Putative associations between certain bacteria and gastric cancer have been described previously; however, the mechanisms underlying such associations are not thoroughly understood. We aimed to confirm the presence of Fusobacterium nucleatum in the biopsy samples of patients with gastroduodenal diseases, including gastric cancer, with concomitant or without Helicobacter pylori infection.

Three hundred patients with gastroduodenal disorders, including gastritis, duodenal ulcer, or gastric cancer, were included. One hundred and eighty (60%) patients were negative and 120 (40%) positive for H. pylori. Associations between the presence of H. pylori and age, gender, or other demographics were statistically insignificant (p > 0.05). The prevalence of F. nucleatum infection was determined for the two patient categories: 215 patients (72%) were positive for F. nucleatum; of these cases, 95 showed evidence of, and 120 lacked, concomitant H. pylori infection. Gastric biopsies obtained from patients with gastric cancer but negative for H. pylori revealed a significant prevalence of F. nucleatum infection.

Hyperplastic polyps, which represent 30%-93% of all gastric epithelial polyps, are the second most common type of gastric polyps after fundic gland polyps. They were previously considered to have no risk of neoplastic transformation. Recently, an increasing number of cases of gastric hyperplastic polyps (GHPs) combined with neoplastic changes have been reported; however, the specific mechanism underlying their transformation has not been thoroughly explored.

To investigate the clinical, endoscopic, and pathological characteristics of the neoplastic transformation of GHPs and explore the risk factors.

A retrospective analysis was performed on 4010 cases of GHPs diagnosed by gastroscopy and pathological examination at the hospital from 2005 to 2021. In total, 3874, 119, and 17 cases were in the group without intraepithelial neoplasia (IN), with low-grade IN, and with high-grade IN, respectively. The data analysis examined the association of endoscopic and pathological features with risk factors for neoplastic transformation. Factors with significant differences were entered into univariate logistic regression, followed by multivariate logistic regression analysis.

Univariate analysis revealed diameter, multiple polyp presence, redness, rough surface, lobulation, erosion, Yamada classification, location, and gastric mucosa were risk factors for neoplastic transformation. Multivariate analysis showed that age > 65 years [odds ratio (OR) = 1.789; 95% confidence interval (CI): 1.227-2.609; P = 0.003], male sex (OR = 1.680; 95%CI: 1.158-2.438; P = 0.006), multiple polyps (OR = 1.851; 95%CI: 1.230-2.784; P = 0.003), pedunculated or semi-pedunculated shape (OR = 2.722; 95%CI: 1.689-4.388; P < 0.001), and polyp diameter were significantly associated with GHPs that demonstrated neoplastic transformation. Compared with chronic superficial gastritis, autoimmune gastritis, atrophic gastritis, and gastritis with IN were independent risk factors for neoplastic transformation [(OR = 2.672; 95%CI: 1.559-4.579; P < 0.001), (OR = 1.876; 95%CI: 1.134-3.103; P = 0.014), and (OR = 5.299; 95%CI: 3.173-8.849; P < 0.001), respectively].

Male sex, age > 65 years, multiple polyps, pedunculated or semi-pedunculated shape, polyp size > 1 cm, and specific background gastric mucosa are key indicators for predicting neoplastic transformation of GHPs.

This study aimed to examine secular trends, age-period-cohort effects, and geographical differences in gastric cancer (GC) mortality in Korea.

Using cause of death data from the Korean Statistical Information Service for GC from 2000 to 2020, we calculated average annual percentage changes (AAPCs) in the age-standardized mortality of GC in 17 cities and provinces through joinpoint regression. Decomposition of age, period, and cohort effects on GC mortality were elucidated by applying a log-linear model and an intrinsic estimate method. Spatial patterns and the degree of spatial clustering in 250 administrative regions were explored via Moran's I statistics. Stratification by sex was performed for all analyses.

The age-standardized mortality of GC per 100,000 persons declined from 29.0 in 2000 to 7.9 in 2020 (AAPC, -6.28%). Age-period-cohort analyses of GC mortality showed a downward trend among five-year age groups from age 20-89 years across five-year periods from 2005-2020 and five-year birth cohorts from 1920-2000. Overall, the younger birth cohort showed lower mortality rates than the older cohort within the same period. In 2020, clusters of high GC mortality were observed in the central area for men (Chungcheongbuk, Jeollabuk, Gyeongsangbuk, and Gyeongsangnam) and in the eastern area for women (Gyeongsangbuk).

This study identified a downward trend in GC mortality among men and women from 2000 to 2020 in Korea. This trend was mainly attributed to birth cohort rather than period effects. Spatial analysis showed high GC mortality in the Chungcheong and Gyeongsangbuk areas.

Little is known about the effect of Helicobacter pylori eradication on the recurrence of gastric hyperplastic polyps after endoscopic resection. Thus, we evaluated the recurrence rate of gastric hyperplastic polyps based on H. pylori eradication following endoscopic resection.

We retrospectively reviewed the medical records of 201 patients with H. pylori infection who underwent endoscopic resection for gastric hyperplastic polyps at six medical centers. H. pylori status was assessed by histological analysis and a rapid urease test. A total of 149 patients underwent successful H. pylori eradication (eradication group), whereas 52 patients had persistent H. pylori infections (non-eradication group). The recurrence rate of gastric hyperplastic polyps and the risk factors according to H. pylori status were analyzed.

During the mean follow-up period of 18.3 months, recurrent gastric polyps developed after endoscopic resection in 10 patients (19.2% [10/52]) in the non-eradication group and 12 patients (8.1% [12/149]) in the eradication group. The cumulative incidence of recurrent gastric hyperplastic polyps was significantly higher in the non-eradication group than in the eradication group (p = 0.041, log-rank test). In the adjusted analysis, H. pylori eradication reduced the recurrence of gastric hyperplastic polyps (hazard ratio [HR], 0.42; 95% confidence interval [CI], 0.18 to 0.99), whereas anticoagulation therapy increased the risk of recurrence of gastric hyperplastic polyps (HR, 4.91; 95% CI, 1.39 to 17.28).

Successful eradication of H. pylori may reduce the recurrence of gastric hyperplastic polyps in patients after endoscopic mucosal resection.

Helicobacter pylori (H. pylori) infects about half of the world’s population and can lead to premalignant lesions and gastric cancer. Updated data about the correlation of histopathological diagnostics with endoscopic diagnostics are scarce. The objective of this study was to identify the concordance between endoscopic and histopathologic findings, with a focus on premalignant lesions. We performed a cross sectional, retrospective study over a 4-year period (2017−2021) on adult patients with dyspeptic symptoms and positive RUT (rapid urease test) in a single hospital centre, with a total of 133 patients infected with H. pylori being included in the study. Statistical associations between endoscopic appearance and histopathological results were found for atrophic antral gastritis (p = 0.001), intestinal metaplasia of the antrum (p = 0.018), gastric polyps (p < 0.001) and gastric corpus cancer (p = 0.012). Females were more likely to be diagnosed through endoscopy with gastric atrophy or intestinal metaplasia (p = 0.031), while chronic atrophic gastritis in corpus was more prevalent in patients older than 65 (p = 0.024). Overall, our study reveals only 21% concordance between Giemsa stain and RUT, highlighting the importance of combining rapid testing with endoscopic and histopathological diagnostic methods for a more accurate early diagnosis and prevention of gastric cancer.

Esophagogastroduodenoscopic examination shows a large, reddish polyp in the gastric cardia. The polyp decreased in size at 10 months and 22 months after cessation of vonoprazan.

Cancer has long been regarded as one of the world's most fatal diseases, claiming the lives of countless individuals each year. Stomach cancer is a prevalent cancer that has recently reached a high number of fatalities. It continues to be one of the most fatal cancer forms, requiring immediate attention due to its low overall survival rate. Early detection and appropriate therapy are, perhaps, of the most difficult challenges in the fight against stomach cancer. We focused on positive tactics for stomach cancer therapy in this paper, and we went over the most current advancements and progressions of nanotechnology-based systems in modern drug delivery and therapies in great detail. Recent therapeutic tactics used in nanotechnology-based delivery of drugs aim to improve cellular absorption, pharmacokinetics, and anticancer drug efficacy, allowing for more precise targeting of specific agents for effective stomach cancer treatment. The current review also provides information on ongoing research aimed at improving the curative effectiveness of existing anti-stomach cancer medicines. All these crucial matters discussed under one overarching title will be extremely useful to readers who are working on developing multi-functional nano-constructs for improved diagnosis and treatment of stomach cancer.

There is increasing evidence that the eradication of Helicobacter pylori leads to the regression of gastric hyperplastic polyps (GHPs). We performed a systematic review with a meta-analysis of randomized controlled trials and observational studies that assessed the effects of eradication.

We searched the PubMed, Embase, and Cochrane Central Register of Controlled Trials databases for relevant studies with a combination of the terms "Helicobacter pylori" and "polyps." The risk ratio was used to compare the effect of H. pylori eradication/treatment on GHP. We also calculated the pooled disappearance rate of GHP in the H. pylori eradication/treatment group and persistent infection group.

We analyzed data from 6 studies, including 3 RCTs. A total of 58/394 patients were included in the H. pylori treatment/successful eradication group, and 57/302 patients were included in the H. pylori untreated/persistent infection group. The pooled rate of GHP elimination after H. pylori treatment/successful eradication was 59% (95% CI, 43%-75%)/79% (95% CI, 72%-86%). H. pylori treatment/successful eradication significantly increased the GHP elimination rate [ITT: (pooled rate: 58% vs. 0%, RR =22.24, 95% CI, 4.51- 109.78, p = 0.0001), PP: (pooled rate: 65% vs. 0%, RR =22.25, 95% CI, 4.52- 109.37, p = 0.0001)/(pooled rate: 79% vs. 9%, RR =26.87, 95% CI, 1.34-540.5, p = 0.03)].

Our meta-analysis showed that after the eradication of H. pylori, most GHPs are eliminated. Moreover, the treatment/successful eradication of H. pylori increased the GHP elimination rate by more than 20 times that in the control group.

The aim of this study was to study the relationship between the formation of gastric fundic gland polyp and gastric hyperplastic polyp (HP) and the changes of gastric juice microenvironment.

The proton-pump inhibitor (PPI) applications to patients were recorded. Gastric juices and biopsy polyps were collected for pathological examination, H. pylori tests, biomarkers, and MUC1, MUC2, MUC5AC expression measurement.

Among 34,892 patients, the detection rate of gastric fundic gland polyps was significantly higher than that of gastric HPs (p < 0.01). The incidence rate of gastric fundic gland polyp and gastric HP in PPI users (n = 3,886) was higher than that of non-PPI users (p < 0.01). The occurrence of polyp was positively related to the duration of PPI application and the H. pylori-positive rate. The bile reflux rate between fundic gland polys group (17.61%) and HPs (28.67%) was significantly different (p < 0.01). The levels of gastric juice Gastrin-17, epidermal growth factor (EGF) and MUC2 from patients with gastric fundic gland polyps and gastric HPs were higher than those in the control group (p < 0.01). However, patients with gastric fundic gland polyps and HPs had significantly lower gastric juice PGE2 and MUC5AC (p < 0.01).

PPI application, H. pylori infection, and bile reflux are the potential risk factors for formation of fundic gland polyps and HPs. The potential mechanism of polyps' formation can be related to the levels of Gastrin-17, EGF, MUC2, PGE2, and MUC5AC in gastric juice.

Gastric adenocarcinoma and proximal polyposis of the stomach (GAPPS) is a rare familial gastric cancer syndrome with an autosomal dominant pattern of inheritance. It is characterised by fundic gland polyposis of the gastric body and is associated with a significant risk of gastric adenocarcinoma. Unlike sporadic gastric cancer, Helicobacter pylori is usually absent in patients with GAPPS. This opposite-point finding has so far not been fully clarified. Prophylactic total gastrectomy is indicated in all cases of GAPPS with fundic gland polyposis and the presence of any dysplasia. If no dysplasia is found at histology, prophylactic gastrectomy is suggested at between 30 and 35 years of age, or at five years earlier than the age at which the youngest family member developed gastric cancer. Different phenotypes of GAPPS demand an individual approach to particular family members.

Helicobacter pylori infection and hyperplastic polyp are known to have strong connections, but there are not enough randomized controlled trial data.

To evaluate the effect of H. pylori eradication on gastric hyperplastic polyp.

This is an open-labeled, single-center, randomized controlled trial. Patients with hyperplastic polyp and current infection of H. pylori were randomly assigned to eradication or non-eradication groups. All participants underwent follow-up endoscopy to investigate the regression of gastric polyps. Gastric polyp regression was defined as the disappearance of polyps or a reduction of more than 50% in size.

Thirty-two patients were randomized to eradication (n = 17) and non-eradication groups (n = 15). Final included patients were 14 in eradication group and 13 in non-eradication group. All patients showed polyp regression in eradication group, whereas no regression was observed in non-eradication group (P < 0.001). Disappearance of polyp (n = 7) and decrease in size (n = 7) were observed in eradication group. In non-eradication group, no change (n = 5), increase of size (n = 5), and increase of number (n = 3) were observed. Mean regression time was 6.8 months, and disappearance time was 9.8 months. In non-eradication group, hyperglycemia was noted in 50% of progression group but not noted in no change group (P = 0.057).

H. pylori eradication induced regression of hyperplastic polyp, and persistent H. pylori infection was related to progression of gastric polyp.

ClinicalTrials.gov ID: NCT03065868.

The incidence of gastric hyperplastic polyps (HPs) has been on the rise in recent years. The contribution of Helicobacter pylori infection to this trend has remained to be elucidated. The present study aimed to explore the association between HPs and H. pylori in China, an area with a high infection rate of H. pylori. In order to study trends of HPs and H. pylori infection over the past decades, cases encountered from 2009 to 2018 were assessed and a total of 109,150 consecutive patients who underwent esophagogastroduodenoscopy at Qingdao Municipal Hospital (Qingdao, China) were enrolled. The incidence of HPs and the prevalence of H. pylori were determined and their correlation was explored. Gastric HPs were detected in 1,497 patients (1.6%) who received gastric biopsies. The incidence of HPs exhibited a rising trend, with a ~4-fold increase in the annual detection rate from 2009 to 2018. The prevalence of H. pylori infection was inversely associated with the prevalence of HPs (adjusted odds ratio, 0.66). The prevalence of H. pylori in the examined cohort decreased with time (r=-0.76, P=0.011). The decreasing trend of H. pylori infection was negatively correlated with the rising trend of HPs (r=-0.64, P=0.048), further indicating an inverse association between them. The difference in the prevalence of HPs between H. pylori-negative and -positive patients increased with age (r=0.80, P=0.018). The age-associated increase was slower in H. pylori-infected patients. The decline in H. pylori infection with time appeared to not be associated with the birth cohort effect, suggesting the decline was not caused by exposure to environmental factors during an early period of life. The present results indicated that the incidence of gastric HPs increased with the decline in H. pylori infection, demonstrating an inverse association between the occurrence of HPs and the infection.

Gastric cancer is one of the infection associated malignancies. In addition to Helicobacter pylori and Epstein-Barr virus (EBV), other oncoviruses might play potential roles in the development of gastric cancer. Associations of oncoviruses other than EBV with gastric cancer risk are aimed to be comprehensively reviewed and assessed in this systematic review and meta-analysis, to identify any potentially causative oncovirus. It might be informative to identify or deny certain oncoviruses which are candidates of risk factor for gastric cancer. To our knowledge, there is no comprehensive review on oncoviruses other than EBV associated with gastric cancer risk. Positive findings might be helpful to suggest further mechanism investigation and high-risk subpopulation recommendation.

PubMed database will be searched up to Dec 31, 2018. The studies, compared the positivity of any oncovirus other than EBV between cases with histologically proven gastric cancer and healthy or nonmalignant controls, are eligible. The detection of oncovirus either in tissue or blood is acceptable. Selection, quality assessment (Newcastle-Ottawa Scale), and data extraction of eligible studies will be performed by 2 independent reviewers. Pooled prevalence of any oncovirus will be combined by meta-analysis for rate. Pooled odds ratio between gastric cancer cases and controls will be estimated by meta-analysis. Heterogeneity and publication bias will be tested. In sensitivity analysis, the leave-one-out method and exclusion of low power studies will be applied where applicable.

This review was not submitted for any ethical approval due to the literature-based nature. The results will be published in a journal and presented at conferences for academic purposes.Registration number was CRD42015029703 in the PROSPERO International Prospective Register of Systematic Reviews.

To our knowledge, there is no comprehensive review on oncoviruses other than EBV associated with gastric cancer risk. Positive findings might be helpful to suggest further mechanism investigation and high-risk subpopulation recommendation.

Gastric cancer is a multifactorial disease associated with a combination of and environmental factors. Each year, one million new gastric cancer cases are diagnosed worldwide and two-thirds end up losing the battle with this devastating disease. Currently, surgery represents the only effective treatment option for patients with early stage tumors. However, the asymptomatic phenotype of this disease during the early stages poses as a significant limiting factor to diagnosis and often renders treatments ineffective. To address these issues, scientists are focusing on personalized medicine and discovering new ways to treat cancer patients. Emerging therapeutic options include the transient receptor potential (TRP) channels. Since their discovery, TRP channels have been shown to contribute significantly to the pathophysiology of various cancers, including gastric cancer. This review will summarize the current knowledge about gastric cancer and provide a synopsis of recent advancements on the role and involvement of TRP channels in gastric cancer as well as a discussion of the benefits of targeting TPR channel in the clinical management of gastric cancer.