Type Ⅰ and type Ⅱ Helicobacter pylori infection status and their impact on gastrin and pepsinogen level in a gastric cancer prevalent area

BACKGROUND Type I Helicobacter pylori(H.pylori)infection causes severe gastric inflammation and is a predisposing factor for gastric carcinogenesis.However,its infection status in stepwise gastric disease progression in this gastric cancer prevalent area has not been evaluated;it is also not known its impact on commonly used epidemiological gastric cancer risk markers such as gastrin-17(G-17)and pepsinogens(PGs)during clinical practice.AIM To explore the prevalence of type I and type II H.pylori infection status and their impact on G-17 and PG levels in clinical practice.METHODS Thirty-five hundred and seventy-two hospital admitted patients with upper gastrointestinal symptoms were examined,and 523 patients were enrolled in this study.H.pylori infection was confirmed by both 13C-urea breath test and serological assay.Patients were divided into non-atrophic gastritis(NAG),nonatrophic gastritis with erosion(NAGE),chronic atrophic gastritis(CAG),peptic ulcers(PU)and gastric cancer(GC)groups.Their serological G-17,PG I and PG II values and PG I/PG II ratio were also measured.RESULTS A total H.pylori infection rate of 3572 examined patients was 75.9%,the infection rate of 523 enrolled patients was 76.9%,among which type I H.pylori infection accounted for 72.4%(291/402)and type II was 27.6%;88.4%of GC patients were H.pylori positive,and 84.2%of them were type I infection,only 11.6%of GC patients were H.pylori negative.Infection rates of type I H.pylori in NAG,NAGE,CAG,PU and GC groups were 67.9%,62.7%,79.7%,77.6%and 84.2%,respectively.H.pylori infection resulted in significantly higher G-17 and PG II values and decreased PG I/PG II ratio.Both types of H.pylori induced higher G-17 level,but type I strain infection resulted in an increased PG II level and decreased PG I/PG II ratio in NAG,NAGE and CAG groups over uninfected controls.Overall PG I levels showed no difference among all disease groups and in the presence or absence of H.pylori;in stratified analysis,its level was increased in GC and PU patients in H.pylori and type I H.pylori-positive groups.CONCLUSION Type I H.pylori infection is the major form of infection in this geographic region,and a very low percentage(11.6%)of GC patients are not infected by H.pylori.Both types of H.pylori induce an increase in G-17 level,while type I H.pylori is the major strain that affects PG I and PG IIs level and PG I/PG II ratio in stepwise chronic gastric disease.The data provide insights into H.pylori infection status and indicate the necessity and urgency for bacteria eradication and disease prevention in clinical practice.

Association between Helicobacter pylori infection,mismatch repair,HER2 and tumor-infiltrating lymphocytes in gastric cancer

BACKGROUND The influence of Helicobacter-pylori(H.pylori)infection and the characteristics of gastric cancer(GC)on tumor-infiltrating lymphocyte(TIL)levels has not been extensively studied.Analysis of infiltrating-immune-cell subtypes as well as survival is necessary to obtain comprehensive information.AIM To determine the rates of deficient mismatch-repair(dMMR),HER2-status and H.pylori infection and their association with TIL levels in GC.METHODS Samples from 503 resected GC tumors were included and TIL levels were evaluated following the international-TILs-working-group recommendations with assessment of the intratumoral(IT),stromal(ST)and invasive-border(IB)compartments.The density of CD3,CD8 and CD163 immune cells,and dMMR and HER2-status were determined by immunohistochemistry(IHC).H.pylori infection was evaluated by routine histology and quantitative PCR(qPCR)in a subset of samples.RESULTS dMMR was found in 34.4%,HER2+in 5%and H.pylori-positive in 55.7%of samples.High IT-TIL was associated with grade-3(P=0.038),while ST-TIL with grade-1(P<0.001),intestinal-histology(P<0.001)and no-recurrence(P=0.003).dMMR was associated with high TIL levels in the ST(P=0.019)and IB(P=0.01)compartments,and STCD3(P=0.049)and ST-CD8(P=0.05)densities.HER2-was associated with high IT-CD8(P=0.009).H.pylorinegative was associated with high IT-TIL levels(P=0.009)when assessed by routine-histology,and with high TIL levels in the 3 compartments(P=0.002-0.047)and CD8 density in the IT and ST compartments(P=0.001)when assessed by qPCR.A longer overall survival was associated with low IT-CD163(P=0.003)and CD8/CD3(P=0.001 in IT and P=0.002 in ST)and high IT-CD3(P=0.021),ST-CD3(P=0.003)and CD3/CD163(P=0.002).CONCLUSION TIL levels were related to dMMR and H.pylori-negativity.Low CD8/CD3 and high CD163/CD3 were associated with lower recurrence and longer survival.

Helicobacter pylori infection, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer and early gastric cancer

AIM: To evaluate the histological features of gastric mucosa, including Helicobacter pylori infection in patients with early gastric cancer and endoscopically found superficial gastritis, gastric erosion, erosive gastritis, gastric ulcer. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of all the patients. Giemsa staining, improved toluidine-blue staining, and Hpylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of gastric mucosa inflammation, gastric glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: The overall prevalence of H pylori infection in superficial gastritis was 28.7%, in erosive gastritis 57.7%, in gastric erosion 63.3%, in gastric ulcer 80.8%, in early gastric cancer 52.4%. There was significant difference (P<0.05), except for the difference between early gastric cancer and erosive gastritis. H pylori infection rate in antrum, corpus, angulus of patients with superficial gastritis was 25.9%, 26.2%, 25.2%, respectively; in patients with erosive gastritis 46.9%, 53.5%, 49.0%, respectively; in patients with gastric erosion 52.4%, 61.5%, 52.4%, respectively; in patients with gastric ulcer 52.4%, 61.5%, 52.4%, respectively; in patients with early gastric cancer 35.0%, 50.7%, 34.6%, respectively. No significant difference was found among the different site biopsies in superficial gastritis, but in the other diseases the detected rates were higher in corpus biopsy (P<0.05). The grades of mononuclear cell infiltration and polymorphonuclear cell infiltration, in early gastric cancer patients, were significantly higher than that in superficial gastritis patients, lower than that in gastric erosion and gastric ulcer patients (P<0.01); however, there was no significant difference compared with erosive gastritis. The grades of mucosa glandular atrophy and intestinal metaplasia were significantly highest in early gastric cancer, lower in gastric ulcer, the next were erosive gastritis, gastric erosion, the lowest in superficial gastritis (P<0.01). Furthermore, 53.3% and 51.4% showed glandular atrophy and intestinal metaplasia in angular biopsy specimens, respectively; but only 40.3% and 39.9% were identified in antral biopsy, and 14.1% and 13.6% in corpus biopsy; therefore, the angulus was more reliable for the diagnosis of glandular atrophy and intestinal metaplasia compared with antrum and corpus (P<0.01). The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pyloripositivity was 50.7%, 34.1%; of erosive gastritis 76.1%, 63.0%; of gastric erosion 84.8%, 87.8%; of gastric ulcer 80.6%, 90.9%; and of early gastric cancer 85.5%, 85.3%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis with H pylorinegativity was 9.9%, 6.9%; of erosive gastritis 42.5%, 42.1%; of gastric erosion 51.1%, 61.9%; of gastric ulcer 29.8%, 25.5%; and of early gastric cancer 84.0%, 86.0%, respectively. The positivity rate of glandular atrophy and intestinal metaplasia of superficial gastritis, erosive gastritis, gastric erosion, and gastric ulcer patients with H pylon positivity was significantly higher than those with H pylori negativity (P<0.01); however, there was no significant difference in patients with early gastric cancer with or without H pylori infection. CONCLUSION: The progression of the gastric pre-cancerous lesions, glandular atrophy and intestinal metaplasia in superficial gastritis, gastric erosion, erosive gastritis and gastric ulcer was strongly related to H pylori infection. In depth studies are needed to evaluate whether eradication of H pylori infection will really diminish the risk of gastric cancer.

Loss of FHIT expression in gastric mucosa of patients with family histories of gastric cancer and Helicobacter pylori infection

AIM: To answer the question whether FHIT gene expression is affected by the family history of gastric carcinoma and the presence of Helicobacter pylori (Hpylori) in the gastric mucosa of patients with dyspepsia.METHODS: FHIT gene expression in two different topographic sites of the gastric mucosa of twenty-one patients with dyspepsia and with or without familial gastric carcinoma, infected or not infected with H pylori, was evaluated by reverse transcription-PCR (RT-PCR) and IMAGE QUANT methods. A rapid urease test and histopathological examination were used to determine H pylori colonization.RESULTS: In the gastric mucosa of patients with family histories of gastric carcinoma, the amount of FHIT protein mRNA was reduced down to 32%, and for patients with H pylori colonization, to 24% in comparison to controls with dyspepsia and without cancer in the family. FHIT expression was independent of the topography of specimens (corpus vsantrum), and for the control patients it was less sensitive to infection with H pylori. A considerable statistical difference in FHIT levels was observed in the gastric mucosa from the corpus of patients with family histories of gastric carcinoma in respect to H pylori colonization (P = 0.06). Macroscopic evaluation of the gastric mucosa demonstrated that pathologic changes classified according to the Sydney system had no significant influence on FHIT expression within each tested group of patients.CONCLUSION: Loss of FHIT expression was observed in patients with dyspepsia and family histories of gastric carcinoma, especially those infected with H pylori. Such results may constitute an early indication of the development of gastric carcinoma, which is associated with family factors including heredity and H pylori infection. The loss of the FHIT gene may serve as a marker for early diagnosis and prevention of gastric carcinoma, especially in context of early monitoring of H pylori infection in individuals with a record of familial stomach cancer.

Endoscopic Kyoto classification of Helicobacter pylori infection and gastric cancer risk diagnosis

Recent advances in endoscopic technology allow detailed observation of the gastric mucosa.Today,endoscopy is used in the diagnosis of gastritis to determine the presence/absence of Helicobacter pylori(H.pylori)infection and evaluate gastric cancer risk.In 2013,the Japan Gastroenterological Endoscopy Society advocated the Kyoto classification,a new grading system for endoscopic gastritis.The Kyoto classification organized endoscopic findings related to H.pylori infection.The Kyoto classification score is the sum of scores for five endoscopic findings(atrophy,intestinal metaplasia,enlarged folds,nodularity,and diffuse redness with or without regular arrangement of collecting venules)and ranges from 0 to 8.Atrophy,intestinal metaplasia,enlarged folds,and nodularity contribute to gastric cancer risk.Diffuse redness and regular arrangement of collecting venules are related to H.pylori infection status.In subjects without a history of H.pylori eradication,the infection rates in those with Kyoto scores of 0,1,and≥2 were 1.5%,45%,and 82%,respectively.A Kyoto classification score of 0 indicates no H.pylori infection.A Kyoto classification score of 2 or more indicates H.pylori infection.Kyoto classification scores of patients with and without gastric cancer were 4.8 and 3.8,respectively.A Kyoto classification score of 4 or more might indicate gastric cancer risk.

Helicobacter pylori infection causes gastric cancer? A review of the epidemiological,meta-analytic, and experimental evidence

Since the discovery of Carnpylobacter-like organisms （Helicobacter pylori） more than two decades ago the possibility of a relationship with gastric cancer has been postulated, tested and supposedly proven. There have been numerous human studies of various designs from many countries around the world. Several meta-analyses have been published and more recently a small number of experimental animal studies were reported looking at the association between Helicobacter pylori infection and gastric cancer. Over the years, the human epidemiological studies have produced conflicting results; the metaanalyses have as one would expect produced similar pooled estimates; while the early experimental animal studies require replication. The exact mechanisms by which H pylori might cause gastric cancer are still under investigation and remain to be elucidated.

Helicobacter pylori in gastric cancer: Features of infection and their correlations with long-term results of treatment

BACKGROUND Helicobacter pylori(H.pylori)is a spiral-shaped bacterium responsible for the development of chronic gastritis,gastric ulcer,gastric cancer(GC),and MALTlymphoma of the stomach.H.pylori can be present in the gastric mucosa(GM)in both spiral and coccoid forms.However,it is not known whether the severity of GM contamination by various vegetative forms of H.pylori is associated with clinical and morphological characteristics and long-term results of GC treatment.AIM To establish the features of H.pylori infection in patients with GC and their correlations with clinical and morphological characteristics of diseases and long-term results of treatment.METHODS Of 109 patients with GC were included in a prospective cohort study.H.pylori in the GM and tumor was determined by rapid urease test and by immunohistochemically using the antibody to H.pylori.The results obtained were compared with the clinical and morphological characteristics and prognosis of GC.Statistical analysis was performed using the Statistica 10.0 software.RESULTS H.pylori was detected in the adjacent to the tumor GM in 84.5%of cases,of which a high degree of contamination was noted in 50.4%of the samples.Coccoid forms of H.pylori were detected in 93.4%of infected patients,and only coccoid-in 68.9%.It was found that a high degree of GM contamination by the coccoid forms of H.pylori was observed significantly more often in diffuse type of GC(P=0.024),in poorly differentiated GC(P=0.011),in stage T3-4(P=0.04)and in N1(P=0.011).In cases of moderate and marked concentrations of H.pylori in GM,a decrease in 10-year relapse free and overall survival from 55.6%to 26.3%was observed(P=0.02 and P=0.07,respectively).The relationship between the severity of the GM contamination by the spiral-shaped forms of H.pylori and the clinical and morphological characteristics and prognosis of GC was not revealed.CONCLUSION The data obtained indicates that H.pylori may be associated not only with induction but also with the progression of GC.

From Helicobacter pylori infection to gastric cancer:Current evidence on the immune response

Gastric cancer(GC)is the result of a multifactorial process whose main components are infection by Helicobacter pylori(H.pylori),bacterial virulence factors,host immune response and environmental factors.The development of the neoplastic microenvironment also depends on genetic and epigenetic changes in oncogenes and tumor suppressor genes,which results in deregulation of cell signaling pathways and apoptosis process.This review summarizes the main aspects of the pathogenesis of GC and the immune response involved in chronic inflammation generated by H.pylori.

Immune response to Helicobacter pylori infection and gastric cancer development

Gastric adenocarcinoma is a global health concern,and Helicobacter pylori(H.pylori)infection is the main risk factor for its occurrence.Of note,the immune response against the pathogen seems to be a determining factor for gastric oncogenesis,and increasing evidence have emphasized several host and bacterium factors that probably influence in this setting.The development of an inflammatory process against H.pylori involves a wide range of mechanisms such as the activation of pattern recognition receptors and intracellular pathways resulting in the production of proinflammatory cytokines by gastric epithelial cells.This process culminates in the establishment of distinct immune response profiles that result from the cytokine-induced differentiation of T naïve cells into specific T helper cells.Cytokines released from each type of T helper cell orchestrate the immune system and interfere in the development of gastric cancer in idiosyncratic ways.Moreover,variants in genes such as single nucleotide polymorphisms have been associated with variable predispositions for the occurrence of gastric malignancy because they influence both the intensity of gene expression and the affinity of the resultant molecule with its receptor.In addition,various repercussions related to some H.pylori virulence factors seem to substantially influence the host immune response against the infection,and many of them have been associated with gastric tumorigenesis.

Is Helicobacter pylori infection protective against esophageal cancer?

Helicobacter pylori(H.pylori)infection affects a substantial proportion of the global population and causes various gastric disorders,including gastric cancer.Recent studies have found an inverse relationship between H.pylori infection and eso-phageal cancer(EC),suggesting a protective role against EC.This editorial focuses on the possible mechanisms underlying the role of H.pylori infection in EC and explores the role of gut microbiota in esophageal carcinogenesis and the prac-ticality of H.pylori eradication.EC has two major subtypes:Esophageal squamous cell carcinoma(ESCC)and esophageal adenocarcinoma(EAC),which have different etiologies and risk factors.Gut microbiota can contribute to EC via inflammation-induced carcinogenesis,immunomodulation,lactagenesis,and genotoxin production.H.pylori infection is said to be inversely related to EAC,protecting against EAC by inducing atrophic gastritis,altering serum ghrelin levels,and triggering cancer cell apoptosis.Though H.pylori infection has no significant association with ESCC,COX-2-1195 polymorphisms and endogenous nitrosamine production can impact the risk of ESCC in H.pylori-infected in-dividuals.There are concerns regarding a plausible increase in EC after H.pylori eradication treatments.However,H.pylori eradication is not associated with an increased risk of EC,making it safe from an EC perspective.

Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P < 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P < 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.

Evaluation of the relationship between dietary factors,CagA-positive Helicobacter pylori infection,and RUNX3 promoter hypermethylation in gastric cancer tissue

AIM:To evaluate the relationship among Helicobacter pylori(H.pylori) infection,CagA status,and dietary factors with RUNX3 promoter hypermethylation.METHODS:Gastric cancer tissue samples were collected from 184 South Korean patients.All patients were interviewed following a semi-quantitative food frequency questionnaire.The average frequencies of intake and portion sizes of 89 common food items were documented,and total intakes of calories,nutrients,vitamins,and minerals were calculated for each subject.DNA was extracted from gastric cancer tissue samples,and amplification of the HSP60 gene was performed to detect H.pylori infection.Nested polymerase chain reaction(PCR) was used to detect the presence of the CagA gene.RUNX3 gene expression was measured by reverse transcription-PCR,and RUNX3 methylation status was evaluated by methylation-specific PCR.The odds ratios(ORs) and 95%CI associated with RUNX3 promoter hypermethylation status were estimated for each of the food groups,lifestyle factors,and the interaction between dietary and lifestyle factors with CagA status of H.pylori infection.RESULTS:Overall,164 patients(89.1%) were positive for H.pylori DNA,with the CagA gene detected in 59(36%) of these H.pylori-positive samples.In all,106(57.6%) patients with gastric cancer demonstrated CpG island hypermethylation at the RUNX3 promoter.RUNX3 expression was undetectable in 52(43.7%) of the 119 gastric cancer tissues sampled.A high consumption of eggs may increase the risk of RUNX3 methylation in gastric cancer patients,having a mean OR of 2.15(range,1.14-4.08).A significantly increased OR of 4.28(range,1.19-15.49) was observed with a high consumption of nuts in patients with CagA-positive H.pylori infection.High intakes of carbohydrate,vitamin B1,and vitamin E may decrease the risk of RUNX3 methylation in gastric cancer tissue,particularly in CagA-or H.pylori-negative infection,with OR of 0.41(0.19-0.90),0.42(0.20-0.89),and 0.29(0.13-0.62),respectively.A high consumption of fruits may protect against RUNX3 methylation.CONCLUSION:These results suggest that the CagA status of H.pylori infection may be a modifier of dietary effects on RUNX3 methylation in gastric cancer tissue.

Helicobacter pylori infection following partial gastrectomy for gastric cancer

Gastric remnants are an inevitable consequence of partial gastrectomy following resection for gastric cancer.The presence of gastric stumps is itself a risk factor for redevelopment of gastric cancer.Helicobacter pylori(H.pylori)infection is also a well-known characteristic of gastric carcinogenesis.H.pylori colonization in the remnant stomach therefore draws special interest from clinicians in terms of stomach cancer development and pathogenesis;however,the H.pylori-infected gastric remnant is quite different from the intact organ in several aspects and researchers have expressed conflicting opinions with respect to its role in pathogenesis.For instance,H.pylori infection of the gastric stump produced controversial results in several recent studies.The prevalence of H.pylori infection in the gastric stump has varied among recent reports.Gastritis developing in the remnant stomach presents with a unique pattern of inflammation that is different from the pattern seen in ordinary gastritis of the intact organ.Bilerefluxate also has a significant influence on the colonization of the stomach stump,with several studies reporting mixed results as well.In contrast,the elimination of H.pylori from the gastric stump has shown a dramatic impact on eradication rate.H.pylori elimination is recognized to be important for cancer prevention and considerable agreement of opinion is seen among researchers.To overcome the current discrepancies in the literature regarding the role of H.pylori in the gastric stump,further research is required.

Dynamic expression of pepsinogen C in gastric cancer, precancerous lesions and Helicobacter pylori associated gastric diseases

AIM:To investigate the relationship between the expression of pepsinogen C (PGC) and gastric cancer, precancerous diseases, and Helicobacter pylori (H pylori) infection. METHODS: The expression of PGC was determined by immunohistochemistry method in 430 cases of gastric mucosa. H3 Pylori infection was determined by HE staining, PCR and ELISA in 318 specimens. RESULTS: The positive rate of PGC expression in 54 cases of normal gastric mucosa was 100%. The positive rates of PGC expression in superficial gastritis or gastric ulcer or erosion, atrophic gastritis or gastric dysplasia and gastric cancer decreased significantly in sequence (P<0.05; 100%/89.2% vs 14.3%/15.2% vs 2.4%). The over-expression rate of PGC in group of superficial gastritis with H pyloriinfection was higher than that in group without H pylori infection (P<0.05; x2= 0.032 28/33 vs 15/25). The positive rate of PGC expression in group of atrophic gastritis with H pylori infection was lower than that in group without H pylori infection (P<0.01; x2 = 0.003 4/61 vs9/30), and in dysplasia and gastric cancer. CONCLUSION: The level of PGC expression has a close relationship with the degree of malignancy of gastric mucosa and development of gastric lesions. There is a relationship between H pylori infection and expression of antigen PGC in gastric mucosa, the positive rate of PGC expression increases in early stage of gastric lesions with H pylori infection such as gastric inflammation and decreases during the late stage such as precancerous diseases and gastric cancer. PGC-negative cases with H py/ori-positive gastric lesions should be given special attention.

Gastric mucosa in Mongolian and Japanese patients with gastric cancer and Helicobacter pylori infection

AIM: To investigate the characteristics of gastric cancer and gastric mucosa in a Mongolian populationby comparison with a Japanese population.METHODS: A total of 484 Mongolian patients with gastric cancer were enrolled to study gastric cancer characteristics in Mongolians. In addition, a total of 208 Mongolian and 3205 Japanese consecutive outpatients who underwent endoscopy, had abdominal complaints, no history of gastric operation or Helicobacter pylori eradication treatment, and no use of gastric secretion inhibitors such as histamine H2-receptor antagonists or proton pump inhibitors were enrolled. This study was conducted with the approval of the ethics committees of all hospitals. The triple-site biopsy method was used for the histologic diagnosis of gastritis and H. pylori infection in all Mongolian and Japanese cases. The infection rate of H. pylori and the status of gastric mucosa in H. pylori-infected patients were compared between Mongolian and Japanese subjects. Age(± 5 years), sex, and endoscopic diagnosis were matched between the two countries.RESULTS: Approximately 70% of Mongolian patients with gastric cancer were 50-79 years of age, and approximately half of the cancers were located in the upper part of the stomach. Histologically, 65.7% of early cancers exhibited differentiated adenocarcinoma, where as 73.9 % of advanced can cersdisplayed undifferentiated adenocarcinoma. The infection rate of H. pylori was higher in Mongolian than Japanese patients(75.9% vs 4 8. 3 %, P<0.0001). When stratified by age, the prevalence was highest among young patients, and tended to decrease in patients aged 50 years or older. The anti-East-Asian Cag Aspecific antibody was negative in 99.4% of H. pyloripositive Mongolian patients. Chronic inflammation, neutrophil activity, glandular atrophy, and intestinal metaplasia scores were significantly lower in Mongolian compared to Japanese H. pylori-positive patients(P < 0.0001), with the exception of the intestinal metaplasia score of specimen from the greater curvature of the upper body. The type of gastritis changed from antrumpredominant gastritis to corpus-predominant gastritis with age in both populations.CONCLUSION: Gastric cancer was located in the upper part of the stomach in half of the Mongolian patients; Mongolian patients were infected with non-East-Asiantype H. pylori.

The relationship between malignant biological molecule expression during the pathological process of gastric cancer and helicobacter pylori infection

Objective:To study the relationship between malignant biological molecule expression during the pathological process of gastric cancer and helicobacter pylori (HP) infection.Methods:A total of 78 cases of gastric cancer specimens that were surgically removed in our hospital between May 2013 and June 2015 were selected as the research material, the gastric cancer tissue and the tissue adjacent to carcinoma were collected, rapid urease test kits were used to test HP, and fluorescent quantitative PCR kits were used to determine the mRNA expression of proliferation- and invasion-related genes.Results:EZH2, c-myc, PIK3CD, Vav3 and UHRF1 mRNA expression in gastric cancer tissue were significantly higher than those in the tissue adjacent to carcinoma while Mst1, ING5, RASAL and E-cadherin mRNA expression were significantly lower than those in the tissue adjacent to carcinoma;EZH2, c-myc, PIK3CD, Vav3 and UHRF1 mRNA expression in HP-positive gastric cancer tissue were significantly higher than those in HP-negative gastric cancer tissue while Mst1, ING5, RASAL and E-cadherin mRNA expression were significantly lower than those in HP-negative gastric cancer tissue.Conclusion: Helicobacter pylori have regulating effect on the expression of proliferation- and invasion-related malignant biological molecules during the pathological process of gastric cancer.

Correlation study between helicobacter pylori infection and tumor malignancy in patients with gastric cancer

Objective:To study the correlation between helicobacter pylori infection and tumor malignancy in patients with gastric cancer.Methods:A total of 119 patients with gastric cancer treated in our hospital between May 2013 and December 2015 were collected and divided into HP-positive group (n=89) and HP-negative group (n=30) according to the combination of helicobacter pylori infection or not. RIA method was used to detect the serum angiogenesis index levels;fluorescence quantitative PCR (RT-PCR) was used to detect the mRNA expression of autophagy genes and proliferation genes in tumor tissues.Results:Serum angiogenesis indexes bFGF, VEGF and MMP-9 levels of HP-positive group were significantly higher than those of HP-negative groups;autophagy genes Beclin1, BNIP3, pULK and PI3KC3 mRNA expression in tumor tissues of HP-positive group were significantly lower than those of HP-negative group, pro-apoptotic genes Bax and p53 mRNA expression were significantly lower than those of HP-negative group, and anti-apoptotic genes PIK3CD, CIP2A and I2PP2A mRNA expression were significantly higher than those of HP-negative group. Conclusion:Helicobacter pylori infection can promote angiogenesis and cell proliferation in lesions of patients with gastric cancer.

Effect of depression on Helicobacter pylori infection in patients with gastric cancer and its correlation with oncogene expression

Objective: To study the effect of depression on Helicobacter pylori (H. pylori) infection in patients with gastric cancer and its correlation with oncogene expression. Methods: A total of 82 patients who accepted radical operation for gastric cancer in Zigong Third People's Hospital between March 2015 and February 2017 were selected as the research subjects and divided into depression group and non-depression group according to the preoperative HAMD scores, and helicobacter pylori infection as well as the mRNA expression of proliferation genes and invasion genes in gastric cancer lesions was detected. Results: The positive rate of H. pylori in gastric cancer lesions of depression group was significantly higher than that of non-depression group;LOXL2, RAB1A, UHRF1, Slug and ADAM8 mRNA expression in gastric cancer lesions of depression group were significantly higher than those of non-depression group while MTS1, NOX, E-cadherin and TIMP1 mRNA expression were significantly lower than those of non-depression group;LOXL2, RAB1A, UHRF1, Slug and ADAM8 mRNA expression in H. pylori-positive gastric cancer lesions of depression group were significantly higher than those in H. pylori-negative gastric cancer lesions of depression group while MTS1, NOX, E-cadherin and TIMP1 mRNA expression were significantly lower than those in H. pylori-negative gastric cancer lesions of depression group. Conclusion: Depression can increase the H. pylori infection rate and promote the proliferation and invasion of cancer cells in gastric cancer lesions.

Helicobacter pylori eradication for primary prevention of gastric cancer:progresses and challenges

Gastric cancer remains a significant global health challenge,causing a substantial number of cancer-related deaths,particularly in China.While the exact causes of gastric cancer are still being investigated,Helicobac-ter pylori(H.pylori)infection has been identified as the primary risk factor,which triggers chronic inflammation and a multistage progression of gastric lesions that may lead to carcinogenesis over a long latency time.Since the 1990s,numerous efforts have focused on assessing the effectiveness of H.pylori eradication in preventing new cases of gastric cancer among both the general population and patients who have undergone early-stage cancer treatment.This body of work,including several community-based interventions and meta-analyses,has shown a reduction in both the incidence of and mortality from gastric cancer following H.pylori treatment,alongside a decreased risk of metachronous gastric cancer.In this review,we seek to consolidate current knowledge on the effects of H.pylori treatment on gastric cancer prevention,its systemic consequences,cost-effectiveness,and the influence of antibiotic resistance and host characteristics on treatment outcomes.We further discuss the potential for precision primary prevention of H.pylori treatment and comment on the efficient implementation of test-and-treat policies and allocation of health resources towards minimizing the burden of gastric cancer globally.

Non-improvement of atrophic gastritis in cases of gastric cancer after successful Helicobacter pylori eradication therapy

BACKGROUND Helicobacter pylori(H.pylori)infection is closely related to the development of gastric cancer(GC).However,GC can develop even after H.pylori eradication.Therefore,it would be extremely useful if GC could be predicted after eradication.The Kyoto classification score for gastritis(GA)is closely related to cancer risk.However,how the score for GC changes after eradication before onset is not well understood.AIM To investigate the characteristics of the progression of Kyoto classification scores for GC after H.pylori eradication.METHODS Eradication of H.pylori was confirmed in all patients using either the urea breath test or the stool antigen test.The Kyoto classification score of GC patients was evaluated by endoscopy at the time of event onset and three years earlier.In ad-dition,the modified atrophy score was evaluated and compared between the GC group and the control GA group.RESULTS In total,30 cases of early GC and 30 cases of chronic GA were evaluated.The pathology of the cancer cases was differentiated adenocarcinoma,except for one case of undifferentiated adenocarcinoma.The total score of the Kyoto classifi-cation was significantly higher in the GC group both at the time of cancer onset and three years earlier(4.97 vs 3.73,P=0.0034;4.2 vs 3.1,P=0.0035,respectively).The modified atrophy score was significantly higher in the GC group both at the time of cancer onset and three years earlier and was significantly improved only in the GA group(5.3 vs 5.3,P=0.5;3.73 vs 3.1,P=0.0475,respectively).CONCLUSION The course of the modified atrophy score is useful for predicting the onset of GC after eradication.Patients with severe atrophy after H.pylori eradication require careful monitoring.