Premalignant Gastric Lesions Research Articles

Virulence Genes of Helicobacter pylori Increase the Risk of Premalignant Gastric Lesions in a Colombian Population.

Background Genetic variability of Helicobacter pylori is associated with various gastrointestinal diseases; however, little is known about interaction with sociodemographic in the development of premalignant lesions in Colombian patients. Methods An analytical study was conducted including cases (patients with gastric atrophy, intestinal metaplasia, and gastric dysplasia) and controls (patients with nonatrophic gastritis). Sociodemographic information was obtained using a questionnaire. Histopathological diagnosis was performed according to the Sydney System. The cagA and vacA genotypes were established using polymerase chain reaction in paraffin blocks. The effect of each variable on the study outcome (premalignant lesion) is presented as odds ratio (OR) and 95% CI. A p value of <0.05 was considered as statistically significant. Results The vacA/s1m1 genotype increases the risk of developing premalignant lesions of the stomach (OR: 3.05, 95% IC: 1.57–5.91, p=0.001). Age and educational level showed a positive interaction with the s1m1 genotype (adjusted OR: 3.68, 95% CI: 1.73–7.82, p=0.001). The cagA genotype was not correlated to the development of premalignant lesions of the stomach (OR: 1.32, 95% CI: 0.90–1.94, p=0.151). Conclusions The vacA genotype, age, and educational level are indicators of the risk of developing premalignant lesions of the stomach in the study population. Significance Statement. Genetic variability of H. pylori and sociodemographic information could be used to predict the risk of premalignant lesions in stomach in Colombian population.

Academy of Medicine, Singapore clinical guideline on endoscopic surveillance and management of gastric premalignant lesions

Gastric cancer (GC) has a good prognosis, if detected at an early stage. The intestinal subtype of GC follows a stepwise progression to carcinoma, which is treatable with early detection and intervention using high-quality endoscopy. Premalignant lesions and gastric epithelial polyps are commonly encountered in clinical practice. Surveillance of patients with premalignant gastric lesions may aid in early diagnosis of GC, and thus improve chances of survival. An expert professional workgroup was formed to summarise the current evidence and provide recommendations on the management of patients with gastric premalignant lesions in Singapore. Twenty-five recommendations were made to address screening and surveillance, strategies for detection and management of gastric premalignant lesions, management of gastric epithelial polyps, and pathological reporting of gastric premalignant lesions.

The Differences of Pepsinogen I and H. Pylori Levels in Patients With Gastric Premalignant Lesion

Background: Gastric cancer is the fifth most common cancer worldwide, precancerous lesions is triggered by H. pylori infection and any other factors. Recent reports confirmed that serum pepsinogens are a valuable biomarker gastric cancer even before the discovery of H. pylori. Research Methods: This study is a cross-sectional study involving 80 confirmed patients with Gastric Premalignant Lesion at Adam Malik General Hospital, Permata Bunda General Hospital, Medan, on April-November 2018. These two variables is sought using the Mann Whitney test (normality test P &lt; 0,05). H. pylori were diagnosed by positive result of examination of Carbon-14 urea breath test (C-UBT) or Campylobacter-like organism (CLO). Examination of Pepsinogen I measured by Abbott ARCHITECT Pepsinogen I Reagent Kit (Abbott Laboratories Inc., Chicago, IL, USA). Result: Of the 60 participants who confirmed has gastritis premalignant lesion according to the inclusion criteria. From the table of characteristic descriptive, it was found that 48 patients were male (60%) and 32 patients were female (40%). From CLO and 14C-UBT, it was found 35 patients were H. pylori-positive (43,8%) and 45 patients were H. pylori-negative (56,3%). Mean age was 51.03 ± 10.97 years. Mean levels of Pepsinogen I was 44.28 ± 21.77. From the second table, it was found that 35 (43,8%) patients with H. pylori-positive has 47.84 mean levels of Pepsinogen I, and 45 (56,3%) patients with H. pylori-negative has 34,79 mean levels of Pepsinogen I. The results of Mann Whitney's correlation analysis found a significant correlation between Pepsinogen (PG) I and H. Pylori in patients with Gastric Premalignant Lesion (p &lt; 0,05). Conclusion : It was found that there was a correlation between Pepsinogen (PG) I levels and H. Pylori in patients with Gastric Premalignant Lesion (p &lt; 0,05).

Preneoplastic Gastric Lesions and Helicobacter Pylori in Endoscopic Detection and Early Diagnosis of Gastric Cancer in Lebanese Population. A Retrospective Study from 2019-2020

Gastric cancer (GC) ranks as the fifth leading cause of cancer worldwide and is the fourth leading cause of cancer mortality. Premalignant gastric lesions (PGL) are considered as the most significant risk factor for GC. The purpose of this study.

Differential Expression of Tissular miRNA-155 in Pediatric Gastritis.

Background: MicroRNA molecules, among them the intensely studied miRNA-155 (miR-155), are regarded as potential biomarkers of chronic gastric inflammation and premalignant lesion progression. However, literature data are scarce in terms of pediatric studies and in the evaluation of the predictive role of miRNA in early gastric inflammation. This study aims to assess the differential expression of miR-155 in relation to pediatric gastritis. Methods: The present research was conducted on 192 patients with chronic dyspeptic symptoms who underwent upper digestive endoscopy. Bioptic samples were harvested for histopathological analysis and tissue miR-155 depiction. MiR-155 expression analysis was carried out through quantitative real-time polymerase chain reaction (qRT-PCR). The study population was divided into two groups: controls (93 patients) and study group (99 patients) with inflammatory modifications. Results: MiR-155 expression was augmented in patients with gastritis but did not differ significantly from controls (p = 0.16). An increase in miR-155 expression was noted in relation to chronic gastritis, H. pylori infection, or increase in gastritis severity, but these variations were not important (p = 0.30, p = 0.44, and p = 0.45, respectively). Conclusions: According to our study, pediatric gastritis increases, but does not greatly influence, miR-155 expression. Dynamic evaluation of miR-155 might enlighten its prognostic role in pediatric gastritis.

Probiotics mitigate Helicobacter pylori-induced gastric inflammation and premalignant lesions in INS-GAS mice with the modulation of gastrointestinal microbiota.

Dysbiosis of gastric microbiota including Helicobacter pylori (H. pylori) infection is associated with the development of stomach cancer. Probiotics have been shown to attenuate H. pylori-induced gastritis, although their role in cancer prevention remains unclear. Thus, we aimed to explore the effects of probiotics on H. pylori-induced carcinogenesis and the alterations of gastrointestinal microbiota. Male INS-GAS mice were randomly allocated to H. pylori-infected and non-infected groups. After 4 weeks, probiotic combination (containing Lactobacillus salivarius and Lactobacillus rhamnosus) was administered in drinking water for 12 weeks. Stomachs were collected for RNA-Sequencing and the differentially expressed genes were validated using RT profiler PCR array. 16S rRNA gene sequencing was performed to assess the alterations of gastrointestinal microbiota. Probiotics significantly alleviate H. pylori-induced gastric pathology, including reduced infiltration of inflammation and lower incidence of precancerous lesions. RNA-Sequencing results showed that probiotics treatment decreased expressions of genes involved in pro-inflammatory pathways, such as NF-κB, IL-17, and TNF signaling pathway. Of note, probiotics did not suppress the growth of H. pylori, but dramatically reshaped the structure of both gastric and gut microbiota. The microbial diversity was increased in H. pylori-infected group after probiotics treatment. While gastric cancer-associated genera Lactobacillus and Staphylococcus were enriched in the stomach of H. pylori-infected group, the beneficial short-chain fatty acids-producing bacteria, including Bacteroides, Alloprevotella, and Oscellibacter, were more abundant in mice treated with probiotics. Additionally, probiotics restored the H. pylori-induced reduction of anti-inflammatory bacterium Faecalibaculum in the gut. Probiotics therapy can protect against H. pylori-associated carcinogenesis probably through remodeling gastrointestinal microbiota, which in turn prevent host cells from malignant transformation.

SLC26A9 deficiency causes gastric intraepithelial neoplasia in mice and aggressive gastric cancer in humans

BackgroundSolute carrier family 26 member (SLC26A9) is a Cl− uniporter with very high expression levels in the gastric mucosa. Here, we describe morphological and molecular alterations in gastric mucosa of slc26a9−/− mice and in selective parietal cell-deleted slc26a9fl/fl/Atp4b-Cre mice and correlate SLC26A9 expression levels with morphological and clinical parameters in a cohort of gastric cancer (GC) patients.MethodsThe expression patterns of genes related to transport and enzymatic function, proliferation, apoptosis, inflammation, barrier integrity, metaplasia and neoplasia development were studied by immunohistochemistry (IHC), quantitative RT-PCR, in situ hybridization and RNA microarray analysis. SLC26A9 expression and cellular/clinical phenotypes were studied in primary human GC tissues and GC cell lines.ResultsWe found that both complete and parietal cell-selective Slc26a9 deletion in mice caused spontaneous development of gastric premalignant and malignant lesions. Dysregulated differentiation of gastric stem cells in an inflammatory environment, activated Wnt signaling, cellular hyperproliferation, apoptosis inhibition and metaplasia were observed. Analysis of human gastric precancerous and cancerous tissues revealed that SLC26A9 expression progressively decreased from atrophic gastritis to GC, and that downregulation of SLC26A9 was correlated with patient survival. Exogenous expression of SLC26A9 in GC cells induced upregulation of the Cl−/HCO3− exchanger AE2, G2/M cell cycle arrest and apoptosis and suppressed their proliferation, migration and invasion.ConclusionsOur data indicate that SLC26A9 deletion in parietal cells is sufficient to trigger gastric metaplasia and the development of neoplastic lesions. In addition, we found that SLC26A9 expression decreases during human gastric carcinogenesis, and that exogenous SLC26A9 expression in GC cells reduces their malignant behavior.Graphical abstract

Serum antibodies to selected Helicobacter pylori antigens are associated with active gastritis in patients seen at the University Teaching Hospital in Lusaka, Zambia.

Little is known about specific bacterial characteristics of Helicobacter pylori (H. pylori) infection influencing gastric carcinogenesis in Zambia. The aim of this study was to evaluate the associations between pre-selected H. pylori antibodies with gastric cancer, premalignant lesions and active gastritis. This was cross-sectional study with multiple comparisons of patients with gastric cancer (GC), gastric premalignant (GP) lesions and active or chronic gastritis. A fluorescent bead-based antibody multiplex serology assay was used to quantify antibodies to thirteen immunogenic H. pylori antigens. Logistic regression models were used to examine the associations. Included were 295 patients with: 59 GC, 27 GP lesions, 48 active and 161 chronic gastritis. Overall, 257/295 (87%) were H. pylori positive. H. pylori seropositivity was not associated with sex, age, body mass index, socio-economic status, HIV infection, alcohol consumption or cigarette smoking (p-values all above 0.05). When compared to the patients with chronic gastritis, the presence of catalase and cinnamyl alcohol dehydrogenase (Cad) antibodies was positively associated with GP lesions (OR 3.53; 95% CI 1.52-8.17 and OR 2.47; 95% CI 1.08-5.67 respectively). However, seropositivity to Cad antibodies was significantly lower in GC patients (OR 0.28; 95% CI 0.09-0.83). Compared to chronic, active gastritis was significantly associated with (p<0.05) H. pylori sero-positivity (OR 9.46; 95% CI 1.25-71.52) and specific antibodies including cytotoxin-associated gene A, vacuolating cytotoxin A, Helicobacter cysteine-rich protein C, hypothetical protein HP0305 and outer membrane protein HP1564. Among Zambian patients seen at a single center, antibodies to H. pylori (CagA, VacA, Omp, HcpC, HP0305 and HpaA) were associated with active gastritis.

Effect of Helicobacter pylori Eradication on Gastric Cancer Prevention: Updated Report From a Randomized Controlled Trial With 26.5 Years of Follow-up

Helicobacter pylori infection is considered as the most important risk factor in the pathogenesis of gastric cancer. This study aims to evaluate the long-term effects of H pylori eradication treatment on the incidence and mortality of gastric cancer among a high-risk population. This prospective, randomized, placebo-controlled trial was conducted in a high-risk area in southern China in July 1994. A total of 1630 asymptomatic, H pylori-infected individuals were randomly assigned to receive standard triple therapy for H pylori eradication (n= 817) or placebo (n= 813), and were followed up until December 2020. The primary outcome was incidence of gastric cancer. Total and cause-specific mortalities were the secondary outcomes. During 26.5 years of follow-up, 21 participants (2.57%) in the treatment arm and 35 (4.31%) in the placebo arm were diagnosed with gastric cancer. Participants receiving H pylori treatment had a lower incidence of gastric cancer compared with their placebo counterparts (hazard ratio [HR], 0.57; 95% CI, 0.33-0.98). More obvious risk reduction was observed among those without premalignant gastric lesions (HR, 0.37; 95% CI, 0.15-0.95) and those without dyspepsia symptoms at baseline (HR, 0.44; 95% CI, 0.21-0.94). Furthermore, compared with 32 cases of gastric cancer observed among 527 participants with persistent H pylori infection in the placebo group, only 16 were identified in 625 subjects with successful eradication in the treatment group (HR, 0.46; 95% CI, 0.26-0.83). However, there were no statistically significant differences for any mortality end points between the 2 groups. Eradication of H pylori might confer a long-term protection against gastric cancer in high-risk populations, especially for infected individuals without precancerous gastric lesions at baseline.

The Association of Trefoil Factors with Gastric Cancer and Premalignant Lesions: A Cross-Sectional Population-Based Cohort Study.

A lack of research on the association of trefoil factors (TFF) with gastric cancer and premalignant lesions (PML) in the general population is an important obstacle to the application of TFFs for gastric cancer screening. We aimed to analyze the association of TFFs with gastric cancer and PMLs in a general population. We evaluated 3,986 adults residing in Wuwei, China. We collected baseline characteristics and gastric cancer risk factors, including TFFs, endoscopic diagnosis, and pathologic information. Three logistic regression models were generated to analyze the association between TFFs and gastric cancer, as well as PMLs. Adjusted odds ratio (OR) and 95% confidence intervals (95% CI) were calculated to determine the strength of association. Compared with pepsinogen (PG) and anti-Helicobacter pylori immunoglobulin G antibody (Hp-IgG), TFFs had significant association with gastric cancer and PMLs after adjusting for biomarkers and risk factors (P < 0.05). The ORs (95% CI) for TFF1 (1.67; 1.27-2.20), TFF2 (2.66; 2.01-3.51), and TFF3 (1.32; 1.00-1.74) were larger than the ORs for PGI (0.79; 0.61-1.03), PGI/II (1.00; 0.76-1.31), and Hp-IgG (0.99; 0.73-1.35) in the gastric cancer group. In the intestinal metaplasia (IM) group, not only the TFF3 serum level was the highest, but also the OR (1.92; 1.64-2.25) was the highest. TFFs were associated with risk of gastric cancer and PMLs. Serum TFFs can improve the screening of high-risk populations for gastric cancer.

Brand interchangeability of pepsinogen tests in the real-world setting after eradication of Helicobacter pylori: a community-based study

BackgroundSerum pepsinogen (PG) is recommended as a screening test for premalignant gastric lesions. However, real-world evidence demonstrating its applicability and equivalence between different test brands is limited.MethodsMass screening began in 2018 in a high-risk Taiwanese population after eradication of Helicobacter pylori, with the first stage of two PG tests (GastroPanel®, Helsinki, Finland and LZ-Test®, Tokyo, Japan) and the second stage of endoscopy. A positive test was defined as PG-I < 30 ng/mL or PG-I/II ratio < 3 for GastroPanel® and PG-I ≤ 70 ng/mL and PG-I/II ratio ≤ 3 for LZ-Test®. Index lesions included atrophic gastritis and intestinal metaplasia. Test performance was evaluated based on the participation rate, positivity rate, referral rate, positive predictive value (PPV), and the detection rate.ResultsAmong 7616 eligible participants, 5117 (67.2%) received PG tests and 284 (5.6%) tested positive. Of those who tested positive, 105 (37.0%) underwent endoscopy. Overall PPVs for atrophic gastritis and intestinal metaplasia were 12.4% and 18.9%, respectively, with detection rates of 2.5 and 3.9 per 1000, respectively. Correlations of numerical measures between tests were high and the agreements of test results were substantial. The PPVs (16.3% vs. 16.3% and 23.8% vs. 21.3%, P = 1.00 and 0.71, respectively), detection rates (2.5 vs. 2.5 and 3.7 vs. 3.3 per 1000, P = 1.00 and 0.27, respectively), and the stage distributions of gastritis were all comparable, which were confirmed by multiple regression analyses.ConclusionsPG testing is effective for mass screening after eradication of H. pylori. Tests from different manufacturers, even using different analytical methods and cutoff criteria, can perform equivalently.

Gastroscopic results for the asymptomatic, average-risk population in Northern China: a cross-sectional study of 60,519 adults

Background Studies on average-risk individuals undergoing gastroscopy screening in China are scarce. Objective To determine and compare the prevalence of lesions found by gastroscopy and the association between sex, age, Helicobacter pylori infection and gastric premalignant lesions. Methods Gastroscopy results were analysed for 60,519 individuals enrolled from January 2013 to December 2019. Results The median age was 49.84 years (SD, 9.47 years) for women and 48.90 years (SD, 8.82 years) for men, and the ratio of females to males was 35.10% (n = 21,240) to 64.90% (n = 39,279). The most common lesions detected by endoscopy were chronic gastritis, reflux oesophagitis, duodenitis and gastric polyps, detected in 24.48%, 10.28%, 3.96% and 3.61%, respectively. Oesophageal cancer and gastric cancer were detected in 0.33% and 0.47% of patients, respectively. The prevalence of chronic gastritis increased with age and was higher in males than in females (26.47% [n = 10396] versus 20.80% [n = 4417], p < .001). The prevalence of gastric ulcers was highest in the elderly group, and the H. pylori infection rate of gastric ulcer patients was 47.28%. The prevalence of gastric polyps was higher in females than in males (5.47% [n = 1161] versus 2.61% [n = 1024], p < .001), and the H. pylori infection rate in inflammatory polyp patients was higher than that in fundic gland polyp patients (28.32% [n = 442] versus 7.29% [n = 29], p < .001). Conclusion The prevalence of upper gastrointestinal endoscopic lesions is high in the asymptomatic population undergoing physical examination and is associated with sex, age, and H. pylori infection.

Evaluation of the association between gastric cancer and plasma selenium in Zambian adults: a case-control study.

There is some evidence that Selenium (Se) is protective against gastric carcinogenesis, but these data are inconsistent. With a predicted increase in gastric cancer cases in Africa over the next 20 years, there is an urgent need to identify strategies that could be employed to prevent the surge. The objective of our study was to investigate the association between gastric cancer and plasma Se levels in Zambian adults. Our method used a case–control study with cases having either confirmed gastric cancer or premalignancies and controls having none. In addition, we measured antibodies against Helicobacter pylori and human immunodeficiency virus. Data were analysed with Stata 15 software using standard statistical methods. Using a normal reference range for Se of 0.9–1.9 μmol/L, 140/159 (88%) study participants had Se deficiency. Plasma Se levels were similar in all the three groups; 0.33 (interquartile range (IQR) 0.14–0.64) μmol/L for patients with gastric cancer, 0.38 (IQR 0.21–0.60) μmol/L for premalignant lesions and 0.28 (IQR 0.14–0.64) μmol/L in controls, (p-values = 0.35 and 0.34, respectively). In conclusion, we found no association between plasma Se levels and gastric cancer or premalignant lesions among adult Zambian adults.

Toll-Like Receptor 1 Locus Re-examined in a Genome-Wide Association Study Update on Anti–Helicobacter pylori IgG Titers

A genome-wide significant association between anti-Helicobacter pylori (H pylori) IgG titers and Toll-like receptor (TLR1/6/10) locus on 4p14 was demonstrated for individuals of European ancestry, but not uniformly replicated. We re-investigated this association in an updated genome-wide association study (GWAS) meta-analysis for populations with low gastric cancer incidence, address potential causes of cohort heterogeneity, and explore functional implications of genetic variation at the TLR1/6/10 locus. The dichotomous GWAS (25% individuals exhibiting highest anti-H pylori IgG titers vs remaining 75%) included discovery and replication sampls of, respectively, n= 15,685 and n= 9676, all of European ancestry. Longitudinal analysis of serologic data was performed on H pylori-eradicated subjects (n= 132) and patients under surveillance for premalignant gastric lesions (n= 107). TLR1/6/10 surface expression, TLR1 mRNA, and cytokine levels were measured in leukocyte subsets of healthy subjects (n= 26) genotyped for TLR1/6/10 variants. The association of the TLR1/6/10 locus with anti-H pylori IgG titers (rs12233670; β=-0.267 ± SE 0.034; P= 4.42× 10-15) presented with high heterogeneity and failed replication. Anti-H pylori IgG titers declined within 2-4 years after eradication treatment (P= 0.004), and decreased over time in patients with premalignant gastric lesions (P < 0.001). Variation at the TLR1/6/10 locus affected TLR1-mediated cytokine production and TLR1 surface expression on monocytes (P= 0.016) and neutrophils (P= 0.030), but not mRNA levels. The association between anti-H pylori IgG titers and TLR1/6/10 locus was not replicated across cohorts, possibly owing to dependency of anti-H pylori IgG titers on therapy, clearance, and antibody decay. H pylori-mediated immune cell activation is partly mediated via TLR1 signaling, which in turn is affected by genetic variation.

Clinical relevance of virulence genes in Helicobacter pylori isolates recovered from adult dyspeptic patients in Turkey

PurposeBacterial virulence factors play a major role in the pathogenesis of Helicobacter pylori infection. The aims of this study were to evaluate virulence genes in H. pylori isolates and to compare the presence of these genes and associated clinical pathologies. MethodsA total of 148 H. pylori isolates, recovered from adult dyspeptic patients, were used. The patients, from whom the isolates were obtained, were assigned to two groups by their endoscopic findings, which manifested as chronic gastritis or peptic ulcer. The presence of gastric atrophy and intestinal metaplasia was recorded for each patient, based on histopathological examination. Analyses of the virulence genes were performed by the polymerase chain reaction technique. ResultsThe patients had a mean age of 47 ​± ​15 years and 86 (58%) of them were female. Based on endoscopic examination, 103 (69.6%) patients were diagnosed with chronic gastritis and 45 (30.4%) with peptic ulcer. Histopathological examination revealed intestinal metaplasia in 30 (20%) patients and gastric atrophy in 12 (8%) patients. The prevalence rates of cagA, cagE, iceA1, iceA2, and babA2 were determined to be 87%, 74%, 58%, 26%, and 95%, respectively. The most prevalent vacA alleles were s1/s1a (82%/97%) and the least prevalent allele was s2 (20%). A new vacA genotype (s1as1bs1c) was detected, for the first time, in 18 (12%) isolates. No significant difference was found between the patient groups with chronic gastritis and peptic ulcer for the prevalences of the virulence genes (p ​> ​0.05). Furthermore, intestinal metaplasia and gastric atrophy showed no significant correlation with the virulence genes (p ​> ​0.05). ConclusionsIt is thoughted that H. pylori isolates with predominant cagA, cagE, VacA (s1, s1a), and babA2 virulence genes are associated with gastroduodenal diseases. However, there is no correlation between gastric premalignant lesions and virulence genes.

Association Between Serum Midkine Level and Gastric Precancerous Lesion in Patients with Gastritis.

Gastric cancer is the fifth most common malignancy and the third highest cancer-related mortality worldwide after lung and colorectal cancers. The gastric carcinogenesis is started with precancerous lesion. Prompt diagnosis and management of gastric precancerous lesion may prevent disease progression. Midkine is a growth factor associated with various cancers and proposed as a marker for detecting gastric precancerous lesion. The aim of the study is to determine the association between serum midkine level and gastric precancerous lesion in patients with gastritis. A cross sectional study was conducted at Haji Adam Malik general hospital. Subjects were obtained by consecutive sampling. Inclusion criteria were patients aged 18 years or older, diagnosed with gastritis from gastroscopy and histopathology results, and willing to cooperate in the study. Each subjects underwent interview and endoscopic examination. Serum midkine level was determined using enzyme-linked immunosorbent assay (ELISA) method. Chi square, receiver operating characteristic (ROC) curve, and logistic regression tests were applied. A total of 160 subjects were enrolled with 29.4% had gastric precancerous lesion. Serum midkine level was associated with gastric premalignant lesion. Cut off point for serum midkine level was 252 pg/mL with area under the curve of 0.816 (p<0.001). It's sensitivity, specificity, and accuracy in diagnosing gastric precancerous lesion were 74.5%, 71.7%, and 72.5%, respectively. Helicobacter pylori infection, high serum midkine level, heavy alcohol drinker, and family history of gastric cancer were risk factors for gastric precancerous lesion. Serum midkine level is associated with gastric premalignant lesion in patients with gastritis and has good diagnostic values.

Are ABO blood groups associated with premalignant gastric lesions and helicobacter pylori?

Are ABO blood groups associated with premalignant gastric lesions and helicobacter pylori?

Comparison of the gastric biopsy results of Afghan refugees and Turkish people

Helicobacter pylori- (H. pylori) infection is one of the effective factors in the development of gastric premalignant lesions, and it is known that socioeconomic conditions are closely related to H. pylori infection. Our aim was to show whether there were differences regarding H. pylori infection and gastric histopathological findings between humans who had to manage an exhausting escape out of their own country and residents of a coastal town in the black sea region of Turkey. Endoscopic findings of Turkish and Afghan patients who underwent gastroscopy for various reasons, gastric biopsies, and their histopathological results (H. pylori, intestinal metaplasia, and gastric atrophy) and some biochemical parameters were retrospectively screened from the hospital online data system. A total of 222 patients, 41 Afghan and 181 Turkish, were included in the study. There were no significant differences regarding age and gender of the patients between the groups. The percentage of the patients with intestinal metaplasia and H. pylori infection was higher in the group of the Afghan patients than in Turkish patients. Afghan refugees had similar rates of atrophic gastritis (23.1% versus 21.5%; p=0.834), when compared to resident controls. Risk factors of gastric cancer include the presence of H. pylori infection, atrophic gastritis, and intestinal metaplasia. This study supports the knowledge that socioeconomic factors such as low economic conditions and poor health infrastructure are one of the major causes of widespread global H. pylori infection status.

Autophagy mediates ER stress and inflammation in Helicobacter pylori-related gastric cancer

ABSTRACT Autophagy is a cellular degradation mechanism, which is triggered by the bacterium Helicobacter pylori. A single nucleotide polymorphism (SNP) in the autophagy gene ATG16L1 (rs2241880, G-allele) has been shown to dysregulate autophagy and increase intestinal endoplasmic reticulum (ER) stress. Here, we investigate the role of this SNP in H. pylori-mediated gastric carcinogenesis and its molecular pathways. ATG16L1 rs2241880 was genotyped in subjects from different ethnic cohorts (Dutch and Australian) presenting with gastric (pre)malignant lesions of various severity. Expression of GRP78 (a marker for ER stress) was assessed in gastric tissues. The effect of ATG16L1 rs2241880 on H. pylori-mediated ER stress and pro-inflammatory cytokine induction was investigated in organoids and CRISPR/Cas9 modified cell lines. Development of gastric cancer was associated with the ATG16L1 rs2241880 G-allele. Intestinal metaplastic cells in gastric tissue of patients showed increased levels of ER-stress. In vitro models showed that H. pylori increases autophagy while reducing ER stress, which appeared partly mediated by the ATG16L1 rs2241880 genotype. H. pylori-induced IL-8 production was increased while TNF-α production was decreased, in cells homozygous for the G-allele. The ATG16L1 rs2241880 G-allele is associated with progression of gastric premalignant lesions and cancer. Modulation of H. pylori-induced ER stress pathways and pro-inflammatory mediators by ATG16L1 rs2441880 may underlie this increased risk.

Is intestinal metaplasia the point of no return in the progression of gastric carcinogenesis?

Is intestinal metaplasia the point of no return in the progression of gastric carcinogenesis?