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  • 1
    Abstract: Evidence indicates that gaining weight in adult life is associated with an elevated risk of colorectal cancer; however, biological mechanisms that may explain this association remain unclear. We evaluated the mediation effect of 20 different biomarkers on the relationship between adult weight gain and colorectal cancer, using data from a prospective nested case-control study of 452 incident cases diagnosed between 1992 and 2003 and matched within risk sets to 452 controls within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. The proportions of mediated effects (%) were estimated on the basis of differences in percent effect changes in conditional logistic regression models with and without additional adjustment for individual biomarkers. Greater adult weight gain (〉/=300 g/year vs. 〈300 g/year) was associated with a higher risk of colon cancer (multivariable-adjusted relative risk = 1.54, 95% confidence interval: 1.07, 2.24) but not rectal cancer (relative risk = 1.07, 95% confidence interval: 0.68, 1.66). This association was accounted for mostly by attained waist circumference (reduction of 61%) and by the biomarkers soluble leptin receptor (reduction of 43%) and glycated hemoglobin (reduction of 28%). These novel data suggest that the observed association between adult weight gain and colon cancer could be primarily explained by attained abdominal fatness and biomarkers of metabolic dysfunction.
    Type of Publication: Journal article published
    PubMed ID: 28387787
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  • 2
    Keywords: EXPOSURE ; BIOMARKERS ; BREAST ; HUMANS ; smoking ; VALIDITY ; ENDOMETRIAL ; HEMOGLOBIN ADDUCTS ; glycidamide
    Abstract: Acrylamide, classified in 1994 by IARC as 'probably carcinogenic' to humans, was discovered in 2002 in some heat-treated, carbohydrate-rich foods. The association between dietary acrylamide intake and epithelial ovarian cancer risk (EOC) has been previously studied in one case-control and three prospective cohort studies which obtained inconsistent results, and could not further examine histological subtypes other than serous EOC. The present study was carried out in the European Prospective Investigation into Cancer and Nutrition (EPIC) sub-cohort of women (n=325,006). Multivariate Cox proportional hazards models were used to assess the association between questionnaire-based acrylamide intake and EOC risk. Acrylamide was energy-adjusted using the residual method, and was evaluated both as a continuous variable (per 10microg/day) and in quintiles; when subgroups by histological EOC subtypes were analyzed, acrylamide intake was evaluated in quartiles. During a mean follow-up of 11 years, 1,191 incident EOC cases were diagnosed. At baseline, the median acrylamide intake in EPIC was 21.3 mug/day. No associations, and no evidence for a dose-response were observed between energy-adjusted acrylamide intake and EOC risk (HR10microg/day:1.02, 95%CI:0.96-1.09; HRQ5vsQ1:0.97, 95%CI:0.76-1.23). No differences were seen when invasive EOC subtypes (582 serous, 118 endometrioid, and 79 mucinous tumors) were analyzed separately. This study did not provide evidence that acrylamide intake, based on food intake questionnaires, was associated with risk for EOC in EPIC. Additional studies with more reliable estimates of exposure based on biomarkers may be needed.
    Type of Publication: Journal article published
    PubMed ID: 25300475
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  • 3
    Abstract: Diets high in red or processed meat have been associated positively with some cancers, and several possible underlying mechanisms have been proposed, including iron-related pathways. However, the role of meat intake in adult glioma risk has yielded conflicting findings because of small sample sizes and heterogeneous tumour classifications. The aim of this study was to examine red meat, processed meat and iron intake in relation to glioma risk in the European Prospective Investigation into Cancer and Nutrition study. In this prospective cohort study, 408 751 individuals from nine European countries completed demographic and dietary questionnaires at recruitment. Multivariable Cox proportional hazards models were used to examine intake of red meat, processed meat, total dietary iron and haem iron in relation to incident glioma. During an average follow-up of 14.1 years, 688 incident glioma cases were diagnosed. There was no evidence that any of the meat variables (red, processed meat or subtypes of meat) or iron (total or haem) were associated with glioma; results were unchanged when the first 2 years of follow-up were excluded. This study suggests that there is no association between meat or iron intake and adult glioma. This is the largest prospective analysis of meat and iron in relation to glioma and as such provides a substantial contribution to a limited and inconsistent literature.
    Type of Publication: Journal article epub ahead of print
    PubMed ID: 27845960
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  • 4
    Abstract: PURPOSE: There is inconsistent evidence regarding the relationship between higher intake of nuts, being an energy-dense food, and weight gain. We investigated the relationship between nut intake and changes in weight over 5 years. METHODS: This study includes 373,293 men and women, 25-70 years old, recruited between 1992 and 2000 from 10 European countries in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Habitual intake of nuts including peanuts, together defined as nut intake, was estimated from country-specific validated dietary questionnaires. Body weight was measured at recruitment and self-reported 5 years later. The association between nut intake and body weight change was estimated using multilevel mixed linear regression models with center/country as random effect and nut intake and relevant confounders as fixed effects. The relative risk (RR) of becoming overweight or obese after 5 years was investigated using multivariate Poisson regressions stratified according to baseline body mass index (BMI). RESULTS: On average, study participants gained 2.1 kg (SD 5.0 kg) over 5 years. Compared to non-consumers, subjects in the highest quartile of nut intake had less weight gain over 5 years (-0.07 kg; 95% CI -0.12 to -0.02) (P trend = 0.025) and had 5% lower risk of becoming overweight (RR 0.95; 95% CI 0.92-0.98) or obese (RR 0.95; 95% CI 0.90-0.99) (both P trend 〈0.008). CONCLUSIONS: Higher intake of nuts is associated with reduced weight gain and a lower risk of becoming overweight or obese.
    Type of Publication: Journal article epub ahead of print
    PubMed ID: 28733927
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  • 5
    Keywords: CANCER ; CELLS ; CELL ; Germany ; MODEL ; MODELS ; FOLLOW-UP ; SYSTEM ; cohort study ; DISEASE ; DISEASES ; EPIDEMIOLOGY ; RISK ; RISK-FACTORS ; ASSOCIATION ; NO ; LYMPHOMA ; HEALTH ; WOMEN ; etiology ; risk factors ; DIETARY ; UNITED-STATES ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; FRUIT ; nutrition ; VEGETABLES ; CALIBRATION ; B-CELL LYMPHOMA ; MULTIPLE-MYELOMA ; NON-HODGKINS-LYMPHOMA ; ONCOLOGY ; DIETARY FACTORS ; ASSOCIATIONS ; IMMUNE-SYSTEM ; non-Hodgkin lymphoma ; INTERVAL ; FRUITS ; methods ; function ; prospective ; prospective study ; RISK-FACTOR ; HODGKIN LYMPHOMA ; B-CELL ; N-NITROSO COMPOUNDS ; DRINKING-WATER NITRATE
    Abstract: 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
    Type of Publication: Journal article published
    PubMed ID: 17443415
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  • 6
    Keywords: CANCER ; carcinoma ; INFORMATION ; COHORT ; DEATH ; incidence ; RISK ; SITE ; SITES ; GENE ; INFECTION ; DOWN-REGULATION ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; MOLECULE ; NO ; PROGRESSION ; DIFFERENCE ; PROMOTER ; MUTATION ; smoking ; RATES ; FRANCE ; MUTATIONS ; ADHESION ; case-control studies ; ADHESION MOLECULE ; EPIC ; HELICOBACTER-PYLORI ; nutrition ; SMOKERS ; METHYLATION ; E-cadherin ; ONCOLOGY ; case-control study ; RE ; INCREASE ; gastric cancer ; PROMOTER POLYMORPHISM ; HAPLOTYPE ; prospective ; Helicobacter pylori ; ENGLAND ; block ; GENE POLYMORPHISMS ; GENE POLYMORPHISM ; POSITION ; gastric adenocarcinoma ; CDH1 ; E-CADHERIN GENE
    Abstract: 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. (c) 2008 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 18342503
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  • 7
    Keywords: CANCER ; CELLS ; AGENTS ; CELL ; MODEL ; MODELS ; neoplasms ; FOLLOW-UP ; SYSTEM ; COHORT ; cohort study ; EPIDEMIOLOGY ; HISTORY ; incidence ; RISK ; INFECTION ; MECHANISM ; primary ; RISK-FACTORS ; mechanisms ; T cell ; T-CELL ; ASSOCIATION ; DISORDER ; SUSCEPTIBILITY ; NO ; LYMPHOMA ; CARE ; DESIGN ; PLASMA ; AGE ; WOMEN ; etiology ; MEN ; risk factors ; leukemia ; Jun ; diabetes ; ABNORMALITIES ; INFECTIONS ; EPIC ; nutrition ; immunosuppression ; non-hodgkin's lymphoma ; CHRONIC LYMPHOCYTIC-LEUKEMIA ; MULTIPLE-MYELOMA ; VIRAL-INFECTION ; insulin ; MELLITUS ; AGENT ; AUTOIMMUNITY ; multiple myeloma ; DISORDERS ; MEDICAL HISTORY ; INCREASE ; T-CELL LYMPHOMA ; prospective studies ; methods ; SUBTYPES ; metabolic syndrome ; BODY-MASS INDEX ; prospective ; prospective study ; RISK-FACTOR ; CANCERS ; B-CELL ; ENGLAND ; ENVIRONMENTAL-FACTORS ; host ; INCREASES ; viral ; European Prospective Investigation into Cancer ; non-Hodgkin ; neoplasm ; INTERLEUKIN-6 GENE
    Abstract: 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
    Type of Publication: Journal article published
    PubMed ID: 18443270
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  • 8
    Keywords: CANCER ; BLOOD ; COHORT ; cohort studies ; cohort study ; POPULATION ; RISK ; MARKER ; BIOMARKERS ; colon ; ASSOCIATION ; NO ; HEALTH ; WOMEN ; colorectal cancer ; MEN ; PROSPECTIVE COHORT ; COLORECTAL-CANCER ; cancer risk ; FRANCE ; COLON-CANCER ; MULTIVARIATE ; UNITED-STATES ; case-control studies ; GLUCOSE ; nutrition ; BETA-CELL FUNCTION ; ONCOLOGY ; case-control study ; REGRESSION ; RE ; INCREASE ; LEVEL ; biomarker ; INSULIN-RESISTANCE ; metabolic syndrome ; USA ; prospective ; cancer research ; CANCER-RISK ; NOV ; HEMOGLOBIN ; TYPE-2 DIABETES-MELLITUS ; European Prospective Investigation into Cancer ; CHRONIC OXIDATIVE STRESS ; GLUCOSE TOXICITY ; RECTAL CANCERS ; SERUM C-PEPTIDE
    Abstract: 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. (Cancer Epidemiol Biomarkers Prev 2008;17(11):3108-15)
    Type of Publication: Journal article published
    PubMed ID: 18990751
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  • 9
    Keywords: CANCER ; MODEL ; MODELS ; SUPPORT ; COHORT ; DEATH ; DISEASE ; EXPOSURE ; MORTALITY ; RISK ; TIME ; POLYMORPHISMS ; hippocampus ; CARE ; CIGARETTE-SMOKING ; smoking ; RATES ; DAMAGE ; RISK FACTOR ; PREVALENCE ; LIPID-PEROXIDATION ; CONSUMPTION ; EPIC ; nutrition ; CORTEX ; USA ; prospective ; INCREASED RISK ; RISK-FACTOR ; lipid ; amyotrophic lateral sclerosis ; INVESTIGATE ; 33 ; FORMALDEHYDE ; SPORADIC ALS
    Abstract: Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrolment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2-32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure. Ann Neurol 2009;65:378-385
    Type of Publication: Journal article published
    PubMed ID: 19399866
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  • 10
    Keywords: RECEPTOR ; CANCER ; BLOOD ; POPULATION ; RISK ; GENE ; GENES ; BIOMARKERS ; colon ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; ADENOMAS ; HEALTH ; colorectal cancer ; REDUCED RISK ; COLORECTAL-CANCER ; GENOTYPES ; COLON-CANCER ; POPULATIONS ; UNITED-STATES ; case-control studies ; CALCIUM ; nutrition ; RECTAL-CANCER ; SERUM ; case control study ; case-control study ; REGRESSION ; colon cancer ; VARIANT ; interaction ; LEVEL ; biomarker ; EPIDEMIOLOGIC EVIDENCE ; GENOTYPE ; USA ; prospective ; rectal cancer ; cancer research ; colorectal ; vitamin D ; VITAMIN-D ; LOGISTIC-REGRESSION ; D METABOLITES ; vitamin D receptor ; 25-HYDROXYVITAMIN-D ; RECTAL CANCERS ; Genetic ; VITAMIN ; CONFIDENCE ; CRC ; Logistic regression ; D-RECEPTOR ; DIETARY CALCIUM
    Abstract: Increased levels of vitamin D and calcium may play a protective role in colorectal cancer (CRC) risk. It has been suggested that these effects may be mediated by genetic variants of the vitamin D receptor (VDR) and the calcium sensing receptor (CASR). However, current epidemiologic evidence from European populations for a role of these genes in CRC risk is scarce. In addition, it is not clear whether these genes may modulate CRC risk independently or by interaction with blood vitamin D concentration wild-type bb, the BB genotype of the VDR BsmI polymorphism was associated with a reduced risk of CRC [RR, 0.76; 95% confidence interval (CI), 0.59-0.98). The association was observed for colon cancer (RR, 0.69; 95% CI, 0.45-0.95) but not rectal cancer (RR, 0.97; 95% CI, 0.62-1.49). The Fok1 and CASR genotypes were not associated with CRC risk in thisand level of dietary calcium intake. A case-control study was conducted nested within the European Prospective Investigation into Cancer and Nutrition. CRC cases (1,248) were identified and matched to 1,248 control subjects. Genotyping for the VDR (BsmI: rs1544410; Fok1: rs2228570) and CASR (rs1801725) genes was done by Taqman, and serum vitamin D (25OHD) concentrations were measured. Conditional logistic regression was used to estimate the incidence rate ratio (RR). Compared with the study. No interactions were noted for any of the polymorphisms with serum 25OHD concentration or level of dietary calcium. These results confirm a role for the BsmI polymorphism of the VDR gene in CRC risk, independent of serum 25OHD concentration and dietary calcium intake. (Cancer Epidemiol Biomarkers Prev 2009;18(9):2485-91)
    Type of Publication: Journal article published
    PubMed ID: 19706842
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