Risk Factor For Gastric Cancer Research Articles

Helicobacter pylori promotes gastric cancer progression by activating the TGF-β/Smad2/EMT pathway through HKDC1.

Helicobacter pylori (H. pylori) infection is widely acknowledged as the primary risk factor for gastric cancer, facilitating its progression via the Correa cascade. Concurrently, Hexokinase Domain Containing 1 (HKDC1) has been implicated in the mediation of aerobic glycolysis, contributing to tumorigenesis across various cancers. However, the precise role of HKDC1 in the inflammatory transformation associated with H. pylori-induced gastric cancer remains elusive. In this study, transcriptome sequencing revealed a significant correlation between HKDC1 and H. pylori-induced gastric cancer. Subsequent validation using qRT-PCR, immunohistochemistry, and Western blot analysis confirmed elevated HKDC1 expression in both human and murine gastritis and gastric tumors. Moreover, in vitro and in vivo experiments demonstrated that H. pylori infection up-regulates TGF-β1 and p-Smad2, thereby activating the epithelial-mesenchymal transition (EMT) pathway, with HKDC1 playing a pivotal role. Suppression of HKDC1 expression or pharmacological inhibition of TGF-β1 reversed EMT activation, consequently reducing gastric cancer cell proliferation and metastasis. These results underscore HKDC1's essential contribution to H. pylori-induced gastric cancer progression via EMT activation.

More powerful dysregulation of Helicobacter pylori East Asian-type CagA on intracellular signalings.

Chronic infection by Helicobacter pylori strains expressing cytotoxin-associated gene A (CagA) are the strongest risk factor for gastric cancer. CagA can be classified into East Asian-type and Western-type (CagAE and CagAW), with CagAE being more closely associated with gastric cancer. This study aimed to investigate the impact of CagAE on intracellular signaling pathways to explain its high oncogenicity. Mutant H. pylori strains expressing either CagAE or CagAW were generated by transforming CagAE/W-expression plasmid into CagA-deleted G27 strain (G27ΔCagA). In human gastric epithelial cells (GES-1) infection, CagAE induced more severe cytopathic changes, including higher interleukin-8 (IL-8) secretion, reduced cell viability, more pronounced "hummingbird phenotype" alterations, and increased cell migration and invasion compared to CagAW. Transcriptome analysis revealed that CagAE had a stronger effect on the up-regulation of key intracellular processes, including tumor necrosis factor-ɑ (TNF-ɑ) signal pathway via nuclear factor kappa-B (NF-κB), inflammatory response, interferon-γ (IFN-γ) response, hypoxia, ultraviolet (UV) response, and Kirsten Rat Sarcoma Viral Oncogene Homolog (KRAS) signaling. A significant upregulation of hypoxia-related genes was a notable feature of CagAE. GES-1 cells infected with CagAE exhibited more severe intracellular hypoxia and higher levels of reactive oxygen species (ROS) than those infected with CagAW. Inhibition of hypoxia-inducible factor-1α (HIF-1α), which blocks hypoxia signaling, mitigated CagAE-induced cell migration, emphasizing the role of hypoxia in mediating CagAE effects. The study provides transcriptome evidence of CagA-associated intracellular regulation during H. pylori infection, demonstrating that CagAE exerts stronger effects on intracellular signaling than CagAW. These findings offer insights into the heightened carcinogenic potential of CagAE in H. pylori-induced gastric cancer.

Racial/ethnic differences in risk factors for non-cardia gastric cancer: an analysis of the Multiethnic Cohort (MEC) Study.

Gastric cancer (GC) incidence rates show notable differences by racial/ethnic groups in the US. We sought to determine whether stratification by race/ethnicity would reveal unique risk factors for development of non-cardia gastric cancer (NCGC) for US population. Analysis included 1,112 incident cases of NCGC and 190,883 controls from the Multiethnic Cohort Study, a prospective US cohort study that recruited individuals living in Hawaii and California, aged 45-75years from 5 races/ethnicities. Descriptive analysis and Cox regression models examined the association of risk factors for GC and calculate hazard ratios for each race/ethnicity, adjusting for sociodemographic and dietary variables. Increasing age and male sex were risk factors for NCGC for most race/ethnicities. Higher risk was associated with: GC family history for Latino and Japanese American individuals [HRs range from 1.75 to 1.98]; foreign-born for Japanese American individuals [HR: 1.52, 95% CI 1.11-2.09]; lower education for African American, Japanese American, and Native Hawaiian individuals [HRs range from 1.30 to 1.74]; daily alcohol consumption for African American individuals[HR: 1.56, 95% CI 1.04-2.35]; current smoking for Latino and Japanese American individuals [HRs range from 1.89 to 1.94]; sodium consumption in the highest quartile for White individuals [HR: 2.55, 95% CI 1.23-5.26] compared to the lowest quartile; fruit consumption in the 2nd, 3rd, and 4th highest quartile for Native Hawaiian individuals [HRs range from 2.19 to 2.60] compared to the lowest quartile; diabetes for African American individuals [HR: 1.79, 95% CI 1.21-2.64]; and gastric/duodenal ulcers for Native Hawaiian individuals [HR: 1.82, 95% CI 1.04-3.18]. Analyses by racial/ethnic group revealed differing risk factors for NCGC. Increased knowledge of the varying pathways to GC can support personalized GC prevention strategies and risk stratification tools for early detection.

Long non-coding RNA AC010457.1 promotes the growth and EMT of gastric cancer via the PI3K/AKT axis

Gastric cancer (GC) is a malignancy with a relatively high mortality rate. This study aimed to ascertain the prognostic significance of long non-coding RNA (lncRNA) AC010457.1 in GC and elucidate its role in disease progression. The Cancer Genome Atlas (TCGA) database was used to screen the prognosis-associated differentially expressed lncRNAs in GC patients. Kaplan-Meier curves, univariate and multivariate Cox regression analyses were applied to assess the prognostic significance of AC010457.1. In vitro and in vivo functional assays were performed to evaluate the effects of AC010457.1 on cellular proliferation and metastasis. Mechanistic investigations, including Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, Western blotting (WB), Immunofluorescence (IF), and Immunohistochemistry (IHC), were used to explore the signaling pathways activated by AC010457.1. We demonstrated that AC010457.1 was abnormally upregulated in GC tissues, and that this aberrant upregulation was associated with a poor prognosis for GC patients. The functional experiments proved that the downregulated of AC010457.1 hindered GC cell proliferation, migration, and invasive potential. Furthermore, KEGG analysis revealed a significant association between AC010457.1 and the PI3K/AKT signaling pathway, which was further corroborated by WB analysis. Rescue experiments provided additional confirmation that AC010457.1 regulated PI3K/AKT promote GC proliferation, migration, and epithelial-mesenchymal transition (EMT). Collectively, our findings suggest that AC010457.1 overexpression serves as a distinct prognostic risk factor in GC and may represent a promising therapeutic target for the treatment of this malignancy.

Development and validation of a relatively accurate gastric cancer high-risk group screening scoring system in urban residents.

Our study aimed to develop a relatively accurate gastric cancer (GC) screening score system for urban residents and to validate the screening efficacy. The present study included a derivation cohort (n = 3406) and a validation cohort (n = 868) of urban residents. Applying the full-stack engineering intelligent system platform of Hualian Health Big Data of Shandong University, the clinical physical examination data of subjects were collected. Univariate and multivariate analyses were used to identify risk factors for GC, and subsequently, an optimal prediction rule was established to create three distinct scoring systems. In the GC-risk scoring system I, age, plateletocrit (PCT), carcinoembryonic antigen (CEA), glucose, albumin, creatinine were independent risk factors of GC, with scores ranging from 0 to 28 and optimal cut-off was 15.5. The second scoring system consisted of age, PCT, RDW-CV, CEA, glucose, albumin, and creatinine, with scores ranging from 0 to 31. The optimal cut-off point was determined to be 15.5. The scoring system III comprise of age, sex, PCT, RDW CV, CEA, glucose, with scores ranging from 0 to 21 and optimal cut-off was 10.5. All three scoring systems demonstrated excellent discrimination for GC, achieving an AUC of 0.884, 0.89, and 0.876, respectively. In external validation, the AUC values were 0.654, 0.658, and 0.714. Notably, the GC-risk scoring system III exhibited the highest screening efficiency. Urban residents benefited from the effective and verified GC-risk scoring systems, which demonstrated excellent performance in identifying individuals with an elevated risk of GC.

Public awareness of gastric cancer risk factors and screening behaviours in Shijiazhuang, China: A community-based survey.

Reducing exposure to risk factors and screening represent 2 major approaches to gastric cancer (GC) prevention, but public knowledge GC risk factors and screening behaviour remain unknown. We aimed to investigate public awareness of GC risk factors, adherence to screening, and barriers hindering screening practices in China. This community-based household survey was conducted within Shijiazhuang, China, and 1490 residents were recruited through a multistage stratified cluster random sampling approach. A self-administered questionnaire was completed which consisted of three sections: demographics, awareness of GC risk factors, and personal screening behaviours. Factors associated with knowledge of risk factors and screening behaviours were evaluated using binary logistic regression analysis. The mean risk factor awareness score of 12 (7, 15) revealed insufficient knowledge in 51.1% of participants. Dietary lifestyle factors were better understood than physical activity and weight-related factors. Marital status (OR 1.967; 95% CI 1.415 to 2.734), higher income (OR 1.197; 95% CI 1.010 to 1.418), and a history of upper gastrointestinal problems (OR 0.048; 95% CI 1.002 to 1.311) were associated with higher awareness. Merely 21.5% underwent GC screening, with higher rates linked to older age (OR 1.642; 95% CI 1.418 to 1.902), higher education (OR 1.398; 95% CI 1.176 to 1.662), a history of upper gastrointestinal problems (OR 3.842; 95% CI 2.833 to 5.209), and moderate (OR 2.077; 95% CI 1.352 to 3.191) and high (OR 2.529; 95% CI 1.311 to 4.878) perceived GC risk. Notably, participants commonly refused gastroscopy due to the absence of symptoms or signs. In Shijiazhuang, more than half of participants demonstrated inadequate knowledge of GC risk factors, and screening participation rates were remarkably low. This emphasizes the need for targeted interventions to enhance GC awareness and significantly improve screening rates.

Risk Factors for Gastric Cancer at RSUP Prof. Dr. I.G.N.G. Ngoerah Year 2018-2023

Gastric cancer is the fifth most common cancer and the fourth most common cause of death due to cancer in the world. The development of gastric cancer tends to be quite slow and takes years, so it is often found in the late stages. The cause of stomach cancer is not known for certain, but it is believed to be caused by many factors. This study aims to determine the risk factors for gastric cancer at RSUP Prof. Dr. I.G.N.G. Ngoerah was diagnosed in 2018-2023. This research was conducted using a retrospective descriptive method using secondary data in the form of medical records on 46 samples of gastric cancer patients who were controls or treated at RSUP Prof. Dr. I.G.N.G. Ngoerah was diagnosed in 2018-2023 The variables studied include the dependent variables, namely age, gender, peptic ulcers, blood type, obesity, alcohol consumption and smoking. The results of the analysis showed that gastric cancer patients at RSUP Prof. Dr. I.G.N.G. The majority are over 50 years old (82.6%), male (58.7%), have no peptic ulcers (89.1%), have blood type A (37%), underweight (50%), are not consume alcohol (97.8%), and do not smoke (97.8%).It can be concluded that the risk factors for gastric cancer patients at RSUP Prof. Dr. I.G.N.G. Ngoerah majority are over 50 years old, male, have no peptic ulcers, have blood type A, are underweight, do not consume alcohol and do not smoke. Keywords: Gastric Cancer, Risk Factors, RSUP Prof. Dr. I.G.N.G. Ngoerah

Endogenous glucocorticoids are required for normal macrophage activation and gastric Helicobacter pylori immunity.

Glucocorticoids are steroid hormones well known for their potent anti-inflammatory effects. However, their immunomodulatory properties are multifaceted. Increasing evidence suggests that glucocorticoid signaling promotes effective immunity and that disruption of glucocorticoid signaling impairs immune function. In this study, we conditionally deleted the glucocorticoid receptor (GR) in the myeloid lineage using the LysM-Cre driver (myGRKO). We examined the impact on macrophage activation and gastric immune responses to Helicobacter pylori, the best-known risk factor of gastric cancer. Our results indicate that, compared with wild type (WT), glucocorticoid receptor knockout (GRKO) macrophages exhibited higher expression of proinflammatory genes in steroid-free conditions. However, when challenged in vivo, GRKO macrophages exhibited aberrant chromatin landscapes and impaired proinflammatory gene expression profiles. Moreover, gastric colonization with H. pylori revealed impaired gastric immune responses and reduced T cell recruitment in myGRKO mice. As a result, myGRKO mice were protected from atrophic gastritis and pyloric metaplasia development. These results demonstrate a dual role for glucocorticoid signaling in preparing macrophages to respond to bacterial infection but limiting their pathogenic activation. In addition, our results support that macrophages are critical for gastric H. pylori immunity.NEW & NOTEWORTHY Signaling by endogenous glucocorticoids primes macrophages toward more robust responses to pathogens. Disruption of glucocorticoid signaling caused dysregulation of the chromatin landscape, blunted proinflammatory gene activation upon bacterial challenge, and impaired the gastric inflammatory response to Helicobacter pylori infection.

Helicobacter pylori induce circ_0046854 to regulate microRNA-511-3p/CSF1 axis and enhance the resistance of gastric cancer to cisplatin.

Helicobacter pylori (HP) is considered a major risk factor for gastric cancer (GC) and during this process, cytotoxin‑associated gene A (CagA) plays in essence. The study mainly focused on the molecular mechanism of circular RNA 0046854 (circ_0046854) in HP-induced GC. Clinically, 56 cases of GC and normal tissues were collected, and the GC tissues were divided into HP-negative GC tissues (HP-) and 33 HP-positive GC tissues (HP+). Tissue expression of circ_0046854, microRNA (miR)-511-3p and colony-stimulating factor 1 (CSF1) was tested. BGC-823/Cisplatin (DDP) resistant strain was induced and cell growth and DDP resistance were detected after HP infection. In vivo experiments were performed using a mouse xenograft model. The relationship between circ_0046854, miR-511-3p and CSF1 was confirmed. GC tissues especially HP+ cancer tissues expressed high circ_0046854 and CSF1 and low miR-511-3p. HP-induced circ_0046854 expression in GC cells through CagA. Inhibition of circ_0046854 or miR-511-3p elevation inhibited the growth and DDP resistance in GC cells. Circ_0046854 acted as a sponge for miR-511-3p, which targeted CSF1. Restoring CSF1 could abolish the inhibitory effect of miR-511-3p overexpression on CagA+ HP-induced GC progression in vitro. Circ_0046854 silencing repressed tumor growth and aggrandized the inhibiting effects of DDP on tumorigenesis in vivo. Circ_0046854/miR-511-3p/CSF1 axis may be involved in the development of HP-induced GC, thus providing new ideas for studying the mechanism of HP-related gastric diseases.

Helicobacter pylori induces GBA1 demethylation to inhibit ferroptosis in gastric cancer.

This research investigates potential therapeutic targets for gastric cancer, focusing on ferroptosis-related genes. Gastric cancer is known for its lower survival rates, necessitating new treatment strategies. This study employed Mendelian randomization to identify ferroptosis-related genes and methylation sites in gastric cancer, examining correlations between Helicobacter pylori infection, GBA1 gene expression, and promoter methylation with single-cell datasets and the TCGA-STAD database. We used Helicobacter pylori-infected gastric cancer cell models and used next-generation sequencing to monitor methylation changes pre- and post-infection. GBA1 expression levels were assessed via qRT-PCR and Western blot both before and after infection. The effect of Helicobacter pylori on GC cell proliferation was analyzed using CCK-8 and EdU assays after knocking down the GBA1 gene. The association between Helicobacter pylori infection and ferroptosis, including its reversibility after GBA1 knockdown, was evaluated using FerrOrange, GSH, MDA, and C11-BODIPY assays. Mass spectrometry measured the impact of Helicobacter pylori and GBA1 knockdown on lipid metabolism. An in vivo subcutaneous tumor-bearing model was also established to confirm these findings. Mendelian randomization analysis revealed that high GBA1 expression and reduced methylation levels of its promoter are risk factors for gastric cancer. Single-cell sequencing and TCGA-STAD datasets indicated a positive correlation between Helicobacter pylori infection and GBA1 expression, with a concurrent negative correlation between GBA1 promoter methylation and GBA1 expression. In gastric cancer cell lines, Helicobacter pylori infection was observed to enhance GBA1 expression and decrease methylation levels at its promoter. Additionally, Helicobacter pylori promoted GC cell proliferation, an effect mitigated by knocking down GBA1. Infection also reduced lipid peroxidation, increased glutathione levels, and impeded ferroptosis in GC cells; however, these effects were reversed following GBA1 knockdown. Changes in sphingolipid metabolism induced by I were detected in GC cell lines. In vivo experiments using a subcutaneous tumor-bearing model demonstrated that Helicobacter pylori infection fosters tumorigenesis in GC cells. Our study demonstrates that Helicobacter pylori infection triggers demethylation and upregulation of GBA1, subsequently inhibiting ferroptosis in gastric cancer cells. These findings suggest that targeting the GBA1 pathway may offer a novel therapeutic approach for managing gastric cancer.

Risk Factors and Prevention of Stomach Cancer, Excluding Helicobacter pylori

Gastric cancer is a significant health problem owing to its high incidence and mortality rate. The risk factors for gastric cancer include both uncontrollable (e.g., age, sex, and genetic predisposition) and controllable factors (e.g., <i>Helicobacter pylori</i> infection, smoking, alcohol consumption, obesity, and high-salt diets). Although treatment of <i>H. pylori</i> infections has been implemented as a primary preventive measure, the risk of gastric cancer may persist, highlighting the need for additional preventive measures. This review discusses various risks and protective factors associated with gastric cancer, studies conducted on these factors, and chemoprevention. Smoking is a risk factor for this disease; thus, is not recommended and current smokers are encouraged to quit because cessation can reduce the risk of gastric cancer. Excessive alcohol intake has been reported to increase the risk of gastric cancer as has the consumption of high-salt foods that can damage the gastric mucosa. Additionally, increasing the intake of fruits and vegetables, known for their protective effects against gastric cancer, can aid in its prevention. Studies on chemopreventive agents, including nonsteroidal anti-inflammatory drugs (e.g., aspirin), statins, and metformin, have been reported; however, evidence of their effectiveness remains insufficient to recommend these agents as preventive treatments. Additional well-planned studies on preventive medications and dietary approaches are necessary.

Gastric Cancer: An Up-to-Date Review with New Insights into Early-Onset Gastric Cancer.

Gastric cancer (GC) is the fifth most frequently diagnosed cancer and the fifth most common cause of cancer death in the world. Regarding the age at which the diagnosis was made, GC is divided into early-onset gastric cancer (EOGC-up to 45 years of age) and conventional GC (older than 45). EOGC constitutes approximately 10% of all GCs. Numerous reports indicate that EOGC is more aggressive than conventional GC and is often discovered at an advanced tumor stage, which has an impact on the five-year survival rate. The median survival rate for advanced-stage GC is very poor, amounting to less than 12 months. Risk factors for GC include family history, alcohol consumption, smoking, Helicobacter pylori, and Epstein-Barr virus infection. It has been shown that a proper diet and lifestyle can play a preventive role in GC. However, research indicates that risk factors for conventional GC are less correlated with EOGC. In addition, the unclear etiology of EOGC and the late diagnosis of this disease limit the possibilities of effective treatment. Genetic factors are considered a likely cause of EOGC, as young patients are less exposed to environmental carcinogens. Research characterizing GC in young patients is scarce. This comprehensive study presents all aspects: epidemiology, risk factors, new treatment strategies, and future directions.

Chronic Atrophic Gastritis and Intestinal Metaplasia: A Latin American Perspective

Gastric cancer (GC), a significant cause of mortality globally, is the leading cause of cancer-related deaths among Latin American men. GC is usually diagnosed at an advanced stage; therefore, therapeutic options are limited, and prognosis is poor. <i>Helicobacter pylori</i> infection remains the primary risk factor for GC; therefore, primary prevention directed toward diagnosis and treatment (“test-and-treat” strategy) is important. Western medicine guidelines recommend esophagogastroduodenoscopy (EGD) for at-risk individuals aged >40 years with regular surveillance in patients with gastric premalignant conditions (GPMC). However, limited availability of EGD in Latin America necessitates development of risk stratification tools to minimize the endoscopic burden. Results from the Chilean “Endoscopic Cohort and Histological Operative Link on Gastric Assessment (OLGA) Staging” (ECHOS study), propose endoscopic surveillance of advanced GPMC (OLGA/Operative Link for Gastric Intestinal Metaplasia [OLGIM] stages III–IV) with reliable risk stratification to facilitate early GC detection. Ensuring high-quality EGD and enhanced diagnostic yield of GPMC is essential. GPMC grading tools, such as the Kimura-Takemoto or Endoscopic Grading of Gastric Intestinal Metaplasia classification, should be incorporated into the regular risk assessment protocol. However, obtaining mapping gastric biopsies using standardized methods such as the updated Sydney System biopsy protocol, followed by grading of chronic atrophic gastritis with or without intestinal metaplasia using the OLGA and OLGIM staging systems are preferred for GC risk stratification. Recent GC prevention strategies recommended in Chile include a “test-and-treat” approach for <i>H. pylori</i> in individuals aged 35–44 years and combined <i>H. pylori</i>/pepsinogen I–II serology and EGD evaluation in patients aged >45 years to optimize the limited preventive resources available in the region.

Unlocking the Potential: Epstein-Barr Virus (EBV) in Gastric Cancer and Future Treatment Prospects, a Literature Review.

Gastric cancer (GC) is a complex disease with various etiologies. While Helicobacter pylori infection is still one of the leading risk factors for GC, increasing evidence suggests a link between GC and other infective agents such as Epstein Bar Virus (EBV). EBV-associated gastric cancer (EBVaGC) is now recognized as a distinct subgroup of GC, and the complex interactions between the virus and gastric mucosa may influence its development. A recent integrative analysis of the genome and proteome of GC tissues by The Cancer Genome Atlas project has identified EBVaGC as a specific subtype characterized by PIK3CA and ARID1A mutations, extensive DNA hyper-methylation, and activation of immune signaling pathways. These molecular characteristics are markers of the unique molecular profile of this subset of GC and are potential targets for therapy. This review aims to provide an overview of the current knowledge on EBVaGC. It will focus on the epidemiology, clinic-pathological features, and genetic characteristics of EBVaGC. Additionally, it will discuss recent data indicating the potential use of EBV infection as a predictive biomarker of response to chemotherapy and immune checkpoint inhibitors. The review also delves into potential therapeutic approaches for EBVaGC, including targeted therapies and adoptive immunotherapy, highlighting the promising potential of EBV as a therapeutic target.

Association between Helicobacter pylori and its eradication and the development of cancer

BackgroundHelicobacter pylori (H. pylori) is a gram-negative gastrointestinal pathogen that colonises the human stomach and is considered a major risk factor for gastric cancer and mucosa-associated lymphoid tissue lymphoma. Furthermore,...

Rapid visual detection of Helicobacter pylori and vacA subtypes by Dual-Target RAA-LFD assay

BackgroundHelicobacter pylori (H. pylori) infects over 50% of the global population and is a significant risk factor for gastric cancer. The pathogenicity of H. pylori is primarily attributed to virulence factors such as vacA. Timely and accurate identification, along with genotyping of H. pylori virulence genes, are essential for effective clinical management and controlling its prevalence. MethodsIn this study, we developed a dual-target RAA-LFD assay for the rapid, visual detection of H. pylori genes (16s rRNA, ureA, vacA m1/m2), using recombinase aided amplification (RAA) combined with lateral flow dipstick (LFD) methods. Both 16s rRNA and ureA were selected as identification genes to ensure reliable detection accuracy. ResultsA RAA-LFD assay was developed to achieve dual-target amplification at a stable 37 °C within 20 min, followed by visualization using the lateral flow dipstick (LFD). The whole process, from amplification to results, took less than 30 min. The 95 % limit of detection (LOD) for 16 s rRNA and ureA, vacA m1, vacA m2 were determined as 3.8 × 10-2 ng/μL, 5.8 × 10-2 ng/μL and 1.4 × 10-2 ng/μL, respectively. No cross-reaction was observed in the detection of common pathogens including Escherichia coli, Klebsiella pneumoniae, Enterococcus faecalis, Staphylococcus aureus, Pseudomonas aeruginosa, and Bacillus subtilis, showing the assay’s high specificity. In the evaluation of the clinical performance of the RAA-LFD assay. A total of 44 gastric juice samples were analyzed, immunofluorescence staining (IFS) and quantitative polymerase chain reaction (qPCR) were used as reference methods. The RAA-LFD results for the 16s rRNA and ureA genes showed complete agreement with qPCR findings, accurately identifying H. pylori infection as confirmed by IFS in 10 out of the 44 patients. Furthermore, the assay successfully genotyped vacA m1/m2 among the positive samples, showing complete agreement with qPCR results and achieving a kappa (κ) value of 1.00. ConclusionThe dual-target RAA-LFD assay developed in this study provides a rapid and reliable method for detecting and genotyping H. pylori within 30 min, minimizing dependency on sophisticated laboratory equipment and specialized personnel. Clinical validation confirms its efficacy as a promising tool for effectively control of its prevalence and aiding in the precise treatment of H. pylori-associated diseases.

Height and cancer risk in East Asians: Evidence from a prospective cohort study and Mendelian randomization analyses

BackgroundHeight is associated with increased cancer risk, but most studies focus on Western populations. We aimed to evaluate this relationship in East Asians. MethodObservational analyses were performed utilizing data from China Kadoorie Biobank (CKB) prospective cohort. Adjusted hazard ratios (HRs) and corresponding 95 % confidence intervals (CIs) were estimated using Cox proportional hazards models. Two-sample Mendelian randomization (MR) analyses explored causal effects between height and cancer using data from Korean Genome and Epidemiology Study (KoGES), Biobank Japan (BBJ), and CKB. ResultsOver a median 10.1-years follow-up, 22,731 incident cancers occurred. In observational analyses, after Bonferroni correction, each 10 cm increase in height was significantly associated with higher risk of overall cancer (HR 1.16, 95 % CI 1.14–1.19, P < 0.001), lung cancer (1.18, 95 % CI 1.12–1.24, P < 0.001), esophageal cancer (1.21, 95 % CI 1.12–1.30, P < 0.001), breast cancer (1.41, 95 % CI 1.31–1.53, P < 0.001), and cervix uteri cancer (1.29, 95 % CI 1.15–1.45, P < 0.001). Each 10 cm increase in height was suggestively associated with increased risk for lymphoma (1.18, 95 % CI 1.04–1.34, P = 0.010), colorectal cancer (1.09, 95 % CI 1.02–1.16, P = 0.010), and stomach cancer (1.07, 95 % CI 1.00–1.14, P = 0.044). In MR analyses, genetically predicted height (per 1 standard deviation increase, 8.07 cm) was suggestively associated with higher risk of lung cancer (odds ratio [OR] 1.17, 95 % confidence interval [CI] 1.02–1.35, P = 0.0244) and gastric cancer (OR 1.14, 95 % CI 1.02–1.29, P = 0.0233). ConclusionsTaller height was significantly related to a higher risk for overall cancer, lung cancer, esophageal cancer, breast cancer, and cervix uteri cancer. Our findings suggest that height may be a potential causal risk factor for lung and gastric cancers among East Asians.

Chronic cigarette smoke exposure masks pathological features of Helicobacter pylori infection while promoting tumor initiation.

Gastric cancer is the fifth most common cancer and the fifth leading cause of cancer deaths worldwide. Chronic infection by the bacterium Helicobacter pylori is the most prominent gastric cancer risk factor, but only 1-3% of infected individuals will develop gastric cancer. Cigarette smoking is another independent gastric cancer risk factor, and H. pylori- infected smokers are at a 2-11-fold increased risk of gastric cancer development, but the direct impacts of cigarette smoke on H. pylori pathogenesis remain unknown. In this study, male C57BL/6 mice were infected with H. pylori and began smoking within one week of infection. The mice were exposed to cigarette smoke (CS) five days/week for 8 weeks. CS exposure had no notable impact on gross gastric morphology or inflammatory status compared to filtered-air (FA) exposed controls in mock-infected mice. However, CS exposure significantly blunted H. pylori- induced gastric inflammatory responses, reducing gastric atrophy and pyloric metaplasia development. Despite blunting these classic pathological features of H. pylori infection, CS exposures increased DNA damage within the gastric epithelial cells and accelerated H. pylori- induced dysplasia onset in the INS-GAS gastric cancer model. These data suggest that cigarette smoking may clinically silence classic clinical symptoms of H. pylori infection but enhance the accumulation of mutations and accelerate gastric cancer initiation.

Gastric polyposis and risk of gastric cancer in patients with familial adenomatous polyposis

BackgroundGastric polyposis is common in familial adenomatous polyposis (FAP) syndrome. However, the incidence and risk factors for gastric cancer (GC) are unclear. We aimed to evaluate the incidence of GC and associated risk factors in a large FAP population. MethodsRetrospective review of patients with FAP undergoing upper endoscopy at Mayo Clinic from 1989 to 2023. Cumulative incidence of GC (95% CIs) were calculated using Kaplan-Meier survival approaches. Associations of clinical characteristics with development of GC were examined using Cox proportional hazards regression. ResultsA total of 337 patients underwent 2502 endoscopies with a median of 10.4 years (IQR, 3.9–17.2) of endoscopic surveillance. At any time during surveillance, 294 patients (87%) had gastric polyps; 200 (59%), fundic gland polyps; 116 (34%), low-grade dysplasia (LGD); and 11 (3.3%), high-grade dysplasia (HGD). Among these, only 6 patients (2%) developed GC—5 with HGD (3 [50%] on previous endoscopy and 2 [33%] at the time of cancer diagnosis) and 1 (16%) with LGD on previous endoscopy. The 10-year cumulative incidence of GC is 0% with no polyps, 1% with polyps, 6% with LGD, 11% with polyps ≥2 cm, and 20% with HGD. Both HGD and polyps ≥2 cm had a strong association with the development of GC (P < .001). ConclusionAlthough the overall risk of GC in FAP is low, outcomes remain poor. GC can be predicted by endoscopic findings and specific GC surveillance guidelines are imperative to improve detection rates and guide timely intervention.

Gastroesophageal Disease and Environmental Exposure: A Systematic Review.

Environmental exposure-associated disease is an active area of study, especially in the context of increasing global air pollution and use of inhalants. Our group is dedicated to the study of exposure-related inflammation and downstream health effects. While many studies have focused on the impact of inhalants on respiratory sequelae, there is growing evidence of the involvement of other systems including autoimmune, endocrine, and gastrointestinal. This systematic review aims to provide a recent update that will underscore the associations between inhalation exposures and upper gastrointestinal disease in the contexts of our evolving environmental exposures. Keywords focused on inhalational exposures and gastrointestinal disease. Primary search identified n = 764 studies, of which n = 64 met eligibility criteria. In particular, there was support for existing evidence that PM increases the risk of upper gastrointestinal diseases. Smoking was also confirmed to be major risk factor. Interestingly, studies in this review have also identified waterpipe use as a significant risk factor for gastroesophageal reflux and gastric cancer. Our systematic review identified inhalational exposures as risk factors for aerodigestive disease, further supporting the association between environmental exposure and digestive disease. However, due to limitations on our review's scope, further studies must be done to better understand this interaction.