TPOAb Indicates neuroendocrine tumor in autoimmune gastritis: A retrospective study of 91 patients.

BACKGROUND: The association between serological indexes and occurrence of complications in patients with autoimmune gastritis (AIG) remains unclear. METHODS: 91 patients with AIG were recruited and their clinical information were collected. The differences between serological indexes and complications of AIG were analyzed. And potential biomarker for early prediction and diagnosis of AIG with complications was explored. RESULTS: AIG patients in our study was 58.12 ± 11.68 years old, containing 31 males and 60 females. G17 was elevated in 49 of 52; PGI/II decreased in 43/49; GPA positive in 48/61; Anemia presented 28 in 80; Vitamin B12 deficiency occurred 23 in 58. Neuroendocrine tumor (NET) was the most common complication in AIG patients, accounting for 27/91. The second was polyps, making up for 14/91. There is also 9/91 of gastric mucosa neoplasia happened in AIG. No significant difference of G7, PGI, PGII, PGI/II and VB12 in AIG was found in different gastric mucosal lesions (P > 0.05). However, AIG patients with TPOAb positive had a higher risk in the occurrence of NET simultaneously (P = 0.0212). Those AIG with NET patients exhibited a significantly higher TPOAb level (P = 0.0078). ROC curve suggested that TPOAb can predict the existence of NET in AIG (AUC = 0.7410, P < 0.05). CONCLUSION: We found that TPOAb can serve as a predictive biomarker of NET in AIG. This accessible test is helpful for endoscopy specialists to pay attention to gastric mucosal lesions in TPOAb-positive AIG patients, improving early diagnosis and intervention of comorbidities ability.

Elevated programmed cell death-1 protein/ligand (PD-1/PD-L1) and variants are associated with susceptibility to multiple myeloma: a case-control study in the Chinese cohort.

Multiple myeloma (MM) is a malignant disorder characterised by progressive immune dysregulation. The importance of programmed cell death protein 1 (PD-1)/programmed cell death ligand 1 (PD-L1) in MM has been documented in various populations, but studies have been limited to the Chinese cohort. In the present study, we examined the role of PD-1/PDL-1 in large cohorts of Chinese patients with MM and healthy controls to reveal a possible association with MM. Three hundred thirty-four MM patients and 202 healthy age-sex-matched subjects were enrolled in the present study. Serum levels of PD-1 and PD-L1 were quantified by ELISA. Percentages of T cells (CD4+ and CD8+ T cells) expressing PD-1 receptor were assessed by flow cytometry. Variants in PD-L1 (rs4143815) and PD-1 gene (rs2227981, rs2227982, rs7421861 and rs11568821) were genotyped by PCR-RFLP method. Patients with multiple myeloma had higher levels of PD-1 and PDL-1 than healthy controls, indicating an important role for programmed cell death protein-1 and its ligand in the pathogenesis of MM. T cells expressing PD-1 receptors were also significantly higher in MM patients than in controls. Mutants for PD-L1 (rs4143815) and PD-1 (rs2227982 and rs7421861) polymorphisms were significantly more common in MM than in HC. Interestingly, PD-L1 (rs4143815) and PD-1 (rs2227982 and rs7421861) variants were linked to higher sPD-L1 and sPD-1 levels, respectively. PD-1/PD-L1 levels are significantly higher in MM patients and could be a promising biomarker for the disease. Variants of PD-L1 and PD-1 are linked to serum-soluble proteins and are associated with the development of MM.

Circ_0000419 acts as a tumor suppressor in gastric cancer development via regulating miR-300/RGMB axis.

OBJECTIVE: Dysregulated circular RNAs (circRNAs) have been verified to function in the development of gastric cancer (GC). The current study was designed to investigate the role of circ_0000419 in GC progression, and the potential mechanistic pathway. METHODS: Relative expression of circ_0000419, microRNA-300 (miR-300) and Repulsive Guidance Molecule B (RGMB) was analyzed by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assay. Cell metastasis, including migration and invasion, was assessed by wound healing and Transwell assays. Glucose consumption and lactate production were examined using kits. The association between miR-300 and circ_0000419 or RGMB was validated by dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assays. Role of circ_0000419 in vivo was determined by xenograft experiment. RESULTS: Circ_0000419 and RGMB were downregulated, while miR-300 was upregulated in GC tissues and cells. Gain of circ_0000419 inhibited migration, invasion and glycolysis in GC cells, which was attenuated by introduction of miR-300 or silencing of RGMB. Circ_0000419 sponged miR-300, and RGMB was direct target of miR-300. Circ_0000419 overexpression could block GC tumor growth in vivo. CONCLUSION: Circ_0000419 inhibited GC cell migration, invasion and glycolysis through regulation of miR-300/RGMB axis, at least in part, affording a molecular target for GC treatment.

Effects on BBPS score with bowel preparation time and dosage.

BACKGROUND: To evaluate the effects on the Boston Bowel Preparation Scale (BBPS) score with different bowel preparation times and dosages. METHODS: Six hundred patients who underwent colonoscopy in the Endoscopy Center of Ningbo No.9 Hospital in 2021 were recruited and randomly assigned to 3 groups: Group A: "4-hour 1 + 2L" bowel preparation regimen; Group B: "6-hour 1 + 2L" bowel preparation regimen; and Group C: "4-hour 0 + 2L" bowel preparation regimen. BBPS score among these groups is compared and analyzed in the Statistical Product and Service Solutions software. RESULTS: There was no difference in baseline characteristics among the three groups of patients (P > .05). There was no significant difference in the BBPS score between Group B and Group C, whereas the BBPS score in Group A was significantly higher than that in Groups B and C (P < .05). CONCLUSION: The "4-hour 1 + 2L" bowel preparation regimen can obtain higher BBPS score for colonoscopy, which is suggested to be the optimal plan for colonoscopy patients of the time and dosage. Definitely, higher BBPS score can improve the quality of colonoscopy diagnosis and treatment consequence.

Genome-Wide Association and Transcriptome-Wide Association Studies Identify Novel Susceptibility Genes Contributing to Colorectal Cancer.

Background: Colorectal cancer (CRC) is among the most common cancers diagnosed worldwide. Although genome-wide association studies have effectively identified the genetic basis of CRC, there is still unexplained variability in genetic risk. Transcriptome-wide association studies (TWAS) integrate summary statistics from CRC genome-wide association studies (GWAS) with gene expression data to prioritize these GWAS findings and uncover additional gene-trait correlations. Methods: First, we carried out a post-GWAS analysis using summary statistics from a large-scale GWAS of CRC (n = 4,562 cases, n = 382,756 controls). Second, combined with the expression weight sets from GTEx (v7), susceptibility genes were identified with the FUSION software. Colocalization, conditional and fine-mapping analyses, phenome-wide association study (pheWAS), and Mendelian randomization were employed to further characterize the observed correlations. Results: In the post-GWAS analyses, we first identified new genome-wide significant associations: three genomic risk loci were identified at 8q24.21 (rs6983267, P = 6.98 × 10-12), 15q13.3 (rs58658771, P = 1.40 × 10-10), and 18q21.1 (rs6507874, P = 1.91 × 10-14). In addition, the TWAS also identified four loci statistically significantly associated with CRC risk, largely explained by expression regulation, including six candidate genes (DUSP10, POU5F1B, C11orf53, COLCA1, COLCA2, and GREM1-AS1). We further discovered evidence that low expression of COLCA2 is correlated with CRC risk with Mendelian randomization. Conclusions: We discovered novel CRC risk loci and candidate functional genes by merging gene expression and GWAS summary data, offering new insight into the molecular processes underlying CRC development. This makes it easier to prioritize potential genes for follow-up functional research in CRC.

Analysis of core genes for colorectal cancer prognosis based on immune and stromal scores.

BACKGROUND: Colorectal cancer (CRC) is one of the most common malignancies.An early diagnosis and an accurate prognosis are major focuses of CRC research. Tumor microenvironment cells and the extent of infiltrating immune and stromal cells contribute significantly to the tumor prognosis. METHODS: Immune and stromal scores were calculated based on the ESTIMATE algorithm using the sample expression profile of the The Cancer Genome Atlas (TCGA) database. GSE102479 was used as the validation database. Differentially expressed genes whose expression was significantly associated with the prognosis of CRC patients were identified based on the immune matrix score. Survival analysis was conducted on the union of the differentially expressed genes. A protein-protein interaction (PPI) network was constructed using the STRING database to identify the closely connected modules. To conduct functional enrichment analysis of the relevant genes, GO and KEGG pathway analyses were performed with Cluster Profiler. Pivot analysis of the ncRNAs and TFs was performed by using the RAID2.0 database and TRRUST v2 database. TF-mRNA regulatory relationships were analyzed in the TRRUST V2 database. Hubgene targeting relationships were screened in the TargetScan, miRTarBase and miRDB databases. The SNV data of the hub genes were analyzed by using the R maftools package. A ROC curve was drawn based on the TCGA database. The proportion of immune cells was estimated using CIBERSORT and the LM22 feature matrix. RESULTS: The results showed that the matrix score was significantly correlated with colorectal cancer stage T. A total of 789 differentially expressed genes and 121 survival-related prognostic genes were identified. The PPI network showed that 22 core genes were related to the CRC prognosis. Furthermore, four ncRNAs that regulated the core prognosis genes, 11 TFs with regulatory effects on the core prognosis genes, and two drugs, quercetin and pseudoephedrine, that have regulatory effects on colorectal cancer were also identified. CONCLUSIONS: We obtained a list of tumor microenvironment-related genes for CRC patients. These genes could be useful for determining the prognosis of CRC patients. To confirm the function of these genes, additional experiments are necessary.

Driving safety assessment for ride-hailing drivers.

Ride-hailing services, which have become increasingly prevalent in the last decade, provide an efficient travel mode by matching drivers and travelers via smartphone apps. Ride-hailing services enable millions of non-traditional taxi drivers to provide travel services, but may also raise safety concerns due to heterogeneity in the driver population. This study evaluated crash risk factors for ride-hailing drivers, including driving history and ride-hailing operational characteristics, using a sample of 189,815 drivers. We utilized the Poisson generalized additive model to accommodate for the potential nonlinear relationship between crash rate and risk factors. Results showed that crash history, the percentage of long-shift bookings, driving distance, operations during peak hours, years of being a ride-hailing driver, and passenger rating were significantly associated with crash risk. Several factors showed nonlinear relationships with crash risk. We adopted the SHapley Additive exPlanation (SHAP) method to assess and visualize the impact of each risk factor. The results indicated that passenger average rating, total driving distance, and crash history were the leading contributing factors. The findings of this study provide critical information for the development of safety countermeasures, driver education programs, as well as safety regulations for the ride-hailing industry.

The SELS rs34713741 Polymorphism Is Associated with Susceptibility to Colorectal Cancer and Gastric Cancer: A Meta-Analysis.

Aims: The selenoprotein S (SELS) gene has been suggested to be an important factor in the development of multiple diseases, including gastric cancer (GC) and colorectal cancer (CRC). However, the association between the SELS gene rs34713741 polymorphism and risk of GC and CRC is inconclusive. Thus, we aimed to investigate the relationship between this polymorphism and the susceptibility to GC and CRC through a meta-analysis. Materials and Methods: Literature was retrieved through the following electronic databases: PubMed, Embase, Web of Science, and Chinese National Knowledge Infrastructure. The pooled odds ratio (OR) and 95% confidence interval (CI) were used to assess the strength of the associations of the alleles of rs4713741 locus with the risk of CRC and GC. Results: Seven studies that collectively included 2331 cases and 2233 controls were utilized for this meta-analysis. Under the allelic and dominant models, the T allele of the SELS rs34713741 polymorphism was significantly associated with CRC risk (allelic model: OR = 1.20, 95% CI = 1.08-1.33, p = 0.0004; dominant model: OR = 1.25, 95% CI = 1.10-1.43, p = 0.001). In addition, all of the genetic models (allelic, dominant, and recessive models) identified the rs34713741 T allele as being significantly associated with GC risk (allelic model: OR = 1.67, 95% CI = 1.30-2.15, p < 0.001; dominant model: OR = 1.70, 95% CI = 1.25-2.30, p = 0.0006; recessive model: OR = 2.39, 95% CI = 1.26-4.50, p = 0.007). Conclusions: The SELS gene rs34713741 T-allele is a highly probable risk factor for both CRC and GC. The results of this study will provide support for using this single nucleotide polymorphism in the diagnosis of GC and CRC.

Polymorphism rs6478109 in the TNFSF15 gene contributes to the susceptibility to Crohn's disease but not ulcerative colitis: a meta-analysis.

OBJECTIVE: Polymorphisms in the tumor necrosis factor superfamily 15 (TNFSF15) gene contribute to susceptibility to inflammatory bowel disease (IBD). However, associations between TNFSF15 rs6478109, rs7869487, and rs7865494 polymorphisms and IBD remain unclear. METHODS: Eligible articles were retrieved from the PubMed, EMBASE, Web of Science, and CNKI databases through 20 March 2020. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to evaluate the relationships of TNFSF15 polymorphisms with IBD susceptibility. RESULTS: Under the recessive model, TNFSF15 rs6478109 was associated with IBD risk (OR = 0.56; 95% CI: 0.35, 0.92). Stratification analyses based on the type of disease-Crohn's disease (CD) or ulcerative colitis (UC)-revealed a significant association under the allelic and recessive models between TNFSF15 rs6478109 and CD (allelic model: OR = 0.84, 95% CI: 0.71, 0.99; recessive model: OR = 0.44, 95% CI: 0.22, 0.87) but not UC. Stratification by ethnicity indicated a significantly decreased risk of IBD in Asian populations with TNFSF15 rs6478109 under the recessive model (OR = 0.56, 95% CI: 0.35, 0.92). CONCLUSIONS: Our meta-analysis suggested that under the allelic and recessive models, the TNFSF15 rs6478109 polymorphism was likely protective for CD but not UC in the Asian population.

CircRNA_0005075 suppresses carcinogenesis via regulating miR-431/p53/epithelial-mesenchymal transition axis in gastric cancer.

This study was aimed to explore the expression and biological function of circRNA_0005075 in gastric cancer (GC) progression and its underlying mechanism. First, the expression level of circRNA_0005075 and microRNA-431 (miR-431) in GC tissues were detected with the quantitative real-time polymerase chain reaction. In addition, after down-regulated the circRNA_0005075 expression by plasmid transfection in GC cells, the Cell Counting Kit-8 (CCK-8), EDU, transwell assay were conducted to evaluate the function of circRNA_0005075 or miR-431 on cell proliferation, metastasis in vitro. Moreover, p53 and Epithelial-mesenchymal transition (EMT) pathway related proteins were also measured with western blotting. Then, our data revealed that CircRNA_0005075 was found to be significantly up-regulated in GC tissues as well as GC cell lines, and the GC patients with higher CircRNA_0005075 expression were more likely to have poor outcomes. Down-regulation of CircRNA_0005075 could significantly suppress the GC cell proliferation and cell metastasis ability, while the addition of miR-431 inhibitors could counteract this effect. Importantly, we discovered that the silencing of circRNA_0005075 could weaken the micro-RNA sponge function for miR-431, and then upregulate the expression of p53 and forbid the EMT signalling pathway, and finally suppress the tumourigenesis of GC. To sum up, CircRNA_0005075 could inhibit cell growth and metastasis of GC through regulating the miR-431/p53/EMT axis. SIGNIFICANCE OF THE STUDY: The research clearly elucidated the potential role and relative regulatory mechanism of circRNA_0005075 in gastric cancer (GC) progression. Briefly, circRNA_0005075 could directly inhibit the expression level of miR-431, then regulate the p53/Epithelial-mesenchymal transition axis, and finally inhibit cell growth and metastasis in GC. Consequently, circRNA_0005075 might act as an oncogene in the GC procession, which provides a promising way for the treatment of GC.

Genetic association between IL23R rs11209026 and rs10889677 polymorphisms and risk of Crohn's disease and ulcerative colitis: evidence from 41 studies.

OBJECTIVE: IL23R plays an important role in the pathogenesis of inflammatory bowel disease (IBD). The IL23R rs11209026 and rs10889677 polymorphisms have been shown to be associated with the development of Crohn's disease (CD) and ulcerative colitis (UC). But the results were inconsistent and inconclusive. So, we aim to investigate the genetic association between rs11209026 and rs10889677 polymorphisms and UC and CD risk by a meta-analysis. METHODS: Literature search was conducted through PubMed, CNKI, and web of science databases. Pooled OR and 95% CI was used to assess the association between the allelic, dominant and recessive models of IL23R rs11209026 and rs10889677 polymorphisms and UC and CD risk. RESULTS: 41 publications with 13,803 patients with CD and 17,446 controls, as well as 5876 patients with UC and 10,053 controls were included in the present study. All the genetic models of rs11209026 polymorphism significantly decrease CD and UC risk (except for the recessive model in UC) (p < 0.05). A subgroup analysis based on ethnicity showed that the allelic (p < 0.00001, OR = 0.65) and dominant models (p < 0.00001, OR = 0.61) of rs11209026 polymorphism were significantly associated with UC risk in Caucasians, but not in Asians (p > 0.05). In addition, the allelic (CD: p < 0.00001, OR = 1.34; UC: p < 0.00001, OR = 1.22) and dominant models (CD: p = 0.002, OR = 1.39; UC: p = 0.01, OR = 1.29), but not the recessive model of rs10889677 polymorphism significantly increase the risk of CD and UC (p > 0.05). A subgroup analysis showed that the genetic models of rs10889677 polymorphism were associated with CD risk in Caucasians (p < 0.05), but not in Asians (p > 0.05). The dominant model of rs10889677 polymorphism was associated with UC risk in Asians (p = 0.04, OR = 1.54), but not in Caucasians (p > 0.05). CONCLUSIONS: Our meta-analysis demonstrated that the rs11209026 polymorphism might be a protective factor against developing IBD, while the rs10889677 polymorphism might be a risk factor for IBD.

MicroRNA-145 Inhibits Cell Migration and Invasion in Colorectal Cancer by Targeting TWIST.

INTRODUCTION: MicroRNAs function as oncogenes or tumor suppressors in the development of various human cancers. We investigated the effect of microRNA-145 (miR-145) on colorectal cancer (CRC) cell invasion and migration. METHODS: The levels of miR-145 in CRC cells were examined by quantitative PCR; Western blotting was used to detect TWIST1 (twist family bHLH transcription factor 1) protein and the epithelial-mesenchymal transition (EMT)-related proteins (E-cadherin, vimentin). Then, we transfected miR-145 mimics or inhibitor into CRC cells and used the wound healing and Transwell invasion assays to investigate their migration and invasive capability, respectively. RESULTS: The miR-145 mimics suppressed CRC cell invasion and migration significantly; in contrast, miR-145 downregulation had the opposite effect. Furthermore, miR-145 regulated TWIST1 levels negatively at transcriptional level. TWIST1 knockdown significantly inhibited the CRC cell migration ability and the number of CRC cells that crossed the Transwell membrane. There was no significant difference in terms of migration and invasive capability after the cells had been transfected with miR-145 mimics or inhibitor plus TWIST1 small interfering RNA (siRNA) as compared to the TWIST1 siRNA-only group. Furthermore, we demonstrate that the inhibition of miR-145 could enhance the capability for lung metastasis in vivo. CONCLUSION: Taken together, these findings indicate that miR-145 acts as a new tumor suppressor by regulating TWIST1 and plays a vital role in the invasive and migration ability of CRC cells.

Prediction of Overall Survival in Gastric Cancer Using a Nine-lncRNA.

Long noncoding RNA (lncRNA) was closely attached to various cancers according to previous studies. In this study we aimed to investigate an lncRNA signature with prognostic value of over survival (OS) outcomes of gastric cancer (GC). Profiles of mRNAs expression and clinical information of 381 GC tissues and 32 nontumor gastric tissues were downloaded from The Cancer Genome Atlas database. Comparison of various lncRNA expression between cancer tissue and normal tissue was made among these data. In the end, a nine-lncRNA signature was discovered using univariate and multivariate Cox regression analyses, with a prospect possibility of the OS in GC patients. Receiver operating characteristic (ROC) was used to evaluate the accuracy of survival model. The gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were used to predict the possible functions and pathways of these lncRNAs. Altogether 720 distinctively expressed lncRNAs were selected between GC and normal tissues. By univariate and multivariate Cox regression analyses, nine lncRNAs were eventually filtered to set a predictive model, distributing patients into high-risk and low-risk groups with extraordinary different OS. Area under the curve of the ROC curve for the nine-lncRNA signature's prediction of 5-year OS was 0.795. Further functional enrichment analyses indicated that these lncRNAs may be associated with biological processes such as protein binding, DNA replication, and cell cycle. Our study identified a nine-lncRNA signature, which could act as a potential prognostic biomarker in the prediction of GC patients' OS.

Diagnostic value of apolipoprotein C-I, transthyretin and apolipoprotein C-III in gastric cancer.

Diagnostic value of apolipoprotein C-I (ApoC-I), transthyretin (TTR) and ApoC-III in gastric cancer were evaluated. Retrospective analysis methods were used to collect 60 patients with gastric cancer first diagnosed in The First Affiliated Hospital of Jiaxing University. There were 60 patients with chronic atrophic gastritis in the benign lesion group and 60 healthy individuals in the control group. The expression levels of serum ApoC-I, TTR and ApoC-III was detected by enzyme-linked immunosorbent assay. Differences existed in the expression levels of ApoC-I, TTR and ApoC-III in the gastric cancer group, benign lesion group and control group (P<0.001), with the expression levels of ApoC-I, TTR and ApoC-III in the gastric cancer group being lower than that of the benign lesion group (P<0.05), and the expression levels of ApoC-I, TTR and ApoC-III in the benign lesion group being lower than that of the control group (P<0.05). The expression levels of ApoC-I, TTR and ApoC-III in the gastric cancer group were to a certain degree correlated with the clinical stage, lymph node metastasis and differentiation of patients in the gastric cancer group (P<0.05). The specificity and negative predictive value of combined detection were proven to be higher than the separate detection of the three factors (P<0.05). The detection of serum ApoC-I, TTR and ApoC-III was of great significance in the diagnosis of gastric cancer and the estimation of its severity. The method of combined detection is worth a further in-depth study as it could improve the specificity of diagnosis and have a higher negative predictive value.

The genetic association between EGF A61G polymorphism (rs4444903) and risk of colorectal cancer: An update meta-analysis and trial sequential analysis.

BACKGROUND: Colorectal cancer was a complex disease with multiple causative factors including genetic and environmental factors, as well as the interaction of the 2 factors. Relationship between epidermal growth factor (EGF) A61G polymorphism and colorectal cancer risk has been widely investigated previously, whereas results derived from these studies were inconclusive and controversial. The aim of this study was to investigate the association between the EGF A61G polymorphism and colorectal cancer using a meta-analysis of existing literature. METHODS: Literature search was conducted from PubMed, EMBASE, China National Knowledge Infrastructure, Wanfang, and Cochrane library databases before July 2017. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate the strength of the association between EGF A61G and colorectal cancer. RESULTS: A total of 9 studies that involved 1448 cases and 1928 healthy controls and found allelic (OR = 1.18, P = .04) and recessive models (OR = 1.36, P = .03) of EGF A61G were significantly associated with the risk of colorectal cancer. Stratification analyses by ethnicity indicated that the EGF 61G significantly increased the risk of colorectal cancer in the Caucasian subgroup (OR = 1.24, P = .02), but not in Asian subgroup (OR = 1.12, P = .08). And the frequency of GG genotype of EGF A61G significantly increased in cases than that in healthy controls in both Caucasian (OR = 1.40, P = .04) and Asian subgroups (OR = 1.27, P = .01). Furthermore, the sample sources and genotyping methods seem to have no influence on the correction of EGF A61G and colorectal cancer susceptibility (P > .05). CONCLUSION: The results indicate that EGF A61G might increase the risk of colorectal cancers.

The genetic association between iNOS and eNOS polymorphisms and gastric cancer risk: a meta-analysis.

OBJECTIVE: There are a number of susceptible factors for an increased risk of gastric cancer. Nitric oxide (NO) is considered to be associated with the development of a range of cancers. In particular, inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) are known to play a central role in the production of NO. Published studies relating to the association between eNOS rs1799983, rs2070744, and iNOS rs2297518 polymorphisms and the risk of gastric cancer risk are conflicting and inconclusive and require further analysis. MATERIALS AND METHODS: This study involved a meta-analysis of case-control studies relating to eNOS rs1799983, rs2070744, and iNOS rs2297518 polymorphisms published prior to January 2018. Literature searches were carried out in PubMed, Embase, Web of Science, the Cochrane Library databases, and the Chinese National Knowledge Infrastructure. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were used to evaluate the strength of association based on genotype data. RESULTS: A total of 1,356 cases and 1,791 controls were included from nine case-control studies involving eNOS rs1799983 (G894T), rs2070744 (T-786C), and iNOS rs2297518 (C150T) polymorphisms. Data analysis indicated that iNOS rs2297518 was a risk factor for Helicobacter pylorus-positive gastric cancer when compared with H. pylorus-negative gastric cancer (p=0.003, OR [95% CI] =2.19 [1.31-3.66]). In addition, the allelic, dominant, and recessive models of eNOS rs2070744 were significantly associated with a risk of gastric cancer (allelic model: p<0.00001, OR [95% CI] =0.23 [0.16-0.34]; dominant model: p<0.00001, OR [95% CI] =0.25 [0.15-0.42]; recessive model: p<0.00001, OR [95% CI] =0.16 [0.08-0.30]). No association was identified between eNOS rs1799983 and the risk of gastric cancer (p>0.05). CONCLUSION: iNOS rs2297518 and eNOS rs2070744 polymorphisms may represent susceptible factors for gastric cancer.