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  • 1
    Keywords: CANCER ; MODEL ; MODELS ; FOLLOW-UP ; COHORT ; DISEASE ; MORTALITY ; RISK ; RISKS ; AGE ; WOMEN ; OBESITY ; smoking ; COUNTRIES ; TOBACCO ; GLUCOSE ; BODY ; DIABETES-MELLITUS ; nutrition ; pancreatic cancer ; RELATIVE RISK ; physical activity ; MASS INDEX ; PANCREATIC-CANCER ; PHYSICAL-ACTIVITY ; HEIGHT ; WAIST ; INTERVAL ; pancreatic ; INSULIN-RESISTANCE ; PARTICIPANTS ; anthropometry ; prospective ; RISK-FACTOR ; BODY-FAT DISTRIBUTION ; hip ; MALE SMOKERS
    Abstract: Tobacco smoking is the only established risk factor for pancreatic cancer. Results from several epidemiologic studies have suggested that increased body mass index and/or lack of physical activity may be associated with an increased risk of this disease. We examined the relationship between anthropometry and physical activity recorded at baseline and the risk of pancreatic cancer in the European Prospective Investigation into Cancer and Nutrition (n = 438,405 males and females age 19-84 years and followed for a total of 2,826,070 person-years). Relative risks (RR) were calculated using Cox proportional hazards models stratified by age, sex, and country and adjusted for smoking and self-reported diabetes and, where appropriate, height. In total, there were 324 incident cases of pancreatic cancer diagnosed in the cohort over an average of 6 years of follow-up. There was evidence that the RR of pancreatic cancer was associated with increased height [RR, 1.74; 95% confidence interval (95% CI), 1.20-2.52] for highest quartile compared with lowest quartile (P-trend = 0.001). However, this trend was primarily due to a low risk in the lowest quartile, as when this group was excluded, the trend was no longer statistically significant (P = 0.27). A larger waist-to-hip ratio and waist circumference were both associated with an increased risk of developing the disease (RR per 0.1, 1.24; 95% CI, 1.04-1.48; P-trend = 0.02 and RR per 10 cm, 1.13; 95% CI, 1.01-1.26; P-trend = 0.03, respectively). There was a nonsignificant increased risk of pancreatic cancer with increasing body mass index (RR, 1.09; 95% CI, 0.95-1.24 per 5 kg/m(2)), and a nonsignificant decreased risk with total physical activity (RR, 0.82; 95% CI, 0.50-1.35 for most active versus inactive). Future studies should consider including measurements of waist and hip circumference, to further investigate the relationship between central adiposity and the risk of pancreatic cancer
    Type of Publication: Journal article published
    PubMed ID: 16702364
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  • 2
    Keywords: CANCER ; CELLS ; LUNG ; MODEL ; lung cancer ; LUNG-CANCER ; COHORT ; EXPOSURE ; TIME ; CARCINOGENESIS ; STAGE ; prevention ; CIGARETTE-SMOKING ; smoking ; COUNTRIES ; RATES ; PARAMETERS ; TRANSFORMATION ; PROJECT ; EPIC ; nutrition ; mechanistic model ; INITIATION ; DEPENDENCE ; TOBACCO-SMOKE ; 2-MUTATION MODEL ; PROMOTION ; prospective ; EUROPEAN COUNTRIES ; ATOMIC-BOMB SURVIVORS ; EXPANSION ; CIGARETTE-SMOKE ; BRITISH DOCTORS DATA ; CLONAL EXPANSION MODEL ; P53 MUTATION SPECTRUM ; SOMATIC MUTATIONS ; STATE-VECTOR MODEL
    Abstract: A stochastic two-stage cancer model is used to analyse the relation between lung cancer and cigarette smoking. The model contains the main rate-limiting stages of carcinogenesis, which include initiation, promotion (clonal expansion of initiated cells), malignant transformation and a lag time for tumour formation. Various data sets were used to test the model. These include the data of a large prospective collaborative project carried out in 10 different European countries, the European Prospective Investigation into Cancer and Nutrition (EPIC). This new data set has not been modelled before. The model is also tested on other published data from CPS-II (Cancer Prevention Study II) of the American Cancer Society and the British doctors' study. The analyses indicate that the EPIC data are best described with smoking dependence on the rates of malignant transformation and clonal expansion. With increasing smoking rates, saturation effects in the two exposure rate-dependent model parameters were observed. The results find confirmation in the biological literature, where both mutational effects and promotional effects of cigarette smoke are documented
    Type of Publication: Journal article published
    PubMed ID: 16410261
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  • 3
    Keywords: CANCER ; Germany ; LUNG ; FOLLOW-UP ; INFORMATION ; lung cancer ; LUNG-CANCER ; COHORT ; cohort study ; EPIDEMIOLOGY ; EXPOSURE ; MORTALITY ; occupation ; POPULATION ; RISK ; RISKS ; REDUCTION ; RISK-FACTORS ; ASSOCIATION ; HUMANS ; WOMEN ; MEN ; risk factors ; smoking ; COUNTRIES ; cancer risk ; POPULATIONS ; DIET ; VALIDITY ; EPIC ; nutrition ; SMOKERS ; RELATIVE RISK ; exercise ; physical activity ; REGRESSION ; ASSOCIATIONS ; PHYSICAL-ACTIVITY ; INTERVAL ; SUBTYPES ; prospective ; UNIT ; RISK-FACTOR ; CANCER-RISK ; sports ; occupations ; ACTIVITY QUESTIONNAIRE
    Abstract: Research conducted predominantly in male populations on physical activity and lung cancer has yielded inconsistent results. We examined this relationship among 416,277 men and women from the European Prospective Investigation into Cancer and Nutrition (EPIC). Detailed information on recent recreational, household and occupational physical activity, smoking habits and diet was assessed at baseline between 1992 and 2000. Relative risks (RR) were estimated using Cox regression. During 6.3 years of follow-up we identified 607 men and 476 women with incident lung cancer. We did not observe an inverse association between recent occupational, recreational or household physical activity and lung cancer risk in either males or females. However, we found some reduction in lung cancer risk associated with sports in males (adjusted RR = 0.71; 95% confidence interval 0.50-0.98; highest tertile vs. inactive group), cycling (RR = 0.73; 0.54-0.99) in females and non-occupational vigorous physical activity. For occupational physical activity, lung cancer risk was increased for unemployed men (adjusted RR = 1.57; 1.20-2.05) and men with standing occupations (RR = 1.35; 1.02-1.79) compared with sitting professions. There was no evidence of heterogeneity of physical activity associations across countries, or across any of the considered cofactors. For some histologic subtypes suggestive sex-specific reductions, limited by subgroup sizes, were observed, especially with vigorous physical activity. In total, our study shows no consistent protective associations of physical activity with lung cancer risk. It can be assumed that the elevated risks found for occupational physical activity are not produced mechanistically by physical activity itself but rather reflect exposure to occupation-related lung cancer risk factors. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16894558
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  • 4
    Keywords: CANCER ; carcinoma ; Germany ; FOLLOW-UP ; INFORMATION ; COHORT ; EPIDEMIOLOGY ; RISK ; INFECTION ; RISK-FACTORS ; ASSOCIATION ; HEALTH ; REDUCED RISK ; risk factors ; cancer risk ; RECRUITMENT ; DIET ; STOMACH ; adenocarcinoma ; case-control studies ; TOBACCO ; ALCOHOL ; CARDIA ; EPIC ; ESOPHAGUS ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; nutrition ; STOMACH-CANCER ; case-control study ; ASSOCIATIONS ; DIGESTIVE-TRACT ; gastric cancer ; LEVEL ; case control studies ; INTERVAL ; methods ; PROFILES ; prospective ; EVALUATE ; odds ratio ; RISK-FACTOR ; CANCER-RISK ; Helicobacter pylori ; cardia cancer ; socioeconomic position
    Abstract: Objectives To evaluate the association of socioeconomic position with adenocarcinoma of the oesophagus and stomach. Methods The European Prospective Investigation into Cancer and Nutrition (EPIC) cohort comprises about 520000 participants mostly aged 35-70 years. Information on diet and lifestyle was collected at recruitment. After an average follow-up of 6.5 years, 268 cases with adenocarcinoma of the stomach and 56 of the oesophagus were confirmed. We examined the effect of socioeconomic position on cancer risk by means of educational data and a computed Relative Index of Inequality (RII). In a nested case-control study, adjustment for Helicobacter pylori (H. pylori) infection was performed. Results Higher education was significantly associated with a reduced risk of gastric cancer [vs lowest level of education, hazard ratio (HR): 0.64, 95% Confidence intervals (CI): 0.43-0.981. This effect was more pronounced for cancer of the cardia (HR: 0.42, 95% CI: 0.20-0.89) as compared to non-cardia gastric cancer (HR: 0.66, 95% CI: 0.36-1.22). Additionally, the inverse association of educational level and gastric cancer was stronger for cases with intestinal (extreme categories, HR: 0.13, 95% CI: 0.04-0.44) rather than diffuse histological subtype (extreme categories, HR: 0.71 95% CI: 0.37-1.40). In the nested case-control study, inverse but statistically non-significant associations were found after additional adjustment for H. pylori infection [highest vs lowest level of education: Odds ratio (OR) 0.53, 95% CI: 0.24-1.18]. Educational level was non-significantly, inversely associated with carcinoma of the oesophagus. Conclusion A higher socioeconomic position was associated with a reduced risk of gastric adenocarcinoma, which was strongest for cardia cancer or intestinal histological subtype, suggesting different risk profiles according to educational level. These effects appear to be explained only partially by established risk factors
    Type of Publication: Journal article published
    PubMed ID: 17227779
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  • 5
    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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  • 6
    Keywords: SURVIVAL ; COHORT ; EPIDEMIOLOGY ; RISK ; RISK-FACTORS ; HEALTH ; POPULATIONS ; INEQUALITIES ; DETERMINANTS ; PHYSICAL-ACTIVITY ; METAANALYSIS ; socioeconomic status ; SOCIOECONOMIC-STATUS ; Educational level ; Pancreatic cancer incidence
    Abstract: Introduction: Until now, studies examining the relationship between socioeconomic status and pancreatic cancer incidence have been inconclusive. Aim: To prospectively investigate to what extent pancreatic cancer incidence varies according to educational level within the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Methods: In the EPIC study, socioeconomic status at baseline was measured using the highest level of education attained. Hazard ratios by educational level and a summary index, the relative indices of inequality (Rh), were estimated using Cox regression models stratified by age, gender, and center and adjusted for known risk factors. In addition, we conducted separate analyses by age, gender and geographical region. Results: Within the source population of 407, 944 individuals at baseline, 490 first incident primary pancreatic adenocarcinoma cases were identified in 9 European countries. The crude difference in risk of pancreatic cancer according to level of education was small and not statistically significant (RII = 1.14, 95% CI 0.80-1.62). Adjustment for known risk factors reduced the inequality estimates to only a small extent. In addition, no statistically significant associations were observed for age groups (adjusted RII 〈= (60) (years) = 0.85, 95% CI 0.44-1.64, adjusted RII〉 60 years = 1.18, 95% CI 0.73-1.90), gender (adjusted RIImale = 1.20, 95% CI 0.68-2.10, adjusted RIIfemale = 0.96, 95% CI 0.56-1.62) or geographical region (adjusted RIINorthern Europe = 1.14, 95% CI 0.81-1.61, adjusted RIIMiddle (Europe) = 1.72, 95% CI 0.93-3.19, adjusted RIISouthern Europe = 0.75, 95% CI 0.32-1.80). Conclusion: Despite large educational inequalities in many risk factors within the EPIC study, we found no evidence for an association between educational level and the risk of developing pancreatic cancer in this European cohort.
    Type of Publication: Journal article published
    PubMed ID: 20829145
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  • 7
    Keywords: CANCER ; BLOOD ; RISK ; ENZYMES ; GENE ; GENES ; ACTIVATION ; DNA ; CARCINOGENESIS ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; AGE ; CIGARETTE-SMOKING ; COUNTRIES ; GENOTYPES ; COLORECTAL CANCERS ; LINKAGE DISEQUILIBRIUM ; adenocarcinoma ; case-control studies ; TOBACCO ; GASTRIC-CANCER ; nutrition ; SMOKERS ; case-control study ; VARIANT ; TOBACCO-SMOKE ; GSTM1 ; GSTT1 ; gastric cancer ; S-TRANSFERASE M1 ; case control studies ; INTERVAL ; ENZYME ; GENETIC-POLYMORPHISM ; LOCUS ; FAMILY-HISTORY ; prospective ; ALLELE FREQUENCIES ; COMPOUND ; EPOXIDE HYDROLASE POLYMORPHISMS ; EUROPEAN COUNTRIES ; HIGH-INCIDENCE AREA ; INCREASED RISK ; NEVER SMOKERS ; odds ratio ; T1 NULL GENOTYPES ; tobacco smoke ; UNIT
    Abstract: Metabolizing enzymes, which often display genetic polymorphisms, are involved in the activation of compounds present in tobacco smoke that may be relevant to gastric carcinogenesis. We report the results of a study looking at the association between risk of gastric adenocarcinoma and polymorphisms in genes CYP1A1, CYP1A2, EPHX1, and GSTT1. A nested case-control study was carried out within the European Prospective Investigation into Cancer and Nutrition, developed in 10 European countries. The study includes 243 newly diagnosed cases of histologically confirmed gastric adenocarcinoma and 946 controls matched by center, age, sex, and date of blood collection. Genotypes were determined in nuclear DNA from WBCs. We found an increased risk of gastric cancer for homozygotes for C (histidine) variant in Y113H of EPHX1 (odds ratio, 1.91; 95% confidence interval, 1.19-3.07) compared with subjects with TC/TT. There was also a significant increased risk for smokers carrying at least one variant allele A in Ex7+129C 〉 A (m4) of CYP1A1 and never smokers with null GSTT1 and allele A in the locus -3859G 〉 A of CYP1A2. Most of these genes are involved in the activation and detoxification of polycyclic aromatic hydrocarbons, suggesting a potential role of these compounds in gastric carcinogenesis
    Type of Publication: Journal article published
    PubMed ID: 17164366
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  • 8
    Keywords: CANCER ; LUNG-CANCER ; SUPPORT ; COHORT ; RISK ; GENE ; GENES ; validation ; DNA ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; antibodies ; antibody ; NO ; HEALTH ; REPAIR ; COLORECTAL-CANCER ; cancer risk ; microsatellite instability ; adenocarcinoma ; EPIC ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; DNA repair ; TP53 ; RE ; prospective studies ; XPD POLYMORPHISMS ; gastric cancer ; XRCC1 ; GC ; ALLELES ; LEVEL ; DNA repair genes ; prospective ; prospective study ; CANCER-RISK ; Helicobacter pylori ; intestinal metaplasia ; ENGLAND ; CHINESE POPULATION ; HOGG1 SER326CYS POLYMORPHISM ; OGG1 ; chronic atrophic gastritis ; pepsinogen ; RATIO ; GENE POLYMORPHISMS ; GENE POLYMORPHISM ; neoplasm ; gastric adenocarcinoma ; severe chronic atrophic gastritis
    Abstract: Background The contribution of genetic variation in DNA repair genes to gastric cancer (GC) risk remains essentially unknown. The aim of this study was to explore the relative contribution of DNA repair gene polymorphisms to GC risk and severe chronic atrophic gastritis (SCAG). Method A nested case control study within the EPIC cohort was performed including 246 gastric adenocarcinomas and 1175 matched controls. Controls with SCAG (n 91), as defined by low pepsinogen A (PGA) levels, and controls with no SCAG (n 1061) were also compared. Twelve polymorphisms at DNA repair genes (MSH2, MLH1, XRCC1, OGG1 and ERCC2) and TP53 gene were analysed. Antibodies against Helicobacter pylori were measured. Results No association was observed for any of these polymorphisms with stomach cancer risk. However, ERCC2 K751Q polymorphism was associated with an increased risk for non-cardial neoplasm [odds ratio (OR) 1.78; 95 confidence interval (CI) 1.023.12], being ERCC2 K751Q and D312N polymorphisms associated with the diffuse type. ERCC2 D312N (OR 2.0; 95 CI 1.093.65) and K751Q alleles (OR 1.82; 95 CI 1.013.30) and XRCC1 R399Q (OR 1.69; 95 CI 1.022.79) allele were associated with an increased risk for SCAG. Conclusion Our study supports a role of ERCC2 in non-cardial GC but not in cardial cancer. A concordant result was observed for subjects with low PGA levels. XRCC1 allele was associated also with SCAG. This is the first prospective study suggesting that individual variation in DNA repair may be relevant for gastric carcinogenesis, a finding that will require further confirmation validation in larger independent studies
    Type of Publication: Journal article published
    PubMed ID: 18641418
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  • 9
    Keywords: CANCER ; evaluation ; MODEL ; MODELS ; COHORT ; DISEASE ; EXPOSURE ; incidence ; RISK ; validation ; IMPACT ; ASSOCIATION ; HEALTH ; WOMEN ; colorectal cancer ; MEN ; COLORECTAL-CANCER ; FISH ; REGION ; MEASUREMENT ERROR ; FRANCE ; REGIONS ; VARIABILITY ; DIET ; DIETARY ; SERIES ; OUTCOMES ; EPIC ; nutrition ; CALIBRATION ; FOOD ; DIETARY-INTAKE ; HETEROGENEITY ; MULTICENTER COHORT ; REGRESSION ; INCREASE ; DIETARY QUESTIONNAIRE ASSESSMENTS ; ENERGY-INTAKE ; LEVEL ; methods ; NUTRITIONAL EPIDEMIOLOGY ; CANCER INCIDENCE ; prospective ; ENGLAND ; SET ; outcome ; ERRORS ; RATIO ; VALUES ; European Prospective Investigation into Cancer ; hazard ratio ; CONFIDENCE-INTERVALS ; multicentre study ; TIME-SCALE
    Abstract: 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): 0.950.99] and 0.93 (0.880.98), 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 dietdisease relationship caused by differential impact of measurement errors across cohorts
    Type of Publication: Journal article published
    PubMed ID: 18180242
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  • 10
    Keywords: CANCER ; tumor ; carcinoma ; MODEL ; COHORT ; RISK ; POLYMORPHISMS ; WOMEN ; colorectal cancer ; RISK FACTOR ; TOBACCO ; ALCOHOL-CONSUMPTION ; LIFE-STYLE FACTORS ; RECTAL-CANCER ; ASSOCIATIONS ; METAANALYSIS ; INCREASED RISK ; COLON TUMORS ; Tumor Location ; TUMOR MICROSATELLITE INSTABILITY
    Abstract: BACKGROUND & AIMS: There has been consistent evidence for a relationship between smoking and colorectal cancer (CRC), although it is not clear whether the colon or rectum is more sensitive to the effects of smoking. We investigated the relationships between cigarette smoking and risk of CRC and tumor location. METHODS: We analyzed data from 465,879 participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) study; 2,741 developed CRC during the follow-up period (mean 8.7 years). Cox proportional hazard regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs). RESULTS: The risk of colon carcinoma was increased among ever smokers (HR 1.18, 95%CI 1.06-1.32) and former cigarette smokers (HR 1.21, 95%CI 1.08-1.36), compared with never smokers; the increased risk for current smokers was of borderline significance (HR 1.13, 95%CI 0.98-1.31). When stratified for tumor location, the risk of proximal colon cancer was increased for former (HR 1.25, 95%CI 1.04-1.50) and current smokers (HR 1.31, 95%CI 1.06-1.64), but the risks for cancers in the distal colon or rectum were not. Subsite analyses showed a non-significant difference between the proximal and distal colon (p=0.45) for former smokers and a significant difference for current smokers (p=0.02). For smokers that had stopped smoking for at least 20 years, the risk of developing colon cancer was similar to that of never smokers. CONCLUSIONS: Ever smokers have an increased risk of colon cancer, which appeared to be more pronounced in the proximal than the distal colon location.
    Type of Publication: Journal article published
    PubMed ID: 21029790
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