influencing cancer risk and therapeutic outcomes. Local tissue microbiota may impact the transition from premalignant states to malignancy. Characterization of the intratumoral microbiota increasingly reveals distinct microbiomes that may influence tumor growth, immune responses, and treatment efficacy. Various bacteria species have been reported to modulate cancer therapies through mechanisms such as altering drug metabolism and shaping the tumor microenvironment (TME). For instance, gut or intratumoral bacterial enzymatic activity can convert prodrugs into active forms, enhancing therapeutic effects or, conversely, inactivating small-molecule chemotherapeutics. Specific bacterial species have also been linked to improved responses to immunotherapy, underscoring the microbiome's role in treatment outcomes. Furthermore, unique microbial signatures in cancer patients, compared with healthy individuals, demonstrate the diagnostic potential of microbiota. Beyond the gut, tumor-associated and local microbiomes also affect therapy by influencing inflammation, tumor progression, and drug resistance. This review explores the multifaceted relationships between microbiomes and cancer, focusing on their roles in modulating the TME, immune activation, and treatment efficacy. The diagnostic and therapeutic potential of bacterial members of microbiota represents a promising avenue for advancing precision oncology and improving patient outcomes. By leveraging microbial biomarkers and interventions, new strategies can be developed to optimize cancer diagnosis and treatment.

The demonstration that Helicobacter pylori is a pathogenic bacterium with marked carcinogenic potential has paved the way for new preventive approaches for gastric cancer. Although decades of research have uncovered complex interactions of H. pylori with epithelial cells, current insights have refined our view on H. pylori-associated carcinogenesis. Specifically, the cell-type-specific effects on gastric stem and progenitor cells deep in gastric glands provide a new view on the ability of the bacteria to colonize long-term, manipulate host responses and promote gastric pathology. Furthermore, new, large-scale epidemiological data have shed light on factors that determine why only a subset of carriers progress to gastric cancer. Currently, technological advances have brought yet another revelation: H. pylori is far from the only microorganism able to colonize the stomach. Instead, the stomach is colonized by a diverse gastric microbiota, and there is emerging evidence for the occurrence and pathological effect of dysbiosis resulting from an aberrant interplay between H. pylori and the gastric mucosa. With the weight of this evidence mounting, here we consider how the lessons learned from H. pylori research inform and synergize with this emerging field to bring a more comprehensive understanding of the role of microbes in gastric carcinogenesis.

Although Helicobacter pylori (H. pylori) eradication therapy is important for preventing gastric cancer (GC), the occurrence of GC after H. pylori eradication remains a problem. In this study, the aim was to identify risk factors for GC after H. pylori eradication by comparing long-term histological, endoscopic, and serological evaluations of patients with and without GC.

Patients who underwent H. pylori eradication therapy at Oita University Hospital between June 1997 and August 2013 and were followed for at least 3 years with long-term endoscopy, histology, and serum biochemical tests were included, and the GC (215 cases) and non-GC (11 cases) groups were compared.

The GC group was older than the non-GC group at the time of eradication, had lower serum pepsinogen I/II levels, had severe endoscopic atrophic changes, had higher activity at the antrum, and inflammation and intestinal metaplasia (IM) at the corpus on updated Sydney system scoring. On long-term follow-up after eradication, the GC group had a wider range of endoscopic mucosal atrophy and a lower serum pepsinogen I/II ratio at any time point.

Endoscopic mucosal atrophy and the serum pepsinogen I/II ratio are useful predictors of GC in patients post H. pylori eradication at any time point.

Projections of future gastric cancer incidence and the demand for health-care services for gastric cancer patients by geographic area will assist local authorities in determining health-care needs, allocating medical resources, and planning services. This study aims to project the future incidence of gastric cancer, estimate the number of patients per medical institution, and decompose the net changes in cases to assess the impact of population aging by geographic area. Our projections are based on population-based cancer registry data, census data from 2000 to 2020, and the projected population for 2025-2045 in Kanagawa, Japan. We classified Kanagawa into urban, town, outer city, and rural areas based on geographic and population features. The number of medical institutions providing gastric cancer treatment was used to estimate the number of patients per medical institution. We projected a decrease of 25%, 52%, and 5% in gastric cancer cases in towns, outer cities, and rural areas from 2020 to 2045, respectively. However, cases are expected to increase by 9% in urban areas, primarily due to population aging. The annual number of gastric cancer patients per medical institution in urban areas is expected to increase from 54 to 59, while numbers in other areas are predicted to decline from 2020 to 2045. Our long-term projections indicate that the number of older gastric cancer patients will continue to increase in urban areas. While current measures effectively reduce gastric cancer risk, they need to be revised to address the impact of population aging.

Objective The characteristics of gastric cancer in patients with atrophic mucosa and no apparent history of Helicobacter pylori eradication have not been thoroughly investigated. Therefore, this study examined the clinicopathological characteristics of gastric cancer in these patients. Methods We retrospectively examined the endoscopic and pathological characteristics of gastric cancer in patients who underwent endoscopic submucosal dissection. Patients We divided the patients into 2 groups: those with gastric atrophy and no history of eradication (group A; n=102) and those with a history of eradication (group B; n=161). In group A, patients were further divided into mild atrophy (group C) and severe atrophy (group D) groups, while group B was further divided into those who underwent eradication treatment >5 years ago (group E) and those who underwent eradication 1-5 years ago (group F). Results Group A comprised significantly older individuals (75±8.0 vs. 71±7.5 years old, p<0.001) with a higher frequency of elevated gastric cancer than group B (32.4% vs. 17.4%, p=0.006). Compared with group E, group A was older and had a greater incidence of elevated gastric cancer. The incidence of gastric cancer in the U or M region was lower in group C than in group D. Conclusion Gastric cancer in patients with gastric atrophy and no history of eradication was associated with an older age and higher frequency of elevated-type morphology than in those with a history of eradication.

Gastric cancer (GC) is the third leading reason of death in men and the fourth in women. Studies have documented an inhibitory function of melatonin on the proliferation, progression and invasion of GC cells. MicroRNAs (miRNAs) are small, non-coding RNAs that play an important function in regulation of biological processes and gene expression of the cells. Some studies reported that melatonin can suppress the progression of GC by regulating the exosomal miRNAs. Thus, melatonin represents a promising potential therapeutic agent for subjects with GC. Herein, we evaluate the existing data of both in vivo and in vitro studies to clarify the molecular processes involved in the therapeutic effects of melatonin in GC. The data emphasize the critical function of melatonin in several signaling ways by which it may inhibit cancer cell proliferation, decrease chemo-resistance, induce apoptosis as well as limit invasion, angiogenesis, and metastasis. This review provides a resource that identifies some of the mechanisms by which melatonin controls GC enlargement. In light of the findings, melatonin should be considered a novel and testable therapeutic mediator for GC treatment.

The omentum is a common site of peritoneal metastasis in various cancers, including gastric cancer. It contains immune cell aggregates known as milky spots, which provide a microenvironment for peritoneal immunity by regulating innate and adaptive immune responses. In this study, we investigated gene expression profiles in cells from omental milky spots of patients with gastric cancer (n = 37) by RNA sequencing analysis and classified the patients into four groups (G1-4). Notably, significant differences were observed between the groups in terms of macroscopic type, lymphatic invasion, venous invasion, and pathological stage (pStage). G3, which was enriched in genes related to acquired immunity, showed earlier tumor stages (macroscopic type 0, Ly0, V0, and pStage I) and a better prognosis. In contrast, G4 showed enrichment of genes related to neutrophils and innate immunity; G1 and G2 showed no enrichment of innate or adaptive immune-related genes, suggesting an immune desert microenvironment. Cytometric analysis revealed significantly more T and B cells and fewer neutrophils in G3. Accordingly, the immune microenvironment in omental milky spots may vary depending on the stage of gastric cancer progression. When univariate Cox proportional hazards regression models were used to search for prognostically relevant genes specific to G3, 23 potential prognostic genes were identified as common genes associated with relapse-free survival and overall survival. In addition, the multivariate Cox proportional hazards model using these prognostic genes and clinicopathological information showed that combining the B cell marker CD19 and Ly had a high predictive accuracy for prognosis. Based on this study's results, it is possible that tumor progression, such as lymphatic and/or venous infiltration of tumor cells, may affect the immune cell composition and proportions in omental milky spots of patients with gastric cancer and analysis of gene expression in omental milky spots may help to predict gastric cancer prognosis.

Genetic abnormalities specific to post-Helicobacter pylori eradication gastric cancer (GC), especially those associated with undifferentiated post-eradication GC, are unknown. We conducted next-generation sequencing of GC diagnosed either before or after eradication to investigate the carcinogenesis of post-eradication GC.

Five cases of post-eradication differentiated GC [HP(-)-D group], five cases of H. pylori-positive differentiated GC [HP(+)-D group], four cases of post-eradication undifferentiated GC [HP(-)-U group], and six cases of H. pylori-positive undifferentiated GC [HP(+)-U group] underwent analysis. DNA was extracted from tumor samples, and non-tumor samples of all subjects. Next-generation target sequencing was conducted using the Ion AmpliSeq Library Kit 2.0 with the Ion AmpliSeq Cancer Hotspot Panel v2. Next-generation targeted sequencing results of the cancer part were subtracted from the results of the non-cancer part.

The HP(-)-D group displayed significantly fewer SNPs in hotspot than the other groups (p < 0.01). Definitive DNA mutations were identified by sequencing of cancerous and non-cancerous tissues. 5 of 20 patients had specific somatic mutations, with different TP53 mutations in the HP(+)-D and HP(-)-U groups, CTNNB1 mutations in the HP(+)-U group, and ATM mutations in the HP(+)-U group, but no mutations in the HP(-)-D group.

Several definite genetic mutations involved in GC were observed. Mutations were less frequent in post-eradication differentiated GC. However, because of small number of cases analyzed to identify carcinogenic differences, further analysis with a large number of cases and with strictly grading GC samples is needed.

Genetic abnormalities specific to post-Helicobacter pylori eradication gastric cancer (GC), especially those associated with undifferentiated post-eradication GC, are unknown. We conducted next-generation sequencing of GC diagnosed either before or after eradication to investigate the carcinogenesis of post-eradication GC.

Five cases of post-eradication differentiated GC [HP(-)-D group], five cases of H. pylori-positive differentiated GC [HP(+)-D group], four cases of post-eradication undifferentiated GC [HP(-)-U group], and six cases of H. pylori-positive undifferentiated GC [HP(+)-U group] underwent analysis. DNA was extracted from tumor samples, and non-tumor samples of all subjects. Next-generation target sequencing was conducted using the Ion AmpliSeq Library Kit 2.0 with the Ion AmpliSeq Cancer Hotspot Panel v2. Next-generation targeted sequencing results of the cancer part were subtracted from the results of the non-cancer part.

The HP(-)-D group displayed significantly fewer SNPs in hotspot than the other groups (p < 0.01). Definitive DNA mutations were identified by sequencing of cancerous and non-cancerous tissues. 5 of 20 patients had specific somatic mutations, with different TP53 mutations in the HP(+)-D and HP(-)-U groups, CTNNB1 mutations in the HP(+)-U group, and ATM mutations in the HP(+)-U group, but no mutations in the HP(-)-D group.

Several definite genetic mutations involved in GC were observed. Mutations were less frequent in post-eradication differentiated GC. However, because of small number of cases analyzed to identify carcinogenic differences, further analysis with a large number of cases and with strictly grading GC samples is needed.

Screening for, and treating, Helicobacter pylori in the general population or patients with early gastric neoplasia could reduce incidence of, and mortality from, gastric cancer. We updated a meta-analysis of randomized controlled trials (RCTs) examining this issue.

We searched the literature through October 4, 2024, identifying studies examining effect of eradication therapy on incidence of gastric cancer in H pylori-positive adults without gastric neoplasia at baseline or H pylori-positive patients with gastric neoplasia undergoing endoscopic mucosal resection (EMR) in either RCTs or observational studies. The control arm received placebo or no eradication therapy in RCTs and no eradication therapy in observational studies. Follow-up was ≥2 years. We estimated relative risks (RR) of gastric cancer incidence and mortality.

Eleven RCTs and 13 observational studies were eligible. For RCTs, RR of gastric cancer was lower with eradication therapy in healthy H pylori-positive individuals (8 RCTs, 0.64; 95% confidence interval [CI], 0.48-0.84) and H pylori-positive patients with gastric neoplasia undergoing EMR (3 RCTs, 0.52; 95% CI, 0.38-0.71). RR of death from gastric cancer was lower with eradication therapy in healthy H pylori-positive individuals (5 RCTs, 0.78; 95% CI, 0.62-0.98). In observational studies, RR of future gastric cancer was lower with eradication therapy in H pylori-positive subjects without gastric neoplasia at baseline (11 studies, 0.56; 95% CI, 0.43-0.73) and H pylori-positive patients with gastric neoplasia undergoing EMR (2 studies, 0.19; 95% CI, 0.06-0.61).

This meta-analysis provides further evidence that administering eradication therapy prevents gastric cancer in H pylori-positive individuals, with consistency in results among studies of different design.

This study investigated the oral microbiome signatures associated with upper gastrointestinal (GI) and pancreaticobiliary cancers.

Saliva samples from cancer patients and age- and sex-matched healthy controls were analyzed using 16S rRNA-targeted sequencing, followed by comprehensive bioinformatics analysis.

Significant dissimilarities in microbial composition were observed between cancer patients and controls across esophageal cancer (EC), gastric cancer (GC), biliary tract cancer (BC), and pancreatic cancer (PC) groups (R2 = 0.067, = 0.075, = 0.068, and = 0.044; p = 0.001, = 0.001, = 0.002, and = 0.004, respectively). Additionally, the oral microbiome composition significantly differed by the four cancer sites (p = 0.001 for EC vs. GC, EC vs. BC, EC vs. PC, GC vs. BC, and GC vs. PC; p = 0.013 for BC vs. PC). We built oral metagenomic classifiers to predict cancer and selected specific microbial taxa with diagnostic properties. For EC, the classifier differentiated cancer patients and controls with good accuracy (area under the curve [AUC] = 0.791) and included three genera: Akkermansia, Escherichia-Shigella, and Subdoligranulum. For GC, the classifier exhibited high discriminative power (AUC = 0.961); it included five genera (Escherichia-Shigella, Gemella, Holdemanella, Actinomyces, and Stomatobaculum) and three species (Eubacterium sp. oral clone EI074, Ruminococcus sp. Marseille-P328, and Leptotrichia wadei F0279). However, microbial taxa with diagnostic features for BC and PC were not identified.

These findings suggested that the oral microbiome composition may serve as an indicator of tumorigenesis in upper GI and pancreaticobiliary cancers. The development of oral metagenomic classifiers for EC and GC demonstrates the potential value of microbial biomarkers in cancer screening.

Objective In recent years, there has been a growing focus on health risks associated with alcohol consumption. The present study investigated whether or not the genetic variant of aldehyde dehydrogenase 2 (ALDH2) influences the risk of gastric cancer among individuals identified as hazardous drinkers using the Alcohol Use Disorders Identification Test (AUDIT), which provides a comprehensive assessment of hazardous drinking behavior. Patients We enrolled men with hazardous drinking behavior (AUDIT score ≥8) who had undergone gastric cancer screening (either endoscopy or a barium X-ray examination of the upper gastrointestinal tract) between April 2013 and March 2020 within 1 year from entry and who had subsequently undergone at least one more gastric cancer screening up to March 2021. Functional single-nucleotide polymorphisms of ALDH2 (rs671) were measured using a direct TaqMan polymerase chain reaction method with unprocessed saliva. Results A total of 246 men were enrolled, comprising 193 individuals with active ALDH2 (ALDH2*1/*1) and 53 with less-active ALDH2 (ALDH2*1/*2). The cumulative incidence of gastric cancer in the less-active group was higher than in the active ALDH2 group (p=0.01, hazard ratio: 4.6, 95% confidence interval: 1.2-16.7). Alcohol consumption was lower in the less-active ALDH2 group than in the active ALDH2 group, although no marked difference was observed in the AUDIT score. Conclusion In individuals with hazardous drinking behavior, a heightened risk of gastric cancer was observed among those with less-active ALDH2 variants, even when their alcohol consumption was comparatively lower than in those with active ALDH2 variants.

Helicobacter pylori (H. pylori), the dominating cause of gastric cancer, most often infects children initiating inflammation in the antral part and spreads orally to the oxyntic mucosa. Traditionally, eradication of H. pylori has been based upon a combination of antibiotics together with a proton pump inhibitor (PPI) to reduce gastric destruction of the antibiotics. Recently it has been shown that the more efficient inhibitors of acid secretion, the potassium-competitive acid blockers (PCABs) in combination with amoxicillin alone gave highly sufficient H. pylori eradication.

To further elucidate the importance of gastric acidity we studied the literature for the connection between gastric acidity and the presence of H. pylori.

It is well-known that H. pylori is dependent of some acidity in the surroundings to neutralize NH3 produced by its urease, explaining the loss of H. pylori in total oxyntic atrophy. With adequate dosing PCABs can induce almost complete anacidity for 24-h which probably is necessary for H. pylori eradication. Even a short period with hypergastrinemia may induce mutations in the target cell of gastrin, the enterochromaffin-like (ECL) cell which may contribute to the relatively short interval between H. pylori eradication and gastric cancer in the users of profound acid inhibitors.

The use of PCABs alone dosed sufficiently seems promising for H. pylori eradication, but a combination with a gastrin antagonist would be preferable.

Accurate detection of Helicobacter pylori and its antimicrobial resistance is essential for eradication of the infections. The aim of this study was to compare five different CE-IVD marked assays in detection of H. pylori from 268 clinical stool samples. Samples were considered positive for H. pylori when at least three of the five tests were positive. Amplified IDEIA Hp StAR (Oxoid) and Premier Platinum HpSA PLUS (Meridian Bioscience Inc.) assays showed sensitivity of 100% [95% CI (confidence interval): 87-100] and LIAISON® Meridian H. pylori SA (DiaSorin) of 83.3% (95% CI: 66-93). Specificities of the assays were 94.5% (95% CI: 91-97), 95.4%; (95% CI: 92-97), and 97.1% (95% CI: 94-99) respectively. Amplidiag® H. pylori + ClariR (Mobidiag) assay showed 93.3% (95% CI: 78-99) and Allplex™ H. pylori & ClariR Assay (Seegene Inc.) 36.7% (95% CI: 22-55) sensitivity, while specificity of both was 97.9% (95% CI: 95-99). The Amplidiag® and Allplex™ assays concordantly detected clarithromycin resistance in positive for H. pylori samples. The Amplidiag® assay showed the highest accuracy, namely 97.4% (95% CI: 95-99). These data provide helpful information for planning laboratory diagnostics of H. pylori and detection of clarithromycin resistance from stool samples.

Gastric cancer (GC) has benefited from treatment improvements such as minimally invasive surgery, molecular-targeted drugs, and immune check point inhibitors. However, the prognosis of advanced GC is still unfavorable. Minimally invasive pre-treatment detection of drug sensitivity (MI-PDDS) has increasing importance in view of improved chemotherapy. Gastric biopsy specimens are obtained with relative ease but have not been considered an appropriate source for generating cell lines because of their minute amounts. We therefore materialized the idea of MI-PDDS using biopsy-derived cell lines obtained from endoscopic biopsy specimens. Here, a cell line designated TCC-GC1-C1 was established from a biopsy specimen of a histologically confirmed adenocarcinoma of the stomach. The cell line showed the ability of forming spheroid with deeply stained nuclei and disturbed cellular morphology indicative of malignancy. Single-nucleotide polymorphism (SNP) genotyping of the cell line revealed a duplication of chromosome19q and a deletion of chromosome 8p. A drug screening test with 221 anticancer drugs showed that the cell line had high sensitivity to the proteasome inhibitor (Carfilzomib) and the fibroblast growth factor receptor inhibitor (Erdafitinib), with a low IC50 value of under 0.1 μM. Our MI-PDDS approach holds promise in making a treatment decision for advanced GC.