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  • 1
    Keywords: CANCER ; FOLLOW-UP ; COHORT ; EXPOSURE ; RISK ; NITRIC-OXIDE ; INFECTION ; ASSOCIATION ; antibodies ; antibody ; PLASMA ; NUMBER ; cancer risk ; DIETARY ; INDIVIDUALS ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; DIETARY-INTAKE ; INCREASE ; IRON ; LEVEL ; prospective ; MEAT INTAKE ; RED MEAT ; CANCER-RISK ; Helicobacter pylori ; N-NITROSO COMPOUNDS ; HEME ; processed meat
    Abstract: The risk of gastric cancer (GC) associated with dietary intake of nitrosodimethylamine (NDMA) and endogenous formation of nitroso compounds (NOCs) was investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC). The study included 521 457 individuals and 314 incident cases of GC that had occurred after 6.6 average years of follow-up. An index of endogenous NOC (ENOC) formation was estimated using data of the iron content from meat intake and faecal apparent total NOC formation according to previous published studies. Antibodies to Helicobacter pylori and vitamin C levels were measured in a sub-sample of cases and matched controls included in a nested case-control within the cohort. Exposure to NDMA was 〈 1 mu g on average compared with 93 mu g on average from ENOC. There was no association between NDMA intake and GC risk (HR, 1.00; 95% CI, 0.7-1.43). ENOC was significantly associated with non-cardia cancer risk (HR, 1.42; 95% CI, 1.14-1.78 for an increase of 40 mu g/day) but not with cardia cancer (HR, 0.96; 95% CI, 0.69-1.33). Although the number of not infected cases is low, our data suggest a possible interaction between ENOC and H.pylori infection (P for interaction = 0.09). Moreover, we observed an interaction between plasma vitamin C and ENOC (P 〈 0.02). ENOC formation may account for our previously reported association between red and processed meat consumption and gastric cancer risk
    Type of Publication: Journal article published
    PubMed ID: 16571648
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  • 2
    Keywords: CANCER ; carcinoma ; Germany ; FOLLOW-UP ; INFORMATION ; COHORT ; EPIDEMIOLOGY ; RISK ; INFECTION ; RISK-FACTORS ; ASSOCIATION ; HEALTH ; REDUCED RISK ; risk factors ; cancer risk ; RECRUITMENT ; DIET ; STOMACH ; adenocarcinoma ; case-control studies ; TOBACCO ; ALCOHOL ; CARDIA ; EPIC ; ESOPHAGUS ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; STOMACH-CANCER ; case-control study ; ASSOCIATIONS ; DIGESTIVE-TRACT ; gastric cancer ; LEVEL ; case control studies ; INTERVAL ; methods ; PROFILES ; prospective ; EVALUATE ; odds ratio ; RISK-FACTOR ; CANCER-RISK ; Helicobacter pylori ; cardia cancer ; socioeconomic position
    Abstract: Objectives To evaluate the association of socioeconomic position with adenocarcinoma of the oesophagus and stomach. Methods The European Prospective Investigation into Cancer and Nutrition (EPIC) cohort comprises about 520000 participants mostly aged 35-70 years. Information on diet and lifestyle was collected at recruitment. After an average follow-up of 6.5 years, 268 cases with adenocarcinoma of the stomach and 56 of the oesophagus were confirmed. We examined the effect of socioeconomic position on cancer risk by means of educational data and a computed Relative Index of Inequality (RII). In a nested case-control study, adjustment for Helicobacter pylori (H. pylori) infection was performed. Results Higher education was significantly associated with a reduced risk of gastric cancer [vs lowest level of education, hazard ratio (HR): 0.64, 95% Confidence intervals (CI): 0.43-0.981. This effect was more pronounced for cancer of the cardia (HR: 0.42, 95% CI: 0.20-0.89) as compared to non-cardia gastric cancer (HR: 0.66, 95% CI: 0.36-1.22). Additionally, the inverse association of educational level and gastric cancer was stronger for cases with intestinal (extreme categories, HR: 0.13, 95% CI: 0.04-0.44) rather than diffuse histological subtype (extreme categories, HR: 0.71 95% CI: 0.37-1.40). In the nested case-control study, inverse but statistically non-significant associations were found after additional adjustment for H. pylori infection [highest vs lowest level of education: Odds ratio (OR) 0.53, 95% CI: 0.24-1.18]. Educational level was non-significantly, inversely associated with carcinoma of the oesophagus. Conclusion A higher socioeconomic position was associated with a reduced risk of gastric adenocarcinoma, which was strongest for cardia cancer or intestinal histological subtype, suggesting different risk profiles according to educational level. These effects appear to be explained only partially by established risk factors
    Type of Publication: Journal article published
    PubMed ID: 17227779
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  • 3
    Keywords: CANCER ; BLOOD ; RISK ; ENZYMES ; GENE ; GENES ; ACTIVATION ; DNA ; CARCINOGENESIS ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; AGE ; CIGARETTE-SMOKING ; COUNTRIES ; GENOTYPES ; COLORECTAL CANCERS ; LINKAGE DISEQUILIBRIUM ; adenocarcinoma ; case-control studies ; TOBACCO ; GASTRIC-CANCER ; nutrition ; SMOKERS ; case-control study ; VARIANT ; TOBACCO-SMOKE ; GSTM1 ; GSTT1 ; gastric cancer ; S-TRANSFERASE M1 ; case control studies ; INTERVAL ; ENZYME ; GENETIC-POLYMORPHISM ; LOCUS ; FAMILY-HISTORY ; prospective ; ALLELE FREQUENCIES ; COMPOUND ; EPOXIDE HYDROLASE POLYMORPHISMS ; EUROPEAN COUNTRIES ; HIGH-INCIDENCE AREA ; INCREASED RISK ; NEVER SMOKERS ; odds ratio ; T1 NULL GENOTYPES ; tobacco smoke ; UNIT
    Abstract: Metabolizing enzymes, which often display genetic polymorphisms, are involved in the activation of compounds present in tobacco smoke that may be relevant to gastric carcinogenesis. We report the results of a study looking at the association between risk of gastric adenocarcinoma and polymorphisms in genes CYP1A1, CYP1A2, EPHX1, and GSTT1. A nested case-control study was carried out within the European Prospective Investigation into Cancer and Nutrition, developed in 10 European countries. The study includes 243 newly diagnosed cases of histologically confirmed gastric adenocarcinoma and 946 controls matched by center, age, sex, and date of blood collection. Genotypes were determined in nuclear DNA from WBCs. We found an increased risk of gastric cancer for homozygotes for C (histidine) variant in Y113H of EPHX1 (odds ratio, 1.91; 95% confidence interval, 1.19-3.07) compared with subjects with TC/TT. There was also a significant increased risk for smokers carrying at least one variant allele A in Ex7+129C 〉 A (m4) of CYP1A1 and never smokers with null GSTT1 and allele A in the locus -3859G 〉 A of CYP1A2. Most of these genes are involved in the activation and detoxification of polycyclic aromatic hydrocarbons, suggesting a potential role of these compounds in gastric carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 17164366
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  • 4
    Keywords: CANCER ; carcinoma ; FOLLOW-UP ; COHORT ; cohort study ; RISK ; SITE ; INFECTION ; ASSOCIATION ; antibodies ; WOMEN ; MEN ; COUNTRIES ; DIET ; STOMACH ; adenocarcinoma ; case-control studies ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; CALIBRATION ; case-control study ; INCREASE ; case control studies ; HELICOBACTER-PYLORI INFECTION ; prospective ; Helicobacter pylori ; intake ; FOODS
    Abstract: It is considered that fruit and vegetable (F&V) protect against oesophagus and gastric cancer (GC). However, 2 recent meta-analyses suggest that the strength of association on GC seems to he weaker for vegetables than for fruit and weaker in cohort than in case-control studies. No evidence exists from cohort studies about adenocarcinoma of oesophagus (ACO). In 521,457 men and women participating in the EPIC cohort in 10 European countries, information of diet and lifestyle was collected at baseline. After an average of 6.5 years of follow-up, a total of 330 GC and 65 ACO, confirmed and classified by a panel of pathologists, was used for the analysis. We examined the relation between F&V intake and GC and ACO. A calibration study in a sub-sample was used to control diet measurement errors. In a sub-sample of cases and a random sample of controls, antibodies against Helicobacter pylori (Hp) were measured and interactions with F&V were examined in a nested case-control study. We observed no association with total vegetable intake or specific groups of vegetables and GC risk, except for the intestinal type, where a negative association is possible regarding total vegetable (calibrated HR 0.66; 95% CI 0.35-1.22 per 100 g increase) and onion and garlic intake (calibrated HR 0.70; 95% CI 0.38-1.29 per 10 g increase). No evidence of association between fresh fruit intake and GC risk was observed. We found a negative but non significant association between citrus fruit intake and the cardia site (calibrated HR 0.77; 95% CI 0.47-1.22 per 100 g increase) while no association was observed with the non-cardia site. Regarding ACO, we found a non significant negative association for vegetable intake and for citrus intake (calibrated HRs 0.72; 95% Cl 0.32-1.64 and 0.77; 95% CI 0.46-1.28 per 100 and 50 g increase, respectively). It seems that lip infection does not modify the effect of F&V intake. Our study supports a possible protective role of vegetable intake in the intestinal type of GC and the ACO. Citrus fruit consumption may have a role in the protection against cardia GC and ACO. (c) 2005 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16380980
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  • 5
    Keywords: CANCER ; FOLLOW-UP ; COHORT ; POPULATION ; RISK ; INFECTION ; CARCINOGENESIS ; ASSOCIATION ; WOMEN ; MEN ; cancer risk ; DOSE-RESPONSE ; DIETARY ; adenocarcinoma ; ADENOCARCINOMAS ; case-control studies ; CARDIA ; CONSUMPTION ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; case-control study ; DIETARY FACTORS ; ASSOCIATIONS ; INCREASE ; case control studies ; INTERVAL ; prospective ; MEAT INTAKE ; RED MEAT ; JAPANESE ; Helicobacter pylori ; N-NITROSO COMPOUNDS
    Abstract: Background. Dietary factors are thought to have an important role in gastric and esophageal carcinogenesis, but evidence from cohort studies for such a role is lacking. We examined the risks of gastric cancer and esophageal adenocarcinoma associated with meat consumption within the European Prospective Investigation Into Cancer and Nutrition (EPIC) cohort. Methods: A total of 521 457 men and women aged 35-70 years in 10 European countries participated in the EPIC cohort. Dietary and lifestyle information was collected at recruitment. Cox proportional hazard models were used to examine associations between meat intake and risks of cardia and gastric noncardia cancers and esophageal adenocarcinoma. Data from a calibration substudy were used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. In a nested case-control study, we examined interactions between Helicobacter pylori infection status (i.e., plasma H. pylori antibodies) and meat intakes. All statistical tests were two-sided. Results: During a mean follow-up of 6.5 years, 330 gastric adenocarcinoma and 65 esophageal adenocarcinomas were diagnosed. Gastric noncardia cancer risk was statistically significantly associated with intakes of total meat (calibrated HR per 100-g/day increase = 3.52, 95%, CI = 1.96 to 6.34), red meat (calibrated HR per 50-g/day increase = 1.73; 95% CI = 1.03 to 2.88), and processed meat (calibrated HR per 50-g/day increase = 2.45; 95% CI = 1.43 to 4.21). The association between the risk of gastric noncardia cancer and total meat intake was especially large in H. pylori-infected subjects (odds ratio per 100-g/day increase = 5.32; 95% CI = 2.10 to 13.4). Intakes of total, red, or processed meat were not associated with the risk of gastric cardia cancer. A positive but non-statistically significant association was observed between esophageal adenocarcinoma cancer risk and total and processed meat intake in the calibrated model. In this study population, the absolute risk of development of gastric adenocarcinoma within 10 years for a study subject aged 60 years was 0.26% for the lowest quartile of total meat intake and 0.33% for the highest quartile of total meat intake. Conclusion: Total, red, and processed meat intakes were associated with an increased risk of gastric noncardia cancer, especially in H. pylori antibody-positive subjects, but not with cardia gastric cancer
    Type of Publication: Journal article published
    PubMed ID: 16507831
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  • 6
    Keywords: CANCER ; LUNG-CANCER ; SUPPORT ; COHORT ; RISK ; GENE ; GENES ; validation ; DNA ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; antibodies ; antibody ; NO ; HEALTH ; REPAIR ; COLORECTAL-CANCER ; cancer risk ; microsatellite instability ; adenocarcinoma ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; DNA repair ; TP53 ; RE ; prospective studies ; XPD POLYMORPHISMS ; gastric cancer ; XRCC1 ; GC ; ALLELES ; LEVEL ; DNA repair genes ; prospective ; prospective study ; CANCER-RISK ; Helicobacter pylori ; intestinal metaplasia ; ENGLAND ; CHINESE POPULATION ; HOGG1 SER326CYS POLYMORPHISM ; OGG1 ; chronic atrophic gastritis ; pepsinogen ; RATIO ; GENE POLYMORPHISMS ; GENE POLYMORPHISM ; neoplasm ; gastric adenocarcinoma ; severe chronic atrophic gastritis
    Abstract: Background The contribution of genetic variation in DNA repair genes to gastric cancer (GC) risk remains essentially unknown. The aim of this study was to explore the relative contribution of DNA repair gene polymorphisms to GC risk and severe chronic atrophic gastritis (SCAG). Method A nested case control study within the EPIC cohort was performed including 246 gastric adenocarcinomas and 1175 matched controls. Controls with SCAG (n 91), as defined by low pepsinogen A (PGA) levels, and controls with no SCAG (n 1061) were also compared. Twelve polymorphisms at DNA repair genes (MSH2, MLH1, XRCC1, OGG1 and ERCC2) and TP53 gene were analysed. Antibodies against Helicobacter pylori were measured. Results No association was observed for any of these polymorphisms with stomach cancer risk. However, ERCC2 K751Q polymorphism was associated with an increased risk for non-cardial neoplasm [odds ratio (OR) 1.78; 95 confidence interval (CI) 1.023.12], being ERCC2 K751Q and D312N polymorphisms associated with the diffuse type. ERCC2 D312N (OR 2.0; 95 CI 1.093.65) and K751Q alleles (OR 1.82; 95 CI 1.013.30) and XRCC1 R399Q (OR 1.69; 95 CI 1.022.79) allele were associated with an increased risk for SCAG. Conclusion Our study supports a role of ERCC2 in non-cardial GC but not in cardial cancer. A concordant result was observed for subjects with low PGA levels. XRCC1 allele was associated also with SCAG. This is the first prospective study suggesting that individual variation in DNA repair may be relevant for gastric carcinogenesis, a finding that will require further confirmation validation in larger independent studies
    Type of Publication: Journal article published
    PubMed ID: 18641418
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  • 7
    Keywords: CANCER ; carcinoma ; RISK ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; adenocarcinoma ; nutrition ; S-TRANSFERASE M1 ; CYTOCHROME-P450 2E1
    Type of Publication: Journal article published
    PubMed ID: 16702391
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  • 8
    Keywords: CANCER ; BLOOD ; carcinoma ; FOLLOW-UP ; EPIDEMIOLOGY ; POPULATION ; RISK ; SITE ; SITES ; ASSOCIATION ; antibodies ; PLASMA ; AGE ; cancer risk ; POPULATIONS ; STOMACH ; adenocarcinoma ; case-control studies ; ESOPHAGUS ; meat ; nutrition ; SUBSITE ; ONCOLOGY ; case-control study ; REGRESSION ; METAANALYSIS ; LEVEL ; case control studies ; analysis ; methods ; prospective ; odds ratio ; CANCER-RISK ; CIRCULATING LEVELS ; Helicobacter pylori ; stomach cancer ; SERUM PEPSINOGEN-I ; chronic atrophic gastritis ; pepsinogen ; SEROPOSITIVITY
    Abstract: Helicobacter pylori (H. pylori), atrophic gastritis, dietary and lifestyle factors have been associated with gastric cancer (GC). These factors have been evaluated in a large case-control study nested in the European Prospective Investigation into Cancer and Nutrition carried out in 9 countries, including the Mediterranean area. Participants, enrolled in 1992-1998, provided life-style and dietary information and a blood sample (360,000; mean follow-up: 6.1 years). For 233 GC cases diagnosed after enrolment and their 910 controls individually-matched by center, gender, age and blood donation date H. pylori antibodies (antilysate and antiCagA) and plasma Pepsinogen A (PGA) were measured by ELISA methods. Severe chronic atrophic gastritis (SCAG) was defined as PGA circulating levels 〈 22 mu g/l. Overall, in a conditional logistic regression analysis adjusted for education, smoke, weight and consumption of total vegetables, fruit, red and preserved meat, H. pylori seropositivity was associated with GC risk. Subjects showing only antibodies anti-H. pylori lysate, however, were not at increased risk, while those with antiCagA antibodies had a 3.4-fold increased risk. Overall, the odds ratio associated with SCAG was 3.3 (95% CI 2.2-5.2). According to site, the risk of noncardia GC associated with CagA seropositivity showed a further increase (OR 6.5; 95% CI 3.3-12.6); on the other hand, a ten-fold increased risk of cardia GC was associated with SCAG (OR 11.0; 95% C1 3.0-40.9). These results support the causal relationship between H. pylori CagA+ strains infection, and GC in these European populations even after taking into account dietary habits. This association was limited to distal GC, while serologically defined SCAG was strongly associated with cardia GC, thus suggesting a divergent risk pattern for these 2 sites. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17131317
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  • 9
    Keywords: CANCER ; MODEL ; SUPPORT ; COHORT ; DISEASE ; DISEASES ; incidence ; NEW-YORK ; POPULATION ; RISK ; SITE ; INDEX ; ASSOCIATION ; lifestyle ; DECREASE ; CIGARETTE-SMOKING ; smoking ; COUNTRIES ; cancer risk ; DIET ; STOMACH ; adenocarcinoma ; TOBACCO ; ALCOHOL ; ALCOHOL-CONSUMPTION ; body mass index ; CARDIA ; cigarette smoking ; CONSUMPTION ; EPIC ; EPIC study ; ESOPHAGUS ; European Prospective Investigation into Cancer and Nutrition ; FRUIT ; gastric cancer,smoking,cohort study ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; HISTOLOGIC TYPE ; meat ; nutrition ; QUESTIONNAIRE ; questionnaires ; SMOKERS ; STOMACH-CANCER ; SUBSITE ; TOBACCO SMOKING ; VEGETABLES
    Abstract: Smoking has recently been recognised as causally associated with the development of gastric cancer (GC). However, evidence on the effect by sex, duration and intensity of smoking, anatomic subsite and cessation of smoking is limited. Our objective was to assess the relation between tobacco use and GC incidence in the European Prospective Investigation into Cancer and Nutrition (EPIC). We studied data from 521,468 individuals recruited from 10 European countries taking part in the EPIC study. Participants completed lifestyle questionnaires that included questions on lifetime consumption of tobacco and diet in 1991-1998. Participants were followed until September 2002, and during that period 305 cases of stomach cancer were identified. After exclusions, 274 were eligible for the analysis, using the Cox proportional hazard model. After adjustment for educational level, consumption of fresh fruit, vegetables and preserved meat, alcohol intake and body mass index (BMI), there was a significant association between cigarette smoking and gastric cancer risk: the hazard ratio (HR) for ever smokers was 1.45 (95% confidence interval [CI] = 1.08-1.94). The HR of current cigarette smoking was 1.73 (95% CI = 1.06-2.83) in males and 1.87 (95% CI = 1.12-3.12) in females. Hazard ratios increased with intensity and duration of cigarette smoked. A significant decrease of risk was observed after 10 years of quitting smoking. A preliminary analysis of 121 cases with identified anatomic site showed that current cigarette smokers had a higher HR of GC in the cardia (HR = 4.10) than in the distal part of the stomach (HR = 1.94). In this cohort, 17.6 % (95% CI = 10.5-29.5 %) of GC cases may be attributable to smoking. Findings from this large study support the causal relation between smoking and gastric cancer in this European population. Stomach cancer should be added to the burden of diseases caused by smoking. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 14520702
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