Risk Of Gastric Cardia Cancer Research Articles

Use of proton pump inhibitors for the risk of gastric cancer.

This study aimed to systematically analyze the association between long-term use of proton pump inhibitors (PPIs) and the risk of gastric cancer (GC). We performed a systematic search of articles on the relationship between long-term use of PPIs and the risk of GC from PubMed and EMBASE. We calculated the pooled odds ratio of GC in PPI users compared to non-PPI users using random-effects models. This meta-analysis included 18 studies from 20 different databases with 4348,905 patients enrolled. In the random effects model, we found that an increased risk of GC among PPI users (OR = 1.94; 95% CI [1.43, 2.64]). The long-term use of PPIs compared with histamine-2 receptor antagonist users did not increase the risk of GC (OR = 1.65; 95% CI [0.92, 2.97]). Stratified analysis showed that PPI users had a significantly increased risk of noncardia GC (OR = 2.53; 95% CI [2.03, 3.15]), but had a relatively small relationship with the risk of gastric cardia cancer. (OR = 1.79; 95% CI [1.06, 3.03]). With the extension of PPI use time, the estimated risk value decreases (<1 year: OR = 6.33, 95% CI [3.76, 10.65]; 1-3 years: OR = 1.82, 95% CI [1.30, 2.55]; >3 years: OR = 1.25, 95% CI [1.00, 1.56]). Despite Helicobacter pylori eradication, the long-term use of PPIs did not alter the increased risk of GC (OR = 2.29; 95% CI [1.57, 3.33]). Our meta-analysis found that PPI use may be associated with an increased risk of GC. Further research on the causal relationship between these factors is necessary.

Genome-wide DNA methylation profiling of gastric cardia cancer.

Aberrant DNA methylation has been found in various cancer types including gastric cancer, yet the genome-wide DNA methylation profile of gastric cardia cancer (GCC) remains unclear. Therefore, we aimed to profile the DNA methylation pattern of GCC and identify promising diagnostic epigenetic biomarkers. We investigated the genome-wide DNA methylation pattern in eight pairs of GCC and adjacent normal tissues using Illumina 850K microarrays. Subsequently, bisulfite-pyrosequencing and quantitative real-time PCR were performed on eight pairs of GCC-adjacent normal tissues for validation. Finally, we performed immunohistochemistry to examine ADHFE1 expression on 126 pairs of GCC-adjacent normal samples. DNAmethylome analysis showed global hypomethylation and local hypermethylation of promoter cytosine-phosphate-guanine (CpG) islands (CGIs) in GCC tissues compared with gastric cardia normal mucosa (P<2.2×10-16 ). Differential methylation analysis identified a total of 91 723 differentially-methylated probes (DMPs), and the candidate gene with the largest average DNA methylation difference mapped to ADHFE1 (mean Δβ=0.53). Subsequently, three DMPs in the ADHFE1 promoter were validated by pyrosequencing. Notably,the mean methylation level of the three candidate DMPs (ADHFE1_cg08090772, ADHFE1_cg19283840, and ADHFE1_cg20295442) was negatively associated with ADHFE1 mRNA expression level (Spearman rho=-0.64, P=0.01). Moreover, both mRNA (P=0.0213) and protein (P<0.0001) expression of ADHFE1 were significantly decreased in GCCs compared with the adjacent normal tissues. Our results reveal DNA methylation aberrations in GCC and that ADHFE1 gene DNA methylation contributes to the risk of GCC, thus providing novel mechanistic insights into gastric cardia cancer carcinogenesis.

Five Serum Trace Elements Associated with Risk of Cardia and Noncardia Gastric Cancer in a Matched Case-Control Study.

BackgroundSerum trace elements have for some time been suggested to influence the development of gastric cancer, but evidence is still lacking.MethodsAll newly diagnosed patients with gastric cancer were compared with healthy controls 1:1 matched by sex, age (±3 years), and place of residence during 2013–2015. The serum concentration of all trace elements was analyzed using inductively coupled plasma mass spectrometry. Heliobacter pylori infections in cases were diagnosed using the rapid urease test, while in controls were detected using the colloidal gold method.ResultsA total of 122 cases of gastric cardia cancer (GCC) and 177 gastric noncardia cancer (NCGC), and 299 matched healthy controls were included. Positive associations were found between serum copper and copper/zinc ratio and risk of overall gastric cancer (OR4th vs 1st quartile: 2.42, 95% CI: 1.10–5.32 for copper; OR4th vs 1st quartile: 11.7, 95% CI: 3.83–35.6 for copper/zinc ratio), and for both GCC and NCGC subtypes. Serum selenium was inversely associated with the risk of NCGC (OR4th vs 1st quartile: 0.18, 95% CI: 0.07–0.51), while molybdenum seems to reduce the risk of GCC (OR4th vs 1st quartile: 0.12, 95% CI: 0.03–0.47). Strong inverse associations were also detected between serum calcium and risk of all groups of gastric cancer (all p for trend<0.05).ConclusionThe current study indicated statistically significant positive associations between serum copper, copper/zinc ratio, and gastric cancer, as well as inverse associations among selenium, molybdenum, and calcium. The results shall be carefully interpreted before further in vivo animal studies show definitive evidence.

Global prevalence of Helicobacter pylori and its effect on human health

Helicobacter pylori infection is non-hereditary disease caused by a bacteria H. pylori that possess gram-negative helical morphology. H. pylori infection can cause variety of gastrointestinal problems, including stomach ulcers, inflammation in stomach linings and cancer. The H. pylori bacterium has infected approximately 50% of the total populations. The frequency of H. pylori infection varies among countries, underdeveloped countries have high ratio of cases of H. pylori whereas its ratio is low in developed countries. Around 70% children of underdeveloped countries may be affected by H. pylori infection. Non-cardia gastric patient have a high chances to be infected by H. pylori however, the risk of gastric cardia cancer is relatively low in the H. pylori infection. Patients with weak metabolic control and poor glycemic condition especially diabetes type 2 patients are more susceptible to H. pylori disease. The Gastroesophageal reflux syndrome and H. pylori infection share an inverse relationship particularly those with CagA-positive strains, are less likely to have risk of Gastroesophageal Reflux Disease (GERD). The association of Non-alcoholic fatty liver disease (NAFLD) with H. pylori infection reveals that Cytotoxic-associated gene A (cagA) negative strain is the leading cause of H. pylori infection in NAFLD. Diagnosis of H. pylori can be performed by upper endoscopy or EGD, Breath test and stool culture. Treating H. pylori medicine with natural ingredient such as probiotic, green tea, honey and olive oil can improve the efficiency of antibacterial drug. This review demonstrates that patients of non-cardia gastritis, diabetes type 2 and NAFLD are more prone to be infected by H. pylori disease the ratio of H. pylori infection in humans can be reduced by improving domestic hygienic and sanitary infrastructure. Keywords: Breath test; Cancer of stomach; Diabetes type 2; Endoscopy; Gastroesophageal reflux disease; Gastric cardia cancer; Helicobacter pylori; Non-cardia gastric cancer; Stomach ulcers; Stool culture http://dx.doi.org/10.19045/bspab.2020.90098

Association between polymorphisms in the CYP1A1, CYP2E1 and GSTM1 genes, and smoking, alcohol and upper digestive tract carcinomas in a high-incidence area of northern China.

Metabolic gene variants, smoking, and alcohol consumption are important upper digestive tract cancer (UDTC) risk factors. However, the gene-gene and gene-environment interactions remain unclear. A case-control study in a high incidence area for upper digestive tract cancer was conducted in China. DNA was extracted from buffy coat samples for PCR or PCR-restriction fragment length polymorphism. Smoking and alcohol drinking status was determined by questionnaires. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the associations. After adjusting for confounding factors, smoking increased esophageal cancer (EC), gastric cardia cancer (GCC) and gastric antral carcinoma (GAC) risk by 3.594, 4.658, and 3.999-fold, respectively. Alcohol consumption increased EC, GCC and GAC risk by 1.953, 2.442 and 1.765-fold, respectively. The cytochrome P4501A1 (CYP1A1) rs4646903 T>C polymorphism increased GCC risk, the cytochrome P4502E1 (CYP2E1) rs2031920 C>T polymorphism increased EC risk, while the GSTM1 null genotype decreased EC risk. An association existed between the following: CYP1A1 rs4646903 and smoking in EC, GCC and GAC; CYP1A1 rs4646903 and alcohol consumption in EC and GCC; CYP2E1 rs2031920 and smoking in EC, GCC and GAC and CYP2E1 rs2031920 and alcohol consumption in EC and GCC. No association was observed between CYP1A1 and CYP2E1. The glutathione S-transferase mu 1 (GSTM1) null genotype decreased EC risk (OR=0.510). Smoking/drinking are upper digestive tract cancer risk factors. The CYP1A1 rs4646903 and CYP2E1 rs2031920 polymorphisms were risk factors of GCC or EC, and the GSTM1 null genotype may serve a protective role against EC. The results of the present study indicated that gene-environment interactions increase the risk of UDTC.

Alcohol drinking and gastric cancer risk: a meta-analysis of observational studies.

BackgroundMany studies investigated the association between alcohol drinking and gastric cancer risk, but the results were controversial. We performed a meta-analysis of observational studies to explore the association.Materials and MethodsWe searched PubMed to identify the relevant studies that reported the association between alcohol drinking and gastric cancer risk up to December 31, 2016. We pooled relative risks (RRs) in random effects model and performed dose-response analysis to quantify the association. Cochran Q test and I2 analyses were used to evaluate the heterogeneity. Meta-regression, subgroup, sensitivity and publication bias analyses were also performed.Results75 studies were included in our study. The pooled RR of high vs low total alcohol drinking was 1.25 (95% CI, 1.15–1.37, P < 0.001), and a nonlinear association was further observed. Subgroup analysis showed that alcohol drinking significantly associated with the risk of gastric noncardia cancer (RR, 1.19; 95% CI, 1.01–1.40, P = 0.033), but not with the risk of gastric cardia cancer (RR, 1.16; 95% CI, 0.98–1.39, P = 0.087). Notably, the pooled RRs of high vs low analyses were 1.13 (95% CI, 1.03–1.24, P = 0.012) for beer drinking, 1.22 (95% CI, 1.06–1.40, P = 0.005) for liquor drinking, and 0.99 (95% CI, 0.84–1.16, P = 0.857) for wine drinking.ConclusionsOur meta-analysis found a nonlinear association between alcohol drinking and gastric cancer risk, and heavy drinking level was strongly related to gastric cancer risk. Beer and liquor had significant positive associations with gastric cancer risk, while wine drinking would not increase gastric cancer risk. These results need to be verified in future research.

Body mass index, serum total cholesterol, and risk of gastric high-grade dysplasia: A case-control study among Chinese adults.

Obesity is related to an increased risk of gastric cardia cancer. However, the influences of excess body weight and serum total cholesterol on the risk of gastric high-grade dysplasia have not been fully characterized.A case-control study was conducted to explore the relationships between body mass index (BMI), serum total cholesterol level, and the risk of gastric high-grade dysplasia in Chinese adults. A total of 893 consecutive patients with gastric high-grade dysplasia (537 men and 356 women) and 902 controls (543 men and 359 women) were enrolled from January 2000 to October 2015. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated, and a multivariate analysis was conducted.After adjusting for age, alcohol consumption, smoking status, family history of gastric cancer or esophageal cancer, and serum total cholesterol level, a BMI ranging from 27.5 to 29.9 was significantly related to an increased risk of gastric high-grade dysplasia in both men (adjusted OR = 1.87, 95% CI = 1.24-2.81) and women (adjusted OR = 2.72, 95% CI = 1.44-5.16). The 2 highest BMI categories (27.5-29.9 and ≥30.0) were identified as risk factors for gastric cardia high-grade dysplasia in both men (BMI = 27.5-29.9: adjusted OR = 1.78, 95% CI = 1.02-3.10; BMI ≥ 30.0: adjusted OR = 2.54, 95% CI = 1.27-5.08) and women (BMI = 27.5-29.9: adjusted OR = 2.88, 95% CI = 1.27-6.55; BMI ≥ 30.0: adjusted OR = 2.77, 95% CI = 1.36-5.64), whereas only a BMI ranging from 27.5 to 29.9 was a risk factor for gastric noncardia high-grade dysplasia in both men (adjusted OR = 1.98, 95% CI = 1.25-3.14) and women (adjusted OR = 2.88, 95% CI = 1.43-5.81). In addition, higher serum total cholesterol was associated with an increased risk of gastric noncardia high-grade dysplasia (adjusted OR = 1.83, 95% CI = 1.25-2.69) in women.Increased BMI was associated with an increased risk of gastric high-grade dysplasia in both men and women, and higher serum total cholesterol increased the risk of gastric noncardia high-grade dysplasia in women.

Abstract 2549: Familial risk of upper gastrointestinal cancers by tumor location

Abstract Background: Upper gastrointestinal (UGI) cancers are within the most common malignancies worldwide. Familial clustering of UGI cancers and the significance of family history have been addressed in the past. We aimed to further elucidate the familial risk based on specified tumor locations. Methods: Using the Swedish Family-Cancer Database, we determined the familial risk of UGI cancer patients diagnosed between 1958 and 2012. Standardized incidence ratio (SIR) was used for calculating concordant and discordant familial cancers risks, stratified by tumor locations. All results were adjusted for sex, age group, period, and socioeconomic status. Results: Risk of esophageal cancer in first-degree relatives (FDRs) of esophageal cancer patients was 2•4-fold higher than that in those without such a family history. Familial risk for concordant cancer in upper and middle third of esophagus was 3•2- and 5•6-fold, respectively. Family history of esophageal cancer in lower part was associated with increased risk of gastric cardia cancer in FDRs and vice versa. Family history of both adenocarcinoma and SCC of esophageal cancer increased the familial risk of concordant (similar) and discordant subtypes. Occurrence of gastric cancer in the body and the antrum of stomach in a FDR were associated with an increased risk of gastric cancer 6- to 7-fold in the same location in family members, respectively. Conclusion: Family history of UGI cancers in some specific locations like upper and middle third of esophagus, body and antrum of stomach can be considered as an important predictive evidence for the same cancers in relatives. Citation Format: Elham Kharazmi, Masoud Babaei, Mahdi Fallah, Thianhui Chen, Kristina Sundquist, Kari Hemminki. Familial risk of upper gastrointestinal cancers by tumor location. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 2549.

Two novel variants on 13q22.1 are associated with risk of esophageal squamous cell carcinoma.

Chromosome 13q22.1 has previously been identified to be a susceptibility locus for pancreatic cancer in Chinese and European ancestry populations. This pleiotropy study aimed to identify novel variants in this region associated with susceptibility to different types of human cancer. To fine-map the 13q22.1 region, imputation analyses were conducted on the basis of the GWAS data of 2,031 esophageal squamous cell cancer (ESCC) cases and 2,044 controls and 5,930 SNPs (625 directly genotyped and 5,305 well imputed). Promising associations were then examined in ESCC (4,146 cases and 4,135 controls), gastric cardia cancer (1,894 cases and 1,912 controls), noncardia gastric cancer (1,007 cases and 2,243 controls), and colorectal cancer (1,111 cases and 1,138 controls). Fine mapping and biochemical analyses were further performed to elucidate the potential function of novel variants. Two novel variants, rs1924966 and rs115797771, were associated with ESCC risk (P = 1.37 × 10(-10) and P = 2.32 × 10(-10), respectively) and were also associated with risk of gastric cardia cancer (P = 0.0003 and P = 0.0018, respectively) but not gastric cancer and colorectal cancer. Fine-mapping revealed another SNP, rs58090485, in strong linkage disequilibrium with rs115797771 (r(2) = 0.94). Functional analysis showed that this SNP disturbs a transcriptional repressor binding to the promoter region of KLF5, which might result in high constitutional expression of KLF5. These results demonstrate that variants mapped on 13q22.1 are associated with the risk of different types of cancer. 13q22.1 might serve as a biomarker for the identification of individuals at risk for ESCC and gastric cardia cancer.

Macronutrient intake and stomach cancer.

This study examines the association between intake of selected macronutrients and the risk of stomach cancer in a Northern American population. Mailed questionnaires were completed between 1994 and 1997 in eight Canadian provinces by 1,181 incident, histologically confirmed cases of stomach cancer and 5,039 population controls. Information on nutrient intake was obtained using a food frequency questionnaire. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were derived through unconditional logistic regression to adjust for potential confounders, including an estimate of total energy intake. Intakes of total fat, saturated fat, and cholesterol were significantly associated with the risk of stomach cancer: The ORs for the highest versus the lowest quartile were 1.58 (95% CI 1.13-2.20), 1.86 (95% CI 1.37-2.52), and 1.75 (95% CI 1.36-2.25), respectively. Total fiber was inversely associated with stomach cancer (p = 0.03). The positive associations with intake of total fat and saturated fat were apparently stronger in women, overweight or obese subjects, and ever smokers. Saturated fat was specifically associated with increased risk of gastric cardia cancer, with an OR of 3.31 (95% CI 1.48-7.43). A diet high in saturated fat appears to increase the risk of stomach cancer, particularly among obese subjects and for gastric cardia cancer.

Total, caffeinated and decaffeinated coffee and tea intake and gastric cancer risk: results from the EPIC cohort study.

Prospective studies examining the association between coffee and tea consumption and gastric cancer risk have shown inconsistent results. We investigated the association between coffee (total, caffeinated and decaffeinated) and tea consumption and the risk of gastric cancer by anatomical site and histological type in the European Prospective Investigation into Cancer and Nutrition study. Coffee and tea consumption were assessed by dietary questionnaires at baseline. Adjusted hazard ratios (HRs) were calculated using Cox regression models. During 11.6 years of follow up, 683 gastric adenocarcinoma cases were identified among 477,312 participants. We found no significant association between overall gastric cancer risk and consumption of total coffee (HR 1.09, 95%-confidence intervals [CI]: 0.84-1.43; quartile 4 vs. non/quartile 1), caffeinated coffee (HR 1.14, 95%-CI: 0.82-1.59; quartile 4 vs. non/quartile 1), decaffeinated coffee (HR 1.07, 95%-CI: 0.75-1.53; tertile 3 vs. non/tertile 1) and tea (HR 0.81, 95%-CI: 0.59-1.09; quartile 4 vs. non/quartile 1). When stratified by anatomical site, we observed a significant positive association between gastric cardia cancer risk and total coffee consumption per increment of 100 mL/day (HR 1.06, 95%-CI: 1.03-1.11). Similarly, a significant positive association was observed between gastric cardia cancer risk and caffeinated coffee consumption (HR 1.98, 95%-CI: 1.16-3.36, p-trend=0.06; quartile 3 vs. non/quartile 1) and per increment of 100 mL/day (HR 1.09, 95%-CI: 1.04-1.14). In conclusion, consumption of total, caffeinated and decaffeinated coffee and tea is not associated with overall gastric cancer risk. However, total and caffeinated coffee consumption may be associated with an increased risk of gastric cardia cancer. Further prospective studies are needed to rule out chance or confounding.

Relationship between body mass index and the risk of early gastric cancer and dysplasia regardless of Helicobacter pylori infection.

Obesity is known to be associated with an increased risk of gastric cardia cancer but not with noncardia cancer. In terms of gastric dysplasia, few studies have evaluated its relationship with obesity. In addition, no study on the relationship between obesity and the risk of gastric cancer has analyzed the status of Helicobacter pylori infection. A case-control study was designed to investigate the relationship between obesity and the risk of gastric cancer and dysplasia adjusted for the status of H. pylori infection in Koreans. Nine hundred ninety-eight gastric cancer patients, 313 gastric dysplasia patients, and 1,288 subjects with normal endoscopic findings were included. As gender differences could be the largest confounding factor, the risk of gastric cancer and dysplasia with an increasing body mass index (BMI) was analyzed in men and women, separately, and was adjusted for age, smoking, drinking, family history of gastric cancer, H. pylori infection, atrophic gastritis, intestinal metaplasia, and serum pepsinogen I/pepsinogen II ratio. Obesity (BMI 25 kg/m(2) or greater but less than 30 kg/m(2)) was associated with increased risk of early gastric cancer [adjusted odds ratio (aOR) 1.657; 95 % confidence interval (CI) 1.086-2.528; P = 0.019] and well or moderately differentiated adenocarcinoma (aOR 1.566; 95 % CI 1.011-2.424; P = 0.044) compared with normal BMI status (BMI < 23 kg/m(2)) in men. Obesity was related to gastric dysplasia (aOR 2.086; 95 % CI 1.011-4.302; P = 0.047) in women. The effect of obesity on gastric cancer showed a gender difference. That is, in men it was related to increased risk of early gastric cancer and well or moderately differentiated adenocarcinoma, but it was associated with gastric dysplasia in women regardless of H. pylori infection in Korea. Further research into this difference is necessary.

Vegetarian Diets and Breast Cancer. Preliminary Results from the AHS-2 Cohort

Vegetarian Diets and Breast Cancer. Preliminary Results from the AHS-2 Cohort

Body mass index and risk of gastric cancer: a meta-analysis.

Overweight and obesity, indicated as increased body mass index, are associated with the risk of some cancers. We carried out a meta-analysis on published cohort and case-control studies to assess the strength of association between body mass index and gastric cancer. Relevant studies were identified through PubMed, Web of Science and Medline electronic databases. Adjusted relative risks (odds ratios) with 95% confidence interval were used to assess the strength of association between body mass index and gastric cancer. Sixteen eligible studies were included in this meta-analysis. Overall, obesity (body mass index ≥ 30 kg/m(2)) was associated with an increased risk of gastric cancer (odds ratio = 1.13, 95% confidence interval = 1.03-1.24) compared with normal weight (body mass index = 18.5 to <25 kg/m(2)), while overweight (body mass index = 18.5 to <30 kg/m(2)) showed no association (odds ratio = 1.04, 95% confidence interval = 0.96-1.12). Specifically, a stratified analysis showed there were associations between obesity and the increased risk of gastric cancer for males (odds ratio = 1.27, 95% confidence interval = 1.09-1.48), non-Asians (odds ratio = 1.14, 95% confidence interval = 1.02-1.28) and both cohort studies (odds ratio = 1.10, 95% confidence interval = 1.00-1.22) and case-control studies (odds ratio = 1.29, 95% confidence interval = 1.03-1.60). Both overweight (odds ratio = 1.22, 95% confidence interval = 1.05-1.42) and obesity (odds ratio = 1.61, 95% confidence interval = 1.15-2.24) were associated with the increased risk of gastric cardia cancer. The results indicated that obesity was associated with the risk of gastric cancer, especially for males and among non-Asians. Both overweight and obesity were associated with the risk of gastric cardia cancer.

Association between gastric cardia adenocarcinoma risk and alcohol flushing response, but not alcohol consumption

The relationship between the development of gastric cardia cancer (GCA) and alcohol consumption remains unclear. Alcohol flushing response reflects an accumulation of the carcinogenic acetaldehyde and has been proved to be a risk factor for many cancers. The main objective of the present study was to assess the impact of alcohol flushing response on GCA risk in a Chinese population in conjunction with lifetime alcohol consumption. The study subjects consist of 281 male patients [130 with GCA and 151 with esophageal squamous cell carcinoma (ESCC)] and 160 non-cancer male controls, matched with respect to age. Conditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (95% CI). There is no significant association between GCA risk and alcohol consumption. However, the adjusted ORs for flushing response of GCA and ESCC was 2.03 (95% CI 1.15-3.56, p=0.014) and 2.32 (95% CI 1.34-4.03, p=0.003), respectively, compared with those reporting no flushing response. Furthermore, compared with non-drinkers, the heavy drinkers and moderate drinkers with current/former flushing response experienced significant GCA risk (heavy drinkers: OR 2.59, 95% CI 1.06-6.31, p=0.037; moderate drinkers: OR 3.11, 95% CI 1.17-8.26, p=0.023), while drinkers without flushing response did not have increased risk. The drinkers with flushing response also had a higher ESCC risk than those without flushing response. In conclusion, alcohol flushing response is a clinically useful biomarker of susceptibility to GCA and ESCC risk from alcohol.

Body Mass Index and Risk of Gastric Cancer: A Meta-analysis of a Population with More Than Ten Million from 24 Prospective Studies

To provide a quantitative assessment of the association between body mass index (BMI) and the risk of gastric cancer, we summarized the evidence from prospective studies. Eligible studies published up to November 30, 2012, were retrieved via computer searches of MEDLINE and EMBASE as well as manual review of references. Summary relative risks (SRR) with their corresponding 95% confidence intervals (CI) were calculated using a random-effects model. A total of 24 prospective studies of BMI and gastric cancer risk with 41,791 cases were included in our analysis. Overall, both overweight (BMI, 25-30 kg/m(2)) and obesity (BMI, ≥30 kg/m(2)) were not associated with risk of total gastric cancer (overweight: SRR, 1.01; 95% CI, 0.96-1.07; obesity: SRR, 1.06; 95% CI, 0.99-1.12). Furthermore, we found increased BMI was positively associated with the risk of gastric cardia cancer (GCC; SRR = 1.21 for overweight and 1.82 for obesity), but not with gastric non-cardia cancer (GNCC; SRR = 0.93 for overweight and SRR = 1.00 for obesity). Similar results were observed in a linear dose-response analysis. On the basis of meta-analysis of prospective studies, we find high BMI is positively associated with the risk of GCCs but not with GNCCs. (i) On the basis of more definite and quantitative evidence than previously available, we found that increasing BMI was not a clear risk factor for total gastric cancer. (ii) Increased BMI was positively associated with risk of GCC but not with GNCCs.

The association of cigarette smoking with gastric cancer: the multiethnic cohort study.

The purpose of this study is to investigate the association of cigarette smoking with gastric cancer. Over 215,000 men and women, representing five ethnic groups (African Americans, Japanese Americans, Latino Americans, Native Hawaiians, and Whites), completed a mailed questionnaire, 1993-1996. After an average follow-up of 7.3 years, 454 men and 242 women were diagnosed with gastric adenocarcinoma. Cox proportional hazard models were used to calculate multivariate-adjusted hazard ratios and 95% confidence intervals. Current cigarette smokers had elevated hazard ratios compared with never smokers among men (HR = 1.98; 95% CI 1.46-2.70) and women (HR = 1.78; 95% CI 1.23-2.57). This positive association was consistent across all five ethnicities. Former smokers had an elevated risk among men, but not among women. There was a significant trend by intensity (cigarettes per day) and duration (years) of smoking among all current smokers. After separation by anatomic location of their tumor, ever smokers had a higher risk for gastric cardia cancer (HR = 2.86; 95% CI 1.66-4.93) than for distal gastric cancer (HR = 1.52; 95% CI 1.25-1.86) among men and women combined. Analysis by histologic tumor type showed a stronger association between current smoking and the intestinal type. Overall, this study shows an association of current cigarette smoking with gastric cancer in both sexes, consistency of this effect across five ethnic groups, evidence for a dose-response effect of smoking in both sexes, a stronger effect for cardia than for distal gastric cancer, and a stronger association for intestinal than for diffuse gastric cancer.

Meat Consumption and Risk of Esophageal and Gastric Cancer in a Large Prospective Study

Red and processed meats could increase cancer risk through several potential mechanisms involving iron, heterocyclic amines, polycyclic aromatic hydrocarbons, and N-nitroso compounds. Although there have been multiple studies of meat and colorectal cancer, other gastrointestinal malignancies are understudied. We estimated hazard ratios (HR) and 95% confidence intervals (CI) for the association between meat, meat components, and meat cooking by-products and risk of esophageal or gastric cancer in a large cohort study. During ∼10 years of follow-up, we accrued 215 esophageal squamous cell carcinomas, 630 esophageal adenocarcinomas, 454 gastric cardia adenocarcinomas, and 501 gastric non-cardia adenocarcinomas. Red meat intake was positively associated with esophageal squamous cell carcinoma (HR for the top versus bottom quintile=1.79, 95% CI: 1.07-3.01, P for trend=0.019). Individuals in the highest intake quintile of 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx) had an increased risk for gastric cardia cancer (HR=1.44, 95% CI: 1.01-2.07, P for trend=0.104). Furthermore, those in the highest quintile of 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx), 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), or heme iron intake had a suggestive increased risk for esophageal adenocarcinoma (HR=1.35, 95% CI: 0.97-1.89, P for trend=0.022; HR=1.45, 95% CI: 0.99-2.12, P for trend=0.463; or HR=1.47, 95% CI: 0.99-2.20, P for trend=0.063, respectively). Benzo[a]pyrene, nitrate, and nitrite were not associated with esophageal or gastric cancer. We found positive associations between red meat intake and esophageal squamous cell carcinoma, and between DiMeIQx intake and gastric cardia cancer.

Tea, coffee, carbonated soft drinks and upper gastrointestinal tract cancer risk in a large United States prospective cohort study

The authors investigated the relationship between hot tea, iced tea, coffee and carbonated soft drinks consumption and upper gastrointestinal tract cancers risk in the NIH-AARP Study. During 2,584,953 person-years of follow-up on 481,563 subjects, 392 oral cavity, 178 pharynx, 307 larynx, 231 gastric cardia, 224 gastric non-cardia cancer, 123 Oesophageal Squamous Cell Carcinoma (ESCC) and 305 Oesophageal Adenocarcinoma (EADC) cases were accrued. Hazard ratios (HRs) and 95% confidence intervals (95% CIs) were calculated by multivariate-adjusted Cox regression. Compared to non-drinking, the hazard ratio for hot tea intake of ⩾1 cup/day was 0.37 (95% CI: 0.20, 0.70) for pharyngeal cancer. The authors also observed a significant association between coffee drinking and risk of gastric cardia cancer (compared to <1 cup/day, the hazard ratio for drinking >3 cups/day was 1.57 (95% CI: 1.03, 2.39)), and an inverse association between coffee drinking and EADC for the cases occurring in the last 3 years of follow-up (compared to <1 cup/day, the hazard ratio for drinking >3 cups/day was 0.54 (95% CI: 0.31, 0.92)), but no association in earlier follow-up. In summary, hot tea intake was inversely associated with pharyngeal cancer, and coffee was directly associated with gastric cardia cancer, but was inversely associated with EADC during some follow-up periods.

Jasmine tea consumption and upper gastrointestinal cancer in China.

Epidemiological data on green/jasmine tea and esophageal as well as gastric cancer are limited and inconclusive. In order to study the effect of jasmine tea in upper gastrointestinal (UGI) cancers, we evaluated 600 esophageal squamous cell carcinoma (ESCC), 598 gastric cardia cancer (GCA), and 316 gastric non-cardia cancer (GNCA) cases and 1,514 age-, gender-, and neighborhood-matched controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated from logistic regression adjusted for matching factors and potential confounders. Among controls, 35% of males and 8% of females reported consumption of jasmine tea; other tea consumption was rare. Consumption of jasmine tea (ever vs. never) was not associated with risk of ESCC (OR = 1.15, 95% CI 0.92–1.44), GCA (OR = 1.14, 95% CI 0.88–1.37), or GNCA (OR = 0.85, 95% CI 0.64–1.15) in males and females combined. Among males, cumulative lifetime consumption showed a significant positive dose–response relation with ESCC risk, but not for GCA and GNCA. In exploratory analyses, occupation affected the relation between tea and ESCC such that consumption in males was associated with increased risk only in non-office workers. Overall, we found no evidence for a protective effect of tea in esophageal or gastric cancer. Further studies of the potential effects of thermal damage, tea quality, and water quality on UGI cancers are suggested.