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2007

Variations in plasma phytoestrogen concentrations in European adults

Peeters P.H., Slimani N., van der Schouw Y.T., Grace P.B., Navarro C., Tjonneland A., Olsen A., Clavel-Chapelon F., Touillaud M., Boutron-Ruault M.C., Jenab M., Kaaks R., Linseisen J., Trichopoulou A., Trichopoulos D., Dilis V., Boeing H., Weikert C., Overvad K., Pala V., Palli D., Panico S., Tumino R., Vineis P., Bueno-de-Mesquita H.B., Van Gils C.H., Skeie G., Jakszyn P., Hallmans G., Berglund G., Key T.J., Travis R., Riboli E., Bingham S.A.

J Nutr; 2007; 137(5): 1294-1300

Abstract as provided by PubMed

Dietary phytoestrogens may play a role in chronic disease occurrence. The aim of our study was to assess the variability of plasma concentrations in European populations. We included 15 geographical regions in 9 European countries (Denmark, France, Germany, Greece, Italy, Spain, Sweden, The Netherlands, and UK) and a 16th region, Oxford, UK, where participants were recruited from among vegans and vegetarians. All subjects were participants of the European Prospective Investigation into Cancer and Nutrition (EPIC). Plasma concentrations of 3 isoflavones (daidzein, genistein, and glycitein), 2 metabolites of daidzein [O-desmethylangolensin (O-DMA) and equol] and 2 mammalian lignans (enterodiol and enterolactone) were measured in 1414 participants. We computed geometric means for each region and used multivariate regression analysis to assess the influence of region, adjusted for gender, age, BMI, alcohol intake, smoking status, and laboratory batch. Many subjects had concentrations below the detection limit [0.1 microg/L (0.4 nmol/L)] for glycitein (80%), O-DMA (73%) and equol (62%). Excluding subjects from Oxford, UK, the highest concentrations of isoflavones were in subjects from the Netherlands and Cambridge, UK [2-6 microg/L (7-24 nmol/L); P < 0.05], whereas concentrations for lignans were highest in Denmark [8 microg/L (27 nmol/L); P < 0.05]. Isoflavones varied 8- to 13-fold, whereas lignans varied 4-fold. In the vegetarian/vegan cohort of Oxford, concentrations of isoflavones were 5-50 times higher than in nonvegetarian regions. Region was the most important determinant of plasma concentrations for all 7 phytoestrogens. Despite the fact that plasma concentrations of phytoestrogens in Europe were low compared with Asian populations, they varied substantially among subjects from the 16 different regions

Endogenous androgens and risk of epithelial ovarian cancer: results from the European Prospective Investigation into Cancer and Nutrition (EPIC)

Rinaldi S., Dossus L., Lukanova A., Peeters P.H., Allen N.E., Key T., Bingham S., Khaw K.T., Trichopoulos D., Trichopoulou A., Oikonomou E., Pera G., Larranaga N., Martinez-Garcia C., Ardanaz E., Quiros J.R., Tormo M.J., Tjonneland A., Olsen A., Overvad K., Chang-Claude J., Linseisen J., Schulz M., Boeing H., Van Gils C.H., Bueno-de-Mesquita B.H., Pala V., Palli D., Panico S., Tumino R., Vineis P., Clavel-Chapelon F., Mesrine S., Boutron-Ruault M.C., Lundin E., Agren A., Berglund G., Manjer J., Kumle M., Lund E., Slimani N., Saracci R., Riboli E., Kaaks R.

Cancer Epidemiol Biomarkers Prev; 2007; 16(1): 23-29

Abstract as provided by PubMed

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

Fruit and vegetable consumption and lymphoma risk in the European Prospective Investigation into Cancer and Nutrition (EPIC)

Rohrmann S., Becker N., Linseisen J., Nieters A., Rudiger T., Raaschou-Nielsen O., Tjonneland A., Johnsen H.E., Overvad K., Kaaks R., Bergmann M.M., Boeing H., Benetou V., Psaltopoulou T., Trichopoulou A., Masala G., Mattiello A., Krogh V., Tumino R., Gils C.H., Peeters P.H., Bueno-de-Mesquita H.B., Ros M.M., Lund E., Ardanaz E., Chirlaque M.D., Jakszyn P., Larranaga N., Losada A., Martinez-Garcia C., Agren A., Hallmans G., Berglund G., Manjer J., Allen N.E., Key T.J., Bingham S., Khaw K.T., Slimani N., Ferrari P., Boffetta P., Norat T., Vineis P., Riboli E.

Cancer Causes Control; 2007; 18(5): 537-549

Abstract as provided by PubMed

INTRODUCTION: Lymphomas are a heterogeneous group of malignant diseases of cells of the immune system. The best-established risk factors are related to dys-regulation of immune function, and evidence suggests that factors such as dietary or lifestyle habits may be involved in the etiology. MATERIAL AND METHODS: In the European Prospective Investigation into Cancer and Nutrition (EPIC), 849 lymphoma cases were identified in a median follow-up period of 6.4 years. Fruit and vegetable consumption was estimated from validated dietary questionnaires. Cox proportional hazard models were used to examine the association between fruit and vegetable intake with the risk of lymphomas overall and subentities. RESULTS: There was no overall association between total fruit and vegetable consumption and risk of lymphoma [hazard ratio (HR) = 0.95, 95% confidence interval (CI) 0.78-1.15 comparing highest with lowest quartile]. However, the risk of diffuse large B-cell lymphomas (DLBCL) tended to be lower in participants with a high intake of total vegetables (HR = 0.49, 95% CI 0.23-1.02). CONCLUSION: In this large prospective study, an inverse associations between fruit and vegetable consumption and risk of lymphomas overall could not be confirmed. Associations with lymphoma subentities such as DLBCL warrant further investigation

Haplotype-Based Analysis of Common Variation in the Acetyl-CoA Carboxylase {alpha} Gene and Breast Cancer Risk: A Case-Control Study Nested within the European Prospective Investigation into Cancer and Nutrition

Sinilnikova O.M., McKay J.D., Tavtigian S.V., Canzian F., DeSilva D., Biessy C., Monnier S., Dossus L., Boillot C., Gioia L., Hughes D.J., Jensen M.K., Overvad K., Tjonneland A., Olsen A., Clavel-Chapelon F., Chajes V., Joulin V., Linseisen J., Chang-Claude J., Boeing H., Dahm S., Trichopoulou A., Trichopoulos D., Koliva M., Khaw K.T., Bingham S., Allen N.E., Key T., Palli D., Panico S., Berrino F., Tumino R., Vineis P., Bueno-de-Mesquita H.B., Peeters P.H., Van Gils C.H., Lund E., Pera G., Quiros J.R., Dorronsoro M., Martinez Garcia C., Tormo M.J., Ardanaz E., Hallmans G., Lenner P., Berglund G., Manjer J., Riboli E., Lenoir G.M., Kaaks R.

Cancer Epidemiol Biomarkers Prev; 2007; 16(3): 409-415

Abstract as provided by PubMed

A key fatty acid synthesis enzyme, acetyl-CoA carboxylase alpha (ACC-alpha), has been shown to be highly expressed in human breast cancer and other tumor types and also to specifically interact with the protein coded by one of two major breast cancer susceptibility genes BRCA1. We used a comprehensive haplotype analysis to examine the contribution of the ACC-alpha common genetic variation (allele frequency >5%) to breast cancer in a case-control study (1,588 cases/2,600 controls) nested within the European Prospective Investigation into Cancer and Nutrition. We identified 21 haplotype-tagging polymorphisms efficiently capturing common variation within 325 kb of ACC-alpha and surrounding sequences using genotype data from the HapMap project and our resequencing data. We found an effect on overall risk of breast cancer in homozygous carriers of one common haplotype [odds ratio (OR), 1.74; 95% confidence interval (95% CI), 1.03-2.94]. When the data were subdivided by menopausal status, we found statistical evidence of heterogeneity for two other common haplotypes (P value for heterogeneity = 0.016 and 0.045). In premenopausal women, the carriers of these haplotypes, compared with noncarriers, had an altered risk of breast cancer (OR, 0.70; 95% CI, 0.53-0.92 and OR, 1.35; 95% CI, 1.04-1.76). These findings were not significant after adjustment for multiple testing and therefore should be considered as preliminary and evaluated in larger independent studies. However, they suggest a possible role of the ACC-alpha common sequence variants in susceptibility to breast cancer and encourage studies of other genes involved in fatty acid synthesis. (Cancer Epidemiol Biomarkers Prev 2007;16(3):409-15)

The EPIC nutrient database project (ENDB): a first attempt to standardize nutrient databases across the 10 European countries participating in the EPIC study

Slimani N., Deharveng G., Unwin I., Southgate D.A., Vignat J., Skeie G., Salvini S., Parpinel M., Moller A., Ireland J., Becker W., Farran A., Westenbrink S., Vasilopoulou E., Unwin J., Borgejordet A., Rohrmann S., Church S., Gnagnarella P., Casagrande C., van Bakel M., Niravong M., Boutron-Ruault M.C., Stripp C., Tjonneland A., Trichopoulou A., Georga K., Nilsson S., Mattisson I., Ray J., Boeing H., Ocke M., Peeters P.H., Jakszyn P., Amiano P., Engeset D., Lund E., de Magistris M.S., Sacerdote C., Welch A., Bingham S., Subar A.F., Riboli E.

Eur J Clin Nutr; 2007; 61(9): 1037-1056

Abstract as provided by PubMed

OBJECTIVE: This paper describes the ad hoc methodological concepts and procedures developed to improve the comparability of Nutrient databases (NDBs) across the 10 European countries participating in the European Prospective Investigation into Cancer and Nutrition (EPIC). This was required because there is currently no European reference NDB available. DESIGN: A large network involving national compilers, nutritionists and experts on food chemistry and computer science was set up for the 'EPIC Nutrient DataBase' (ENDB) project. A total of 550-1500 foods derived from about 37,000 standardized EPIC 24-h dietary recalls (24-HDRS) were matched as closely as possible to foods available in the 10 national NDBs. The resulting national data sets (NDS) were then successively documented, standardized and evaluated according to common guidelines and using a DataBase Management System specifically designed for this project. The nutrient values of foods unavailable or not readily available in NDSs were approximated by recipe calculation, weighted averaging or adjustment for weight changes and vitamin/mineral losses, using common algorithms. RESULTS: The final ENDB contains about 550-1500 foods depending on the country and 26 common components. Each component value was documented and standardized for unit, mode of expression, definition and chemical method of analysis, as far as possible. Furthermore, the overall completeness of NDSs was improved (>or=99%), particularly for beta-carotene and vitamin E. CONCLUSION: The ENDB constitutes a first real attempt to improve the comparability of NDBs across European countries. This methodological work will provide a useful tool for nutritional research as well as end-user recommendations to improve NDBs in the future

Alcohol intake and breast cancer risk: the European Prospective Investigation into Cancer and Nutrition (EPIC)

Tjonneland A., Christensen J., Olsen A., Stripp C., Thomsen B.L., Overvad K., Peeters P.H., Van Gils C.H., Bueno-de-Mesquita H.B., Ocke M.C., Thiebaut A., Fournier A., Clavel-Chapelon F., Berrino F., Palli D., Tumino R., Panico S., Vineis P., Agudo A., Ardanaz E., Martinez-Garcia C., Amiano P., Navarro C., Quiros J.R., Key T.J., Reeves G., Khaw K.T., Bingham S., Trichopoulou A., Trichopoulos D., Naska A., Nagel G., Chang-Claude J., Boeing H., Lahmann P.H., Manjer J., Wirfalt E., Hallmans G., Johansson I., Lund E., Skeie G., Hjartaker A., Ferrari P., Slimani N., Kaaks R., Riboli E.

Cancer Causes Control; 2007; 18(4): 361-373

Abstract as provided by PubMed

OBJECTIVE: Most epidemiologic studies have suggested an increased risk of breast cancer with increasing alcohol intake. Using data from 274,688 women participating in the European Prospective Investigation into Cancer and Nutrition study (EPIC), we investigated the relation between alcohol intake and the risk of breast cancer. METHODS: Incidence rate ratios (IRRs) based on Cox proportional hazard models were calculated using reported intake of alcohol, recent (at baseline) and lifetime exposure. We adjusted for known risk factors and stratified according to study center as well as potentially modifying host factors. RESULTS: During 6.4 years of follow up, 4,285 invasive cases of breast cancer within the age group 35-75 years were identified. For all countries together the IRR per 10 g/day higher recent alcohol intake (continuous) was 1.03 (95% confidence interval (CI): 1.01-1.05). When adjusted, no association was seen between lifetime alcohol intake and risk of breast cancer. No difference in risk was shown between users and non-users of HRT, and there was no significant interaction between alcohol intake and BMI, HRT or dietary folate. CONCLUSION: This large European study supports previous findings that recent alcohol intake increases the risk of breast cancer

Serum androgens and prostate cancer among 643 cases and 643 controls in the European Prospective Investigation into Cancer and Nutrition

Travis R.C., Key T.J., Allen N.E., Appleby P.N., Roddam A.W., Rinaldi S., Egevad L., Gann P.H., Rohrmann S., Linseisen J., Pischon T., Boeing H., Johnsen N.F., Tjonneland A., Overvad K., Kiemeney L., Bueno-de-Mesquita H.B., Bingham S., Khaw K.T., Tumino R., Sieri S., Vineis P., Palli D., Quiros J.R., Ardanaz E., Chirlaque M.D., Larranaga N., Gonzalez C., Sanchez M.J., Trichopoulou A., Bikou C., Trichopoulos D., Stattin P., Jenab M., Ferrari P., Slimani N., Riboli E., Kaaks R.

Int J Cancer; 2007; 121(6): 1331-1338

Abstract as provided by PubMed

We examined the hypothesis that serum concentrations of circulating androgens and sex hormone binding globulin (SHBG) are associated with risk for prostate cancer in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition (EPIC). Concentrations of androstenedione, testosterone, androstanediol glucuronide and SHBG were measured in serum samples for 643 prostate cancer cases and 643 matched control participants, and concentrations of free testosterone were calculated. Conditional logistic regression models were used to calculate odds ratios for risk of prostate cancer in relation to the serum concentration of each hormone. After adjustment for potential confounders, there was no significant association with overall risk for prostate cancer for serum total or free testosterone concentrations (highest versus the lowest thirds: OR, 1.02; 95% CI, 0.73-1.41 and OR, 1.07, 95% CI, 0.74-1.55, respectively) or for other androgens or SHBG. Subgroup analyses showed significant heterogeneity for androstenedione by cancer stage, with a significant inverse association of androstenedione concentration and risk for advanced prostate cancer. There were also weak positive associations between free testosterone concentration and risk for total prostate cancer among younger men and risk for high-grade disease. In summary, in this large nested case-control study, concentrations of circulating androgens or SHBG were not strongly associated with risk for total prostate cancer. However, our findings are compatible with a positive association of free testosterone with risk in younger men and possible heterogeneity in the association with androstenedione concentration by stage of disease; these findings warrant further investigation. (c) 2007 Wiley-Liss, Inc

Modified Mediterranean diet and survival after myocardial infarction: the EPIC-Elderly study

Trichopoulou A., Bamia C., Norat T., Overvad K., Schmidt E.B., Tjonneland A., Halkjaer J., Clavel-Chapelon F., Vercambre M.N., Boutron-Ruault M.C., Linseisen J., Rohrmann S., Boeing H., Weikert C., Benetou V., Psaltopoulou T., Orfanos P., Boffetta P., Masala G., Pala V., Panico S., Tumino R., Sacerdote C., Bueno-de-Mesquita H.B., Ocke M.C., Peeters P.H., van der Schouw Y.T., Gonzalez C., Sanchez M.J., Chirlaque M.D., Moreno C., Larranaga N., Van Guelpen B., Jansson J.H., Bingham S., Khaw K.T., Spencer E.A., Key T., Riboli E., Trichopoulos D.

Eur J Epidemiol; 2007; 22(12): 871-881

Abstract as provided by PubMed

Mediterranean diet is associated with lower incidence of coronary heart disease, and two randomised trials indicated that it improves prognosis of coronary patients. These trials, however, relied on a total of 100 deaths and evaluated designer diets in the clinical context. We have evaluated the association of adherence to the modified Mediterranean diet, in which unsaturates were substituted for monounsaturates, with survival among elderly with previous myocardial infarction within the European Prospective Investigation into Cancer and nutrition (EPIC) study. As of December 2003, after a median follow-up of 6.7 years, 2671 EPIC participants from nine countries were 60 years or older and had prevalent myocardial infarction but no stroke or cancer at enrolment, complete information on dietary intakes and important covariates and known survival status. Adherence to the modified Mediterranean diet was assessed through a 10-unit-scale. Mortality ratio in relation to modified Mediterranean diet was estimated through Cox regression controlling for possible confounding. Increased adherence to modified Mediterranean diet by two units was associated with 18% lower overall mortality rate (95% confidence interval 7-27%, fixed effects model). There was no significant heterogeneity by sex, age at enrolment, or country, although the association tended to be less evident among northern Europeans. Associations between food groups contributing to the modified Mediterranean diet and mortality were generally weak. A diet inspired by the Mediterranean pattern that can be easily adopted by Western populations is associated with substantial reduction of total mortality of coronary patients in the community

Lung cancers attributable to environmental tobacco smoke and air pollution in non-smokers in different European countries: a prospective study

Vineis P., Hoek G., Krzyzanowski M., Vigna-Taglianti F., Veglia F., Airoldi L., Overvad K., Raaschou-Nielsen O., Clavel-Chapelon F., Linseisen J., Boeing H., Trichopoulou A., Palli D., Krogh V., Tumino R., Panico S., Bueno-de-Mesquita H.B., Peeters P.H., Lund E.E., Agudo A., Martinez C., Dorronsoro M., Barricarte A., Cirera L., Quiros J.R., Berglund G., Manjer J., Forsberg B., Day N.E., Key T.J., Kaaks R., Saracci R., Riboli E.

Environ Health; 2007; 7

Abstract as provided by PubMed

BACKGROUND: Several countries are discussing new legislation on the ban of smoking in public places, and on the acceptable levels of traffic-related air pollutants. It is therefore useful to estimate the burden of disease associated with indoor and outdoor air pollution. METHODS: We have estimated exposure to Environmental Tobacco Smoke (ETS) and to air pollution in never smokers and ex-smokers in a large prospective study in 10 European countries (European Prospective Investigation into Cancer and Nutrition)(N = 520,000). We report estimates of the proportion of lung cancers attributable to ETS and air pollution in this population. RESULTS: The proportion of lung cancers in never- and ex-smokers attributable to ETS was estimated as between 16 and 24%, mainly due to the contribution of work-related exposure. We have also estimated that 5-7% of lung cancers in European never smokers and ex-smokers are attributable to high levels of air pollution, as expressed by NO2 or proximity to heavy traffic roads. NO2 is the expression of a mixture of combustion (traffic-related) particles and gases, and is also related to power plants and waste incinerator emissions. DISCUSSION: We have estimated risks of lung cancer attributable to ETS and traffic-related air pollution in a large prospective study in Europe. Information bias can be ruled out due to the prospective design, and we have thoroughly controlled for potential confounders, including restriction to never smokers and long-term ex-smokers. Concerning traffic-related air pollution, the thresholds for indicators of exposure we have used are rather strict, i.e. they correspond to the high levels of exposure that characterize mainly Southern European countries (levels of NO2 in Denmark and Sweden are closer to 10-20 ug/m3, whereas levels in Italy are around 30 or 40, or higher).Therefore, further reduction in exposure levels below 30 ug/m3 would correspond to additional lung cancer cases prevented, and our estimate of 5-7% is likely to be an underestimate. Overall, our prospective study draws attention to the need for strict legislation concerning the quality of air in Europe

The association of gastric cancer risk with plasma folate, cobalamin, and methylenetetrahydrofolate reductase polymorphisms in the European prospective investigation into cancer and nutrition

Vollset S.E., Igland J., Jenab M., Fredriksen A., Meyer K., Eussen S., Gjessing H.K., Ueland P.M., Pera G., Sala N., Agudo A., Capella G., Del Giudice G., Palli D., Boeing H., Weikert C., Bueno-de-Mesquita H.B., Carneiro F., Pala V., Vineis P., Tumino R., Panico S., Berglund G., Manjer J., Stenling R., Hallmans G., Martinez C., Dorronsoro M., Barricarte A., Navarro C., Quiros J.R., Allen N., Key T.J., Bingham S., Linseisen J., Kaaks R., Overvad K., Tjonneland A., Buchner F.L., Peeters P.H., Numans M.E., Clavel-Chapelon F., Boutron-Ruault M.C., Trichopoulou A., Lund E., Slimani N., Ferrari P., Riboli E., Gonzalez C.A.

Cancer Epidemiol Biomarkers Prev; 2007; 16(11): 2416-2424

Abstract as provided by PubMed

Previous studies have shown inconsistent associations of folate intake and polymorphisms of the methylenetetrahydrofolate reductase (MTHFR) gene with gastric cancer risk. Our nested case-control study within the European Prospective Investigation into Cancer and Nutrition cohort is the first prospective study of blood folate levels and gastric cancer. Gastric cancer cases (n = 247) and controls (n = 631) were matched for study center, age, sex, and time of blood donation. Two common single nucleotide polymorphisms of the MTHFR gene were determined, as were plasma concentrations of folate, cobalamin (vitamin B12), total homocysteine, and methylmalonic acid (cobalamin deficiency marker) in prediagnostic plasma. Risk measures were calculated with conditional logistic regression. Although no relations were observed between plasma folate or total homocysteine concentrations and gastric cancer, we observed a trend toward lower risk of gastric cancer with increasing cobalamin concentrations (odds ratio, 0.79 per SD increase in cobalamin; P = 0.01). Further analyses showed that the inverse association between cobalamin and gastric cancer was confined to cancer cases with low pepsinogen A levels (marker of severe chronic atrophic gastritis) at the time of blood sampling. The 677 C-->T MTHFR polymorphism was not associated with gastric cancer, but we observed an increased risk with the variant genotype of the 1298 A-->C polymorphism (odds ratio, 1.47 for CC versus AA; P = 0.04). In conclusion, we found no evidence of a role of folate in gastric cancer etiology. However, we observed increased gastric cancer risk at low cobalamin levels that was most likely due to compromised cobalamin status in atrophic gastritis preceding gastric cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(11):2416-24)

2006

No association between polymorphisms in CYP2E1, GSTM1, NAT1, NAT2 and the risk of gastric adenocarcinoma in the European prospective investigation into cancer and nutrition

Agudo A., Sala N., Pera G., Capella G., Berenguer A., Garcia N., Palli D., Boeing H., Del Giudice G., Saieva C., Carneiro F., Berrino F., Sacerdote C., Tumino R., Panico S., Berglund G., Siman H., Stenling R., Hallmans G., Martinez C., Amiano P., Barricarte A., Navarro C., Quiros J.R., Allen N., Key T., Bingham S., Khaw K.T., Linseisen J., Nagel G., Overvad K., Tjonneland A., Olsen A., Bueno-de-Mesquita H.B., Boshuizen H.C., Peeters P.H., Numans M.E., Clavel-Chapelon F., Boutron-Ruault M.C., Trichopoulou A., Lund E., Blaker H., Jenab M., Ferrari P., Norat T., Riboli E., Gonzalez C.A.

Cancer Epidemiol Biomarkers Prev; 2006; 15(5): 1043-1045
Polymorphisms in metabolic genes related to tobacco smoke and the risk of gastric cancer in the European prospective investigation into cancer and nutrition

Agudo A., Sala N., Pera G., Capella G., Berenguer A., Garcia N., Palli D., Boeing H., Del Giudice G., Saieva C., Carneiro F., Berrino F., Sacerdote C., Tumino R., Panico S., Berglund G., Siman H., Stenling R., Hallmans G., Martinez C., Bilbao R., Barricarte A., Navarro C., Quiros J.R., Allen N., Key T., Bingham S., Khaw K.T., Linseisen J., Nagel G., Overvad K., Tjonneland A., Olsen A., Bueno-de-Mesquita H.B., Boshuizen H.C., Peeters P.H., Numans M.E., Clavel-Chapelon F., Boutron-Ruault M.C., Trichopoulou A., Lund E., Offerhaus J., Jenab M., Ferrari P., Norat T., Riboli E., Gonzalez C.A.

Cancer Epidemiol Biomarkers Prev; 2006; 15(12): 2427-2434

Abstract as provided by PubMed

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

Reliability of biomarkers of iron status, blood lipids, oxidative stress, vitamin D, C-reactive protein and fructosamine in two Dutch cohorts

Al-Delaimy W.K., Jansen E.H., Peeters P.H., van der Laan J.D., van Noord P.A., Boshuizen H.C., van der Schouw Y.T., Jenab M., Ferrari P., Bueno-de-Mesquita H.B.

Biomarkers; 2006; 11(4): 370-382

Abstract as provided by PubMed

Biomarkers are widely used in epidemiology, yet there are few reliability studies to assess the appropriateness of using these biomarkers for the assessment of exposure-disease relationships. The aim of the study was to assess the reliability of 20 biomarkers in serum collected from two Dutch centres (Utrecht and Bilthoven) participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) at two points several years apart. Blood samples were collected from 30 men from Bilthoven and 35 women from Utrecht. Ferritin, total iron, total iron-binding capacity, transferrin saturation, transferrin, C-reactive protein, bilirubin, cholesterol, triglycerides, apo lipoprotein-A, apo lipoprotein-B, high-density lipoproteins, low-density lipoproteins, uric acid, creatinine, reactive oxygen metabolites, the ferric-reducing ability of plasma, protein thiol oxidation, fructosamine, and vitamin D biomarkers in serum were analysed from the blood samples at the two points of time. For all biomarkers, except C-reactive protein, there were no substantial changes in the mean levels over time. Uric acid, ferritin, creatinine, HDL, and apo lipoprotein-B levels consistently showed the highest reliability for men and women (intra-class correlation = 0.69-0.86). Among women, the ferric-reducing ability of plasma, and protein thiol oxidation had poor reliability; and among men iron-related biomarkers (except serum ferritin) had poor reliability. With the exception of a few gender-specific differences, most of the 20 biomarkers performed well and can be considered to have sufficient reliability to be used in future cohort studies

Anthropometry, physical activity, and the risk of pancreatic cancer in the European prospective investigation into cancer and nutrition

Berrington de Gonzalez A., Spencer E.A., Bueno-de-Mesquita H.B., Roddam A., Stolzenberg-Solomon R., Halkjaer J., Tjonneland A., Overvad K., Clavel-Chapelon F., Boutron-Ruault M.C., Boeing H., Pischon T., Linseisen J., Rohrmann S., Trichopoulou A., Benetou V., Papadimitriou A., Pala V., Palli D., Panico S., Tumino R., Vineis P., Boshuizen H.C., Ocke M.C., Peeters P.H., Lund E., Gonzalez C.A., Larranaga N., Martinez-Garcia C., Mendez M., Navarro C., Quiros J.R., Tormo M.J., Hallmans G., Ye W., Bingham S.A., Khaw K.T., Allen N., Key T.J., Jenab M., Norat T., Ferrari P., Riboli E.

Cancer Epidemiol Biomarkers Prev; 2006; 15(5): 879-885

Abstract as provided by PubMed

Tobacco smoking is the only established risk factor for pancreatic cancer. Results from several epidemiologic studies have suggested that increased body mass index and/or lack of physical activity may be associated with an increased risk of this disease. We examined the relationship between anthropometry and physical activity recorded at baseline and the risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (n = 438,405 males and females age 19-84 years and followed for a total of 2,826,070 person-years). Relative risks (RR) were calculated using Cox proportional hazards models stratified by age, sex, and country and adjusted for smoking and self-reported diabetes and, where appropriate, height. In total, there were 324 incident cases of pancreatic cancer diagnosed in the cohort over an average of 6 years of follow-up. There was evidence that the RR of pancreatic cancer was associated with increased height [RR, 1.74; 95% confidence interval (95% CI), 1.20-2.52] for highest quartile compared with lowest quartile (P(trend) = 0.001). However, this trend was primarily due to a low risk in the lowest quartile, as when this group was excluded, the trend was no longer statistically significant (P = 0.27). A larger waist-to-hip ratio and waist circumference were both associated with an increased risk of developing the disease (RR per 0.1, 1.24; 95% CI, 1.04-1.48; P(trend) = 0.02 and RR per 10 cm, 1.13; 95% CI, 1.01-1.26; P(trend) = 0.03, respectively). There was a nonsignificant increased risk of pancreatic cancer with increasing body mass index (RR, 1.09; 95% CI, 0.95-1.24 per 5 kg/m(2)), and a nonsignificant decreased risk with total physical activity (RR, 0.82; 95% CI, 0.50-1.35 for most active versus inactive). Future studies should consider including measurements of waist and hip circumference, to further investigate the relationship between central adiposity and the risk of pancreatic cancer

The effect of occasional smoking on smoking-related cancers : In the European Prospective Investigation into Cancer and Nutrition (EPIC)

Bjerregaard B.K., Raaschou-Nielsen O., Sorensen M., Frederiksen K., Tjonneland A., Rohrmann S., Linseisen J., Bergman M.M., Boeing H., Sieri S., Palli D., Tumino R., Sacerdote C., Bueno-de-Mesquita H.B., Buchner F.L., Gram I.T., Braaten T., Lund E., Hallmans G., Agren A., Riboli E.

Cancer Causes Control; 2006; 17(10): 1305-1309

Abstract as provided by PubMed

OBJECTIVE: Most studies on tobacco smoking have focused on daily-smokers. Occasional smokers, who have never smoked daily, have often been included in the reference group of never-smokers. We have investigated the association between occasional smoking and cancer of the bladder, kidney, pancreas, upper aero-digestive tract and lung. METHODS: The study population consisted of 158,488 persons, who provided information on occasional smoking, within the European Prospective Investigation into Cancer and Nutrition (EPIC), 780 of whom developed a smoking-related cancer. We used Cox proportional hazard model, stratified by gender and country to estimate incidence rate ratios (IRR) for smoking-related cancers. RESULTS: The results suggest that occasional smokers have a higher risk of bladder cancer (IRR: 1.92, 95% confidence interval (CI) 0.93-3.98) and of the major smoking-related cancers combined (IRR: 1.24, 95% CI 0.80-1.94) than true never-smokers. Including occasional smokers in the reference group resulted in a lower risk estimate for former and current smokers. CONCLUSIONS: Occasional smoking should be discouraged

Tobacco smoke and bladder cancer--in the European Prospective Investigation into Cancer and Nutrition

Bjerregaard B.K., Raaschou-Nielsen O., Sorensen M., Frederiksen K., Christensen J., Tjonneland A., Overvad K., Chapelon F.C., Nagel G., Chang-Claude J., Bergmann M.M., Boeing H., Trichopoulos D., Trichopoulou A., Oikonomou E., Berrino F., Palli D., Tumino R., Vineis P., Panico S., Peeters P.H., Bueno-de-Mesquita H.B., Kiemeney L., Gram I.T., Braaten T., Lund E., Gonzalez C.A., Berglund G., Allen N., Roddam A., Bingham S., Riboli E.

Int J Cancer; 2006; 119(10): 2412-2416

Abstract as provided by PubMed

The purpose of the present study was to investigate the association between smoking and the development of bladder cancer. The study population consisted of 429,906 persons participating in the European Prospective Investigation into Cancer and Nutrition (EPIC), 633 of whom developed bladder cancer during the follow-up period. An increased risk of bladder cancer was found for both current- (incidence rate ratio 3.96, 95% confidence interval: 3.07-5.09) and ex- (2.25, 1.74-2.91) smokers, compared to never-smokers. A positive association with intensity (per 5 cigarettes) was found among current-smokers (1.18, 1.09-1.28). Associations (per 5 years) were observed for duration (1.14, 1.08-1.21), later age at start (0.75, 0.66-0.85) and longer time since quitting (0.92, 0.86-0.98). Exposure to environmental tobacco smoke (ETS) during childhood increased the risk of bladder cancer (1.38, 1.00-1.90), whereas for ETS exposure as adult no effect was detected. The present study confirms the strong association between smoking and bladder cancer. The indication of a higher risk of bladder cancer for those who start smoking at a young age and for those exposed to ETS during childhood adds to the body of evidence suggesting that children are more sensitive to carcinogens than adults

Polymorphisms of genes coding for insulin-like growth factor 1 and its major binding proteins, circulating levels of IGF-I and IGFBP-3 and breast cancer risk: results from the EPIC study

Canzian F., McKay J.D., Cleveland R.J., Dossus L., Biessy C., Rinaldi S., Landi S., Boillot C., Monnier S., Chajes V., Clavel-Chapelon F., Tehard B., Chang-Claude J., Linseisen J., Lahmann P.H., Pischon T., Trichopoulos D., Trichopoulou A., Zilis D., Palli D., Tumino R., Vineis P., Berrino F., Bueno-de-Mesquita H.B., Van Gils C.H., Peeters P.H.M., Pera G., Ardanaz E., Chirlaque M.D., Quiros J.R., Larranaga N., Martinez-Garcia C., Allen N.E., Key T.J., Bingham S.A., Khaw K.T., Slimani N., Norat T., Riboli E., Kaaks R.

Br J Cancer; 2006; 94(2): 299-307

Abstract as provided by PubMed

Insulin-like growth factor I (IGF-I) stimulates cell proliferation and can enhance the development of tumours in different organs. Epidemiological studies have shown that an elevated level of circulating IGF-I is associated with increased risk of breast cancer, as well as of other cancers. Most of circulating IGF-I is bound to an acid-labile subunit and to one of six insulin-like growth factor binding proteins (IGFBPs), among which the most important are IGFBP-3 and IGFBP-1. Polymorphisms of the IGF1 gene and of genes encoding for the major IGF-I carriers may predict circulating levels of IGF-I and have an impact on cancer risk. We tested this hypothesis with a case-control study of 807 breast cancer patients and 1588 matched control subjects, nested within the European Prospective Investigation into Cancer and Nutrition. We genotyped 23 common single nucleotide polymorphisms in IGF1, IGFBP1, IGFBP3 and IGFALS, and measured serum levels of IGF-I and IGFBP-3 in samples of cases and controls. We found a weak but significant association of polymorphisms at the 5' end of the IGF1 gene with breast cancer risk, particularly among women younger than 55 years, and a strong association of polymorphisms located in the 5' end of IGFBP3 with circulating levels of IGFBP-3, which confirms previous findings. Common genetic variation in these candidate genes does not play a major role in altering breast cancer risk in Caucasians.British Journal of Cancer (2006) 94, 299-307. doi:10.1038/sj.bjc.6602936 www.bjcancer.com Published online 10 January 2006

A comprehensive analysis of the androgen receptor gene and risk of breast cancer: results from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3)

Cox D.G., Blanche H., Pearce C.L., Calle E.E., Colditz G.A., Pike M.C., Albanes D., Allen N.E., Amiano P., Berglund G., Boeing H., Buring J., Burtt N., Canzian F., Chanock S., Clavel-Chapelon F., Feigelson H.S., Freedman M., Haiman C.A., Hankinson S.E., Henderson B.E., Hoover R., Hunter D.J., Kaaks R., Kolonel L., Kraft P., Le Marchand L., Lund E., Palli D., Peeters P.H., Riboli E., Stram D.O., Thun M., Tjonneland A., Trichopoulos D., Yeager M.

Breast Cancer Res; 2006; 8(5): R54

Abstract as provided by PubMed

ABSTRACT: INTRODUCTION: Androgens have been hypothesised to influence risk of breast cancer through several possible mechanisms, including their conversion to estradiol or their binding to the oestrogen receptor and/or androgen receptor (AR) in the breast. Here, we report on the results of a large and comprehensive study of the association between genetic variation in the AR gene and risk of breast cancer in the National Cancer Institute Breast and Prostate Cancer Cohort Consortium (BPC3). METHODS: The underlying genetic variation was determined by first sequencing the coding regions of the AR gene in a panel of 95 advanced breast cancer cases. Second, a dense set of markers from the public database was genotyped in a panel of 349 healthy women. The linkage disequilibrium relationships (blocks) across the gene were then identified, and haplotype-tagging single nucleotide polymorphisms (htSNPs) were selected to capture the common genetic variation across the locus. The htSNPs were then genotyped in the nested breast cancer cases and controls from the Cancer Prevention Study II, European Prospective Investigation into Cancer and Nutrition, Multiethnic Cohort, Nurses' Health Study, and Women's Health Study cohorts (5,603 breast cancer cases and 7,480 controls). RESULTS: We found no association between any genetic variation (SNP, haplotype, or the exon 1 CAG repeat) in the AR gene and risk of breast cancer, nor were any statistical interactions with known breast cancer risk factors observed. CONCLUSION: Among postmenopausal Caucasian women, common variants of the AR gene are not associated with risk of breast cancer

Fish consumption and breast cancer risk. The European Prospective Investigation into Cancer and Nutrition (EPIC)

Engeset D., Alsaker E., Lund E., Welch A., Khaw K.T., Clavel-Chapelon F., Thiebaut A., Chajes V., Key T.J., Allen N.E., Amiano P., Dorronsoro M., Tjonneland A., Stripp C., Peeters P.H., Van Gils C.H., Chirlaque M.D., Nagel G., Linseisen J., Ocke M.C., Bueno-de-Mesquita H.B., Sacerdote C., Tumino R., Ardanaz E., Sanchez M.J., Panico S., Palli D., Trichopoulou A., Kalapothaki V., Benetou V., Quiros J.R., Agudo A., Overvad K., Bjerregaard L., Wirfalt E., Schulz M., Boeing H., Slimani N., Riboli E.

Int J Cancer; 2006; 119(1): 175-182

Abstract as provided by PubMed

There is current interest in fish consumption and marine omega-3 (n-3) fatty acids and breast cancer risk. Some in vitro and animal studies have suggested an inhibitory effect of marine n-3 fatty acids on breast cancer growth, but the results from epidemiological studies that have examined the association between fish consumption and breast cancer risk in humans are inconsistent. We examined fish consumption and breast cancer risk in 310,671 women aged between 25 and 70 yr at recruitment into the European Prospective Investigation Into Cancer and Nutrition (EPIC). The participants completed a dietary questionnaire between 1992-98 and were followed up for incidence of breast cancer for a median of 6.4 yr. Hazard ratio for breast cancer by intake of total and lean and fatty fish were estimated, stratified by study centre and adjusted for established breast cancer risk factors. During follow-up, 4,776 invasive incident breast cancers were reported. No significant associations between intake of total fish and breast cancer risk were observed, hazard ratio (HR) 1.01 (95% confidence interval [CI] 0.99-1.02; p = 0.28 per 10 g fish/day). When examining lean and fatty fish separately, we found a positive significant association only in the highest quintile for fatty fish (HR 1.13, 95% CI 1.01-1.26), but test for trend was not significant (p = 0.10). No associations with breast cancer risk were observed when the study participants were subdivided by menopausal status. Although the period of follow-up is relatively short, the results provide no evidence for an association between fish intake and breast cancer risk

Physical activity and risk of colon and rectal cancers: the European prospective investigation into cancer and nutrition

Friedenreich C., Norat T., Steindorf K., Boutron-Ruault M.C., Pischon T., Mazuir M., Clavel-Chapelon F., Linseisen J., Boeing H., Bergman M., Johnsen N.F., Tjonneland A., Overvad K., Mendez M., Quiros J.R., Martinez C., Dorronsoro M., Navarro C., Gurrea A.B., Bingham S., Khaw K.T., Allen N., Key T., Trichopoulou A., Trichopoulos D., Orfanou N., Krogh V., Palli D., Tumino R., Panico S., Vineis P., Bueno-de-Mesquita H.B., Peeters P.H., Monninkhof E., Berglund G., Manjer J., Ferrari P., Slimani N., Kaaks R., Riboli E.

Cancer Epidemiol Biomarkers Prev; 2006; 15(12): 2398-2407

Abstract as provided by PubMed

We investigated several aspects of the role of physical activity in colon and rectal cancer etiology that remain unclear in the European Prospective Investigation into Nutrition and Cancer. This cohort of 413,044 men and women had 1,094 cases of colon and 599 cases of rectal cancer diagnosed during an average of 6.4 years of follow-up. We analyzed baseline data on occupational, household, and recreational activity to examine associations by type of activity, tumor subsite, body mass index (BMI), and energy intake. The multivariate hazard ratio for colon cancer was 0.78 [95% confidence interval (95% CI), 0.59-1.03] among the most active participants when compared with the inactive, with evidence of a dose-response effect (P(trend) = 0.04). For right-sided colon tumors, the risk was 0.65 (95% CI, 0.43-1.00) in the highest quartile of activity with evidence of a linear trend (P(trend) = 0.004). Active participants with a BMI under 25 had a risk of 0.63 (95% CI, 0.39-1.01) for colon cancer compared with the inactive. Finally, an interaction between BMI and activity (P(interaction) = 0.03) was observed for right-sided colon cancers; among moderately active and active participants with a BMI under 25, a risk of 0.38 (95% CI, 0.21-0.68) was found as compared with inactive participants with BMI >30. No comparable decreased risks were observed for rectal cancer for any type of physical activity for any subgroup analyses or interactions considered. We found that physical activity reduced colon cancer risk, specifically for right-sided tumors and for lean participants, but not rectal cancer

Fruit and vegetable intake and the risk of stomach and oesophagus adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST)

Gonzalez C.A., Pera G., Agudo A., Bueno-de-Mesquita H.B., Ceroti M., Boeing H., Schulz M., Del Giudice G., Plebani M., Carneiro F., Berrino F., Sacerdote C., Tumino R., Panico S., Berglund G., Siman H., Hallmans G., Stenling R., Martinez C., Dorronsoro M., Barricarte A., Navarro C., Quiros J.R., Allen N., Key T.J., Bingham S., Day N.E., Linseisen J., Nagel G., Overvad K., Jensen M.K., Olsen A., Tjonneland A., Buchner F.L., Peeters P.H., Numans M.E., Clavel-Chapelon F., Boutron-Ruault M.C., Roukos D., Trichopoulou A., Psaltopoulou T., Lund E., Casagrande C., Slimani N., Jenab M., Riboli E.

Int J Cancer; 2006; 118(10): 2559-2566

Abstract as provided by PubMed

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 be 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% CI 0.32-1.64 and 0.77; 95% CI 0.46-1.28 per 100 and 50 g increase, respectively). It seems that Hp 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

Meat intake and risk of stomach and esophageal adenocarcinoma within the European Prospective Investigation Into Cancer and Nutrition (EPIC)

Gonzalez Carlos A., Jakszyn Paula, Pera Guillem, Agudo Antonio, Bingham Sheila, Palli Domenico, Ferrari Pietro, Boeing Heiner, del Giudice Giuseppe, Plebani Mario, Carneiro Fatima, Nesi Gabriella, Berrino Franco, Sacerdote Carlotta, Tumino Rosario, Panico Salvatore, Berglund Goran, Siman Henrik, Nyren Olof, Hallmans Goran, Martinez Carmen, Dorronsoro Miren, Barricarte Aurelio, Navarro Carmen, Quiros Jose R., Allen Naomi, Key Timothy J., Day Nicholas E., Linseisen Jakob, Nagel Gabriele, Bergmann Manuela M., Overvad Kim, Jensen Majken K., Tjonneland Anne, Olsen Anja, Bueno-De-Mesquita H.Bas, Ocke Marga, Peeters Petra H.M., Numans Mattijs E., Clavel-Chapelon Francoise, Boutron-Ruault Marie Christine, Trichopoulou Antonia, Psaltopoulou Theodora, Roukos Dimitrios, Lund Eiliv, Hemon Bertrand, Kaaks Rudolf, Norat Teresa, Riboli Elio

J Natl Cancer Inst; 2006; 98(5): 345-354

Abstract as provided by PubMed

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 non-cardia 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 non-cardia 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 non-cardia 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 non-cardia cancer, especially in H. pylori antibody-positive subjects, but not with cardia gastric cancer

TP53 and KRAS2 mutations in plasma DNA of healthy subjects and subsequent cancer occurrence: a prospective study

Gormally E., Vineis P., Matullo G., Veglia F., Caboux E., Le Roux E., Peluso M., Garte S., Guarrera S., Munnia A., Airoldi L., Autrup H., Malaveille C., Dunning A., Overvad K., Tjonneland A., Lund E., Clavel-Chapelon F., Boeing H., Trichopoulou A., Palli D., Krogh V., Tumino R., Panico S., Bueno-de-Mesquita H.B., Peeters P.H., Pera G., Martinez C., Dorronsoro M., Barricarte A., Navarro C., Quiros J.R., Hallmans G., Day N.E., Key T.J., Saracci R., Kaaks R., Riboli E., Hainaut P.

Cancer Res; 2006; 66(13): 6871-6876

Abstract as provided by PubMed

In cancer patients, plasma often contains mutant DNA released by cancer cells. We have assessed the significance of plasma DNA mutations for subsequent cancer development in healthy subjects in a large longitudinal prospective study. The European Prospective Investigation into Cancer and Nutrition study was analyzed with a nested case-control design. Cases were nonsmokers or ex-smokers for >10 years and newly diagnosed with lung, bladder, or upper aerodigestive tract cancers or leukemia accrued after a median follow-up of 6.3 years. Controls were matched 2:1 for follow-up, age, sex, area of recruitment, and smoking status. KRAS2 mutations were detected by mutant-enriched PCR and sequencing (n = 1,098). TP53 mutations were detected by denaturing high-performance liquid chromatography, temporal temperature gradient electrophoresis, and sequencing (n = 550). KRAS2 or TP53 mutations were detected in 13 of 1,098 (1.2%) and 20 of 550 (3.6%) subjects, respectively, 16 of whom developed cancer on average after 18.3 months of follow-up. Among 137 subjects who developed bladder cancer, 5 had KRAS2 mutations [odds ratio (OR), 4.25; 95% confidence interval (95% CI), 1.27-14.15] and 7 had TP53 mutations (OR, 1.81; 95% CI, 0.66-4.97). There was a nonsignificant trend for association between TP53 mutations and bulky adducts in lymphocyte DNA (OR, 2.78; 95% CI, 0.64-12.17). This is the first report of TP53 or KRAS2 mutations in the plasma of healthy subjects in a prospective study, suggesting that KRAS2 mutation is detectable ahead of bladder cancer diagnosis. TP53 mutation may be associated with environmental exposures. These observations have implications for monitoring early steps of carcinogenesis

Endogenous versus exogenous exposure to N-nitroso compounds and gastric cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST) study

Jakszyn P., Bingham S., Pera G., Agudo A., Luben R., Welch A., Boeing H., Del Giudice G., Palli D., Saieva C., Krogh V., Sacerdote C., Tumino R., Panico S., Berglund G., Siman H., Hallmans G., Sanchez M.J., Larranaga N., Barricarte A., Chirlaque M.D., Quiros J.R., Key T.J., Allen N., Lund E., Carneiro F., Linseisen J., Nagel G., Overvad K., Tjonneland A., Olsen A., Bueno-de-Mesquita H.B., Ocke M.O., Peeters P.H., Numans M.E., Clavel-Chapelon F., Trichopoulou A., Fenger C., Stenling R., Ferrari P., Jenab M., Norat T., Riboli E., Gonzalez C.A.

Carcinogenesis; 2006; 27(7): 1497-1501

Abstract as provided by PubMed

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 mug on average compared with 93 mug 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 mug/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

Plasma and dietary carotenoid, retinol and tocopherol levels and the risk of gastric adenocarcinomas in the European prospective investigation into cancer and nutrition

Jenab M., Riboli E., Ferrari P., Friesen M., Sabate J., Norat T., Slimani N., Tjonneland A., Olsen A., Overvad K., Boutron-Ruault M.C., Clavel-Chapelon F., Boeing H., Schulz M., Linseisen J., Nagel G., Trichopoulou A., Naska A., Oikonomou E., Berrino F., Panico S., Palli D., Sacerdote C., Tumino R., Peeters P.H., Numans M.E., Bueno-de-Mesquita H.B., Buchner F.L., Lund E., Pera G., Chirlaque M.D., Sanchez M.J., Arriola L., Barricarte A., Quiros J.R., Johansson I., Johansson A., Berglund G., Bingham S., Khaw K.T., Allen N., Key T., Carneiro F., Save V., Giudice G.D., Plebani M., Kaaks R., Gonzalez C.A.

Br J Cancer; 2006; 95(3): 406-415

Abstract as provided by PubMed

Despite declining incidence rates, gastric cancer (GC) is a major cause of death worldwide. Its aetiology may involve dietary antioxidant micronutrients such as carotenoids and tocopherols. The objective of this study was to determine the association of plasma levels of seven common carotenoids, their total plasma concentration, retinol and alpha- and gamma-tocopherol, with the risk of gastric adenocarcinoma in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC), a large cohort involving 10 countries. A secondary objective was to determine the association of total sum of carotenoids, retinol and alpha-tocopherol on GCs by anatomical subsite (cardia/noncardia) and histological subtype (diffuse/intestinal). Analytes were measured by high-performance liquid chromatography in prediagnostic plasma from 244 GC cases and 645 controls matched by age, gender, study centre and date of blood donation. Conditional logistic regression models adjusted by body mass index, total energy intake, smoking and Helicobacter pylori infection status were used to estimate relative cancer risks. After an average 3.2 years of follow-up, a negative association with GC risk was observed in the highest vs the lowest quartiles of plasma beta-cryptoxanthin (odds ratio (OR)=0.53, 95% confidence intervals (CI)=0.30-0.94, P(trend)=0.006), zeaxanthin (OR=0.39, 95% CI=0.22-0.69, P(trend)=0.005), retinol (OR=0.55, 95% CI=0.33-0.93, P(trend)=0.005) and lipid-unadjusted alpha-tocopherol (OR=0.59, 95% CI=0.37-0.94, P(trend)=0.022). For all analytes, no heterogeneity of risk estimates or significant associations were observed by anatomical subsite. In the diffuse histological subtype, an inverse association was observed with the highest vs lowest quartile of lipid-unadjusted alpha-tocopherol (OR=0.26, 95% CI=0.11-0.65, P(trend)=0.003). These results show that higher plasma concentrations of some carotenoids, retinol and alpha-tocopherol are associated with reduced risk of GC.British Journal of Cancer (2006) 95, 406-415. doi:10.1038/sj.bjc.6603266 www.bjcancer.com Published online 11 July 2006

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