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2008

Dietary fat intake and risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition

Crowe F.L., Key T.J., Appleby P.N., Travis R.C., Overvad K., Jakobsen M.U., Johnsen N.F., Tjonneland A., Linseisen J., Rohrmann S., Boeing H., Pischon T., Trichopoulou A., Lagiou P., Trichopoulos D., Sacerdote C., Palli D., Tumino R., Krogh V., Bueno-de-Mesquita H.B., Kiemeney L.A., Chirlaque M.D., Ardanaz E., Sanchez M.J., Larranaga N., Gonzalez C.A., Quiros J.R., Manjer J., Wirfalt E., Stattin P., Hallmans G., Khaw K.T., Bingham S., Ferrari P., Slimani N., Jenab M., Riboli E.

Am J Clin Nutr; 2008; 87(5): 1405-1413

Abstract as provided by PubMed

BACKGROUND: Findings from early observational studies have suggested that the intake of dietary fat might be a contributing factor in the etiology of prostate cancer. However, the results from more recent prospective studies do not support this hypothesis, and the possible association between different food sources of fat and prostate cancer risk also remains unclear. OBJECTIVE: The objectives were to assess whether intakes of dietary fat, subtypes of fat, and fat from animal products were associated with prostate cancer risk. DESIGN: This was a multicenter prospective study of 142,520 men in the European Prospective Investigation into Cancer and Nutrition (EPIC). Dietary fat intake was estimated with the use of country-specific validated food questionnaires. The association between dietary fat and risk of prostate cancer was assessed by using Cox regression, stratified by recruitment center and adjusted for height, weight, smoking, education, marital status, and energy intake. RESULTS: After a median follow-up time of 8.7 y, prostate cancer was diagnosed in 2727 men. There was no significant association between dietary fat (total, saturated, monounsaturated, and polyunsaturated fat and the ratio of polyunsaturated to saturated fat) and risk of prostate cancer. The hazard ratio for prostate cancer for the highest versus the lowest quintile of total fat intake was 0.96 (95% CI: 0.84, 1.09; P for trend = 0.155). There were no significant associations between prostate cancer risk and fat from red meat, dairy products, and fish. CONCLUSION: The results from this large multicenter study suggest that there is no association between dietary fat and prostate cancer risk

Cytokine gene polymorphisms and the risk of adenocarcinoma of the stomach in the European prospective investigation into cancer and nutrition (EPIC-EURGAST)

Crusius J.B., Canzian F., Capella G., Pena A.S., Pera G., Sala N., Agudo A., Rico F., Del Giudice G., Palli D., Plebani M., Boeing H., Bueno-de-Mesquita H.B., Carneiro F., Pala V., Save V.E., 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., Binghan S., Caldas C., Linseisen J., Kaaks R., Overvad K., Tjonneland A., Buchner F.C., Peeters P.H., Numans M.E., Clavel-Chapelon F., Trichopoulou A., Lund E., Jenab M., Rinaldi S., Ferrari P., Riboli E., Gonzalez C.A.

Ann Oncol; 2008; 19(11): 1894-1902

Abstract as provided by PubMed

BACKGROUND: The relative contribution to gastric cancer (GC) risk of variants in genes that determine the inflammatory response remains mostly unknown and results from genotyping studies are inconsistent. PATIENTS AND METHODS: A nested case-control study within the prospective European Prospective Investigation into Cancer and Nutrition cohort was carried out, including 248 gastric adenocarcinomas and 770 matched controls. Twenty common polymorphisms at cytokine genes [interleukin (IL)1A, IL1B, IL1RN, IL4, IL4R, IL6, IL8, IL10, IL12A, IL12B, lymphotoxin alpha and tumor necrosis factor (TNF)] were analyzed. Antibodies against Helicobacter pylori (Hp) and CagA were measured. RESULTS: IL1RN 2R/2R genotype [odds ratio (OR) 2.43; 95% confidence interval (CI) 1.19-4.96] and allele IL1RN Ex5-35C were associated with an increased risk of Hp(+) non-cardia GC. IL8 -251AA genotype was associated with a decreased risk of Hp(+) non-cardia GC (OR 0.51; 95% CI 0.32-0.81), mainly of the intestinal type. These associations were not modified by CagA status. Carriers of IL1B -580C and TNF -487A alleles did not associate with an increased risk. A moderately increased risk of Hp(+) non-cardia GC for IL4R -29429T variant was observed (OR 1.74; 95% CI 1.15-2.63). CONCLUSION: This prospective study confirms the association of IL1RN polymorphisms with the risk of non-cardia GC and indicates that IL8 -251T>A may modify the risk for GC

Polymorphisms of genes coding for ghrelin and its receptor in relation to anthropometry, circulating levels of IGF-I and IGFBP-3, and breast cancer risk: a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC)

Dossus L., McKay J.D., Canzian F., Wilkening S., Rinaldi S., Biessy C., Olsen A., Tjonneland A., Jakobsen M.U., Overvad K., Clavel-Chapelon F., Boutron-Ruault M.C., Fournier A., Linseisen J., Lukanova A., Boeing H., Fisher E., Trichopoulou A., Georgila C., Trichopoulos D., Palli D., Krogh V., Tumino R., Vineis P., Quiros J.R., Sala N., Martinez-Garcia C., Dorronsoro M., Chirlaque M.D., Barricarte A., van Duijnhoven F.J., Bueno-de-Mesquita H.B., Van Gils C.H., Peeters P.H., Hallmans G., Lenner P., Bingham S., Khaw K.T., Key T.J., Travis R.C., Ferrari P., Jenab M., Riboli E., Kaaks R.

Carcinogenesis; 2008; 29(7): 1360-1366

Abstract as provided by PubMed

Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor, has two major functions: the stimulation of the growth hormone production and the stimulation of food intake. Accumulating evidence also suggests a role of ghrelin in cancer development. We conducted a case-control study on 1359 breast cancer cases and 2389 matched controls, nested within the European Prospective Investigation into Cancer and Nutrition, to examine the association of common genetic variants in the genes coding for ghrelin (GHRL) and its receptor (GHSR) with anthropometric measures, circulating insulin growth factor I (IGF-I) and insulin-like growth factor-binding protein 3 and breast cancer risk. Pair-wise tagging was used to select the 15 polymorphisms that represent the majority of common genetic variants across the GHRL and GHSR genes. A significant increase in breast cancer risk was observed in carriers of the GHRL rs171407-G allele (odds ratio: 1.2; 95% confidence interval: 1.0-1.4; P = 0.02). The GHRL single-nucleotide polymorphism rs375577 was associated with a 5% increase in IGF-I levels (P = 0.01). A number of GHRL and GHSR polymorphisms were associated with body mass index (BMI) and height (P between <0.01 and 0.04). The false-positive report probability (FPRP) approach suggests that these results are noteworthy (FPRP < 0.20). The results presented here add to a growing body of evidence that GHRL variations are associated with BMI. Furthermore, we have observed evidence for association of GHRL polymorphisms with circulating IGF-I levels and with breast cancer risk. These associations, however, might also be due to chance findings and further large studies are needed to confirm our results

The evaluation of the diet/disease relation in the EPIC study: considerations for the calibration and the disease models

Ferrari P., Day N.E., Boshuizen H.C., Roddam A., Hoffmann K., Thiebaut A., Pera G., Overvad K., Lund E., Trichopoulou A., Tumino R., Gullberg B., Norat T., Slimani N., Kaaks R., Riboli E.

Int J Epidemiol; 2008; 37(2): 368-378

Abstract as provided by PubMed

BACKGROUND: International multicentre studies on diet and cancer are relatively new in epidemiological research. They offer a series of challenging methodological issues for the evaluation of the association between dietary exposure and disease outcomes, which can both be quite heterogeneous across different geographical regions. This requires considerable work to standardize dietary measurements at the food and the nutrient levels. METHODS: Within the European Prospective Investigation into Cancer and Nutrition (EPIC), a calibration study was set up to express individual dietary intakes according to the same reference scale. A linear regression calibration model was used to correct the association between diet and disease for measurement errors in dietary exposures. In the present work, we describe an approach for analysing the EPIC data, using as an example the evaluation of the association between fish intake and colorectal cancer incidence. RESULTS: Sex- and country-specific attenuation factors ranged from 0.083 to 0.784, with values overall higher for men compared with women. Hazard ratio estimates of colorectal cancer for a 10 g/day increase in fish intake were 0.97 [95% confidence interval (CI): 0.95-0.99] and 0.93 (0.88-0.98), before and after calibration, respectively. CONCLUSIONS: In a multicentre study, the diet/disease association can be evaluated by exploiting the whole variability of intake over the entire study. Calibration may reduce between-centre heterogeneity in the diet-disease relationship caused by differential impact of measurement errors across cohorts

A Bayesian multilevel model for estimating the diet/disease relationship in a multicenter study with exposures measured with error: The EPIC study

Ferrari P., Carroll R.J., Gustafson P., Riboli E.

Stat Med; 2008; 27(29): 6037-6054

Abstract as provided by PubMed

In a multicenter study, the overall relationship between diet and cancer risk can be broken down into: (a) within-center relationships, which reflect the relationships at the individual level in each of the centers, and (b) a between-center relationship, which captures the association between exposure and disease risk at the aggregate level. In this work, we propose the use of a Bayesian multilevel model that takes into account the within- and between-center levels of evidence, using information at the individual and aggregate level. Correction for measurement error is performed in order to correct for systematic between-center measurement error in dietary exposure, and for attenuation biases in relative risk estimates within centers. The estimation of the parameters is carried out in a Bayesian framework using Gibbs sampling. The model entails a measurement, an exposure, and a disease component. Within the European Prospective Investigation into Cancer and Nutrition (EPIC) the association between lipid intake, assessed through dietary questionnaire and 24-hour dietary recall, and breast cancer incidence was evaluated. This analysis involved 21 534 women and 334 incident breast cancer cases from the EPIC calibration study. In this study, total energy intake was positively associated with breast cancer incidence at the aggregate level, whereas no effect was observed for fat. At the individual level, height was positively related to breast cancer incidence, whereas a weaker association was observed for fat. The use of multilevel models, which constitute a very powerful approach to estimating individual vs aggregate levels of evidence should be considered in multicenter studies. Copyright (c) 2008 John Wiley & Sons, Ltd

CDH1 gene polymorphisms, smoking, Helicobacter pylori infection and the risk of gastric cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC-EURGAST)

Jenab M., McKay J.D., Ferrari P., Biessy C., Laing S., Capella Munar G.M., Sala N., Pena S., Crusius J.B., Overvad K., Jensen M.K., Olsen A., Tjonneland A., Clavel-Chapelon F., Boutron-Ruault M.C., Kaaks R., Linseisen J., Boeing H., Bergmann M.M., Trichopoulou A., Georgila C., Psaltopoulou T., Mattiello A., Vineis P., Pala V., Palli D., Tumino R., Numans M.E., Peeters P.H., Bueno-de-Mesquita H.B., Lund E., Ardanaz E., Sanchez M.J., Dorronsoro M., Navarro Sanchez C., Quiros J.R., Hallmans G., Stenling R., Manjer J., Regner S., Key T., Bingham S., Khaw K.T., Slimani N., Rinaldi S., Boffetta P., Carneiro F., Riboli E., Gonzalez C.

Eur J Cancer; 2008; 44(6): 774-780

Abstract as provided by PubMed

Despite declining incidence rates, gastric cancer (GC) is a major cause of death worldwide. E-Cadherin is an adhesion molecule that is thought to be involved in GC. Germline mutations in the E-Cadherin gene (CDH1) have been identified in hereditary diffuse GC. Also, a promoter polymorphism at position -160 C/A has been suggested to lead to transcriptional down regulation and has been shown to affect GC risk in some studies. However, very little information exists on the GC risk association of other CDH1 polymorphisms and it is unclear whether any associations may be different by GC anatomical sites or histological types. Thus, a case-control study (cases=245/controls=950) nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort was conducted to assess the GC risk association of eight CDH1 gene polymorphisms. None of the CDH1 polymorphisms or haplotypes analysed were associated with GC risk and no differences of effect were observed by Helicobacter pylori infection status. However, three CDH1 polymorphisms in the same haplotype block, including the CDH1-160C/A, interacted with smoking to increase GC risk in smokers but not in never smokers. These findings should be confirmed in larger independent studies

Circulating concentrations of folate and vitamin B12 in relation to prostate cancer risk: results from the European prospective investigation into cancer and nutrition study

Johansson M., Appleby P.N., Allen N.E., Travis R.C., Roddam A.W., Egevad L., Jenab M., Rinaldi S., Kiemeney L.A., Bueno-de-Mesquita H.B., Vollset S.E., Ueland P.M., Sanchez M.J., Quiros J.R., Gonzalez C.A., Larranaga N., Chirlaque M.D., Ardanaz E., Sieri S., Palli D., Vineis P., Tumino R., Linseisen J., Kaaks R., Boeing H., Pischon T., Psaltopoulou T., Trichopoulou A., Trichopoulos D., Khaw K.T., Bingham S., Hallmans G., Riboli E., Stattin P., Key T.J.

Cancer Epidemiol Biomarkers Prev; 2008; 17(2): 279-285

Abstract as provided by PubMed

BACKGROUND: Determinants of one-carbon metabolism, such as folate and vitamin B(12), have been implicated in cancer development. Previous studies have not provided conclusive evidence for the importance of circulating concentrations of folate and vitamin B(12) in prostate cancer etiology. The aim of the present study was to investigate the relationship between prostate cancer risk and circulating concentrations of folate and vitamin B(12) in a large prospective cohort. METHODS: We analyzed circulating concentrations of folate and vitamin B(12) in 869 cases and 1,174 controls, individually matched on center, age, and date of recruitment, nested within the European Prospective Investigation into Cancer and Nutrition cohort. Relative risks (RR) for prostate cancer were estimated using conditional logistic regression models. RESULTS: Overall, no significant associations were observed for circulating concentrations of folate (P(trend) = 0.62) or vitamin B(12) (P(trend) = 0.21) with prostate cancer risk. RRs for a doubling in folate and vitamin B(12) concentrations were 1.03 [95% confidence interval (95% CI), 0.92-1.16] and 1.12 (95% CI, 0.94-1.35), respectively. In the subgroup of cases diagnosed with advanced stage prostate cancer, elevated concentrations of vitamin B(12) were associated with increased risk (RR for a doubling in concentration, 1.69; 95% CI, 1.05-2.72, P(trend) = 0.03). No other subgroup analyses resulted in a statistically significant association. CONCLUSION: This study does not provide strong support for an association between prostate cancer risk and circulating concentrations of folate or vitamin B(12). Elevated concentrations of vitamin B(12) may be associated with an increased risk for advanced stage prostate cancer, but this association requires examination in other large prospective studies. (Cancer Epidemiol Biomarkers Prev 2007;17(2):279-85)

Diabetes and the risk of non-Hodgkin's lymphoma and multiple myeloma in the European Prospective Investigation into Cancer and Nutrition

Khan A.E., Gallo V., Linseisen J., Kaaks R., Rohrmann S., Raaschou-Nielsen O., Tjonneland A., Johnsen H.E., Overvad K., Bergmann M.M., Boeing H., Benetou V., Psaltopoulou T., Trichopoulou A., Masala G., Mattiello A., Grioni S., Tumino R., Vermeulen R.C., Peeters P.H., Bueno-de-Mesquita H.B., Ros M.M., Lund E., Ardanaz E., Chirlaque M.D., Jakszyn P., Larranaga N., Losada A., Becker N., Nieters 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.

Haematologica; 2008; 93(6): 842-850

Abstract as provided by PubMed

BACKGROUND: Non-Hodgkin's lymphomas are a heterogeneous group of neoplasms arising from the lymphopoietic system including a wide range of subtypes of either B-cell or T-cell lymphomas. The few established risk factors for the development of these neoplasms include viral infections and immunological abnormalities, but their etiology remains largely unknown. Evidence suggests that certain medical conditions may be linked, through immunosuppression, to the risk of non-Hodgkin's lymphoma. Multiple myeloma is a neoplasm of plasma cells that accounts for approximately 15% of lymphopoietic cancers. Increases in the incidence of non-Hodgkin's lymphoma and multiple myeloma in the past implicate environmental factors as potential causal agents. DESIGN AND METHODS: In the European Prospective Investigation into Cancer and Nutrition (EPIC), 1,213 histologically confirmed incident cases of non-Hodgkin's lymphoma and multiple myeloma (594 men; 619 women) were identified during a follow-up of 8.5 years. Cox proportional hazard models were used to explore the association between self-reported diabetes, diagnosed after 30 years of age, and the risk of non-Hodgkin's lymphoma overall and multiple myeloma and various lymphoma subtypes. RESULTS: We found no association between a personal history of diabetes and the risk of non-Hodgkin's lymphoma overall in men (HR: 1.28, 95% CI: 0.89-1.84), in women (HR: 0.71, 95% CI: 0.41- 1.24), or in men and women combined (HR: 1.09, 95% CI: 0.80-1.47). Among the B-non-Hodgkin's lymphoma subtypes, we observed a statistically significant increased risk of B-cell chronic lymphocytic leukemia (HR: 2.0, 95% CI: 1.04-3.86) in men, but not in women (HR: 1.07, 95% CI: 0.33-3.43). CONCLUSIONS: This prospective study did not provide evidence for a role of self-reported diabetes in the etiology of non-Hodgkin's lymphoma overall or multiple myeloma. We found an increased risk of B-cell chronic lymphocytic leukemia among men with diabetes, but not among women. We hypothesize that diabetes may not play a causal role in the etiology of B-cell chronic lymphocytic leukemia, though the underlying pathogenic mechanisms of both disorders may include shared genetic, host and/or environmental susceptibility factors

Smoking and lymphoma risk in the European prospective investigation into cancer and nutrition

Nieters A., Rohrmann S., Becker N., Linseisen J., Ruediger T., Overvad K., Tjonneland A., Olsen A., Allen N.E., Travis R.C., Bingham S., Khaw K.T., Ardanaz E., Redondo M.L., Basterrechea M., Martinez C., Tormo M.J., Rosso S., Tagliabue G., Masala G., Mattiello A., Tumino R., Boeing H., Bergmann M., Kaaks R., Trichopoulou A., Trichopoulos D., Peeters P.H., Bueno-de-Mesquita B., Boffetta P., Brennan P., Ferrari P., Neasham D., Lund E., Berglund G., Manjer J., Hallmans G., Johansson I., Vineis P., Riboli E.

Am J Epidemiol; 2008; 167(9): 1081-1089

Abstract as provided by PubMed

Lymphomas are one of the few cancers that have been increasing in incidence over the past decades. So far, only a few established risk factors have been identified, including immunosuppression and viral infections. Recent evidence suggests etiologic heterogeneity of different lymphoma subtypes. Smoking may affect risk differently, depending on the lymphoma entity. The European Prospective Investigation into Cancer and Nutrition was used to study the role of smoking in the etiology of lymphomas and individual subtypes within a prospective study. Information on baseline and lifetime tobacco smoking by 478,590 participants was collected between 1992 and 2000. Cox proportional hazards regression was used to calculate multivariate-adjusted hazard ratios and 95% confidence intervals. During 3,567,410 person-years of follow-up, 1,371 lymphoma cases (1,304 non-Hodgkin's lymphomas and 67 Hodgkin's lymphomas) were identified. Relative risk for smokers at recruitment was more than twofold higher for Hodgkin's lymphoma (hazard ratio = 2.14, 95% confidence interval: 1.18, 3.87) but was not elevated for non-Hodgkin's lymphoma (hazard ratio = 1.06, 95% confidence interval: 0.94, 1.19) and individual B-cell non-Hodgkin's lymphoma subtypes. In this prospective study, smoking appeared to increase Hodgkin's lymphoma risk consistently in both genders, whereas B-cell non-Hodgkin's lymphoma risk was not associated. Future analysis should involve viral biomarkers and genetic susceptibility markers to elucidate potential mechanisms of smoking-induced carcinogenesis, particularly for Hodgkin's lymphoma

Intake of vegetables, legumes, and fruit, and risk for all-cause, cardiovascular, and cancer mortality in a European diabetic population

Nothlings U., Schulze M.B., Weikert C., Boeing H., van der Schouw Y.T., Bamia C., Benetou V., Lagiou P., Krogh V., Beulens J.W., Peeters P.H., Halkjaer J., Tjonneland A., Tumino R., Panico S., Masala G., Clavel-Chapelon F., de Lauzon B., Boutron-Ruault M.C., Vercambre M.N., Kaaks R., Linseisen J., Overvad K., Arriola L., Ardanaz E., Gonzalez C.A., Tormo M.J., Bingham S., Khaw K.T., Key T.J., Vineis P., Riboli E., Ferrari P., Boffetta P., Bueno-de-Mesquita H.B., van der A D.L., Berglund G., Wirfalt E., Hallmans G., Johansson I., Lund E., Trichopoulo A.

J Nutr; 2008; 138(4): 775-781

Abstract as provided by PubMed

We examined the associations of intake of vegetables, legumes and fruit with all-cause and cause-specific mortality in a population with prevalent diabetes in Europe. A cohort of 10,449 participants with self-reported diabetes within the European Prospective Investigation into Cancer and Nutrition study was followed for a mean of 9 y. Intakes of vegetables, legumes, and fruit were assessed at baseline between 1992 and 2000 using validated country-specific questionnaires. A total of 1346 deaths occurred. Multivariate relative risks (RR) for all-cause mortality were estimated in Cox regression models and RR for cause-specific mortality were derived in a competing risk model. An increment in intake of total vegetables, legumes, and fruit of 80 g/d was associated with a RR of death from all causes of 0.94 [95% CI 0.90-0.98]. Analyzed separately, vegetables and legumes were associated with a significantly reduced risk, whereas nonsignificant inverse associations for fruit intake were observed. Cardiovascular disease (CVD) mortality and mortality due to non-CVD/non-cancer causes were significantly inversely associated with intake of total vegetables, legumes, and fruit (RR 0.88 [95% CI 0.81-0.95] and 0.90 [0.82-0.99], respectively) but not cancer mortality (1.08 [0.99-1.17]). Intake of vegetables, legumes, and fruit was associated with reduced risks of all-cause and CVD mortality in a diabetic population. The findings support the current state of evidence from general population studies that the protective potential of vegetable and fruit intake is larger for CVD than for cancer and suggest that diabetes patients may benefit from a diet high in vegetables and fruits

A food pattern that is predictive of flavonol intake and risk of pancreatic cancer

Nothlings U., Murphy S.P., Wilkens L.R., Boeing H., Schulze M.B., Bueno-de-Mesquita H.B., Michaud D.S., Roddam A., Rohrmann S., Tjonneland A., Clavel-Chapelon F., Trichopoulou A., Sieri S., Rodriguez L., Ye W., Jenab M., Kolonel L.N.

Am J Clin Nutr; 2008; 88(6): 1653-1662

Abstract as provided by PubMed

BACKGROUND: In the Multiethnic Cohort (MEC) study, we showed inverse associations between flavonols and pancreatic cancer risk. OBJECTIVE: We aimed to define a food pattern associated with intakes of quercetin, kaempferol, and myricetin; to examine the association of that pattern with pancreatic cancer risk; and to investigate the associations in an independent study. DESIGN: Reduced rank regression was applied to dietary data for 183 513 participants in the MEC. A food group pattern was extracted and simplified and applied to dietary data of 424 978 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Dietary intake in both studies was assessed by using specially developed questionnaires. Multivariate Cox proportional hazards models were used to estimate relative risks for pancreatic cancer in the MEC (610 cases) and the EPIC (517 cases) studies. RESULTS: The food group pattern consisted mainly of tea, fruit, cabbage, and wine. In the MEC, inverse associations with pancreatic cancer in smokers were observed for the food group pattern [relative risk: 0.59 (95% CI: 0.31, 1.12) when extreme quintiles were compared; P for trend = 0.03]. In the EPIC study, the simplified pattern was not associated with pancreatic cancer risk (P for trend = 0.78). CONCLUSIONS: A food pattern associated with the intake of quercetin, kaempferol, and myricetin was associated with lower pancreatic cancer risk in smokers in a US-based population. However, failure to replicate the associations in an independent study weakens the conclusions and raises questions about the utility of food patterns for flavonols across populations

Bulky DNA adducts, 4-aminobiphenyl-haemoglobin adducts and diet in the European Prospective Investigation into Cancer and Nutrition (EPIC) prospective study

Peluso M., Airoldi L., Munnia A., Colombi A., Veglia F., Autrup H., Dunning A., Garte S., Gormally E., Malaveille C., Matullo G., 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 B.H., Peeters P.H., Kumle M., Agudo A., Martinez C., Dorronsoro M., Barricarte A., Tormo M.J., Quiros J.R., Berglund G., Jarvholm B., Day N.E., Key T.J., Saracci R., Kaaks R., Riboli E., Bingham S., Vineis P.

Br J Nutr; 2008; 100(3): 489-495

Abstract as provided by PubMed

In contrast to some extensively examined food mutagens, for example, aflatoxins, N-nitrosamines and heterocyclic amines, some other food contaminants, in particular polycyclic aromatic hydrocarbons (PAH) and other aromatic compounds, have received less attention. Therefore, exploring the relationships between dietary habits and the levels of biomarkers related to exposure to aromatic compounds is highly relevant. We have investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort the association between dietary items (food groups and nutrients) and aromatic DNA adducts and 4-aminobiphenyl-Hb adducts. Both types of adducts are biomarkers of carcinogen exposure and possibly of cancer risk, and were measured, respectively, in leucocytes and erythrocytes of 1086 (DNA adducts) and 190 (Hb adducts) non-smokers. An inverse, statistically significant, association has been found between DNA adduct levels and dietary fibre intake (P = 0.02), vitamin E (P = 0.04) and alcohol (P = 0.03) but not with other nutrients or food groups. Also, an inverse association between fibre and fruit intake, and BMI and 4-aminobiphenyl-Hb adducts (P = 0.03, 0.04, and 0.03 respectively) was observed. After multivariate regression analysis these inverse correlations remained statistically significant, except for the correlation adducts v. fruit intake. The present study suggests that fibre intake in the usual range can modify the level of DNA or Hb aromatic adducts, but such role seems to be quantitatively modest. Fibres could reduce the formation of DNA adducts in different manners, by diluting potential food mutagens and carcinogens in the gastrointestinal tract, by speeding their transit through the colon and by binding carcinogenic substances

General and abdominal adiposity and risk of death in Europe

Pischon T., Boeing H., Hoffmann K., Bergmann M., Schulze M.B., Overvad K., van der Schouw Y.T., Spencer E., Moons K.G., Tjonneland A., Halkjaer J., Jensen M.K., Stegger J., Clavel-Chapelon F., Boutron-Ruault M.C., Chajes V., Linseisen J., Kaaks R., Trichopoulou A., Trichopoulos D., Bamia C., Sieri S., Palli D., Tumino R., Vineis P., Panico S., Peeters P.H., May A.M., Bueno-de-Mesquita H.B., van Duijnhoven F.J., Hallmans G., Weinehall L., Manjer J., Hedblad B., Lund E., Agudo A., Arriola L., Barricarte A., Navarro C., Martinez C., Quiros J.R., Key T., Bingham S., Khaw K.T., Boffetta P., Jenab M., Ferrari P., Riboli E.

N Engl J Med; 2008; 359(20): 2105-2120

Abstract as provided by PubMed

BACKGROUND: Previous studies have relied predominantly on the body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) to assess the association of adiposity with the risk of death, but few have examined whether the distribution of body fat contributes to the prediction of death. METHODS: We examined the association of BMI, waist circumference, and waist-to-hip ratio with the risk of death among 359,387 participants from nine countries in the European Prospective Investigation into Cancer and Nutrition (EPIC). We used a Cox regression analysis, with age as the time variable, and stratified the models according to study center and age at recruitment, with further adjustment for educational level, smoking status, alcohol consumption, physical activity, and height. RESULTS: During a mean follow-up of 9.7 years, 14,723 participants died. The lowest risks of death related to BMI were observed at a BMI of 25.3 for men and 24.3 for women. After adjustment for BMI, waist circumference and waist-to-hip ratio were strongly associated with the risk of death. Relative risks among men and women in the highest quintile of waist circumference were 2.05 (95% confidence interval [CI], 1.80 to 2.33) and 1.78 (95% CI, 1.56 to 2.04), respectively, and in the highest quintile of waist-to-hip ratio, the relative risks were 1.68 (95% CI, 1.53 to 1.84) and 1.51 (95% CI, 1.37 to 1.66), respectively. BMI remained significantly associated with the risk of death in models that included waist circumference or waist-to-hip ratio (P<0.001). CONCLUSIONS: These data suggest that both general adiposity and abdominal adiposity are associated with the risk of death and support the use of waist circumference or waist-to-hip ratio in addition to BMI in assessing the risk of death

Body size and risk of prostate cancer in the European prospective investigation into cancer and nutrition

Pischon T., Boeing H., Weikert S., Allen N., Key T., Johnsen N.F., Tjonneland A., Severinsen M.T., Overvad K., Rohrmann S., Kaaks R., Trichopoulou A., Zoi G., Trichopoulos D., Pala V., Palli D., Tumino R., Sacerdote C., Bueno-de-Mesquita H.B., May A., Manjer J., Wallstrom P., Stattin P., Hallmans G., Buckland G., Larranaga N., Chirlaque M.D., Martinez C., Redondo Cornejo M.L., Ardanaz E., Bingham S., Khaw K.T., Rinaldi S., Slimani N., Jenab M., Riboli E.

Cancer Epidemiol Biomarkers Prev; 2008; 17(11): 3252-3261

Abstract as provided by PubMed

BACKGROUND: Body size has been hypothesized to influence the risk of prostate cancer; however, most epidemiologic studies have relied on body mass index (BMI) to assess adiposity, whereas only a few studies have examined whether body fat distribution predicts prostate cancer. METHODS: We examined the association of height, BMI, waist and hip circumference, and waist-hip ratio with prostate cancer risk among 129,502 men without cancer at baseline from 8 countries of the European Prospective Investigation into Cancer and Nutrition (EPIC), using Cox regression, with age as time metric, stratifying by study center and age at recruitment, and adjusting for education, smoking status, alcohol consumption, and physical activity. RESULTS: During a mean follow-up of 8.5 years, 2,446 men developed prostate cancer. Waist circumference and waist-hip ratio were positively associated with risk of advanced disease. The relative risk of advanced prostate cancer was 1.06 (95% confidence interval, 1.01-1.1) per 5-cm-higher waist circumference and 1.21 (95% confidence interval, 1.04-1.39) per 0.1-unit-higher waist-hip ratio. When stratified by BMI, waist circumference and waist-hip ratio were positively related to risk of total, advanced, and high-grade prostate cancer among men with lower but not among those with higher BMI (Pinteraction for waist with BMI, 0.25, 0.02, and 0.05, respectively; Pinteraction for waist-hip ratio with BMI, 0.27, 0.22, and 0.14; respectively). CONCLUSIONS: These data suggest that abdominal adiposity may be associated with an increased risk of advanced prostate cancer. This association may be stronger among individuals with lower BMI; however, this finding needs confirmation in future studies

Glycosylated hemoglobin and risk of colorectal cancer in men and women, the European prospective investigation into cancer and nutrition

Rinaldi S., Rohrmann S., Jenab M., Biessy C., Sieri S., Palli D., Tumino R., Mattiello A., Vineis P., Nieters A., Linseisen J., Pischon T., Boeing H., Hallmans G., Palmqvist R., Manjer J., Wirfalt E., Crowe F.L., Khaw K.T., Bingham S., Tjonneland A., Olsen A., Overvad K., Lund E., Skeie G., Clavel-Chapelon F., Boutron-Ruault M.C., de Lauzon-Guillain B., Ardanaz E., Jakszyn P., Ramon Quiros J., Chirlaque M.D., Sanchez M.J., Dorronsoro M., Trichopoulou A., Lagiou P., Trichopoulos D., Bueno-de-Mesquita H.B., van Duijnhoven F.J., Peeters P.H., Slimani N., Ferrari P., Byrnes G.B., Riboli E., Kaaks R.

Cancer Epidemiol Biomarkers Prev; 2008; 17(11): 3108-3115

Abstract as provided by PubMed

Although large-scale prospective cohort studies have related hyperglycemia to increased risk of cancer overall, studies specifically on colorectal cancer have been generally small. We investigated the association between prediagnostic levels of glycosylated hemoglobin (HbA1c), a marker for average glucose level in blood, and colorectal cancer risk in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition cohort. One thousand and twenty-six incident colorectal cancer cases (561 men and 465 women) and 1,026 matched controls were eligible for the study. Multivariate conditional logistic regression was used to estimate odds ratios (ORS) adjusted for possible confounders. Increasing HbA1c percentages were statistically significantly associated with a mild increase in colorectal cancer risk in the whole population [OR, 1.10; 95% confidence interval (CI), 1.01,1.19 for a 10% increase in HbA1c]. In women, increasing HbA1c percentages were associated with a statistically significant increase in colorectal cancer risk (OR, 1.16; 95% CI, 1.01, 1.32 for a 10% increase in HbA1c) and with a borderline statistically significant increase in rectum cancer (OR, 1.22; 95% CI, 0.99,1.50 for a 10% increase in HbA1c). No significant association with cancer risk was observed in men. The results of the current study suggest a mild implication of hyperglycemia in colorectal cancer, which seems more important in women than in men, and more for cancer of the rectum than of the colon

Alcohol consumption and the risk for prostate cancer in the European prospective investigation into cancer and nutrition

Rohrmann S., Linseisen J., Key T.J., Jensen M.K., Overvad K., Johnsen N.F., Tjonneland A., Kaaks R., Bergmann M.M., Weikert C., Naska A., Trichopoulou A., Trichopoulos D., Pala V., Sacerdote C., Palli D., Tumino R., Bueno-de-Mesquita H.B., Vrieling A., Gonzalez C.A., Larranaga N., Navarro C., Barricarte A., Quiros J.R., Martinez-Garcia C., Hallmans G., Stattin P., Manjer J., Wirfalt E., Bingham S., Khaw K.T., Egevad L., Ferrari P., Jenab M., Riboli E.

Cancer Epidemiol Biomarkers Prev; 2008; 17(5): 1282-1287

Abstract as provided by PubMed

Alcohol is a risk factor for several types of cancer. However, the results for prostate cancer have been inconsistent, with most studies showing no association. Within the European Prospective Investigation into Cancer and Nutrition, detailed information were collected from 142,607 male participants on the intake of alcoholic beverages at recruitment (for 100% of the cohort) and over lifetime (for 76% of the cohort) between 1992 and 2000. During a median follow-up of 8.7 years, 2,655 prostate cancer cases were observed. Multivariate Cox proportional hazard models were used to examine the association of alcohol consumption at recruitment and average lifetime alcohol consumption with prostate cancer adjusted for age, center, smoking, height, weight, physical activity, and nonalcohol energy intake. Overall, neither alcohol consumption at baseline nor average lifetime alcohol consumption was associated with the risk for prostate cancer in this cohort of men. Men who consumed >/=60 g alcohol per day had a relative risk of 0.88 [95% confidence interval (95% CI) 0.72-1.08] compared with men with an intake of 0.1-4.9 g/d; the respective relative risk for average lifetime intake was 1.09 (95% CI, 0.86-1.39). For advanced prostate cancer (n = 537), the relative risks for >/=60 and 0.1-4.9 g alcohol per day at baseline were 0.98 (95% CI, 0.66-1.44) and 1.28 (95% CI, 0.79-2-07), respectively, for average lifetime intake. No statistically significant association was observed for alcohol intake from specific alcoholic beverages. Our results indicate no association between the consumption of alcohol and prostate cancer in this cohort of European men. (Cancer Epidemiol Biomarkers Prev 2008;17(5):1282-7)

Dietary fat and breast cancer risk in the European Prospective Investigation into Cancer and Nutrition

Sieri S., Krogh V., Ferrari P., Berrino F., Pala V., Thiebaut A.C., Tjonneland A., Olsen A., Overvad K., Jakobsen M.U., Clavel-Chapelon F., Chajes V., Boutron-Ruault M.C., Kaaks R., Linseisen J., Boeing H., Nothlings U., Trichopoulou A., Naska A., Lagiou P., Panico S., Palli D., Vineis P., Tumino R., Lund E., Kumle M., Skeie G., Gonzalez C.A., Ardanaz E., Amiano P., Tormo M.J., Martinez-Garcia C., Quiros J.R., Berglund G., Gullberg B., Hallmans G., Lenner P., Bueno-de-Mesquita H.B., van Duijnhoven F.J., Peeters P.H., Van Gils C.H., Key T.J., Crowe F.L., Bingham S., Khaw K.T., Rinaldi S., Slimani N., Jenab M., Norat T., Riboli E.

Am J Clin Nutr; 2008; 88(5): 1304-1312

Abstract as provided by PubMed

BACKGROUND: Epidemiologic studies have produced conflicting results with respect to an association of dietary fat with breast cancer. OBJECTIVE: We aimed to investigate the association between fat consumption and breast cancer. DESIGN: We prospectively investigated fat consumption in a large (n = 319,826), geographically and culturally heterogeneous cohort of European women enrolled in the European Prospective Investigation into Cancer and Nutrition who completed a dietary questionnaire. After a mean of 8.8 y of follow-up, 7119 women developed breast cancer. Cox proportional hazard models, stratified by age and center and adjusted for energy intake and confounders, were used to estimate hazard ratios (HRs) for breast cancer. RESULTS: An association between high saturated fat intake and greater breast cancer risk was found [HR = 1.13 (95% CI: 1.00, 1.27; P for trend = 0.038) for the highest quintile of saturated fat intake compared with the lowest quintile: 1.02 (1.00, 1.04) for a 20% increase in saturated fat consumption (continuous variable)]. No significant association of breast cancer with total, monounsaturated, or polyunsaturated fat was found, although trends were for a direct association of risk with monounsaturated fat and an inverse association with polyunsaturated fat. In menopausal women, the positive association with saturated fat was confined to nonusers of hormone therapy at baseline [1.21 (0.99, 1.48) for the highest quintile compared with the lowest quintile; P for trend = 0.044; and 1.03 (1.00, 1.07) for a 20% increase in saturated fat as a continuous variable]. CONCLUSIONS: Evidence indicates a weak positive association between saturated fat intake and breast cancer risk. This association was more pronounced for postmenopausal women who never used hormone therapy

Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study

Vesper H.W., Slimani N., Hallmans G., Tjonneland A., Agudo A., Benetou V., Bingham S., Boeing H., Boutron-Ruault M.C., Bueno-de-Mesquita H.B., Chirlaque D., Clavel-Chapelon F., Crowe F., Drogan D., Ferrari P., Johansson I., Kaaks R., Linseisen J., Lund E., Manjer J., Mattiello A., Palli D., Peeters P.H., Rinaldi S., Skeie G., Trichopoulou A., Vineis P., Wirfalt E., Overvad K., Stromberg U.

J Agric Food Chem; 2008; 56(15): 6046-6053

Abstract as provided by PubMed

Acrylamide exposure was investigated in subgroups of the EPIC study population (510 subjects from 9 European countries, randomly selected and stratified by age, gender, and smoking status) using hemoglobin adducts of acrylamide (HbAA) and its primary metabolite glycidamide (HbGA). Blood samples were analyzed for HbAA and HbGA by HPLC/MS/MS. Statistical models for HbAA and HbGA were developed including body mass index (BMI), educational level, and physical activity. A large variability in acrylamide exposure and metabolism between individuals and country groups was observed with HbAA and HbGA values ranging between 15-623 and 8-377 pmol/g of Hb, respectively. Both adducts differed significantly by country, sex, and smoking status. HbGA values were significantly lower in high alcohol consumers than in moderate consumers. With increasing BMI, HbGA in nonsmokers and HbAA in smokers decreased significantly. In the assessment of potential health effects related to acrylamide exposure, country of origin, BMI, alcohol consumption, sex, and smoking status should be considered

Blood pressure and risk of renal cell carcinoma in the European prospective investigation into cancer and nutrition

Weikert S., Boeing H., Pischon T., Weikert C., Olsen A., Tjonneland A., Overvad K., Becker N., Linseisen J., Trichopoulou A., Mountokalakis T., Trichopoulos D., Sieri S., Palli D., Vineis P., Panico S., Peeters P.H., Bueno-de-Mesquita H.B., Verschuren W.M., Ljungberg B., Hallmans G., Berglund G., Gonzalez C.A., Dorronsoro M., Barricarte A., Tormo M.J., Allen N., Roddam A., Bingham S., Khaw K.T., Rinaldi S., Ferrari P., Norat T., Riboli E.

Am J Epidemiol; 2008; 167(4): 438-446

Abstract as provided by PubMed

Elevated blood pressure has been implicated as a risk factor for renal cell carcinoma (RCC), but prospective studies were confined to men and did not consider the effect of antihypertensive medication. The authors examined the relation among blood pressure, antihypertensive medication, and RCC in the European Prospective Investigation into Cancer and Nutrition (EPIC). Blood pressure was measured in 296,638 women and men, recruited in eight European countries during 1992-1998, 254,935 of whom provided information on antihypertensive medication. During a mean follow-up of 6.2 years, 250 cases of RCC were identified. Blood pressure was independently associated with risk of RCC. The relative risks for the highest versus the lowest category of systolic (>/=160 mmHg vs. <120 mmHg) and diastolic (>/=100 mmHg vs. <80 mmHg) blood pressures were 2.48 (95% confidence interval: 1.53, 4.02) and 2.34 (95% confidence interval: 1.54, 3.55). Risk estimates did not significantly differ according to sex or use of antihypertensive medication. Individuals taking antihypertensive drugs were not at a significantly increased risk unless blood pressure was poorly controlled. These results support the hypothesis that hypertension, rather than its medications, increases the risk of RCC in both sexes, while effective blood pressure control may lower the risk

2007

Serum insulin-like growth factor (IGF)-I and IGF-binding protein-3 concentrations and prostate cancer risk: results from the European Prospective Investigation into Cancer and Nutrition

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

Cancer Epidemiol Biomarkers Prev; 2007; 16(6): 1121-1127

Abstract as provided by PubMed

BACKGROUND: Some studies suggest that elevated serum insulin-like growth factor (IGF)-I concentrations are associated with an increased risk of prostate cancer and, in particular, with an increased risk of advanced-stage prostate cancer. METHODS: We analyzed the association between prediagnostic serum concentrations of IGF-I and IGF-binding protein-3 (IGFBP-3) and prostate cancer risk in a case-control study nested in the European Prospective Investigation into Cancer and Nutrition. This study includes 630 incident prostate cancer cases and 630 matched control subjects. Odds ratios and their 95% confidence intervals (95% CI) were calculated for prostate cancer risk associated with increasing IGF-I and IGFBP-3 concentrations using conditional logistic regression. RESULTS: The risk of total prostate cancer in the highest versus the lowest third of serum peptide concentration was 1.35 (95% CI, 0.99-1.82; Ptrend = 0.08) for IGF-I, 1.39 (95% CI, 1.02-1.89; Ptrend = 0.12) for the IGF-I residuals after adjusting for IGFBP-3, 1.22 (95% CI, 0.92-1.64; Ptrend = 0.38) for IGFBP-3, and 1.01 (95% CI, 0.74-1.37; Ptrend = 0.75) for the IGFBP-3 residuals after adjusting for IGF-I. There was no significant difference in the association of peptide hormones and prostate cancer by stage of disease, although the association of serum IGF-I concentration with risk was slightly stronger for advanced-stage disease; the odds ratio for the highest versus the lowest third was 1.65 (95% CI, 0.88-3.08; Ptrend = 0.21) for IGF-I and 1.76 (95% CI, 0.92-3.40; Ptrend = 0.11) for IGF-I adjusted for IGFBP-3. CONCLUSIONS: In this large nested case-control study, serum IGF-I concentration is not strongly associated with prostate cancer risk, although the results are compatible with a small increase in risk, particularly for advanced-stage disease; no association for IGFBP-3 was observed

Risk of endometrial cancer in relationship to cigarette smoking: Results from the EPIC study

Al-Zoughool M., Dossus L., Kaaks R., Clavel-Chapelon F., Tjonneland A., Olsen A., Overvad K., Boutron-Ruault M.C., Gauthier E., Linseisen J., Chang-Claude J., Boeing H., Schulz M., Trichopoulou A., Chryssa T., Trichopoulos D., Berrino F., Palli D., Mattiello A., Tumino R., Sacerdote C., Bueno-de-Mesquita H.B., Boshuizen H.C., Peeters P.H., Gram I.T., Braaten T., Lund E., Chirlaque M.D., Ardanaz E., Agudo A., Larranaga N., Quiros J.R., Berglund G., Manjer J., Lundin E., Hallmans G., Khaw K.T., Bingham S., Allen N., Key T., Jenab M., Cust A.E., Rinaldi S., Riboli E.

Int J Cancer; 2007; 121(12): 2741-2747

Abstract as provided by PubMed

Current epidemiologic evidence indicates that cigarette smoking reduces the risk of endometrial cancer. We examined data from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort to analyze further aspects of the smoking-endometrial cancer relationship, such as possible modifying effects of menopausal status, HRT use, BMI and parity. In a total of 249,986 women with smoking exposure and menopausal status information, 619 incident endometrial cancer cases were identified during 1.56 million person-years of follow-up. Among postmenopausal women, the hazard ratio (HR) for current smokers versus never smokers was 0.70 (95% CI = 0.53-0.93), while it was 1.75 (95% CI = 1.13-2.70) among premenopausal women at recruitment. After adjustment for risk factors, the HR for postmenopausal women was slightly attenuated to 0.78 (95% CI = 0.59-1.03). No heterogeneity of effect was observed with HRT use or BMI. Among premenopausal women, current smokers of more than 15 cigarettes per day or who smoked for 30 years or more at the time of recruitment had a more than 2-fold increased risk of endometrial cancer compared to never smokers (HR = 2.54; 95% CI = 1.47-4.38 and HR = 2.23; 95% CI = 1.04-4.77, respectively). Past smoking was not associated with endometrial cancer risk, either among pre- or postmenopausal women. In this prospective study, we observed an increased risk of endometrial cancer with cigarette smoking in premenopausal women. The reduction of endometrial cancer risk observed among postmenopausal women does not have direct public health relevance since cigarette smoking is the main known risk factor for cancer. (c) 2007 Wiley-Liss, Inc

Dietary patterns and survival of older Europeans: The EPIC-Elderly Study (European Prospective Investigation into Cancer and Nutrition)

Bamia C., Trichopoulos D., Ferrari P., Overvad K., Bjerregaard L., Tjonneland A., Halkjaer J., Clavel-Chapelon F., Kesse E., Boutron-Ruault M.C., Boffetta P., Nagel G., Linseisen J., Boeing H., Hoffmann K., Kasapa C., Orfanou A., Travezea C., Slimani N., Norat T., Palli D., Pala V., Panico S., Tumino R., Sacerdote C., Bueno-de-Mesquita H.B., Waijers P.M., Peeters P.H., van der Schouw Y.T., Berenguer A., Martinez-Garcia C., Navarro C., Barricarte A., Dorronsoro M., Berglund G., Wirfalt E., Johansson I., Johansson G., Bingham S., Khaw K.T., Spencer E.A., Key T., Riboli E., Trichopoulou A.

Public Health Nutr; 2007; 10(6): 590-598
Pathology findings and validation of gastric and esophageal cancer cases in a European cohort (EPIC/EUR-GAST)

Carneiro F., Moutinho C., Pera G., Caldas C., Fenger C., Offerhaus J., Save V., Stenling R., Nesi G., Mahlke U., Blaker H., Torrado J., Roukos D.H., Sabourin J.C., Boeing H., Palli D., Bueno-de-Mesquita H.B., Overvad K., Bingham S., Clavel-Chapelon F., Lund E., Trichopoulou A., Manjer J., Riboli E., Gonzalez C.A.

Scand. J Gastroenterol; 2007; 42(5): 618-627

Abstract as provided by PubMed

OBJECTIVE: Cardia, non-cardia and intestinal and diffuse subtypes of gastric cancer may have different trends and etiological factors. However, the available information is not always collected in population cancer registries, and heterogeneous criteria have been applied for the histopathological classification of tumors. We describe the pathological features of incident gastric and esophageal cancers identified within the European Prospective Investigation into Cancer and Nutrition (EPIC). MATERIAL AND METHODS: In an investigation on gastric and esophageal cancer (EUR-GAST) in the EPIC project, a validation study of diagnoses reported by EPIC centers was conducted by a European panel of pathologists. Original pathology reports, stained slides of tumors and the respective paraffin blocks were requested from the centers. RESULTS: The whole series encompassed 467 cancer cases (gastric and esophageal cancers). Material was available for histopathological validation in 263 cases (56%); in the remaining cases, information was retrieved from the original reports (n=110; 24%) or codes provided by the EPIC centers (n=94; 20%). Among cases submitted to histopathological validation reported originally as unknown histotype or unknown site, a specific diagnosis was made in 95% and 74% of the cases, respectively. In cases for which only the original reports were available, the respective percentages were 46% and 67%. Gastric adenocarcinomas were classified according to site (cardia (29.4%), non-cardia (48.2%) and unknown (22.4%)) and histological type (intestinal (33.4%), diffuse (33.7%) and mixed, unclassified or unknown (32.9%)). Frequency of cardia was higher in Northern countries (35%) than in Mediterranean countries (18%). CONCLUSIONS: In addition to providing epidemiological data within the EPIC cohort on gastric and esophageal adenocarcinomas, the results reported here confirm the relevance of a validation study, notably for multicenter studies

Plasma adiponectin levels and endometrial cancer risk in pre- and postmenopausal women

Cust A.E., Kaaks R., Friedenreich C., Bonnet F., Laville M., Lukanova A., Rinaldi S., Dossus L., Slimani N., Lundin E., Tjonneland A., Olsen A., Overvad K., Clavel-Chapelon F., Mesrine S., Joulin V., Linseisen J., Rohrmann S., Pischon T., Boeing H., Trichopoulos D., Trichopoulou A., Benetou V., Palli D., Berrino F., Tumino R., Sacerdote C., Mattiello A., Quiros J.R., Mendez M.A., Sanchez M.J., Larranaga N., Tormo M.J., Ardanaz E., Bueno-de-Mesquita H.B., Peeters P.H., Van Gils C.H., Khaw K.T., Bingham S., Allen N., Key T., Jenab M., Riboli E.

J Clin Endocrinol Metab; 2007; 92(1): 255-263

Abstract as provided by PubMed

BACKGROUND: Adiponectin, an adipocytokine secreted by adipose tissue, is decreased in obesity, insulin resistance, type 2 diabetes, and polycystic ovary syndrome, all of which are well-established risk factors for endometrial cancer. METHODS: We conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition to examine the relation between prediagnostic plasma adiponectin levels and endometrial cancer risk. Among pre- and postmenopausal women who were not currently using exogenous hormones, 284 women developed incident endometrial cancer during an average of 5.1 yr of follow-up. Using risk set sampling, 548 control subjects were selected, matched on center, age, menopausal status, phase of menstrual cycle, time of blood draw, and fasting status. Conditional logistic regression models were used to estimate relative risks and 95% confidence intervals. RESULTS: Adiponectin levels were inversely associated with endometrial cancer risk [body mass index-adjusted relative risk for the top vs. bottom quartile = 0.56 (95% confidence interval 0.36-0.86), P(trend) = 0.006]. There was evidence of a stronger inverse association among obese women than among nonobese women (P(heterogeneity) = 0.03). The inverse association also appeared stronger for women who were postmenopausal or perimenopausal than premenopausal at baseline, but this was not statistically significantly heterogeneous (P(heterogeneity) = 0.51). The association remained statistically significant after separate adjustment for other obesity-related physiological risk factors such as C-peptide, IGF binding protein-1, IGF binding protein-2, SHBG, estrone, or free testosterone but only marginally statistically significant after simultaneous adjustment for these factors. CONCLUSIONS: High circulating adiponectin levels are associated with reduced endometrial cancer risk, largely independent of other obesity-related risk factors

Serum levels of C-peptide, IGFBP-1 and IGFBP-2 and endometrial cancer risk; results from the European prospective investigation into cancer and nutrition

Cust A.E., Allen N.E., Rinaldi S., Dossus L., Friedenreich C., Olsen A., Tjonneland A., Overvad K., Clavel-Chapelon F., Boutron-Ruault M.C., Linseisen J., Chang-Claude J., Boeing H., Schulz M., Benetou V., Trichopoulou A., Trichopoulos D., Palli D., Berrino F., Tumino R., Mattiello A., Vineis P., Quiros J.R., Agudo A., Sanchez M.J., Larranaga N., Navarro C., Ardanaz E., Bueno-de-Mesquita H.B., Peeters P.H., Van Gils C.H., Bingham S., Khaw K.T., Key T., Slimani N., Riboli E., Kaaks R.

Int J Cancer; 2007; 120(12): 2656-2664

Abstract as provided by PubMed

We conducted a case-control study nested within the European Prospective Investigation into Cancer and Nutrition, to examine the associations between prediagnostic serum concentrations of C-peptide, insulin-like growth factor binding protein (IGFBP)-1 and IGFBP-2, and endometrial cancer risk. Among pre- and post-menopausal women, who were not currently using exogenous hormones, 286 women developed incident endometrial cancer during an average 5.1 years follow-up. Using risk set sampling, 555 matched control subjects were selected. In conditional logistic regression models adjusted for matching factors only, endometrial cancer risk increased with increasing serum levels of C-peptide (relative risks (RR) for the top vs. bottom quartile = 2.13 [95% confidence interval (CI) 1.33-3.41], p(trend) = 0.001, and decreasing serum levels of IGFBP-2 (RR for the top vs. bottom quartile = 0.56 [95% CI 0.35-0.90], p(trend) = 0.03, but was not significantly associated with IGFBP-1 levels (RR for the top vs. bottom quartile = 0.76 [95% CI 0.47-1.21], p(trend) = 0.25). In BMI-adjusted models, only the C-peptide association remained marginally statistically significant (RR for the top vs. bottom quartile = 1.56 [95% CI 0.94-2.57], p(trend) = 0.05 for C-peptide; 0.84 [95% CI 0.50-1.40], p(trend) = 0.74 for IGFBP-2; and 1.08 [95% CI 0.65-1.78], p(trend) = 0.86 for IGFBP-1 levels). These associations were stronger among nonfasting women (< or =< or =6 hr since last meal; 63% of subjects) but were not evident among fasting women, although the interactions were not statistically significant. The C-peptide-risk association was substantially attenuated after adjustment for free estradiol in postmenopausal women (RR for the top vs. bottom quartile = 1.28 [95% CI 0.67-2.45], p(trend) = 0.42. Our results provide modest support to the hypothesis that hyperinsulinaemia is a risk factor for endometrial cancer

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