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  • 1
    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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  • 2
    Keywords: BLOOD ; COMPONENTS ; cord blood ; LEVEL ; HORMONES ; STEROID-HORMONES ; BLOOD-LEVELS
    Type of Publication: Journal article epub ahead of print
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  • 3
  • 4
    Keywords: CANCER ; LUNG-CANCER ; MORTALITY ; RISK ; SWEDEN ; DATABASE ; GASTRIC-CANCER ; HELICOBACTER-PYLORI ; ATTRIBUTABLE RISKS ; ENDOMETRIAL CANCER ; time trends ; education ; INCIDENCE TRENDS ; SOCIOECONOMIC GROUPS
    Type of Publication: Journal article published
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  • 5
    Keywords: CANCER ; Germany ; human ; incidence ; POPULATION ; RISK ; RISKS ; SITE ; SITES ; IMPACT ; cancer prevention ; prevention ; HEALTH ; lifestyle ; WOMEN ; MEN ; SWEDEN ; cancer risk ; DATABASE ; SIR ; TOBACCO ; ALCOHOL ; FAMILY-CANCER DATABASE ; BRITAIN ; INEQUALITIES ; LONE MOTHERS ; MIDDLE-AGED WOMEN ; NESTED CASE-CONTROL ; NORWEGIAN WOMEN BORN
    Abstract: Limited data are available on the possible changes in cancer risk brought about by widowhood and divorce, an increasing segment of the population. We calculated standardized incidence ratios (SIRs) for cancer among 47,000 widows/widowers and 60,000 divorced people, based on the Swedish Family-Cancer Database. Persons had to be identified with the same civil status in the census of years 1960 and 1970; the comparison group was married people according to the same censuses. Cancers were followed from years 1971 to 1998. Both increased and decreased SIRs were found, and a consistent pattern emerged. The effects on the divorced were always stronger than those in widows/widowers, irrespective of the direction of the effect. Every significant SIR for a cancer site in widows/widowers was accompanied by a more deviant and significant SIR in the divorced. SIRs between divorced men and women (r = 0.83, P 〈 0.0001) and between widows and divorcees correlated (r = 0.70, P 〈 0.0001). The overall cancer risk for the divorced was 0.92-0.94, and it was a balance between increased risks at tobacco-, alcohol-, and human papilloma virus-related sites, and decreased risks at most other sites. The data suggest that the changes in lifestyle on the loss of a spouse impact on the incidence of almost every type of cancer. The effects were so large that a failure to consider marital status in epidemiological studies may be a source to bias. Understanding these lifestyle changes may provide new insight in cancer prevention
    Type of Publication: Journal article published
    PubMed ID: 14504201
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  • 6
    Keywords: CANCER ; EXPRESSION ; carcinoma ; CELL ; Germany ; LUNG ; COMMON ; lung cancer ; LUNG-CANCER ; EXPOSURE ; RISK ; GENE ; GENES ; HYBRIDIZATION ; DNA ; MECHANISM ; primary ; RISK-FACTORS ; mechanisms ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; NO ; AMPLIFICATION ; AGE ; DNA-REPAIR ; REPAIR ; CIGARETTE-SMOKING ; risk factors ; smoking ; PCR ; cancer risk ; DAMAGE ; RISK FACTOR ; REGION ; CARCINOGENS ; adenocarcinoma ; case-control studies ; squamous cell carcinoma ; INDIVIDUALS ; CANCER-RESEARCH ; SMOKERS ; NUCLEOTIDE EXCISION-REPAIR ; CELL CARCINOMA ; case control study ; case-control study ; REGRESSION ; OCCUPATIONAL-EXPOSURE ; CARCINOGEN ; HEAVY ; LUNG ADENOCARCINOMA ; PIGMENTOSUM GROUP-A
    Abstract: Polymorphisms of genes coding for DNA repair can affect lung cancer risk. A common single nucleotide (-4) G-to-A polymorphism was identified previously in the 5' untranslated region of the XPA gene. In a case-control study in European Caucasians, the influence of this polymorphism on primary lung cancer risk overall and according to histologic subtypes was investigated. Four hundred sixty-three lung cancer cases (including 204 adenocarcinoma and 212 squamous cell carcinoma) and 460 tumor-free hospital controls were investigated using PCR amplification and melting point analysis of sequence-specific hybridization probes. Odds ratios (OR) were calculated by multiple logistic regression analysis adjusting for age, gender, smoking habits, and occupational exposure and showed a slightly enhanced risk for all lung cancer cases as well as for squamous cell carcinoma and adenocarcinoma cases. Gene-environment interactions were analyzed with respect to smoking and occupational exposure. A nearly 3-fold increased risk for adenocarcinoma associated with the XPA AA genotype was observed for occupationally exposed individuals (OR, 2.95; 95% confidence interval, 1.42-6.14) and for heavy smokers (OR, 2.52; 95% confidence interval, 1.17-5.42). No genotype-dependent increase in OR was found for nonexposed individuals or those smoking 〈20 pack-years. The significant effect of the XPA polymorphism in heavy smokers and occupationally exposed individuals suggests an important gene-environment interaction for the XPA gene. The underlying mechanisms as to why AA homozygotes are predisposed to lung adenocarcinoma and which specific carcinogens are involved remains to be determined
    Type of Publication: Journal article published
    PubMed ID: 15598786
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  • 7
    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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  • 8
    Keywords: CANCER ; LUNG ; MODEL ; MODELS ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; COHORT ; HISTORY ; RISK ; RISKS ; primary ; RISK-FACTORS ; INTERVENTION ; ASSOCIATION ; BREAST-CANCER ; risk factors ; smoking ; cancer risk ; RISK FACTOR ; DATABASE ; DIETARY ; CANCER-RESEARCH ; FRUIT ; QUESTIONNAIRE ; SMOKERS ; EUROPE ; FOOD ; RELATIVE RISK ; BETA-CAROTENE ; FOOD-FREQUENCY QUESTIONNAIRE ; SUPPLEMENT ; CARDIOVASCULAR-DISEASE ; ASSESSMENT INSTRUMENTS ; COMPOSITION DATABASE ; SERUM MICRONUTRIENTS ; VITAMIN-A ; WOMENS-HEALTH ; YORK-STATE COHORT
    Abstract: Intervention trials with supplemental beta-carotene have observed either no effect or a harmful effect on lung cancer risk. Because food composition databases for specific carotenoids have only become available recently, epidemiological evidence relating usual dietary levels of these carotenoids with lung cancer risk is limited. We analyzed the association between lung cancer risk and intakes of specific carotenoids using the primary data from seven cohort studies in North America and Europe. Carotenoid intakes were estimated from dietary questionnaires administered at baseline in each study. We calculated study-specific multivariate relative risks (RRs) and combined these using a random-effects model. The multivariate models included smoking history and other potential risk factors. During follow-up of up to 7-16 years across studies, 3,155 incident lung cancer cases were diagnosed among 399,765 participants. beta-Carotene intake was not associated with lung cancer risk (pooled multivariate RR = 0.98; 95% confidence interval, 0.87-1.11; highest versus lowest quintile). The RRs for alpha-carotene, lutein/zeaxanthin, and lycopene were also close to unity. beta-Cryptoxanthin intake was inversely associated with lung cancer risk (RR = 0.76; 95% confidence interval, 0.67-0.86; highest versus lowest quintile). These results did not change after adjustment for intakes of vitamin C (with or without supplements), folate (with or without supplements), and other carotenoids and multivitamin use. The associations generally were similar among never, past, or current smokers and by histological type. Although smoking is the strongest risk factor for lung cancer, greater intake of foods high in P-cryptoxanthin, such as citrus fruit, may modestly lower the risk
    Type of Publication: Journal article published
    PubMed ID: 14744731
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  • 9
    Keywords: CANCER ; DIAGNOSIS ; LUNG-CANCER ; HISTORY ; RISK ; GENE ; GENES ; METABOLISM ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; DELETION ; MUTANT ; GLUTATHIONE ; AGE ; smoking ; cancer risk ; CARRIERS ; case-control studies ; TOBACCO ; CANCER-RESEARCH ; M1 ; glutathione-S-transferase ; GLUTATHIONE S-TRANSFERASE ; case-control study ; ENVIRONMENTAL CARCINOGENS ; GSTM1 ; GSTT1 ; METAANALYSIS ; CLASS-MU ; GSTT1 POLYMORPHISMS
    Abstract: The glutathione S-transferase (GST) genes are involved in the metabolism of various carcinogens. Deletion polymorphisms in the genes GSTM1 and GSTT1 and a base transition polymorphism at codon 105 (Ile--〉Val) in GSTP1 were investigated in relation to breast cancer risk. Tobacco smoking and reproductive factors were examined as potential effect modifiers. Individual data from seven case-control studies were pooled within the International Collaborative Study on Genetic Susceptibility to Environmental Carcinogens. To measure the effect of GSTs on breast cancer risk, odds ratios and 95% confidence intervals were computed adjusting for study center and age. The modifying effect was investigated by stratification on variables of smoking habits and reproductive history. A total of 2,048 cases with breast cancer and 1,969 controls were analyzed. The relative odds ratio (95% confidence interval) of breast cancer was 0.98 (0.86-1.12) with the GSTM1 null, 1.11 (0.87-1.41) with the GSTT1 null, 1.01 (0.79-1.28) with GSTP1 heterozygous mutants, and 0.93 (0.62-1.38) with GSTP1 homozygous mutants. Stratification by smoking or reproductive factors did not reveal a modifying effect of these variables, nor was there any association between GSTM1 and age at diagnosis of breast cancer. This is the largest study investigating susceptibility to breast cancer due to polymorphisms in the GST genes. The results conclusively show that single gene GST polymorphisms do not confer a substantial risk of breast cancer to its carriers. Furthermore, GSTs did not interact with smoking or reproductive history to modify cancer risk
    Type of Publication: Journal article published
    PubMed ID: 15342448
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  • 10
    Keywords: CANCER ; Germany ; FOLLOW-UP ; COHORT ; cohort study ; DEATH ; DISEASE ; DISEASES ; MORTALITY ; POPULATION ; RISK ; RISK-FACTORS ; prevention ; AGE ; OBESITY ; risk factors ; smoking ; DIET ; DIETARY ; UNITED-STATES ; PREVALENCE ; body mass index ; MASSES ; RE ; CARDIOVASCULAR-DISEASE ; PHYSICAL-ACTIVITY ; CORONARY-HEART-DISEASE ; INTERVAL ; MEAT CONSUMPTION ; SEVENTH-DAY-ADVENTISTS
    Abstract: Background: The long-term observation of vegetarians in affluent countries can provide insight into the relative effects of a vegetarian diet and lifestyle factors on mortality. Methods: A cohort study of vegetarians and health-conscious persons in Germany was followed-up prospectively for 21 years, including 1,225 vegetarians and 679 health-conscious nonvegetarians. Standardized mortality ratios compared with the German general population were calculated for all causes and specific causes. Within the cohort, Poisson regression modeling was used to investigate the joint effects of several risk factors on overall and cause-specific mortality. Results: Standardized mortality ratios for all-cause mortality was significantly below 100: 59 [95% confidence interval (95% CD, 54-64], predominantly due to a deficit of deaths from circulatory diseases. Within the cohort, vegetarian compared with nonvegetarian diet had no effect on overall mortality [rate ratio (RR), 1.10; 95% CI, 0.89-1.36), whereas moderate and high physical activity significantly reduced risk of death (RR, 0.62, 0.64), adjusted for age, sex, smoking, alcohol intake, body mass index, and educational level. Vegetarian diet was however associated with a reduced RR of 0.70 (95% CI, 0.41-1.18) for ischemic heart disease, which could partly be related to avoidance of meat. Conclusions: Both vegetarians and nonvegetarian health-conscious persons in this study have reduced mortality compared with the general population. Within the study, low prevalence of smoking and moderate or high level of physical activity but not strictly vegetarian diet was associated with reduced overall mortality. The nonsignificant reduction in mortality from ischemic heart diseases in vegetarians compared with health-conscious persons could be explained in part by avoidance of meat intake
    Type of Publication: Journal article published
    PubMed ID: 15824171
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