Risk Of Gastric Cancer Development Research Articles

Gene silencing of Helicobacter pylori through newly designed siRNA convenes the treatment of gastric cancer.

Helicobacter pylori is a gastric pathogen that is responsible for causing chronic inflammation and increasing the risk of gastric cancer development. It is capable of persisting for decades in the harsh gastric environment because of the inability of the host to eradicate the infection. Several treatment strategies have been developed against this bacterium using different antibiotics. But the effectiveness of treating H. pylori has significantly decreased due to widespread antibiotic resistance, including an increased risk of gastric cancer. The small interfering RNAs (siRNA), which is capable of sequence-specific gene-silencing can be used as a new therapeutic approach for the treatment of a variety of such malignancies. In the current study, we rationally designed two siRNA molecules to silence the cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) genes of H. pylori for their significant involvement in developing cancer. We selected a common region of all the available transcripts from different countries of CagA and VacA to design the siRNA molecules. The final siRNA candidate was selected based on the results from machine learning algorithms, off-target similarity, and various thermodynamic properties. Further, we utilized molecular docking and all atom molecular dynamics (MD) simulations to assess the binding interactions of the designed siRNAs with the major components of the RNA-induced silencing complex (RISC) and results revealed the ability of the designed siRNAs to interact with the proteins of RISC complex in comparable to those of the experimentally reported siRNAs. These designed siRNAs should effectively silence the CagA and VacA genes of H. pylori during siRNA mediated treatment in gastric cancer.

The Relationship between Gastroduodenal Pathologies and Helicobacter pylori cagL (Cytotoxin-Associated Gene L) Polymorphism.

The polymorphisms in the region between 58 and 62 amino acids of the 194-amino acid CagL protein (CagL hypervariable motif) affect the binding affinity of CagL to integrin α5β1 (ITGA5B1) receptor in host epithelial cells and have an effect on the development of various gastrointestinal diseases. We aimed to evaluate the associations of gastroduodenal pathologies, with the polymorphisms of cagL gene of Helicobacter pylori (H. pylori) and also associations between vacA genotypes and cagL polymorphisms. A total of 19 gastric cancer, 16 duodenal ulcer, and 26 non-ulcer dyspepsia patients were included in this case-control study. All cases had H. pylori. A fragment of 651 bp from gene cagL (hp0539) and cagA, vacA genes was amplified by polymerase chain reaction. Purified polymerase chain reaction products were sequenced by Sanger sequencing, and nucleotide sequences were translated into amino acid sequences. All of the H. pylori strains had cagL and cagA genes. In the 16 (84%) gastric cancer cases, the D58 amino acid polymorphism was significant than the 4 (15.4%) duodenal ulcer cases (P = .029), and the D58/K59 amino acid polymorphism was significant in 12 (63.1%) of the gastric cancer cases than 1 (3.85%) duodenal ulcer case (P = .008). D58/K59 and DKIGQ (n = 10; 52.63%) were the most common polymorphisms in the gastric cancer and were associated with the vacA genotype s1/m2, respectively (P = .022 and P = .008). The D58/K59 amino acid polymorphism was found to have a significant Odds Ratio (OR) value of 8.9 (P = .0017) in multivariate logistic regression analysis. The risk of gastric cancer development is 8.9 times higher with D58/K59 polymorphism.

Risk of gastric cancer development according to the combination of anti–Helicobacter pylori antibody titer and degree of atrophic gastritis.

297 Background: Helicobacter pylori is known as the main risk factor for gastric cancer. It is also well known that gastric atrophy which is the result of long-term H. pylori infection induces spontaneous regression of H. pylori infection and such atrophic status with negative H. pylori infection is related with high risk of gastric cancer, as in so called “ABC method”. However the implication of anti- H. pylori antibody titer is not well investigated. This study was designed to identify the risk for gastric cancer according to the combination of level of anti- H. pylori antibody titer and gastric atrophy. Methods: Those who had health checkups including upper endoscopy and serum anti- H. pylori antibody test between 2003 and 2018 were enrolled. Among them, those who had positive results for anti- H. pylori antibody were included in this study and those who had followed up for less than 1 year were excluded. Kimura-Takemoto classification C3 or more was defined as gastric atrophy. Individuals were classified into 4 groups: low B (low titer without atrophy), high B (high titer without atrophy), high C (high titer with atrophy), and low C (low titer with atrophy). Their risks for gastric cancer were compared under adjustment with other risk factors. Results: During median 5.7 years of follow-up, among 28,311 subjects, 231 developed new gastric cancer. Among them, 159 were intestinal type, 68 were diffuse type, and 4 were type-unknown. For intestinal type gastric cancer, high C group and low C group showed significantly high risk compared with low B group (high C: aHR 10.516; 95% CI, 6.485-17.054) (low C: aHR 11.191; 95% CI, 7.096-17.649). However, for diffuse type gastric cancer, high B group showed higher risk compared with low B group (aHR, 1.713; 95% CI, 1.021-2.875). When those two factors were taken separately, grade of atrophy was related with the risk for intestinal type gastric cancer (aHR, 2.047; 95% CI, 1.862-2.251), while the level of anti- H. pylori antibody titer was related with the risk for diffuse type gastric cancer (aHR, 1.158; 95% CI, 1.041-1.288). Conclusions: Among those with current H. pylori infection, high anti- H. pylori antibody titer is related with diffuse type gastric cancer. The risk was prominent especially among those without atrophy. Therefore, those with high level of anti- H. pylori antibody titer need to be considered as high risk group even without atrophy and should be considered as good candidates for H. pylori eradication and intensive screening.

Whole Exome Sequencing Study Suggests an Impact of FANCA, CDH1 and VEGFA Genes on Diffuse Gastric Cancer Development.

Gastric cancer (GC) is one of the most common cancer types in the world with a high mortality rate. Hereditary predisposition for GC is not fully elucidated so far. The aim of this study was identification of possible new candidate genes, associated with the increased risk of gastric cancer development. Whole exome sequencing (WES) was performed on 18 DNA samples from adenocarcinoma specimens and non-tumor-bearing healthy stomach tissue from the same patient. Three pathogenic variants were identified: c.1320+1G>A in the CDH1 gene and c.27_28insCCCAGCCCCAGCTACCA (p.Ala9fs) of the VEGFA gene were found only in the tumor tissue, whereas c.G1874C (p.Cys625Ser) in the FANCA gene was found in both the tumor and normal tissue. These changes were found only in patients with diffuse gastric cancer and were absent in the DNA of healthy donors.

The effect of metformin use on gastric cancer in patients with type 2 diabetes: A systematic review and meta-analysis of cohort studies

Introduction: Gastric cancer is one of the main causes of cancer-related deaths in the world. Various studies have so far been conducted to determine the risk of gastric cancer in relation to taking metformin. Therefore, this systematic review and meta-analysis study aims to evaluate the relationship between the administration of metformin in type II diabetes patients and their risk of developing gastric cancer. Materials and Methods: All studies were cohorts. A comprehensive literature searches of the databases, including Cochrane, Web of Science, PubMed, Scopus, and Google Scholar web browser was conducted using standard keywords. Data analysis of this meta-analysis was conducted using STATA 14 software and P<0.05 was considered as a significant level for tests. Results: In a set of 17 cohort studies, including an overall number of 1383404 patients, it was concluded that metformin consumption had reduced the risk of gastric cancer in type II diabetes patients [OR: 0.80 (95% CI: 0.71-0.91)]. In these patients, the impact of metformin on overall survival rates was not statistically significant [OR: 0.71 (95% CI: 0.42-1.18)]. Data analysis revealed the effects of metformin on the risk of gastric cancer development, which involved a reduction [OR: 0.69 (95% CI: 0.44-1.07)] for those who had been taking metformin for less than five years, [OR: 1.04 (95% CI: 0.83-1.30)] for those who had been taking metformin for 5-10 years, and [OR: 0.71 (95% CI: 0.59-0.84)] for the patients who had a history of taking metformin for over 10 years. Conclusion: Metformin administration in type II diabetes patients resulted in the reduction of the risk of gastric cancer, but did not affect the overall survival rates. Furthermore, it was observed that type II diabetes patients, who had been treated by metformin for more than 10 years, had a 29% lower risk for gastric cancer.

Decreasing Incidence of Gastric Cancer with Increasing Time after Helicobacter pylori Treatment: A Nationwide Population-Based Cohort Study.

Background: Treatment of Helicobacter pylori (HP) has been shown to reduce the risk of gastric cancer (GC) development. However, previous studies have focused on patients at high risk of GC. This study aimed to assess the effect of HP treatment on the incidence of GC in the general population. Materials and Methods: Medical records were obtained from the Common Data Model-converted sample Cohort of the National Health Insurance Service of Korea (NHIS-CDM). The target cohort included those who had been prescribed HP treatment and the comparator cohort included those who had not. The association between HP treatment and the risk of GC development was assessed using the Cox proportional hazard model. The incidences of GC according to the period after HP treatment in different age groups were analyzed using proportional trend tests. Results: After large-scale 1:4 propensity score matching, 2735 and 5328 individuals were included in the target and comparator cohorts, respectively. During the median follow-up of 6.5 years, the GC incidence was lower in the HP treatment cohort than in the comparator cohort, but this was statistically insignificant (hazard ratio [HR]: 0.76; 95% confidence interval [CI]: 0.50–1.13; p-value = 0.19). This trend was also observed among the older age (≥65 years, HR: 0.87; 95% CI: 0.44–1.68; p-value = 0.69) and male cohorts (HR: 0.82; 95% CI: 0.51–1.27; p-value = 0.38). Among 58,684 individuals who were treated for HP from the whole NHIS-CDM cohort, the incidence of GC consistently decreased over time and showed a marked decrease with increasing age (p for trend < 0.05). Conclusions: In all age groups of the general population, HP treatment could be recommended to reduce the risk of GC.

Aspirin, metformin, and statin use on the risk of gastric cancer: A nationwide population-based cohort study in Korea with systematic review and meta-analysis.

Background/AimsAlthough several chemopreventive drugs against gastric cancer have been proposed, their effects have not been fully evaluated. We examined the impacts of aspirin, metformin, and statin use on gastric cancer development in a population‐based cohort in Korea.MethodsWe analyzed the association between potential chemopreventive drugs—aspirin, metformin, and statin—and gastric cancer through the Observational Medical Outcomes Partnership Common Data Model‐based Korean nationwide cohort. Use of aspirin, metformin, and statin was defined by ≥365 days of prescriptions for each drug in the general population. To summarize the current evidence, we further performed a systematic review and meta‐analysis of the impact of aspirin, metformin, and statin on gastric cancer development.ResultsAfter propensity score matching, 31,839, 6764, and 10,251 subjects were observed for medians of 4.7, 4.2, and 4.2 years for aspirin, metformin, and statin analysis, respectively. Use of aspirin or statin was associated with lower risks of gastric cancer compared to their non‐use, respectively (hazard ratio [HR] [95% confidence interval [CI]]: aspirin, 0.72 [0.60–0.85], p < 0.01; statin, 0.67 [0.49–0.92], p = 0.01). However, no association was observed between metformin use and gastric cancer development (HR [95% CI]: 0.85 [0.59–1.23], p = 0.40). A subgroup of subjects with diabetes mellitus showed a lower risk of gastric cancer development with statin use. The meta‐analysis showed the highest effect size of gastric cancer development for statin, followed by aspirin and metformin.ConclusionsStatin and aspirin use were associated with significantly reduced risks of gastric cancer development, while the use of metformin was not associated with the gastric cancer risk. The protective effect of statin against gastric cancer was also significant in patients with diabetes mellitus.

Helicobacter pylori Eradication and Gastric Cancer Prevention

Since Warren and Marshall demonstrated Helicobacter pylori (H. pylori) as a cause of gastritis in the early 1980s, H. pylori has been associated with various gastric diseases, including gastric ulcer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, gastric adenoma, gastric adenocarcinoma, and hyperplastic gastric polyps. H. pylori eradication therapy can treat some associated diseases, including low-grade gastric MALT lymphoma, and significantly reduce the risk of peptic ulcer recurrence or progression of atrophic gastritis and intestinal metaplasia. In East Asia, where H. pylori and gastric cancer are prevalent, several studies have been conducted to prove whether the risk of gastric cancer development is reduced through H. pylori eradication therapy. Early studies failed to show the benefits of H. pylori eradication therapy in gastric cancer prevention. However, recent studies with extended follow-up periods have reported reduced risks of gastric cancer after treatment of H. pylori infection. H. pylori eradication therapy effectively prevents gastric cancer even in patients who were treated for early gastric cancer, and can be used in treating hyperplastic gastric polyps. Herein, we reviewed current evidence supporting the benefits of H. pylori eradication therapy to help clinicians understand its impact on gastric cancer prevention and hyperplastic polyp treatment.

Up-regulation of Aquaporin 5 Defines Spasmolytic Polypeptide-Expressing Metaplasia and Progression to Incomplete Intestinal Metaplasia.

Background & AimsMetaplasia in the stomach is highly associated with development of intestinal-type gastric cancer. Two types of metaplasias, spasmolytic polypeptide-expressing metaplasia (SPEM) and intestinal metaplasia (IM), are considered precancerous lesions. However, it remains unclear how SPEM and IM are related. Here we investigated a new lineage-specific marker for SPEM cells, aquaporin 5 (AQP5), to assist in the identification of these 2 metaplasias.MethodsDrug- or Helicobacter felis (H felis) infection-induced mouse models were used to identify the expression pattern of AQP5 in acute or chronic SPEM. Gene-manipulated mice treated with or without drug were used to investigate how AQP5 expression is regulated in metaplastic lesions. Metaplastic samples from transgenic mice and human gastric cancer patients were evaluated for AQP5 expression. Immunostaining with lineage-specific markers was used to differentiate metaplastic gland characteristics.ResultsOur results revealed that AQP5 is a novel lineage-specific marker for SPEM cells that are localized at the base of metaplastic glands initially and expand to dominate glands after chronic H felis infection. In addition, AQP5 expression was up-regulated early in chief cell reprogramming and was promoted by interleukin 13. In humans, metaplastic corpus showed highly branched structures with AQP5-positive SPEM. Human SPEM cells strongly expressing AQP5 were present at the bases of incomplete IM glands marked by TROP2 but were absent from complete IM glands.ConclusionsAQP5-expressing SPEM cells are present in pyloric metaplasia and TROP2-positive incomplete IM and may be an important component of metaplasia that can predict a higher risk for gastric cancer development.

Effect of Ranitidine Intake on the Risk of Gastric Cancer Development.

Gastric cancer is one of the most prevalent cancers globally, with high mortality, particularly in East Asia. Certain ranitidine products contain potentially carcinogenic N-nitrosodimethylamine. We investigated the potential association between gastric cancer risk and ranitidine intake using a nationwide cohort, extracted from the Korean National Health Insurance Service. In this longitudinal study, we employed a 1:1 propensity score matching according to sociodemographic factors. A total of 40,887 subjects were enrolled, of which 906 developed gastric cancer during the follow-up period. We investigated gastric cancer events during the follow-up period using the survival analysis, log-rank test, and Cox proportional hazards regression models to estimate incidence, survival rate, and hazard ratio. The incidence of gastric cancer was 67,422; 67,470; and 67,444 person-years in the control, other histamine-2 blockers, and ranitidine groups, respectively. Because the adjusted hazard ratio of gastric cancer was 0.98 and 1.01 in the other histamine-2 blockers and ranitidine groups, respectively, we could not calculate the likelihood of gastric cancer development in the ranitidine group. Ranitidine intake did not significantly increase the incidence of gastric cancer. Therefore, the relative risk of gastric cancer may be low in patients taking ranitidine products in South Korea.

High-risk individuals for gastric cancer would be missed for surveillance without subtyping of intestinal metaplasia.

The use of Operative Link on Gastritis Assessment (OLGA) and Operative Link on Gastritis Assessment based on Intestinal Metaplasia (OLGIM) staging system is recommended for identifying subjects at risk for developing gastric cancer; usually high-risk lesions are considered only as stages III and IV. Accumulating evidence suggests that incomplete intestinal metaplasia (IM) is important in the development of gastric cancer.Our aim has been to identify the prevalence of incomplete IM in patients with low-risk OLGA/OLGIM stages among a high-risk general population. Healthy adult volunteers aged 40-64years were invited to undergo upper endoscopy within a regional GISTAR pilot study in Kazakhstan (n = 166). Gastric lesions were staged according to OLGA/OLGIM staging system. High iron diamine-alcian blue (HID-AB) was used for subtyping IM. IM prevalence overall was 45.8%. Incomplete IM was present in 52.6% (type II in 30.3% and type III in 22.3%), whereas complete IM was found in 47.4% individuals. The prevalence of OLGIM I and II stage were 39.8 and 4.8%, respectively, whereas OLGIM III was observed in 1.2%. The prevalence of incomplete IM in patients stratified to OLGIM I was 54.5% (type II in 31.8% and type III in 22.7%). High prevalence of incomplete IM was detected not only in subjects with extensive IM, but in those stratified as at the OLGIM I stage. Without IM subtyping, patients with high risk of gastric cancer development would be missed for surveillance.

Applications of machine learning models in the prediction of gastric cancer risk in patients after Helicobacter pylori eradication.

The risk of gastric cancer after Helicobacter pylori (H. pylori) eradication remains unknown. To evaluate the performances of seven different machine learning models in predicting gastric cancer risk after H. pylori eradication. We identified H. pylori-infected patients who had received clarithromycin-based triple therapy between 2003 and 2014 in Hong Kong. Patients were divided into training (n=64238) and validation sets (n=25330), according to period of eradication therapy. The data were used to construct seven machine learning models to predict risk of gastric cancer development within 5years after H. pylori eradication. A total of 26 clinical variables were input into these models. The performances were measured by the area under receiver operating characteristic curve (AUC) analysis. During a mean follow-up of 4.7years, 0.21% of H. pylori-eradicated patients developed gastric cancer. Of the seven machine learning models, extreme gradient boosting (XGBoost) had the best performance in predicting cancer development (AUC 0.97, 95%CI 0.96-0.98), and was superior to conventional logistic regression (AUC 0.90, 95% CI 0.84-0.92). With the XGBoost model, the number of patients considered at high risk of gastric cancer was 6.6%, with miss rate of 1.9%. Patient age, presence of intestinal metaplasia, and gastric ulcer were the heavily weighted factors used by the XGBoost. Based on simple baseline patient information, machine learning model can accurately predict the risk of post-eradication gastric cancer. This model could substantially reduce the number of patients who require endoscopic surveillance.

The updated JSPGHAN guidelines for the management of Helicobacter pylori infection in childhood.

The Japan Pediatric Helicobacter pylori Study Group published the first guidelines on childhood H. pylori infection in 1997. They were later revised by the Japanese Society for Pediatric Gastroenterology, Hepatology and Nutrition (JSPGHAN). The H. pylori eradication rates, when employing triple therapy with amoxicillin and clarithromycin, currently recommended as the first‐line therapy of H. pylori infection in Japan, have substantially decreased, creating an important clinical problem worldwide. In Japanese adults, the “test‐and‐treat” strategy for H. pylori infection is under consideration as an approach for gastric cancer prevention. However, the combined North American and European pediatric guidelines have rejected such a strategy for asymptomatic children. As risk for gastric cancer development is high in Japan, determining whether the “test‐and‐treat” strategy can be recommended in children has become an urgent matter. Accordingly, the JSPGHAN has produced a second revision of the H. pylori guidelines, which includes discussion about the issues mentioned above. They consist of 19 clinical questions and 34 statements. An H. pylori culture from gastric biopsies is recommended, not only as a diagnostic test for active infection but for antimicrobial susceptibility testing to optimize eradication therapy. Based upon antimicrobial susceptibility testing of H. pylori strains (especially involving clarithromycin), an eradication regimen including use of the antibiotics to which H. pylori is susceptible is recommended as the first‐line therapy against H. pylori‐associated diseases. The guidelines recommend against a “test‐and‐treat” strategy for H. pylori infection for asymptomatic children to protect against the development of gastric cancer because there has been no evidence supporting this strategy.

Aspirin, Metformin, and Statin Use on the Risk of Gastric Cancer in a High-Risk Region: A Nationwide Population-Based Cohort Study in Korea with Systematic Review and Meta-Analysis

Objective: Although several chemopreventive drugs against gastric cancer have been proposed, their effects have not been fully evaluated. We examined the impacts of aspirin, metformin, and statin use on gastric cancer development in a population-based cohort in Korea, where gastric cancer is prevalent. Design: We analyzed the association between potential chemopreventive drugs—aspirin, metformin, and statin—and gastric cancer through the Observational Medical Outcomes Partnership Common Data Model-based Korean nationwide cohort. To summarize the current evidence, we further performed a systematic review and meta-analysis of the impact of aspirin, metformin, and statin on gastric cancer development. Results: After propensity-score matching, 66,166, 15,962, and 33,408 subjects were observed for medians of 5.8, 5.3, and 5.3 years for aspirin, metformin, and statin, respectively. Use of aspirin or statin was associated with lower risks of gastric cancer compared to their non-use, respectively (hazard ratio [HR] [95% confidence interval [CI]]: aspirin, 0.84 [0.72–0.97]; statin, 0.66 [0.52–0.82]). However, no association was observed between metformin use and gastric cancer development (HR [95% CI]: 1.00 [0.74–1.34]). A subgroup of subjects with diabetes mellitus showed a lower risk of gastric cancer development with statin use. The meta-analysis showed the highest effect size on gastric cancer development for statin, followed by aspirin and metformin. Conclusion: Statin and aspirin use were associated with significantly reduced risks of gastric cancer development, while the use of metformin was not. The protective effect of statin against gastric cancer was also significant in patients with diabetes mellitus. Funding Statement: This research was supported by a grant from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant number: HI19C0143). Declaration of Interests: None. Ethics Approval Statement: The protocol of the current study was approved by the Institutional Review Board of Kangdong Sacred Heart Hospital (IRB no. 2019-05-014).

Changes in Gastric Microbial Composition before and after Helicobacter pylori Eradication Therapy

Owing to advancements in next-generation sequencing and non-culture-based microbial research techniques, we have recognized that many bacterial taxa other than &lt;i&gt;Helicobacter pylori (H. pylori)&lt;/i&gt; are present in the human stomach. Gastric microbial composition depends on gastric diseases, including gastritis, atrophic gastritis, intestinal metaplasia, and gastric cancer. Although &lt;i&gt;H. pylori&lt;/i&gt; is a major factor associated with gastric cancer development, other bacterial taxa may affect gastric carcinogenesis. Because the risk of gastric cancer development can be reduced through &lt;i&gt;H. pylori&lt;/i&gt; eradication, many investigators have studied the changes in the microbial composition in the stomach after &lt;i&gt;H. pylori&lt;/i&gt; eradication. The gastric microbiome in patients with &lt;i&gt;H. pylori&lt;/i&gt; infection typically shows abundance of &lt;i&gt;H. pylori&lt;/i&gt; and a low microbial diversity index. If we treat &lt;i&gt;H. pylori&lt;/i&gt;-infected patients with antibiotics, microbial diversity increases, and the relative abundance also increases in many bacterial taxa. Several studies suggested that the microbial composition in patients with &lt;i&gt;H. pylori&lt;/i&gt; infection could be restored by &lt;i&gt;H. pylori&lt;/i&gt; eradication therapy; however, there have been inconsistent findings of the abundant bacterial taxa after &lt;i&gt;H. pylori&lt;/i&gt; eradication in patients with atrophic gastritis and intestinal metaplasia. More studies are required to reach a definitive conclusion on restoration of the microbial composition after &lt;i&gt;H. pylori&lt;/i&gt; eradication according to the severity of gastric inflammation.

Endoscopic grading of gastric atrophy on risk assessment of gastric neoplasia: A systematic review and meta-analysis.

Endoscopic examination of gastric atrophy has been developed to determine the extent of atrophy by identifying the atrophic border of gastric mucosa, but its value in predicting the risk of developing gastric neoplasms is not quantified. Thus, this systematic review and meta-analysis aim to assess the incidence risk of gastric neoplasms on the basis of endoscopic grading of gastric atrophy. Two authors independently searched the electronic databases (PubMed, Embase, and the Cochrane Library) from inception through December 31, 2019, without language restriction. The effect size on study outcomes is calculated using random-effects model and presented as risk ratio (RR) with 95% confidence interval (CI). Heterogeneity, publication bias, and quality of included studies were also assessed. Fourteen retrospective studies are identified to perform systematic review and meta-analysis, 11 were cohort studies, and three were cross-sectional research. The pooled RR for developing gastric neoplasms is 3.89 (95% CI 2.92-5.17) among general patients with severe endoscopic atrophy. For patients who underwent endoscopic resection for early gastric neoplasms, nearly two times increased risk of synchronous or metachronous neoplasms is pooled (RR=1.96, 95% CI 1.39-2.75). In terms of the type of endoscopic atrophy, patients with open-type endoscopic atrophy have a higher risk of gastric cancer development (RR 8.02; 95% CI 2.39-26.88) than those with close type. [Correction added on 22 December 2020, after first online publication: '(RR = 7.27; 95% CI 1.64-32.33)' has been corrected to '(RR 8.02; 95% CI 2.39-26.88)'] CONCLUSIONS: Grading endoscopic atrophy according to the Kimura-Takemoto classification can assess the risk of gastric neoplasia development. Patients with severe or open-type endoscopic gastric atrophy at baseline should undergo rigorous surveillance to early detect premalignant lesions and cancer.

The effects of serum levels, and alterations in the genes of binding protein and receptor of vitamin D on gastric cancer.

Due to many biological cell functions of vitamin D including regulation of cell survival, proliferation and differentiation, the metabolism of itself gains importance in the development of several types of cancer. This case-control study was designed to evaluate the risk of gastric cancer development in terms of VDR rs2228570 & rs731236, and VDBP rs7041 polymorphisms, and serum levels of vitamin D. The study consists of 77 gastric cancer patients and 84 healthy individuals. VDR and VDBP gene polymorphisms and vitamin D levels were determined by using PCR-RFLP and HPLC methods. The distribution of VDR or VDBP gene variants were not different in study groups. The serum level of 25-hydroxyvitamin D was significantly lower in gastric cancer patients versus controls (16 ± 6 → 11 ± 6ng/ml) in which male patients have higher levels than females. Although the whole study population lacks normal levels of 25-hydroxyvitamin D, it was found that the risk of the development of gastric cancer was approximately fourfold higher in cases with severe vitamin D (< 10ng/ml) deficiency. Our results indicate that VDR rs731236 & rs2228570 or VDBP rs7041 polymorphisms were not risk factors for the development of gastric cancer individually, however, lower serum levels of vitamin D may be a contributory risk for both predisposition and development of gastric cancer.

Helicobacter pylori infection in rehabilitation staff younger than 35 years: Infection surveillance for three years

Background: Screening for Helicobacter pylori infection is important because of the high risk of gastric cancer development. The H. pylori carrier rate among elderly Japanese patients is still high; therefore, rehabilitation (RH) workers who are in frequent contact with such individuals could be assumed to be at a higher risk of H. pylori infection. Aim/Objective: We surveyed RH workers to investigate the initial occurrence of H. pylori infections in adults. Methods: Urine samples of RH workers aged &lt; 35 years were screened for H. pylori antibodies to confirm infection. H. pylori infection rates were stratified according to the type of RH work and duration of employment. Infection surveillance was performed at six-month intervals for H. pylori-negative individuals. Findings/Results: The H. pylori infection rate among 173 workers was 16.8%. Infection rates were 26.3%, 16.3% and 15.3% among speech, occupational and physiotherapists, respectively. The employment duration was divided into &lt; 24, 24–47, 48–60 and ⩾ 61 months; the respective infection rates were 5.0%, 12.0%, 17.6% and 28.6%. However, no new H. pylori infection was detected in a total of seven surveillance studies of H. pylori-negative workers over a three-year period. Discussion: The results of the initial examination showed that the infection rate increased with the duration of employment. However, subsequent surveillance detected no new H. pylori infections.

Somatometric and Index Indicators for Assessing the Physical State of Patients with Gastric Cancer

The purpose of the research was to study physical health of patients with gastric cancer, the identification of markerspredictors of gastric cancer.Material and methods. This article presents the results of a survey with 150 patients diagnosed with stomach cancer. The research was conducted on the basis of the department of oncoabdominal surgery of Krasnoyarsk Regional Clinical Oncological Hospital named after A.I. Kryzhanovskiy in the period from 2016 to 2017. Patients with established gastric cancer, awaiting for surgical treatment, were examined using anthropometric methods of research. We evaluated the physical status of patients of different age diagnosed with stomach cancer. We also calculated body mass index and Tanner’s index of sexual dimorphism (1968), according to the last we determined the type of gender dimorphism. Distribution of healthy men and women in the population of the Krasnoyarsk Territory was taken for comparison.Results. We have obtained the following markers: overweight and obesity, sex inversion in men of the II period of adulthood and the elderly to gynecomorphy, and in women of the II period of adulthood – to mesomorphy.Conclusions. These markers are used for assessment of the physical status of patients with stomach cancer. They, together with the already known risk factors of gastric cancer development, will help to identify groups with an increased risk for gastric cancer development at the stage of medical examination of the population.

Risk of gastric cancer development after eradication of Helicobacter pylori.

Helicobacter pylori (H. pylori) infection is the most important risk factor for gastric cancer (GC) development through the Correa’s gastric carcinogenesis cascade. However, H. pylori eradication alone does not eliminate GC, as pre-neoplastic lesions (atrophic gastritis, intestinal metaplasia and dysplasia) may have already developed in some patients. It is therefore necessary to identify patients at high-risk for gastric cancer after H. pylori eradication to streamline the management plan. If the patients have not undergone endoscopy with histologic assessment, the identification of certain clinical risk factors and non-invasive testing (serum pepsinogen) can predict the risk of atrophic gastritis. For those with suspected atrophic gastritis, further risk stratification by endoscopy with histologic assessment according to validated histologic staging systems would be advisable. Patients with higher stages may require long-term endoscopic surveillance. Apart from secondary prevention to reduce deaths by diagnosing GC at an early stage, identifying medications that could potentially modify the GC risk would be desirable. The potential roles of a number of medications have been suggested by various studies, including proton pump inhibitors (PPIs), aspirin, statins and metformin. However, there are currently no randomized clinical trials to address the impact of these medications on GC risk after H. pylori eradication. In addition, most of these studies failed to adjust for the effect of concurrent medications on GC risk. Recently, large population-based retrospective cohort studies have shown that PPIs were associated with an increased GC risk after H. pylori eradication, while aspirin was associated with a lower risk. The roles of other agents in reducing GC risk after H. pylori eradication remain to be determined.