High Risk Of Gastric Cancer Research Articles

Gastric Mucosal Status and Risk of Gastric Cancer in High-Risk Individuals: A Population-Based, Multicenter Prospective Study in China.

This study explored the distributions of gastric mucosal status and their links to gastric cancer within urban high-risk individuals in China. From 2014 to 2015, a questionnaire survey was administered among individuals aged 40 to 69 years, residing for over 3 years in seven selected cities across China. Utilizing the questionnaire data, high-risk individuals for gastric cancer were screened. These identified high-risk individuals were invited to undergo endoscopy, followed by pathological examinations conducted for those with suspicious lesions. Prior cancer patients and those newly diagnosed with gastric cancer were excluded, and the remaining endoscopic participants were prospectively followed up until December 2021. The prospective study followed 8911 individuals at high risk of gastric cancer for a median duration of 6.77 years. The incidence density of gastric cancer was 58.55 per 100,000 person-years. At baseline, the distributions of subjects across normal gastric mucosa, gastritis/ulcer/polyp, atrophic gastritis/intestinal metaplasia, and intraepithelial neoplasia groups were 47.09%, 36.27%, 9.57%, and 7.07%, respectively. Compared with normal gastric mucosa, the hazard ratios (HRs) for gastric cancer in the other groups were 0.89 [95% confidence interval (95%CI): 0.38-2.08], 1.52 (95%CI: 0.50-4.66), and 4.63 (95%CI: 1.98-10.82). When using the 40-54 age group as the reference, the HR for 55-69 age group was 3.49 (95%CI: 1.52-7.98). Among high-risk individuals with gastric cancer, the proportions of individuals exhibiting different gastric mucosal status inversely correlated with the severity of mucosal lesions, whereas the risk of gastric cancer progressively escalated with the increasing severity of mucosal lesions and advancing age.

Implementation of the updated Sydney system biopsy protocol improves the diagnostic yield of gastric preneoplastic conditions: Results from a real-world study

BackgroundThe updated Sydney system biopsy protocol (USSBP) standardizes the sampling of gastric biopsies for the detection of preneoplastic conditions (e.g., gastric intestinal metaplasia [GIM]), but the real-world diagnostic yield is not well-described. AimTo determine whether regular application of USSBP is associated with higher detection of chronic atrophic gastritis (CAG), GIM and autoimmune gastritis (AIG). MethodsWe performed a real-world retrospective study at an academic urban tertiary hospital in Chile. We manually reviewed medical records from consecutive patients undergoing esophagogastroduodenoscopy (EGD) from January to December 2017. Seven endoscopists who performed EGDs were categorized into two groups (USSBP ‘regular’ and USSBP ‘infrequent’) based on USSBP adherence, using minimum 20% adherence as the prespecified threshold. Multivariable logistic regression models were used to estimate the odds ratios (aOR) and 95% confidence intervals (CI) for the association between endoscopist groups and the likelihood of diagnosing CAG, GIM or AIG. Results1206 patients were included in the study (mean age: 58.5; 65.3% female). The USSBP regular group demonstrated a higher likelihood of detecting CAG (20% vs. 5.3%; aOR 4.03, 95%CI: 2.69–6.03), GIM (12.2% vs. 3.4%; aOR 3.91, 95%CI: 2.39–6.42) and AIG (2.9% vs. 0.8%; aOR 6.52, 95%CI: 1.87–22.74) compared to infrequent group. Detection of advanced-stage CAG (Operative Link for Gastritis Assessment stage III/IV) was significantly higher in the USSBP regular vs. infrequent group (aOR 5.84, 95%CI: 2.23–15.31). ConclusionsRoutine adherence to USSBP increases the detection rates of preneoplastic conditions, including CAG, GIM and AIG. Standardized implementation of USSBP should be considered in high gastric cancer risk populations.

Pepsinogen and Helicobacter pylori: Serum biomarkers for gastric cancer risk in a diverse United States population

BackgroundSerum Pepsinogen (PG) and Helicobacter pylori (Hp) have potential as biomarkers to identify persons at high risk for gastric cancer (GC) in low incidence populations. We explored the use of these biomarkers in a diverse US population. MethodsSingle institution study using serum samples from 32 newly diagnosed GC (before treatment) and 60 non-cancer participants. ELISA-based PG-I, PG-II, Hp IgG, and Hp virulence seromarker (CagA, VacA) tests were conducted to examine differences between GC and non-GC participants. ResultsMedian age was 58 (IQR 48–68); 56 % were females; 30.1 % were white, 14.8 % black, 28.7 % Hispanic, 6.1 % Asian and 18.2 % other/unknown race/ethnicity. Median values of Hp (47.9 vs 12.6 U/mL, p = 0.003) and pepsinogen ratio (PGR=PGI/PGII) (4.0 vs 7.5, p = 0.003) differed between GC and non-GC. Performance of pepsinogen tests using “standard” cut-offs (PGI ≤ 70 ng/mL and PGR ≤ 3) were highly specific (91.7 %), but not sensitive (34.4 %), while Hp IgG test using “standard” cut-off (≥ 30 U/mL) was sensitive (78.8 %), but less specific (41.2 %). Optimized cut-off values identified in our population using Youden’s Index were PGR ≤ 5.2 and Hp ≥ 17.5 U/mL. Using a combination of these values resulted in a significant increase in test sensitivity (87.9 %) with lower specificity (50.8 %). ConclusionThe combination of pepsinogens and Hp show promise as biomarkers of GC risk in a racially and ethnically diverse US population. Optimal biomarker cut-off points for US populations may differ from those established in East Asia. By adjusting cut-offs there is potential to design GC risk stratification tools tailored specifically for the diverse population within the US.

Data-driven rapid detection of Helicobacter pylori infection through machine learning with limited laboratory parameters in Chinese primary clinics

BackgroundHelicobacter pylori (H. pylori) is a significant global health concern, posing a high risk for gastric cancer. Conventional diagnostic and screening approaches are inaccessible, invasive, inaccurate, time-consuming, and expensive in primary clinics. ObjectiveThis study aims to apply machine learning (ML) models to detect H. pylori infection using limited laboratory parameters from routine blood tests and to investigate the association of these biomarkers with clinical outcomes in primary clinics. MethodsA retrospective analysis with three ML and five ensemble models was conducted on 1409 adults from Hubei Provincial Hospital of Traditional Chinese Medicine. evaluating twenty-three blood test parameters and using the C14 urea breath test as the gold standard for diagnosing H. pylori infection. ResultsIn our comparative study employing three different feature selection strategies, Random Forest (RF) model exhibited superior performance over other ML and ensemble models. Multiple evaluation metrics underscored the optimal performance of the RF model (ROC = 0.951, sensitivity = 0.882, specificity = 0.906, F1 = 0.906, accuracy = 0.894, PPV = 0.908, NPV = 0.880) without feature selection. Key biomarkers identified through importance ranking and shapley additive Explanations (SHAP) analysis using the RF model without feature selection include White Blood Cell Count (WBC), Mean Platelet Volume (MPV), Hemoglobin (Hb), Red Blood Cell Count (RBC), Platelet Crit (PCT), and Platelet Count (PLC). These biomarkers were found to be significantly associated with the presence of H. pylori infection, reflecting the immune response and inflammation levels. ConclusionAbnormalities in key biomarkers could prompt clinical workers to consider H. pylori infection. The RF model effectively identifies H. pylori infection using routine blood tests, offering potential for clinical application in primary clinics. This ML approach can enhance diagnosis and screening, reducing medical burdens and reliance on invasive diagnostics.

Whole-genome sequences of Helicobacter pylori isolated from patients with high risk of gastric cancer in the Andes of Nariño, Colombia.

We sequenced the complete genomes of 16 Helicobacter pylori isolates obtained from patients residing in Nariño, Colombia. These isolates were collected from patients presenting various gastric lesions classified according to the Correa cascade classification. The genomic characterization of these isolates provides valuable insights into the structure, composition, and pathogenicity.

Characterizing the post-traumatic growth trajectory in gastric cancer survivors: a population-based longitudinal study.

Post-traumatic growth can improve the quality of life of cancer survivors. The objective of this study was to investigate post-traumatic growth heterogeneity trajectory in perioperative gastric cancer survivors, and to identify characteristics that predict membership for each trajectory. Gastric cancer survivors (n = 403) were recruited before surgery, their baseline assessment (including post-traumatic growth and related characteristics) was completed, and post-traumatic growth levels were followed up on the day they left the intensive care unit, at discharge, and 1month after discharge. Latent growth mixture mode was used to identify the heterogeneous trajectory of post-traumatic growth, and the core predictors of trajectory subtypes were explored using a decision tree model. Three post-traumatic growth development trajectories were identified among gastric cancer survivors: stable high of PTG group (20.6%), fluctuation of PTG group (44.4%), persistent low of PTG group (35.0%). The decision tree model showed anxiety, coping style, and psychological resilience-which was the primary predictor-might be used to predict the PTG trajectory subtypes of gastric cancer survivors. There was considerable variability in the experience of post-traumatic growth among gastric cancer survivors. Recognition of high-risk gastric cancer survivors who fall into the fluctuation or persistent low of PTG group and provision of psychological resilience-centered support might allow medical professionals to improve patients' post-traumatic growth and mitigate the impact of negative outcomes.

Comparative effectiveness of sodium-glucose cotransporter-2 inhibitors for new-onset gastric cancer and gastric diseases in patients with type 2 diabetes mellitus: a population-based cohort study

ObjectiveTo compare the risks of gastric cancer and other gastric diseases in patients with type-2 diabetes mellitus (T2DM) exposed to sodium-glucose cotransporter 2 inhibitors (SGLT2I), dipeptidyl peptidase-4 inhibitors (DPP4I) or glucagon-like peptide-1 receptor agonists (GLP1a).DesignThis was a population-based cohort study of prospectively collected data on patients with T2DM prescribed SGLT2I, DPP4I or GLP1a between January 1st 2015 and December 31st 2020 from Hong Kong. The outcomes were new-onset gastric cancer, peptic ulcer (PU), acute gastritis, non-acute gastritis, and gastroesophageal reflux disease (GERD). Propensity score matching (1:1) using the nearest neighbour search was performed, and multivariable Cox regression was applied. A three-arm comparison between SGLT2I, DPP4I and GLP1a was conducted using propensity scores with inverse probability of treatment weighting.ResultsA total of 62,858 patients (median age: 62.2 years old [SD: 12.8]; 55.93% males; SGLT2I: n = 23,442; DPP4I: n = 39,416) were included. In the matched cohort, the incidence of gastric cancer was lower in SGLT2I (Incidence rate per 1000 person-year, IR: 0.32; 95% confidence interval, CI 0.23–0.43) than in DPP4I (IR per 1000 person-year: 1.22; CI 1.03–1.42) users. Multivariable Cox regression found that SGLT2I use was associated with lower risks of gastric cancer (HR 0.30; 95% CI 0.19–0.48), PU, acute gastritis, non-acute gastritis, and GERD (p < 0.05) compared to DPP4I use. In the three-arm analysis, GLP1a use was associated with higher risks of gastric cancer and GERD compared to SGLT2I use.ConclusionsThe use of SGLT2I was associated with lower risks of new-onset gastric cancer, PU, acute gastritis, non-acute gastritis, and GERD after matching and adjustments compared to DPP4I use. SGLT2I use was associated with lower risks of GERD and gastric cancer compared to GLP1a use.Graphical abstract

Clinical Characteristics of Patients With Previous Helicobacter pylori Infection-Induced Atrophic Gastritis.

Patients with atrophic gastritis unrelated to autoimmune gastritis (AIG) and without active Helicobacter pylori (H.pylori)infection or previous eradication therapy are considered to have previous Helicobacter pylori infection-induced atrophic gastritis (PHIG). This study aimed to clarify the clinical characteristics of patients with PHIG. Consecutive patients who underwent upper gastrointestinal endoscopy during the study period were enrolled in the study. Pepsinogen and gastrin levels, H. pylori serology, and endoscopic atrophic grade were assessed. Patients were divided into five groups based on their H. pylori status and disease history (PHIG, without H. pylori infection, with active H. pylori infection, with successful H. pylori eradication, and AIG). Their gastric cancer risk status was classified according to the ABC method of serological gastric cancer screening. Of 536 consecutive patients who underwent upper gastrointestinal endoscopy during the study period, 318 were included (31 with PHIG, 77 without H. pylori infection, 101 with active H. pylori infection, 80 with successful H. pylori eradication, and 29 with AIG). Of the 31 patients with PHIG, 21 (68%) were H. pylori-seronegative,and 20 (65%) were classified as group A (normal pepsinogen, H. pylori-seronegative). Patients with PHIG accounted for 90.1% of the patients at high risk for gastric cancer misclassified as group A. The pepsinogen and H. pylori serological profiles of patients with PHIG were similar to those of patients with successful H. pylori eradication more than six years previously. A receiver-operating characteristic curve (ROC) analysis that included 13 patients with AIG and without active H. pylori infection and no previous eradication therapy and 31 patients with PHIG revealed that an endoscopic atrophy grade of O-III or greater according to the Kimura-Takemoto classification can predict AIG. Two-thirds of the patients with PHIG were misclassified as being at low risk (group A) according to the ABC method, suggesting that endoscopy is necessary for group A patients. The results of the serological evaluation of PHIG indicated that patients with PHIG may have experienced spontaneous H. pylori eradication, possibly because of the use of antibiotics for other conditions. Autoimmune gastritis should be considered in the presence of grade 0-III or greater gastric mucosal atrophy in patients with suspected PHIG, even if the autoantibody and histological findings are not available.

Helicobacter pylori Treatment and Gastric Cancer Risk Among Individuals With High Genetic Risk for Gastric Cancer

Helicobacter pylori treatment and nutrition supplementation may protect against gastric cancer (GC), but whether the beneficial effects only apply to potential genetic subgroups and whether high genetic risk may be counteracted by these chemoprevention strategies remains unknown. To examine genetic variants associated with the progression of gastric lesions and GC risk and to assess the benefits of H pylori treatment and nutrition supplementation by levels of genetic risk. This cohort study used follow-up data of the Shandong Intervention Trial (SIT, 1989-2022) and China Kadoorie Biobank (CKB, 2004-2018) in China. Based on the SIT, a longitudinal genome-wide association study was conducted to identify genetic variants for gastric lesion progression. Significant variants were examined for incident GC in a randomly sampled set of CKB participants (set 1). Polygenic risk scores (PRSs) combining independent variants were assessed for GC risk in the remaining CKB participants (set 2) and in an independent case-control study in Linqu. H pylori treatment and nutrition supplementation. Primary outcomes were the progression of gastric lesions (in SIT only) and the risk of GC. The associations of H pylori treatment and nutrition supplementation with GC were evaluated among SIT participants with different levels of genetic risk. Our analyses included 2816 participants (mean [SD] age, 46.95 [9.12] years; 1429 [50.75%] women) in SIT and 100 228 participants (mean [SD] age, 53.69 [11.00] years; 57 357 [57.23%] women) in CKB, with 147 GC cases in SIT and 825 GC cases in CKB identified during follow-up. A PRS integrating 12 genomic loci associated with gastric lesion progression and incident GC risk was derived, which was associated with GC risk in CKB (highest vs lowest decile of PRS: hazard ratio [HR], 2.54; 95% CI, 1.80-3.57) and further validated in the analysis of 702 case participants and 692 control participants (mean [SD] age, 54.54 [7.66] years; 527 [37.80%] women; odds ratio, 1.83; 95% CI, 1.11-3.05). H pylori treatment was associated with reduced GC risk only for individuals with high genetic risk (top 25% of PRS: HR, 0.45; 95% CI, 0.25-0.82) but not for those with low genetic risk (HR, 0.81; 95% CI, 0.50-1.34; P for interaction = .03). Such effect modification was not found for vitamin (P for interaction = .93) or garlic (P for interaction = .41) supplementation. The findings of this cohort study indicate that a high genetic risk of GC may be counteracted by H pylori treatment, suggesting primary prevention could be tailored to genetic risk for more effective prevention.

Autoimmune conditions and gastric cancer risk in a population-based study in the United Kingdom

BackgroundAlthough overall incidence of gastric cancer is decreasing, incidence has been increasing among young people in some Western countries. This trend may stem from the increase in autoimmune conditions.MethodsA nested case-control study of gastric cancer in UK Clinical Practice Research Datalink. Up to ten cancer-free controls were matched to cases by age and sex. Conditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI) for associations between analyzable autoimmune conditions (n = 34) and gastric cancer with Bonferroni correction. We evaluated associations between pernicious anaemia and other conditions. A meta-analysis of published prospective studies and ours was conducted.ResultsAmong 6586 cases (1156 cardia, 1104 non-cardia, and 4334 overlapping/unspecified tumours) and 65,687 controls, any autoimmune condition was associated with gastric cancer (OR = 1.10; 95% CI: 1.01–1.20). Individuals with pernicious anaemia had higher gastric cancer risk than those without (OR = 2.75; 2.19–3.44). Among controls, pernicious anaemia was associated with seven other conditions (OR range: 2.21–29.80). The pooled estimate for any autoimmune condition and gastric cancer was 1.17 (1.14–1.21; n = 47,126 cases).ConclusionAutoimmunity increases gastric cancer risk. Some autoimmune conditions may be indirectly associated with gastric cancer via pernicious anaemia. Pernicious anaemia could be considered for gastric cancer risk stratification and screening.

Hotspots and trends of risk factors in gastric cancer: A visualization and bibliometric analysis.

The lack of specific symptoms of gastric cancer (GC) causes great challenges in its early diagnosis. Thus it is essential to identify the risk factors for early diagnosis and treatment of GC and to improve the survival rates. To assist physicians in identifying changes in the output of publications and research hotspots related to risk factors for GC, constructing a list of key risk factors, and providing a reference for early identification of patients at high risk for GC. Research articles on risk factors for GC were searched in the Web of Science core collection, and relevant information was extracted after screening. The literature was analyzed using Microsoft Excel 2019, CiteSpace V, and VOSviewer 1.6.18. A total of 2514 papers from 72 countries and 2507 research institutions were retrieved. China (n = 1061), National Cancer Center (n = 138), and Shoichiro Tsugane (n = 36) were the most productive country, institution, or author, respectively. The research hotspots in the study of risk factors for GC are summarized in four areas, namely: Helicobacter pylori (H. pylori) infection, single nucleotide polymorphism, bio-diagnostic markers, and GC risk prediction models. In this study, we found that H. pylori infection is the most significant risk factor for GC; single-nucleotide polymorphism (SNP) is the most dominant genetic factor for GC; bio-diagnostic markers are the most promising diagnostic modality for GC. GC risk prediction models are the latest current research hotspot. We conclude that the most important risk factors for the development of GC are H. pylori infection, SNP, smoking, diet, and alcohol.

Bibliometric and visualized analysis of global research on microRNAs in gastric cancer: from 2013 to 2023.

Gastric cancer (GC) imposes a heavy burden on global public health, and microRNAs (miRNAs) play a crucial role in the diagnosis and treatment of GC. Therefore, it is necessary to clarify the hotspots and frontiers in the field of miRNAs in GC to guide future research. A total of 2,051 publications related to miRNAs in GC from January 2013 to December 2023 were searched from the Web of Science Core Collection database. CiteSpace was used to identify research hotspots and delineate developmental trends. In the past decade, China, Nanjing Medical University, and Ba Yi were the most contributing research country, institute, and author in this field, respectively. The role of miRNAs as biomarkers in GC, the mechanism of miRNAs in the progression of GC, and the impact of the mutual effects between miRNAs and Helicobacter pylori on GC have been regarded as the research hotspots. The mechanisms of miRNAs on glucose metabolism and the application of the roles of circular RNAs as miRNA sponges in GC treatment will likely be frontiers. Overall, this study called for strengthened cooperation to identify targets and therapeutic regimes for local specificity and high-risk GC types, and to promote the translation of research results into clinical practice.

Modifiable and Non-Modifiable Factors Associated with Gastric Cancer

Numerous studies have investigated the associations between dietary components, behavioral patterns, and susceptibility to gastric cancer (GC). Diet and lifestyle cover a spectrum of both protective and harmful factors associated with GC. Additionally, non-modifiable factors such as age, gender, blood type, family history, and genetic predispositions may influence GC development. This review aims to explore the interplay between modifiable and non-modifiable factors, along with dietary habits and lifestyle practices, in relation to GC risk and the potential underlying mechanisms. We have synthesized the primary findings of observational studies (case-control and cohort), systematic reviews, and meta-analyses pertaining to preventive and deleterious factors affecting the incidence of gastric cancer. A literature search was conducted on Google Scholar, MEDLINE (PubMed), ScienceDirect, and Scopus for articles published in English from 2001 to 2024. The main search terms included body weight and body fat; diet; fruits and vegetables; meats and processed meats; fried and fast foods; milk and dairy products; salty foods; food and dietary patterns; fat and sweets intake; alcohol consumption; smoking; physical activity; age; sex; family history; blood type; genetics; and medication, and the risk of gastric cancer. Unhealthy dietary patterns, consumption of fried and fast foods, salty foods, alcohol, and smoking have been associated with an increased risk of GC. Non-modifiable factors such as advanced age, male sex, family history, genetics, and blood type A were linked to an elevated risk of GC. Conversely, physical activity and high consumption of fresh fruits and vegetables may prevent GC occurrence due to the presence of antioxidants, fiber, and polyphenols. While many studies have demonstrated that dietary patterns loaded with red and processed meats were associated with a high risk of GC, others have yielded inconclusive results. Controversial findings regarding the relationship between body weight and body fat, medications, milk and dairy products, and fat and sweets consumption with the risk of GC were also observed. Adequate diet modification and addressing preventable factors may play a pivotal role in reducing the incidence of gastric cancer.

Association between glycemic status and the risk of gastric cancer in pre/peri-and postmenopausal women: A nationwide cohort study

PurposeThis study aimed to assess the correlation between glycemic status (prediabetes and type 2 diabetes mellitus) and the risk of gastric cancer according to menopausal status. MethodsA total of 982,559 pre/peri-menopausal and 1445,419 postmenopausal women aged ≥ 40, who underwent the Korean national health screening in 2009, were included and followed up until 2018. Hazard ratio (HR) and 95% confidence interval (CI) were calculated for development of gastric cancers according to hyperglycemic status in both groups using Cox proportional hazards models. ResultsOver a mean follow-up period of 8.3 years, 3259 (0.33%) pre/peri-menopausal women and 13,245 (0.92%) postmenopausal women were diagnosed with gastric cancer. In postmenopausal women, only diabetes mellitus conferred a higher risk of gastric cancer compared to normal glycemic status (HR, 1.15; 95% CI, 1.09–1.20), with an increasing trend of gastric cancers from prediabetes to diabetes (P for trend < 0.001) observed regardless of menopausal status. Obesity, smoking, and heavy alcohol consumption was associated with increased gastric cancer risk mainly in the postmenopausal period. ConclusionsThe risk of gastric cancer escalates with deteriorating glycemic status in a dose-response manner. Diabetes mellitus is linked with an elevated risk of gastric cancer in postmenopausal women.

Adding salt to food at table as an indicator of gastric cancer risk among adults: a prospective study

BackgroundWhile dietary salt intake has been linked with gastric cancer risk in Asian studies, findings from Western populations are sparse and limited to case—control studies. Our aim was to evaluate the frequency of adding salt to food at table in relation to gastric cancer risk among UK adults.MethodsWe evaluated associations between the frequency of adding salt to food and the risk of gastric cancer in the UK Biobank (N = 471,144) using multivariable Cox regression. Frequency of adding salt to food was obtained from a touchscreen questionnaire completed at baseline (2006–2010). 24-h urinary sodium excretion was estimated using INTERSALT formulae. Cancer incidence was obtained by linkage to national cancer registries.ResultsDuring a median follow-up period of 10.9 years, 640 gastric cancer cases were recorded. In multivariable models, the gastric cancer risk among participants reporting adding salt to food at table “always” compared to those who responded “never/rarely” was HR = 1.41 (95% CI: 1.04, 1.90). There was a positive linear association between estimated 24-h urinary sodium levels and the frequency of adding salt to food (p-trend <0 .001). However, no significant association between estimated 24-h urinary sodium with gastric cancer was observed (HR = 1.19 (95% CI: 0.87, 1.61)).Conclusions“Always adding salt to food” at table was associated with a higher gastric cancer risk in a large sample of UK adults. High frequency of adding salt to food at table can potentially serve as a useful indicator of salt intake for surveillance purposes and a basis for devising easy-to-understand public health messages.

Laparoscopic sleeve gastrectomy combined with Toupet fundoplication (T-sleeve): A short report of a Japanese obesity patient with gastroesophageal reflux disease.

Laparoscopic sleeve gastrectomy (LSG) is the most frequently performed procedure in bariatric-metabolic surgery (BMS) worldwide, accounting for approximately 90% of BMS procedures in Japan. While numerous studies have reported on the safety and efficacy of LSG, gastroesophageal reflux disease (GERD) remains a major postoperative complication. Although Roux-en-Y gastric bypass (RYGB) is preferred for severe obesity with GERD, it is less suitable for Japanese patients who have a higher risk of gastric cancer due to the remnant stomach which is difficult to observe with esophago-gastro-duodenoscopy. To address de novo and exacerbation GERD after LSG, we conducted LSG with Toupet fundoplication (T-sleeve) for Japanese patients with severe obesity. In our first T-sleeve case, the patient demonstrated sufficient weight loss and improved GERD following surgery. Hence, we suggest that T-sleeve is a feasible option for Japanese patients with obesity and concurrent GERD.

Severe induction of aberrant DNA methylation by nodular gastritis in adults.

Nodular gastritis (NG) is characterized by marked antral lymphoid follicle formation, and is a strong risk factor for diffuse-type gastric cancer in adults. However, it is unknown whether aberrant DNA methylation, which is induced by atrophic gastritis (AG) and is a risk for gastric cancer, is induced by NG. Here, we analyzed methylation induction by NG. Gastric mucosal samples were obtained from non-cancerous antral tissues of 16 NG and 20 AG patients with gastric cancer and 5 NG and 6 AG patients without, all age- and gender-matched. Genome-wide methylation analysis and expression analysis were conducted by a BeadChip array and RNA-sequencing, respectively. Clustering analysis of non-cancerous antral tissues of NG and AG patients with gastric cancer was conducted using methylation levels of 585 promoter CpG islands (CGIs) of methylation-resistant genes, and a large fraction of NG samples formed a cluster with strong methylation induction. Promoter CGIs of CDH1 and DAPK1 tumor-suppressor genes were more methylated in NG than in AG. Notably, methylation levels of these genes were also higher in the antrum of NG patients without cancer. Genes related to lymphoid follicle formation, such as CXCL13/CXCR5 and CXCL12/CXCR4, had higher expression in NG, and genes involved in DNA demethylation TET2 and IDH1, had only half the expression in NG. Severe aberrant methylation, involving multiple tumor-suppressor genes, was induced in the gastric antrum and body of patients with NG, in accordance with their high gastric cancer risk.

Facilitators of and barriers to gastric cancer and precursor diagnosis among South Texas residents: Social determinants of health.

Latinos/Hispanics are at higher risk for developing gastric cancer (GC) compared with non-Hispanic whites, and social determinants of health (SDoH) are thought to contribute. This study addressed SDoH and their interactions contributing to disparities in the testing and treatment of Helicobacter pylori (HP) infection and diagnosis of GC and its known precursors, among Latinos/Hispanics relative to non-Latinos at two affiliated but independent health systems in San Antonio, Texas, using a mixed methods approach. Secondary data abstraction and analysis showed that GCs represented 2.6% (n = 600) of our population. Men and older individuals were at higher GC risk. Individuals with military insurance were 2.7 times as likely to be diagnosed as private insurance. Latinos/Hispanics had significantly (24%) higher GC risk than Whites. Poverty and lack of insurance contributed to GC risk among the minorities classified as other (Asians, Native Americans, Multiracial; all p < 0.01). All SDoH were associated with H. pylori infection (p < 0.001). Qualitative analysis of patient and provider interviews showed providers reporting insurance as a major care barrier; patients reported appointment delays, and lack of clinic staff. Providers universally agreed treatment of H. pylori was necessary, but disagreed on its prevalence. Patients did not report discussing H. pylori or its cancer risk with providers. These data indicate the importance of considering SDoH in diagnosis and treatment of GC and its precursors, and educating providers and patients on H. pylori risks for GC.

Cold snaring biopsies to increase screening efficacy during endoscopic surveillance of patients at high risk of diffuse gastric cancer.

Cold snaring biopsies to increase screening efficacy during endoscopic surveillance of patients at high risk of diffuse gastric cancer.

Poor oral health was associated with higher risk of gastric cancer: Evidence from 1431677 participants.

In recent years, the association between oral health and the risk of gastric cancer (GC) has gradually attracted increased interest. However, in terms of GC incidence, the association between oral health and GC incidence remains controversial. Periodontitis is reported to increase the risk of GC. However, some studies have shown that periodontitis has no effect on the risk of GC. Therefore, the present study aimed to assess whether there is a relationship between oral health and the risk of GC. To assess whether there was a relationship between oral health and the risk of GC. Five databases were searched to find eligible studies from inception to April 10, 2023. Newcastle-Ottawa Scale score was used to assess the quality of included studies. The quality of cohort studies and case-control studies were evaluated separately in this study. Incidence of GC were described by odds ratio (OR) and 95% confidence interval (CI). Funnel plot was used to represent the publication bias of included studies. We performed the data analysis by StataSE 16. A total of 1431677 patients from twelve included studies were enrolled for data analysis in this study. According to our analysis, we found that the poor oral health was associated with higher risk of GC (OR = 1.15, 95%CI: 1.02-1.29; I2 = 59.47%, P = 0.00 < 0.01). Moreover, after subgroup analysis, the outcomes showed that whether tooth loss (OR = 1.12, 95%CI: 0.94-1.29; I2 = 6.01%, P > 0.01), gingivitis (OR = 1.19, 95%CI: 0.71-1.67; I2 = 0.00%, P > 0.01), dentures (OR = 1.27, 95%CI: 0.63-1.19; I2 = 68.79%, P > 0.01), or tooth brushing (OR = 1.25, 95%CI: 0.78-1.71; I2 = 88.87%, P > 0.01) had no influence on the risk of GC. However, patients with periodontitis (OR = 1.13, 95%CI: 1.04-1.23; I2 = 0.00%, P < 0.01) had a higher risk of GC. Patients with poor oral health, especially periodontitis, had a higher risk of GC. Patients should be concerned about their oral health. Improving oral health might reduce the risk of GC.