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  • 1
    Keywords: CANCER ; CANCER CELLS ; CELLS ; BLOOD ; CELL ; human ; LUNG ; DIAGNOSIS ; FOLLOW-UP ; EXPOSURE ; PROTEIN ; PROTEINS ; PATIENT ; DNA ; CARCINOGENESIS ; ASSOCIATION ; HUMANS ; DESIGN ; PLASMA ; AGE ; MUTATION ; genetics ; smoking ; leukemia ; bladder cancer ; BLADDER-CANCER ; PCR ; CANCER-CELLS ; MUTATIONS ; RECRUITMENT ; CANCER-PATIENTS ; ADDUCTS ; case-control studies ; CANCER PATIENTS ; nutrition ; MULTICENTER ; lung neoplasms ; TP53 ; ADULT ; prospective studies ; PROTOONCOGENE ; HEALTHY-SUBJECTS ; INTERVAL ; CANCER DEVELOPMENT ; prospective ; prospective study ; healthy subjects ; female ; Male ; CANCERS ; LIQUID ; EXPOSURES ; Aged ; Middle Aged ; CANCER-DIAGNOSIS ; Genes,p53 ; Longitudinal Studies ; Proto-Oncogene Proteins ; Urinary Bladder Neoplasms
    Abstract: 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
    Type of Publication: Journal article published
    PubMed ID: 16818665
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  • 2
  • 3
    Keywords: CANCER ; LUNG ; DEATH ; DISEASE ; POPULATION ; RISK ; SAMPLE ; SAMPLES ; TUMORS ; TIME ; PATIENT ; DNA ; treatment ; PLASMA ; COUNTRIES ; leukemia ; BLADDER ; cancer risk ; CANCER-PATIENTS ; CANCER PATIENTS ; EPIC ; European Prospective Investigation into Cancer and Nutrition ; nutrition ; SMOKERS ; EUROPE ; ORAL CAVITY ; ORAL-CANCER ; PULMONARY ; SERUM ; molecular repidemiology ; plasmatic DNA ; prospective studies
    Abstract: Levels of plasma DNA concentrations in cancer patients have been shown to be higher than the plasma DNA concentrations found in healthy subjects. The value of plasma DNA levels for development of neoplastic or pulmonary disease was evaluated in a large prospective study. Plasma samples (n = 1, 184) were analyzed from 776 controls, 359 cases of cancer (lung, bladder, oral cavity, pharynx, larynx, leukemia) and 49 deaths from chronic obstructive pulmonary disease (COPD), including never smokers and ex-smokers, from 9 countries across Europe. The amount of plasma DNA was variable across the European Prospective Investigation into Cancer and Nutrition (EPIC) centers. High DNA concentrations in some centers might be due to the type of population recruited and/or the treatment of the samples. An elevated and statistically significant odds ratio (OR) was found for COPID deaths (OR = 2.53; 95% CI = 1.06-6.02), while nonsignificant increased ORs were present for oral cancers, cancers of the pharynx and larynx and leukemia. When the analyses were stratified by time since recruitment (below or above 36 months), the increased ORs were limited to the more recent period of recruitment, i.e., a time elapsed between blood drawing and disease onset lower than 36 months. This was particularly true for COPID deaths (OR = 12.7; 95% CI = 1.57-103) and leukemia (OR = 2.37; 95% Cl = 1.20-4.67). (C) 2004 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 15252845
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  • 4
    Keywords: ENERGIES ; CANCER ; MODEL ; COHORT ; EPIDEMIOLOGY ; POPULATION ; RISK ; colon ; ASSOCIATION ; ACID ; ACIDS ; NO ; hormone ; ENERGY ; AGE ; WOMEN ; colorectal cancer ; MEN ; smoking ; COLORECTAL-CANCER ; COUNTRIES ; PROSTATE-CANCER ; cancer risk ; FIBER ; FRANCE ; COLON-CANCER ; MULTIVARIATE ; fatty acids ; FATTY-ACIDS ; DIETARY ; CANCER-RESEARCH ; CONSUMPTION ; European Prospective Investigation into Cancer and Nutrition ; FRUIT ; nutrition ; QUESTIONNAIRE ; CALIBRATION ; FOOD ; ASSOCIATIONS ; colon cancer ; WEIGHT ; CORONARY-HEART-DISEASE ; DIETARY-INTAKE MEASUREMENTS ; EPIC PROJECT ; HEIGHT
    Abstract: A link between unsaturated fatty acids or phytonutrients and reduced risk of colorectal cancer has been suggested. However, the effects of higher intake of dietary sources of these nutrients, such as the nuts and seeds food group, are less clear. The objective of this study was to determine the effects of nut and seed intake on colorectal cancer risk within the European Prospective Investigation into Cancer and Nutrition study, a large prospective cohort study involving 10 European countries. Total nut and seed intake was determined from country-specific dietary questionnaires. The data set included 478,040 subjects (141,988 men, 336,052 women) with a total of 855 (327 men, 528 women) colon and 474 (215 men, 259 women) rectal cancer cases. A multivariate Cox proportional hazards model, stratified by center and controlled for fruit intake, dietary fiber, energy, height, weight, sex, age, physical activity, and smoking, was used. The data show no association between higher intake of nuts and seeds and risk of colorectal, colon, and rectal cancers in men and women combined, but a significant inverse association was observed in subgroup analyses for colon cancer in women at the highest (〉6.2 g/d) versus the lowest (nonconsumers; hazard ratio, 0.69;, 95% confidence interval, 0.50-0.95) category of intake and for the linear effect of log-transformed intake (hazard ratio, 0.89; 95% confidence interval, 0.80-0.98), with no associations in men. It is not evident from this data why there may be a stronger association in women or why it may be limited to the colon, suggesting that much, further research is necessary
    Type of Publication: Journal article published
    PubMed ID: 15466975
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  • 5
    Keywords: CANCER ; BLOOD ; LUNG ; EMPHYSEMA ; LUNG-CANCER ; DEATH ; DISEASE ; DISEASES ; EXPOSURE ; HEPATOCELLULAR-CARCINOMA ; POPULATION ; RISK ; BIOMARKERS ; ASSOCIATION ; FREQUENCY ; WOMEN ; CIGARETTE-SMOKING ; leukemia ; BLADDER-CANCER ; ADDUCTS ; TOBACCO ; INDIVIDUALS ; PERIPHERAL-BLOOD ; nutrition ; DNA-ADDUCTS ; TOBACCO-SMOKE ; CHEMICAL CARCINOGENS ; protein adducts ; LEVEL ; ADDUCT ; AFLATOXIN EXPOSURE ; biomarker ; case control studies ; ENVIRONMENTAL TOBACCO-SMOKE ; HEMOGLOBIN ADDUCTS ; INTERVAL
    Abstract: The aim of this study was to evaluate whether biomarkers of environmental tobacco smoke exposure [i.e, 4-aminobiphenyl-hemoglobin (4-ABP-Hb) adducts] were predictive of the risk of tobacco-related cancers and diseases. We did a case control study nested within the European Prospective Investigation into Cancer and Nutrition, involving 190 controls and 149 cases (incident cancer of the lung, bladder, pharynx, larynx, oral cavity, leukemias, and chronic obstructive pulmonary disease or emphysema deaths). All individuals were never smokers or ex smokers for 〉 10 years. 4-ABP-Hb adducts were analyzed in peripheral blood collected before the onset of the disease (median, 7 years). Overall, 4-ABP-Hb adducts were higher, although not statistically significantly so, in cases (as a whole) than controls. In the control population, high fruit and vegetable consumption significantly lowered the frequency of detectable adducts (Fisher's exact test, P = 0.025). Restricting the analysis to women, 4-ABP-Hb adducts were higher in cases than controls (Mann-Whitney P = 0.036) and the odds ratio (OR) for the presence/absence of adducts was 2.42 [95% confidence interval (95% CI), 1.18-4.981. Moreover, the association of adducts with the individual cancer types was stronger in women than in the whole study population, although statistically significant only for leukemias (OR, 2.77; 95% CI, 1.06-7.20). The results provide some evidence that women may be more susceptible to environmental tobacco smoke, as suggested by their higher adduct levels. The most important finding of this prospective study is that, at least in women, 4-ABP-Hb adducts may help identify subjects at high risk of cancers related to environmental tobacco smoke exposure
    Type of Publication: Journal article published
    PubMed ID: 16172219
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  • 6
    Keywords: CANCER ; INFORMATION ; SUPPORT ; COHORT ; EXPOSURE ; LONG-TERM ; RISK ; ACTIVATION ; DNA ; AIR ; ASSOCIATION ; VARIANTS ; BREAST-CANCER ; NO ; HEALTH ; lifestyle ; MUTATION ; PROSPECTIVE COHORT ; COLORECTAL-CANCER ; bladder cancer ; BLADDER-CANCER ; cancer risk ; acetylation ; METABOLIC-ACTIVATION ; COLON-CANCER ; MUTATIONS ; gene-environment interaction ; CARCINOGENS ; DIET ; DIETARY ; NETHERLANDS ; case-control studies ; CONSUMPTION ; EPIC ; nutrition ; QUESTIONNAIRE ; ONCOLOGY ; case-control study ; REGRESSION ; VARIANT ; prospective studies ; LEVEL ; methods ; GENOTYPE ; prospective ; MEAT INTAKE ; RISK-FACTOR ; VARIABLES ; CANCER-RISK ; ENGLAND ; AMINE ; N-acetyltransferase ; GENE-ENVIRONMENT INTERACTIONS ; N-ACETYLATION
    Abstract: Objective The suspect carcinogens, heterocyclic amines (HAAs), found in well-done meat require host-mediated metabolic activation before inducing DNA mutations. The role of SULT1A1 and of NAT2 on the activation of HAAs suggests that NAT2 rapid acetylator genotype and SULT1A1 allele variants can have an effect on HAA carcinogenicity. Methods Data were collected as part of a case-control study nested within the EPIC cohort, the Gen Air investigation. EPIC is a prospective study designed to investigate the relationship between nutrition and cancer. Information was collected through a non-dietary questionnaire on lifestyle variables and through a dietary questionnaire. The subjects were restricted to non-smokers. We calculated the matched odds ratio for bladder cancer risk using logistic regression, controlling for potential confounders. Results There were 227 bladder cases and 612 controls matched 1:3. Meat intake and NAT2 genotype were not independently associated with bladder cancer risk. A significant relationship was observed between bladder cancer risk and consumption of meat only among subjects with the rapid NAT2 genotype (odds ratios [OR] 2.9, 95% CI 1.0-7.9 for the 2nd quartile of meat intake; 3.6, 95% CI 1.3-9.7 for the 3rd quartile; and 3.5, 95% CI 1.2-9.7 for the 4th quartile), and was not present among subjects with the slow genotype. An interaction between NAT2 and meat intake was found in logistic regression (P = 0.034). No association was observed for SULT1A *1/2 genotype (1.0; 95% CI 0.7-1.5) and for SULT1A1 *2/2 genotype (0.9; 95% CI 0.5-1.7). Conclusions These results are suggestive of a role of meat intake and NAT2 on bladder cancer risk. They support the hypothesis that among subjects with the rapid NAT2 acetylation genotype higher levels of HAAs exposure are a bladder cancer risk factor. We did not observe an effect of SULT1A1 allele variants on this cancer. The present study adds new information on the possible long-term adverse effects of diets with high meat intake
    Type of Publication: Journal article published
    PubMed ID: 18264785
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  • 7
    Keywords: CANCER ; MODEL ; SUPPORT ; COHORT ; DISEASE ; DISEASES ; incidence ; NEW-YORK ; POPULATION ; RISK ; SITE ; INDEX ; ASSOCIATION ; lifestyle ; DECREASE ; CIGARETTE-SMOKING ; smoking ; COUNTRIES ; cancer risk ; DIET ; STOMACH ; adenocarcinoma ; TOBACCO ; ALCOHOL ; ALCOHOL-CONSUMPTION ; body mass index ; CARDIA ; cigarette smoking ; CONSUMPTION ; EPIC ; EPIC study ; ESOPHAGUS ; European Prospective Investigation into Cancer and Nutrition ; FRUIT ; gastric cancer,smoking,cohort study ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; HISTOLOGIC TYPE ; meat ; nutrition ; QUESTIONNAIRE ; questionnaires ; SMOKERS ; STOMACH-CANCER ; SUBSITE ; TOBACCO SMOKING ; VEGETABLES
    Abstract: Smoking has recently been recognised as causally associated with the development of gastric cancer (GC). However, evidence on the effect by sex, duration and intensity of smoking, anatomic subsite and cessation of smoking is limited. Our objective was to assess the relation between tobacco use and GC incidence in the European Prospective Investigation into Cancer and Nutrition (EPIC). We studied data from 521,468 individuals recruited from 10 European countries taking part in the EPIC study. Participants completed lifestyle questionnaires that included questions on lifetime consumption of tobacco and diet in 1991-1998. Participants were followed until September 2002, and during that period 305 cases of stomach cancer were identified. After exclusions, 274 were eligible for the analysis, using the Cox proportional hazard model. After adjustment for educational level, consumption of fresh fruit, vegetables and preserved meat, alcohol intake and body mass index (BMI), there was a significant association between cigarette smoking and gastric cancer risk: the hazard ratio (HR) for ever smokers was 1.45 (95% confidence interval [CI] = 1.08-1.94). The HR of current cigarette smoking was 1.73 (95% CI = 1.06-2.83) in males and 1.87 (95% CI = 1.12-3.12) in females. Hazard ratios increased with intensity and duration of cigarette smoked. A significant decrease of risk was observed after 10 years of quitting smoking. A preliminary analysis of 121 cases with identified anatomic site showed that current cigarette smokers had a higher HR of GC in the cardia (HR = 4.10) than in the distal part of the stomach (HR = 1.94). In this cohort, 17.6 % (95% CI = 10.5-29.5 %) of GC cases may be attributable to smoking. Findings from this large study support the causal relation between smoking and gastric cancer in this European population. Stomach cancer should be added to the burden of diseases caused by smoking. (C) 2003 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 14520702
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  • 8
    Keywords: CANCER ; LUNG ; DIAGNOSIS ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; COHORT ; EXPOSURE ; MORTALITY ; RISK ; TIME ; AIR-POLLUTION ; ASSOCIATION ; AGE ; smoking ; COUNTRIES ; RECRUITMENT ; ADDUCTS ; case-control studies ; EPIC ; nutrition ; SMOKERS ; case-control study ; air pollution ; case control studies ; INTERVAL ; GENDER ; occupational exposures ; prospective study ; EXPOSURES ; SO2 ; AMBIENT ; POLLUTANTS
    Abstract: To estimate the relationship between air pollution and lung cancer, a nested case-control study was set up within EPIC (European Prospective Investigation on Cancer and Nutrition). Cases had newly diagnosed lung cancer, accrued after a median follow-up of 7 years among the EPIC exsmokers (since at least 10 years) and never smokers. Three controls per case were matched. Matching criteria were gender, age (+/- 5 years), smoking status, country of recruitment and time elapsed between recruitment and diagnosis. We studied residence in proximity of heavy traffic roads as an indicator of exposure to air pollution. In addition, exposure to air pollutants (NO2, PM10, SO2) was assessed using concentration data from monitoring stations in routine air quality monitoring networks. Cotinine was measured in plasma. We found a nonsignificant association between lung cancer and residence nearby heavy traffic roads (odds ratio = 1.46, 95% confidence interval, CI, 0.89-2.40). Exposure data for single pollutants were available for 197 cases and 556 matched controls. For NO2 we found an odds ratio of 1.14 (95% CI, 0.78-1.67) for each increment of 10 mu g/m(3), and an odds ratio of 1.30 (1.02-1.66) for concentrations greater than 30 mu g/m(3). The association with NO2 did not change after adjustment by cotinine and additional potential confounders, including occupational exposures. No clear association was found with other pollutants. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16463382
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  • 9
    Keywords: CANCER ; LUNG-CANCER ; COHORT ; DNA adducts ; EXPOSURE ; RISK ; DNA ; BIOMARKERS ; colon ; RATS ; CONTRAST ; BINDING ; ASSOCIATION ; COLORECTAL-CANCER ; BLADDER-CANCER ; cancer risk ; POLYCYCLIC AROMATIC-HYDROCARBONS ; COLON-CANCER ; MULTIVARIATE ; ADDUCTS ; CARCINOGENS ; DIET ; DIETARY ; ALCOHOL ; EPIC ; nutrition ; SMOKERS ; FOOD ; GUIDELINES ; VITAMIN-E ; DNA-ADDUCTS ; REGRESSION ; air pollution ; prospective studies ; N-NITROSAMINES ; LEVEL ; biomarker ; analysis ; prospective ; prospective study ; correlation ; BMI ; CANCER-RISK ; ENGLAND ; non-smokers ; AMINE ; gastrointestinal ; European Prospective Investigation into Cancer ; fibre intake ; haemoglobin adducts ; RESISTANT STARCH
    Abstract: 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
    Type of Publication: Journal article published
    PubMed ID: 18275627
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  • 10
    Keywords: ENERGIES ; CANCER ; MODEL ; FOLLOW-UP ; POPULATION ; RISK ; ASSOCIATION ; hormone ; ENERGY ; AGE ; WOMEN ; colorectal cancer ; MEN ; PROSPECTIVE COHORT ; smoking ; COLORECTAL-CANCER ; cancer risk ; FISH ; FIBER ; COLON-CANCER ; DOSE-RESPONSE ; Jun ; DIET ; DIETARY ; UNITED-STATES ; ALCOHOL-CONSUMPTION ; nutrition ; ASSOCIATIONS ; RE ; ENERGY-INTAKE ; EPIC CALIBRATION ; PHYSICAL-ACTIVITY ; INTERVAL ; TESTS ; alcohol consumption ; MEAT INTAKE ; DIETARY CARCINOGENS ; GENETIC SUSCEPTIBILITY ; N-NITROSATION ; RED MEAT
    Abstract: Background. Current evidence suggests that high red meat intake is associated with increased colorectal cancer risk. High fish intake may be associated with a decreased risk, but the existing evidence is less convincing. Methods: We prospectively followed 478040 men and women from 10 European countries who were free of cancer at enrollment between 1992 and 1998. Information on diet and lifestyle was collected at baseline. After a mean follow-up of 4.8 years, 1329 incident colorectal cancers were documented. We examined the relationship between intakes of red and processed meat, poultry, and fish and colorectal cancer risk using a proportional hazards model adjusted for age, sex, energy (nonfat and fat sources), height, weight, work-related physical activity, smoking status, dietary fiber and folate, and alcohol consumption, stratified by center. A calibration substudy based on 36994 subjects was used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. All statistical tests were two-sided. Results: Colorectal cancer risk was positively associated with intake of red and processed meat (highest [〉 160 g/day] versus lowest [〈 20 g/day] intake, HR = 1.35, 95% CI = 0.96 to 1.88; P-trend = .03) and inversely associated with intake of fish (〉 80 g/day versus 〈 10 g/day, HR = 0.69, 95% CI = 0.54 to 0.88; P-trend 〈 .001), but was not related to poultry intake. Correcting for measurement error strengthened the associations between colorectal cancer and red and processed meat intake (per 100-g increase HR = 1.25, 95% CI = 1.09 to 1.41, P-trend = .001 and HR = 1.55, 95% CI = 1.19 to 2.02, P-trend = .001 before and after calibration, respectively) and for fish (per 100 g increase HR = 0.70, 95% CI = 0.57 to 0.87, P-trend 〈 .001 and HR = 0.46, 95% CI = 0.27 to 0.77, P-trend = .003; before and after correction, respectively). In this study population, the absolute risk of development of colorectal cancer within 10 years for a study subject aged 50 years was 1.71% for the highest category of red and processed meat intake and 1.28% for the lowest category of intake and was 1.86% for subjects in the lowest category of fish intake and 1.28% for subjects in the highest category of fish intake. Conclusions: Our data confirm that colorectal cancer risk is positively associated with high consumption of red and processed meat and support an inverse association with fish intake
    Type of Publication: Journal article published
    PubMed ID: 15956652
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