Odds Ratio Of Gastric Cancer Research Articles

Aspirin but not statins is inversely related to gastric cancer with a duration-risk effect: Results from the Stomach Cancer Pooling Project Consortium.

Aspirin and statins have been suggested to have potential chemopreventive effects against gastric cancer (GC), although the results of previous studies have been inconsistent. This study therefore aimed to investigate the association between the use of aspirin and statins and GC. A pooled analysis of seven case-control studies within the Stomach Cancer Pooling Project, including 3220 cases and 9752 controls, was conducted. Two-stage modeling analyses were used to estimate the association between aspirin and statin use and GC after adjusting for potential confounders. The pooled odds ratio (OR) of GC for aspirin users versus nonusers was 0.72 (95% confidence interval [CI], 0.54-0.95). The protective effect of aspirin appeared stronger in individuals without a GC family history (OR, 0.60; 95% CI, 0.37-0.95), albeit with borderline heterogeneity between those with and without a family history (p = .064). The OR of GC decreased with increasing duration of aspirin use, with an OR of 0.41 (95% CI, 0.18-0.95) for durations of ≥15 years. An inverse, nonsignificant association with the risk of GC was observed for the use of statins alone (OR, 0.79; 95% CI, 0.52-1.18). These findings suggest that aspirin use, particularly long-term use, is associated with a reduced risk of GC, whereas a similar association was not observed with statins, possibly because of the low frequency of use.

Dietary intake of vitamin C and gastric cancer: a pooled analysis within the Stomach cancer Pooling (StoP) Project

BackgroundPrevious studies suggest that dietary vitamin C is inversely associated with gastric cancer (GC), but most of them did not consider intake of fruit and vegetables. Thus, we aimed to evaluate this association within the Stomach cancer Pooling (StoP) Project, a consortium of epidemiological studies on GC.MethodsFourteen case–control studies were included in the analysis (5362 cases, 11,497 controls). We estimated odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for the association between dietary intake of vitamin C and GC, adjusted for relevant confounders and for intake of fruit and vegetables. The dose–response relationship was evaluated using mixed-effects logistic models with second-order fractional polynomials.ResultsIndividuals in the highest quartile of dietary vitamin C intake had reduced odds of GC compared with those in the lowest quartile (OR: 0.64; 95% CI: 0.58, 0.72). Additional adjustment for fruit and vegetables intake led to an OR of 0.85 (95% CI: 0.73, 0.98). A significant inverse association was observed for noncardia GC, as well as for both intestinal and diffuse types of the disease. The results of the dose–response analysis showed decreasing ORs of GC up to 150–200 mg/day of vitamin C (OR: 0.54; 95% CI: 0.41, 0.71), whereas ORs for higher intakes were close to 1.0.ConclusionsThe findings of our pooled study suggest that vitamin C is inversely associated with GC, with a potentially beneficial effect also for intakes above the currently recommended daily intake (90 mg for men and 75 mg for women).

Association between Gout and Gastric Cancer: A Nested Case-Control Study Using a National Health Sample Cohort.

Given the global significance of gout and gastric cancer (GC) as major health problems with interrelated impacts, we examined the development of GC in Korean patients with gout. We conducted a nested case-control study using data from 10,174 GC patients and 40,696 control patients from the Korean National Health Insurance Service-National Sample Cohort database. Propensity score matching (1:4) with propensity score overlap-weighted adjustment was used to reduce selection bias and estimate the odds ratio (OR) and 95% confidence intervals (CIs) for the association between gout and GC. An adjusted OR for GC was not significantly higher in patients with gout than in control patients (1.02; 95% CI, 0.93-1.12; p = 0.652). Additionally, no association between gout and GC was observed in subgroup analyses such as sex, age, level of income, region of residence, or Charlson Comorbidity Index score. In conclusion, these results suggest that gout is not a significant independent risk factor for GC among the Korean population. Additional investigation is required to establish a causal association between gout and GC, and to generalize these results to general populations.

Leisure-time physical activity and gastric cancer risk: a pooled study within the StoP project

Abstract Background Although physical activity (PA) has been recognized as a favourable factor in the prevention of various diseases, including certain forms of cancer, the relationship between PA and gastric cancer (GC) is not yet fully comprehended. For this reason, this study aims provide data from a pooled analysis of case-control studies within the Stomach cancer Pooling (StoP) Project to estimate the association between leisure-time PA and the occurrence of GC. Methods Six case-control studies from StoP project collected data on leisure-time PA, for a total of 2,343 cases and 8,614 controls. Subjects were classified into three leisure-time PA categories, either none/low, intermediate or high, based on study-specific tertiles. We used a two-stage approach. Firstly, we applied multivariable logistic regression models to obtain study-specific odds ratios (ORs) and corresponding 95% confidence intervals (CIs) then, we used a random-effect models to obtain pooled effect estimates. Heterogeneity was assessed using Q and I2 statistics. We performed stratified analyses according to demographic, lifestyle and clinical covariates. Results The meta-analysis showed ORs of GC with no significant differences between intermediate vs low and high vs low PA level (OR 1.05 [95%CI 0.76-1.45]; OR 1.23 [95%CI 0.78-1.94], respectively). GC risk estimates did not strongly differ across strata of selected covariates except for age ≤ 55 years old (high vs low level: OR 0.72 [95%CI 0.55-0.94]). Conclusions An association between leisure time PA and GC, apart from some suggestion of decreased risk below age 55, was not found. This may reflect specific characteristics of GC at younger age, or the presence of a cohort effect mediating and interacting with socioeconomic determinants of GC. Key messages • An association between leisure time PA and GC, apart from some suggestion of decreased risk below age 55, was not found. • GC risk estimates did not strongly differ across strata of selected covariates except for age ≤ 55 years old.

Leisure-time physical activity and gastric cancer risk: A pooled study within the Stomach cancer Pooling (StoP) Project.

Although physical activity (PA) has been recognized as a favourable factor in the prevention of various diseases, including certain forms of cancer, the relationship between PA and gastric cancer (GC) is not yet fully understood. This study aims to provide data from a pooled analysis of case-control studies within the Stomach cancer Pooling (StoP) Project to estimate the association between leisure-time PA and the occurrence of GC. Six case-control studies from StoP project collected data on leisure-time PA, for a total of 2,343 cases and 8,614 controls. Subjects were classified into three leisure-time PA categories, either none/low, intermediate or high, based on study-specific tertiles. We used a two-stage approach. Firstly, we applied multivariable logistic regression models to obtain study-specific odds ratios (ORs) and corresponding 95% confidence intervals (CIs) then, we used a random-effect models to obtain pooled effect estimates. We performed stratified analyses according to demographic, lifestyle and clinical covariates. The meta-analysis showed ORs of GC with no significant differences between intermediate vs low and high vs low PA level (OR 1.05 [95%CI 0.76-1.45]; OR 1.23 [95%CI 0.78-1.94], respectively). GC risk estimates did not strongly differ across strata of selected covariates except for age ≤ 55 years old (high vs low level: OR 0.72 [95%CI 0.55-0.94]) and for control population-based studies (high vs low level: OR 0.79 [95%CI 0.68-0.93]). No association was found between leisure time PA and GC, apart from a slight suggestion of decreased risk below age 55 and in control population-based studies. These results may reflect specific characteristics of GC at a younger age, or the presence of a cohort effect mediating and interacting with socioeconomic determinants of GC The different distribution of PA levels among hospitalized controls could have led to an underestimated effect of PA on GC risk.

Chronic metformin intake and gastric cancer: A pooled analysis within the Stomach cancer Pooling (StoP) Project

IntroductionThe association between chronic use of metformin and risk of gastric cancer (GC) has been investigated with contradicting results. We aimed to study the association between chronic use of metformin and GC by using data from the Stomach cancer Pooling (StoP) Project, an epidemiological consortium of case-control studies on GC. MethodsData from three studies of the StoP Project with available information on metformin intake were analyzed.Multivariable logistic regression models were used to estimate study-specific odds ratios (ORs) and 95% confidence intervals (CIs) for the association between chronic use of metformin and GC risk. Analyses were adjusted for sex, age, socioeconomic status, body mass index, smoking status, alcohol drinking status, and history of diabetes. Study-specific ORs and 95% CIs were then pooled with a random-effects model.The dose-response relationship between the duration of metformin intake and GC was assessed with a one-stage logistic model, and the duration of intake was modelled using second-order fractional polynomials. ResultsThe OR of GC in metformin users versus non-users was 1.01 (95% CI=0.61, 1.67). The association between metformin and GC did not change among different strata of study participants’ characteristics or when restricting the analyses to those with a history of diabetes.The dose-response analysis showed a slightly reducing trend in the OR of GC and a borderline significant association with increasing duration of metformin intake. ConclusionsThe results of our study do not clearly support an association between chronic use of metformin and GC, warranting further research.

Serum Total Bile Acids in Relation to Gastrointestinal Cancer Risk: A Retrospective Study.

BackgroundBile acids (BAs) have been proposed to promote gastrointestinal cells carcinogenesis. However, studies on serum total bile acid (TBA) levels and gastrointestinal cancers (GICs) risk are rare.MethodsWe conducted a retrospective case–control study from 2015 to 2019 at the First Affiliated Hospital of Air Force Military Medical University, in which 4,256 GICs cases and 1,333 controls were recruited. Patients’ demographic, clinical and laboratory data were collected. The odds ratios (ORs) with 95% confidence intervals (CIs) were estimated using binary logistic regression models.ResultsPositive associations were observed between serum TBA levels and risks of esophageal cancer (EC), gastric cancer (GC) and colorectal cancer (CRC). Overall, ORs of EC, GC and CRC risk rose with the TBA levels increasing. After adjustment for potential confounders, the OR of TBA-positive for EC risk was 4.89 (95% CI: 3.20-7.49), followed by GC (OR: 3.92, 95% CI: 2.53-6.08), and CRC (OR: 3.32, 95% CI: 2.04-5.11). Patients aged 60 years or older have a higher risk of GICs, especially for EC patients. Males are associated with a higher risk of GC, while females are associated with a higher risk of CRC. Preoperative serum TBA positive and negative was significantly different in the presence or absence of hematogenous metastasis among EC patients (P=0.014), and lymph node metastasis among GC patients (P=0.018).ConclusionsThis retrospective study showed positive associations between serum TBA level and GICs risk, and a higher serum TBA level constitutes a risk factor for GICs.

Association between triglyceride-glucose index and gastric carcinogenesis: a health checkup cohort study.

We aimed to investigate the association between the triglyceride-glucose (TyG) index and gastric carcinogenesis, including precancerous conditions such as dysplasia, atrophic gastritis, and intestinal metaplasia. Patients who received an upper endoscopic assessment at a medical center were included. The enrolled patients were divided into four categories according to their TyG index quartile (Q). To evaluate the relationship between increase of TyG index and gastric cancer, we analyzed the patients who received a health checkup twice. Moreover, receiver-operating characteristic curve analysis was used to establish cut-off value of the TyG index for gastric cancer. Of 127,564 enrolled patients, 43,525 (34.1%) and 186 (0.1%) were diagnosed with precancerous conditions and gastric cancer, respectively. The odds ratios (ORs) of precancerous conditions given TyG index progressively increased across quartiles: using Q1 as the reference: Q2 (OR = 1.403, P < 0.001), Q3 (OR = 1.646, P < 0.001), and Q4 (OR = 1.656, P < 0.001). The ORs of gastric cancer also increased according to the quartiles: Q2 (OR = 1.619, P = 0.045), Q3 (OR = 2.180, P = 0.004), and Q4 (OR = 2.363, P = 0.001). Moreover, the increase in TyG index between baseline and follow-up tests was more significant in gastric cancer group than in control group (P = 0.001). The optimal cut-off value for predicting gastric cancer was 9.73. The TyG index may be a novel predictive biomarker for gastric carcinogenesis. Notably, increase in the TyG index is significantly associated with gastric cancer.

Vitamin D Status and Gastric Cancer: A Cross-Sectional Study in Koreans.

Sufficient vitamin D levels are associated with reduced Helicobacter pylori infections, which can cause gastric carcinogenesis. We examined associations between vitamin D concentrations and gastric cancer (GC) prevalence in a Korean population. We analyzed data of 33,119 adults using serum 25-hydroxyvitamin D (25(OH)D) concentrations as a biomarker of vitamin D status. Participants were classified with GC if previously diagnosed as such by a physician. After controlling for age, sex and body mass index (model A), odds ratio (OR) for GC was 0.81 (95% confidence interval [CI]: 0.70, 0.95), with a 5-ng/mL increment in total 25(OH)D concentrations. In fully adjusted models (model B), the OR for GC was 0.84 (95% CI: 0.72, 0.98), with a 5-ng/mL increment in total vitamin D. Following the classification of vitamin D concentrations into three categories or for GC in model A was 0.52 (95% CI: 0.30, 0.92) comparing between higher (≥20 ng/mL) and lower (<12 ng/mL) total 25(OH)D concentrations. In model B OR for GC was 0.57 (95% CI: 0.32, 1.00) comparing between higher and lower total 25(OH)D concentrations. Our results suggested that high vitamin D concentration was associated with lower ORs of GC in Korean adults.

Epstein Barr virus antibody reactivity and gastric cancer: A population-based case-control study

BackgroundIn contrast to the recognized role of Helicobacter pylori in the etiology of non-cardia gastric cancer (GC), there is still insufficient epidemiological evidence for the involvement of Epstein-Barr virus (EBV) in gastric carcinogenesis. We aimed to evaluate the relation of antibody profile and antibody reactivity intensity against four individual EBV proteins to GC risk. MethodsWe used information from 281 GC cases and 2071 age and sex frequency matched controls recruited in the frame of the MCC-Spain multicase-control study, between 2008 and 2013. Sociodemographic, lifestyle and environmental factors were assessed in face-to-face interviews. Antibody responses to four EBV proteins (EBNA-1, ZEBRA, EA-D, and VCA-p18) were analyzed by multiplex serology. Odds ratios (OR) and 95% confidence intervals were calculated by using logistic regression mixed models to evaluate the association of seropositivity and antibody reactivity against EBV proteins with GC, adjusting for GC risk factors. Stratified analyses by tumor location (cardia vs. non-cardia) and morphology (intestinal vs. diffuse) were done. ResultsAmong controls, seropositivity for EA-D, ZEBRA, EBNA-1 and VCA-p18 was 85%, 91%, 97% and 99%, respectively. Even though seropositivity for none of the studied proteins was associated with a higher GC risk, increasing antibody reactivity against EBNA-1 and VCA-p18 was associated with higher OR of GC. This association was present for cardia and non-cardia cancer cases, and for intestinal and diffuse types. ConclusionOur results support the hypothesis that EBV may play a role in GC etiology, and highlight the importance of evaluating specific antibodies and the dose-response relations when studying widespread infections.

Serum pepsinogen 1 and anti-Helicobacter pylori IgG antibodies as predictors of gastric cancer risk in Finnish males.

Serum pepsinogen 1 (SPG1) and anti-Helicobacter pylori serology have been used for gastric risk stratification in Asia. To assess utility of these markers in a Western population. SPG1 measurements were available for 21895 Finnish male smokers in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. We used Cox proportional hazards models adjusted for potential confounders to estimate gastric cancer hazard ratios (HR) and 95% confidence intervals (95% CI) for low SPG1 (<25μg/L). In a subset (n=3555) with anti-H. pylori serology, these markers jointly defined the following: Group A (H. pylori[-], SPG1[normal]; reference group), Group B (H. pylori[+], SPG1[normal]), Group C (H. pylori[+], SPG1[low]) and Group D (H.pylori[-], SPG1[low]). Odds ratios (ORs) and 95% CI were calculated using multivariate logistic regression. There were 329 gastric cancers diagnosed an average of 13.9years after baseline. Pre-diagnostic low SPG1 was significantly associated with increased gastric cancer risk (HR 2.68, 95% CI 1.99-3.61). Among subjects with both SPG1 and H.pylori serology, groups B, C and D had increased gastric cancer ORs (95% CI) of 1.79 (1.21-2.64), 3.85 (2.36-6.28) and 6.35 (2.20-18.34), respectively. CagA seropositives had significantly higher ORs than CagA seronegatives within group B (Pheterogeneity =0.01). For groups B and C, repeat SPG1 level at 3years did not further stratify gastric cancer risk. Low SPG1 was associated with increased gastric cancer risk in our large Finnish cohort. A single measurement of SPG1 along with H. pylori whole cell and CagA serology provides potentially useful prediction of gastric cancer risk.

High mitochondrial DNA copy number was associated with an increased gastric cancer risk in a Chinese population

Mitochondrial DNA (mtDNA) copy number (mtCN) may be a potential biomarker in relation to cancer risk. However, the role of mtCN in gastric cancer remains uncertain. We examined the association between peripheral blood leukocytes mtCN level and gastric cancer risk in a case-control study including 984 gastric cancer cases and 984 controls. We measured relative mtCN level by real-time quantitative PCR-based assay, and used logistic regression models to assess the association between mtCN and risk of gastric cancer. The mtCN level in gastric cancer cases was significantly higher than that in controls (median value: 6.53 vs 4.12, P = 1.79 × 10-5 ). Compared with those with low mtCN, the risk for gastric cancer was 1.29 (95% confidence interval [CI] = 1.02-1.63) in the median group and 1.74 (95%CI = 1.39-2.18) in the high mtCN group (P for trend = 1.51 × 10-6 ). Because relative telomere length (RTL) has been associated with gastric cancer risk in our previous study, we also evaluated the combined effects of mtCN and RTL on gastric cancer risk. Multivariable regression model revealed that the effects of mtCN and RTL were independent on gastric cancer risk. Compared with those in the lowest risk group by combining mtCN and RTL, the odds ratio for gastric cancer was 4.30 (95%CI = 2.79-6.63) in the highest risk group. Our results suggest that mtDNA may be implicated in gastric carcinogenesis and mtCN as well as RTL may serve as joint susceptible biomarkers for gastric cancer.

Abstract 2272: A prospective study of urinary prostaglandin E2 metabolite, Helicobacter pylori antibodies, and gastric cancer risk

Abstract Background. Previous studies suggest that a stable end-product of prostaglandin E2, the urinary metabolite PGE-M, is excreted in the urine and can be used as an index of systemic prostaglandin E2 (PGE2) production. In the present study we investigate the PGE-M, Helicobacter pylori (H. pylori), and gastric cancer association. Methods. The present analysis included 359 prospectively ascertained gastric cancer cases and 700 individually matched controls from two population-based prospective cohort studies, the Shanghai Women’s Health Study and Shanghai Men’s Health Study. Urinary PGE-M was measured by a liquid chromatography/tandem mass spectrometric method. Sero-positivity to 15 H. pylori recombinantly expressed fusion proteins was detected by H. pylori multiplex serology. Results. Adjusting for H. pylori, increasing PGE-M was associated with higher risk of gastric cancer (Quartile 4 vs. 1, OR=1.76, 95% CI: 1.17-2.66, Ptrend =0.004). This association remained after excluding those diagnosed within two years from sample collection (OR=1.73, 95% CI: 1.12-2.65, Ptrend =0.007). However it was no longer present among individuals with 10 or more years of follow-up (2-4.9 years, OR=3.15, 95% CI: 1.11-8.91; 5-9.9 years, OR=2.23, 95% CI: 1.22-4.06; ≥10 years, OR=0.73, 95% CI: 0.31-1.70). The association of PGE-M with gastric cancer risk was not modified by H. pylori status, but added predictive ability beyond H. pylori; compared to H. pylori-negative individuals with below-median PGE-M levels, H. pylori-positive individuals with above-median PGE-M levels had a 5-fold increase in the odds ratio of gastric cancer (OR=5.08, 95% CI: 2.47-10.43). Conclusion. In China, higher PGE-M levels may indicate an increased risk of gastric cancer independent of the risk conferred by H. pylori infection status, particularly for cancers diagnosed within 10 years of sample collection. Citation Format: Tianyi Wang, Hui Cai, Wei Zheng, Angelika Michel, Michael Pawlita, Ginger Milne, Yong-Bing Xiang, Yu-Tang Gao, Hong-Lan Li, Nathaniel Rothman, Qing Lan, Xiao-Ou Shu, Meira Epplein. A prospective study of urinary prostaglandin E2 metabolite, Helicobacter pylori antibodies, and gastric cancer risk [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2272. doi:10.1158/1538-7445.AM2017-2272

Dietary Flavonols Intake and Risk of Esophageal and Gastric Cancer: A Meta-Analysis of Epidemiological Studies.

Background: Esophageal cancer (EC) and gastric cancer (GC) are common cancers and leading causes of cancer deaths worldwide. Many studies have investigated the association between dietary flavonols intake and the risk of EC and GC, but the results are inconsistent. Hence, we conducted a systematic analysis of relevant population-based studies to assess the association and derive a more precise estimation. Methods: The Cochrane, PubMed and Embase databases were searched to identify articles published through January 2016 that met the predetermined inclusion criterion. Twelve studies involving 4593 patients and 519,378 controls were included. Results: The summary odds ratios (ORs) of EC, GC and the two combined were respectively 0.88 (95% CI: 0.73–1.08), 0.80 (95% CI: 0.70–0.91) and 0.83 (95% CI: 0.74–0.92) for the highest category of dietary flavonols intake compared with the lowest. No significant heterogeneities were observed in these studies. Further analysis showed that the pooled ORs of EC and GC for cohort, population-based case-control and hospital-based case-control studies were 0.90 (95% CI: 0.61–1.34), 0.92 (95% CI: 0.72–1.18), 0.68 (95% CI: 0.38–1.24) and 0.83 (95% CI: 0.65–1.06), 0.84 (95% CI: 0.45–1.59), 0.70 (95% CI: 0.56–0.88). The subgroup analyses revealed a significant association of flavonol intake with a reduced risk of noncardia gastric adenocarcinoma but not gastric cardia adenocarcinoma. Moreover, significant inverse associations of flavonol intake with GC risk were observed in women but not in men, in smokers but not in nonsmokers, in European populations but not in American populations. Similarly, a significant inverse association of flavonols intake with EC risk was also observed in smokers but not in nonsmokers. Conclusion: High intake of dietary flavonols is significantly related to a reduced risk of GC, especially in women and smokers.

Statins Attenuate Helicobacter pylori CagA Translocation and Reduce Incidence of Gastric Cancer: In Vitro and Population-Based Case-Control Studies.

Gastric cancer is the second leading cause of cancer-related death worldwide. The correlation of Helicobacter pylori and the etiology of gastric cancer was substantially certain. Cholesterol-rich microdomains (also called lipid rafts), which provide platforms for signaling, are associated with H. pylori-induced pathogenesis leading to gastric cancer. Patients who have been prescribed statins, inhibitors of 3-hydroxy-3-methyl glutaryl coenzyme A (HMG-CoA) reductase, have exhibited a reduced risk of several types of cancer. However, no studies have addressed the effect of statins on H. pylori-associated gastric cancer from the antineoplastic perspective. In this study, we showed that treatment of gastric epithelial cells with simvastatin reduced the level of cellular cholesterol and led to attenuation of translocation and phosphorylation of H. pylori cytotoxin-associated gene A (CagA), which is recognized as a major determinant of gastric cancer development. Additionally, a nationwide case-control study based on data from the Taiwanese National Health Insurance Research Database (NHIRD) was conducted. A population-based case-control study revealed that patients who used simvastatin exhibited a significantly reduced risk of gastric cancer (adjusted odds ratio (OR) = 0.76, 95% confidence interval (CI) = 0.70–0.83). In patients exhibiting H. pylori infection who were prescribed simvastatin, the adjusted OR for gastric cancer was 0.25 (95% CI = 0.12–0.50). Our results combined an in vitro study with a nationwide population analysis reveal that statin use might be a feasible approach to prevent H. pylori-associated gastric cancer.

Increased deaths from gastric cancer in communities living close to waste landfills

Background: Municipal waste landfills (MWLs) have been linked with some malignancies, but data about gastric cancer (GC) are still uncertain. Methods: Number of deaths from GC, death rates, and odds ratios (ORs) were calculated considering all residents in the 258 towns in the Apulia Region (4,099,547 subjects, years 2006–2009), living within 3 km from each of the 16 regional MWLs (n = 716,404) or in control areas (n = 3,383,143). Results: Males living close to MWLs showed a higher death rate for GC, a twofold higher mean number of GC deaths and higher adjusted ORs of GC, compared with controls areas. Conclusions: In a large population and over a wide time period, an increased risk of death from GC has been shown in males living in communities close to MWLs. Primary prevention policies acting through more sustainable waste management might probably partially reduce deaths from GC in areas with MWLs.

Dietary Fiber Intake Reduces Risk for Gastric Cancer: A Meta-analysis

The association between dietary fiber intake and gastric cancer risk has been investigated by many studies, with inconclusive results. We conducted a meta-analysis of case-control and cohort studies to analyze this association. Relevant studies were identified by searching PubMed and Embase through October 2012. We analyzed 21 articles, which included 580,064 subjects. Random-effects models were used to estimate summary relative risks. Dose-response, subgroup, sensitivity, meta-regression, and publication bias analyses were performed. The summary odds ratios of gastric cancer for the highest, compared with the lowest, dietary fiber intake was 0.58 (95% confidence interval, 0.49-0.67) with significant heterogeneity among studies (P < .001, I(2)= 62.2%). Stratified analysis for study design, geographic area, source and type of fiber, Lauren's classification, publication year, sample size, and quality score of study yielded consistent results. Dose-response analysis associated a 10-g/day increment in fiber intake with a significant (44%) reduction in gastric cancer risk. Sensitivity analysis restricted to studies with control for conventional risk factors produced similar results, and omission of any single study had little effect on the combined risk estimate. In a meta-analysis, we show that dietary fiber intake is associated inversely with gastric cancer risk; the effect probably is independent of conventional risk factors. The direction of the protective association of dietary fiber was consistent among all studies, but the absolute magnitude was less certain because of heterogeneity among the studies. Further studies therefore are required to establish this association.

Polymorphism of the salt sensitivity gene angiotensinogen and gastric cancer risk

A high-salt diet is a risk factor for gastric cancers other than those caused by Helicobacter pylori. The angiotensinogen (AGT) M235T polymorphism has been associated with salt sensitivity. The aim of the present study was to clarify the association between the AGT M235T polymorphism and gastric cancer. The AGT M235T polymorphism was genotyped using PCR-RFLP analysis in 206 gastric cancers and 210control biopsies. A logistic-regression analysis was performed to identify an odds ratio to determine whether a correlation exists between genetic polymorphism and risk in patients with gastric cancer as compared to the control samples. Statistical significance was determined using the Mann Whitney U and Chi-square tests. The genotype distribution was found to be MM=9 (4.4%), MT=57 (27.7%), and TT=140 (67.9%) in samples from patients with gastric cancer and MM=8 (3.8%), MT=60 (28.6%) and TT=142 (67.6%) in the control samples. The odds ratio of gastric cancer of the MM genotype associated with the T carrier was 1.0 (0.4-2.7) (P=0.95). The distribution pattern of AGT M235T polymorphism in the gastric cancer cases and controls was not found to be significantly different in this study. Thus, it can be concluded that other sites of AGT polymorphism or other salt sensitivity genes may be associated with gastric cancer.

No associations of Toll-like receptor 2 (TLR2) -196 to -174del polymorphism with the risk of Helicobacter pylori seropositivity, gastric atrophy, and gastric cancer in Japanese

Recently, the association between gastric cancer risk and a functional polymorphism of Toll-like receptor 2 (TLR2), -196 to -174del, was reported for a Japanese population. This study aimed to confirm the associations of the polymorphism with the risk of gastric cancer, as well as Helicobacter pylori seropositivity and the risk of gastric atrophy in Japanese. The study subjects were 583 histologically diagnosed gastric cancer patients and 1636 age- and sex-frequency-matched control outpatients who visited Aichi Cancer Center Hospital from the years 2001 to 2005. Serum anti-H. pylori IgG antibody and pepsinogens were measured to evaluate H. pylori infection and gastric atrophy, respectively. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by a logistic model. The age- and sex-adjusted ORs of gastric cancer were 1.13 (95% CI: 0.88-1.46) for ins/del, 1.17 (95% CI: 0.79-1.73) for del/del, and 1.14 (95% CI: 0.89-1.45) for ins/del + del/del, relative to the ins/ins genotype compared with gastric atrophy controls; none of these findings were statistically significant. The TLR2 -196 to 174del polymorphism was not significantly associated with either H. pylori seropositivity or gastric atrophy. Our study did not reproduce the association between gastric cancer risk and the TLR2 -196 to -174del polymorphism in Japanese. Further examinations with sufficient numbers of study subjects are required to verify our findings.

Toll‐Like Receptor 4 +3725 G/C Polymorphism, Helicobacter pylori Seropositivity, and the Risk of Gastric Atrophy and Gastric Cancer in Japanese

Toll-like receptor 4 (TLR4) Asp299Gly and Thr399Ile polymorphisms were reported to be a risk factor of gastric carcinoma or its precursors in Caucasian and Indian population, but these polymorphisms are absent in Japanese. We investigated the associations of TLR4+3725 G/C polymorphism, another functional polymorphism of TLR4, with risk of gastric cancer and gastric atrophy in Japanese. Study subjects were 583 histologically diagnosed gastric cancer patients and age- and sex-matched 1592 control outpatients, who visited Aichi Cancer Center Hospital from 2001 to 2005. Serum anti-H. pylori IgG antibody and pepsinogens were measured to evaluate H. pylori infection and gastric atrophy, respectively. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by a logistic model. Among the seropositive subjects, the age- and sex-adjusted OR of gastric atrophy was 1.17 (95%CI: 0.91-1.50) for G/C, 1.20 (95%CI: 0.76-1.89) for C/C, and 1.18 (95%CI: 0.93-1.49) for G/C+C/C relative to G/G genotype. The age- and sex-adjusted OR of severe gastric atrophy among H. pylori seropositive subjects was 1.43 (95%CI: 0.99-2.06) for G/C, 1.47 (95%CI: 0.76-2.88) for C/C, and 1.43 (95%CI: 1.01-2.04) for G/C+C/C. The OR of gastric cancer compared with gastric atrophy controls was not statistically significant. Our study found that TLR4+3725 G/C polymorphism was a risk factor of severe gastric atrophy in H. pylori seropositive Japanese. Our results underscored the significance of the variations in host innate immunity due to TLR4 polymorphism as genetic predispositions to gastric precancerous lesions in Eastern Asian populations with the same backgrounds.