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  • 1
    Keywords: ENERGIES ; CANCER ; Germany ; human ; MODEL ; MODELS ; FOLLOW-UP ; COHORT ; EPIDEMIOLOGY ; RISK ; RISK-FACTORS ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; TRIAL ; hormone ; HEALTH ; ENERGY ; AGE ; WOMEN ; HORMONE REPLACEMENT THERAPY ; OBESITY ; risk factors ; COUNTRIES ; cancer risk ; RISK FACTOR ; EPIC ; EPIC study ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; POSTMENOPAUSAL WOMEN ; MASS INDEX ; PH ; WEIGHT ; body weight ; fat distribution ; HEIGHT ; ADIPOSITY ; breast neoplasm ; HORMONE-REPLACEMENT THERAPY ; METAANALYSIS
    Abstract: The evidence for anthropometric factors influencing breast cancer risk is accumulating, but uncertainties remain concerning the role of fat distribution and potential effect modifiers. We used data from 73,542 premenopausal and 103,344 postmenopausal women from 9 European countries, taking part in the EPIC study. RRs from Cox regression models were calculated, using measured height, weight, BMI and waist and hip circumferences; categorized by cohort wide quintiles; and expressed as continuous variables, adjusted for study center, age and other risk factors. During 4.7 years of follow-up, 1,879 incident invasive breast cancers were identified. In postmenopausal women, current HRT modified the body size-breast cancer association. Among nonusers, weight, BMI and hip circumference were positively associated with breast cancer risk (all P-trend less than or equal to 0.002); obese women (BMI 〉 30) had a 31% excess risk compared to women with BMI 〈 25. Among HRT users, body measures were inversely but nonsignificantly associated with breast cancer. Excess breast cancer risk with HRT was particularly evident among lean women. Pooled RRs per height increment of 5 cm were 1.05 (95% CI 1.00-1.16) in premenopausal and 1.10 (95% CI 1.05-1.16) in postmenopausal women. Among premenopausal women, hip circumference was the only other measure significantly related to breast cancer (P-trend = 0.03), after accounting for BMI. In postmenopausal women not taking exogenous hormones, general obesity is a significant predictor of breast cancer, while abdominal fat assessed as waist-hip ratio or waist circumference was not related to excess risk when adjusted for BMI. Among premenopausal women, weight and BMI showed nonsignificant inverse associations with breast cancer. (C) 2004 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15252848
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  • 2
    Keywords: RECEPTOR ; CANCER ; GROWTH ; GROWTH-FACTOR ; proliferation ; tumor ; CELL-PROLIFERATION ; PATHWAY ; RISK ; GENE ; GENES ; PROTEIN ; TUMORS ; RELEASE ; PATIENT ; BINDING ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; COLORECTAL-CANCER ; PROSTATE-CANCER ; cancer risk ; case-control studies ; SOMATOSTATIN ; CANCER PATIENTS ; nutrition ; FACTOR-I ; BINDING PROTEIN ; SERUM ; SINGLE ; IGF-I ; BINDING-PROTEIN ; case-control study ; ASSOCIATIONS ; RE ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; cell proliferation ; development ; GROWTH-FACTOR-I ; BINDING PROTEIN-3 ; LEVEL ; case control studies ; GENOTYPE DATA ; FACTOR (IGF)-I ; PREMENOPAUSAL WOMEN ; IGFBP3 ; insulin-like growth factor ; PLASMA-LEVELS ; SERUM-LEVELS
    Abstract: Insulin-like growth factor-I (IGF-I) stimulates cell proliferation and can enhance the development of tumors in different organs. Epidemiologic studies have shown that an elevated level of circulating IGF-I is associated to increased risk of breast cancer as well as other cancers. Genetic variants affecting the release or biological action of growth hormone (GH), the main stimulator of IGF-I production, may predict circulating levels of IGF-I and have an effect on cancer risk. We tested this hypothesis with a large case-control study of 807 breast cancer patients and 1,588 matched control subjects nested within the European Prospective Investigation into Cancer and Nutrition. We genotyped 22 common single nucleotide polymorphisms in 10 genes involved in GH production and action (GHRH, GHRHR, SST, SSTR1-SSTR5, POU1F1, and GH1), and in parallel, we measured serum levels of IGF-I and IGFBP-3, its major binding protein, in samples of cases and controls. SST and SSTR2 polymorphisms showed weak but statistically significant associations with breast cancer risk. SSTR5 polymorphisms were associated with IGF-I levels, whereas one polymorphism in GHRHR and one in POU1F1 were associated with IGFBP-3 levels. Our conclusion is that common genetic variation in the GH synthesis pathway, as measured by single nucleotide polymorphisms selected in the present study, is not a major determinant of IGF-I and IGFBP-3 circulating levels, and it does not play a major role in altering breast cancer risk
    Type of Publication: Journal article published
    PubMed ID: 16214911
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  • 3
    Keywords: CANCER ; RISK ; INFECTION ; STOMACH ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; STOMACH-CANCER ; UNIT ; RISK-FACTOR ; Helicobacter pylori ; stomach cancer
    Type of Publication: Journal article published
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  • 4
    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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  • 5
    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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  • 6
    Keywords: CANCER ; BLOOD ; Germany ; COHORT ; RISK ; MICE ; ASSOCIATION ; BREAST-CANCER ; hormone ; AGE ; ovarian cancer ; OVARIAN-CANCER ; WOMEN ; cancer risk ; case-control studies ; VALIDITY ; nutrition ; dehydroepiandrosterone ; POSTMENOPAUSAL WOMEN ; SERUM ; case-control study ; REGRESSION ; ASSOCIATIONS ; DETERMINANTS ; development ; LEVEL ; case control studies ; SERUM-LEVELS ; SULFATE ; HORMONES ; DEHYDROEPIANDROSTERONE-SULFATE ; TESTOSTERONE ; prospective ; STEROID-HORMONES ; INCREASED RISK ; odds ratio ; CANCER-RISK ; OVARIAN ; BODY-MASS-INDEX
    Abstract: Few epidemiologic studies have examined the hypothesis that circulating androgens are involved in the development of ovarian cancer. We investigated the association between prediagnostic serum levels of androgens and sex hormone-binding globulin (SHBG) and ovarian cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort. One hundred and ninety-two ovarian cancer cases and 346 matched controls not using exogenous hormones at baseline blood donation were eligible for the study. Serum levels of testosterone, androstenedione, dehydroepiandrosterone sulfate, and SHBG were measured by direct immunoassays. Free testosterone (fT) was calculated according to mass action laws. Multivariate conditional logistic regression was used to estimate odds ratios adjusted for possible confounders. Overall, there was no association between serum concentrations of androgens or SHBG and ovarian cancer risk. In postmenopausal women, fT concentrations were inversely related to risk [highest versus lowest tertile odds ratio 0.45 (0.24-0.86); P-trend = 0-01]. Among women diagnosed before the age of 55 years, there was a negative association with SHBG and a positive association with fT and ovarian cancer risk, although these associations were not statistically significant. The present study suggests that circulating androgens and SHBG levels are not strongly associated with ovarian cancer risk, although levels of fT may be associated with an increased risk among women diagnosed at relatively young age. The heterogeneity of results on the associations of fT with ovarian cancer risk in postmenopausal women deserves further investigation
    Type of Publication: Journal article published
    PubMed ID: 17220328
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  • 7
    Keywords: CANCER ; BLOOD ; Germany ; RISK ; METABOLISM ; ASSOCIATION ; BREAST-CANCER ; DESIGN ; NUMBER ; AGE ; WOMEN ; REPRODUCIBILITY ; etiology ; cancer risk ; EPIC ; nutrition ; ESTRADIOL ; POSTMENOPAUSAL WOMEN ; SERUM ; ONCOLOGY ; REGRESSION ; ESTROGEN ; LEVEL ; analysis ; PHASE ; PREMENOPAUSAL ; TESTOSTERONE ; prospective ; STEROID-HORMONES ; VARIABLES ; CANCER-RISK ; BINDING GLOBULIN ; ENGLAND ; steroids ; SEX-HORMONES ; postmenopausal ; androgens ; FREE TESTOSTERONE ; ESTROGENS
    Abstract: Epidemiological data show that reproductive and hormonal factors are involved in the etiology of endometrial cancer, but there is little data on the association with endogenous sex hormone levels. We analyzed the association between prediagnostic serum concentrations of sex steroids and endometrial cancer risk in the European Prospective Investigation into Cancer and Nutrition using a nested case-control design of 247 incident endometrial cancer cases and 481 controls, matched on center, menopausal status, age, variables relating to blood collection, and, for premenopausal women, phase of menstrual cycle. Using conditional regression analysis, endometrial cancer risk among postmenopausal women was positively associated with increasing levels of total testosterone, free testosterone, estrone, total estradiol, and free estradiol. The odds ratios (ORs) for the highest versus lowest tertile were 2.66 (95% confidence interval (CI) 1.50-4.72; P=0.002 for a continuous linear trend) for estrone, 2.07 (95% Cl 1.20-3.60; P=0.001) for estradiol, and 1.66 (95% Cl 0.98-2.82; P=0.001) for free estradiol. For total and free testosterone, ORs for the highest versus lowest tertile were 1.44 (95% Cl 0.88-2.36; P=0.05) and 2.05 (95% Cl 1.23-3.42; P=0.005) respectively. Androstenedione and dehydroepiandrosterone sulfate were not associated with risk. Sex hormone-binding globulin was significantly inversely associated with risk (OR for the highest versus lowest tertile was 0.57, 95% Cl 0.34-0.95; P=0.004). In premenopausal women, serum sex hormone concentrations were not clearly associated with endometrial cancer risk, but numbers were too small to draw firm conclusions. In conclusion, relatively high blood concentrations of estrogens and free testosterone are associated with an increased endometrial cancer risk in postmenopausal women
    Type of Publication: Journal article published
    PubMed ID: 18509001
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  • 8
    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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  • 9
    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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  • 10
    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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