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  • 1
    Keywords: CANCER ; Germany ; INFORMATION ; EXPOSURE ; RISK ; GENE ; METABOLISM ; PATIENT ; HETEROCYCLIC AMINES ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY ; AGE ; CIGARETTE-SMOKING ; colorectal cancer ; smoking ; COLORECTAL-CANCER ; cancer risk ; genetic polymorphism ; CARCINOGENS ; case-control studies ; TOBACCO ; INDIVIDUALS ; CONSUMPTION ; meat ; ONCOLOGY ; case-control study ; REGRESSION ; RE ; ALLELE ; CARCINOGEN ; SUBSTRATE ; case control studies ; INTERVAL ; ENZYME ; analysis ; GENOTYPE ; MEAT CONSUMPTION ; USA ; odds ratio ; RISK-FACTOR ; CANCER-RISK ; colorectal ; LOGISTIC-REGRESSION ; N-ACETYLTRANSFERASE-1 ; NAT2 GENETIC POLYMORPHISMS ; SULFOTRANSFERASE 1A1 ; SULT1A1
    Abstract: Several procarcinogens that are present in cooked red meat and tobacco smoke are substrates for sulfotransferase 1A1 (SULT1A1). The association between environmental exposures and colorectal cancer risk may be modified by individual differences in the metabolism. Thus, we investigated the effect of a common polymorphism in the SULT1A1 gene associated with decreased enzyme activity on the susceptibility to colorectal cancer in a population-based case-control study. Patients (505) and 604 age- and sex-matched controls provided detailed risk factor information and were genotyped for SULT1A1 G638A using a fluorescence-based melting curve analysis method. Multivariate logistic regression analysis was used to estimate colorectal cancer risk associated with environmental exposures by SULT1A1 genotype. SULT1A1 genotype was not an independent risk factor for colorectal cancer. Risk of colorectal cancer associated with frequent consumption of red meat was significantly elevated among carriers of the SULT1A1*2 allele but not increased among subjects with the SULT1A1*1/*1 genotype (odds ratio (OR) 2.1, 95% confidence interval (CI) 1.1-4.1 and OR 1.0, 95% CI 0.5-2.1, respectively). Colorectal cancer risk associated with 30+ pack-years of active smoking was higher among carriers of the SULT1A1*2 allele (OR 1.7, 95 % CI 1.0-3.2) than among individuals with the SULT1A1*1/*1 genotype (OR 1.1, 95% CI 0.6-2.1). Our results do not support a main effect of SULT1A1 genotype with regard to colorectal cancer but suggest that individuals with the low activity SULT1A1*2 allele may be at higher risk following carcinogen exposure than those with the SULT1A1*1/*1 genotype. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 17013894
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  • 2
    Keywords: CANCER ; Germany ; RISK ; BREAST ; breast cancer ; BREAST-CANCER ; prevention ; AGE ; WOMEN ; cancer risk ; UNITED-STATES ; case-control studies ; POSTMENOPAUSAL WOMEN ; breast neoplasms ; premenopause ; YOUNG-WOMEN ; ADULT ; case-control study ; population-based case-control study ; RE ; WEIGHT ; BODY-SIZE ; PHYSICAL-ACTIVITY ; HEIGHT ; case control studies ; INTERVAL ; DIFFERENT PERIODS ; MASS ; PREMENOPAUSAL WOMEN ; OVERWEIGHT ; body weight changes ; RELATIVE WEIGHT
    Abstract: Studies have shown fairly consistent results regarding an inverse relationship between overweight and premenopausal breast cancer risk, but reported effects of weight changes have been inconsistent. Data was analysed on weight, weight changes, height and body build for 558 premenopausal women with breast cancer and 1116 controls below 51 years who participated in a population-based case-control study in Germany from 1992 to 1995. Larger body build at menarche conferred a protective effect, when compared with smaller build [odds ratio (OR) 0.69, 95% confidence interval (CI) 0.49, 0.96]. In comparison with the lowest quartile, higher quartiles of weight gain from the lowest adult weight to current weight conferred a significant protective effect to those who attained their lowest adult weight after but not before the (median) age of 21, with OR and 95% CI of 0.52 (0.32, 0.83), 0.50 (0.30, 0.81), 0.56 (0.34, 0.94) for second, third and fourth quartiles respectively. Our findings are consistent with studies that found weight gain to be protective against premenopausal breast cancer and suggest that this effect may be more pronounced for women who were lean in adolescence and early adulthood. European Journal of Cancer Prevention 14:419-426 (c) 2005 Lippincott Williams & Wilkins
    Type of Publication: Journal article published
    PubMed ID: 16030434
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  • 3
    Keywords: CANCER ; Germany ; DISEASE ; RISK ; RISKS ; GENE ; transcription ; ASSOCIATION ; FREQUENCY ; polymorphism ; SUSCEPTIBILITY ; ALPHA ; BREAST ; breast cancer ; BREAST-CANCER ; ASSAY ; NUMBER ; WOMEN ; cancer risk ; REGION ; LENGTH ; case-control study ; PROMOTER POLYMORPHISM ; ESTROGEN ; ALLELES ; case control studies ; INTERVAL ; GENETIC-POLYMORPHISM ; PREMENOPAUSAL WOMEN ; NO ASSOCIATION ; HORMONE LEVELS ; AGE 40 YEARS ; AUSTRALIAN WOMEN ; METABOLISM GENE CYP17 ; STEROID 17-ALPHA-HYDROXYLASE/17,20 LYASE
    Abstract: Introduction Studies on the association between the cytochrome P450c17 alpha gene (CYP17) 5 '-untranslated region MspA1 genetic polymorphism and breast cancer risk have yielded inconsistent results. Higher levels of estrogen have been reported among young nulliparous women with the A2 allele. Therefore we assessed the impact of CYP17 genotypes on the risk of premenopausal breast cancer, with emphasis on parity. Methods We used data from a population-based case-control study of women aged below 51 years conducted from 1992 to 1995 in Germany. Analyses were restricted to clearly premenopausal women with complete information on CYP17 and encompassed 527 case subjects and 904 controls, 99.5% of whom were of European descent. The MspA1 polymorphism was analyzed using PCR-RFLP (PCR-restriction fragment length polymorphism) assay. Results The frequencies of the variant allele among the cases and controls were 43% and 41%, respectively. Overall, CYP17 A1/A2 and A2/A2 genotypes compared with the A1/A1 genotype were not associated with breast cancer, with adjusted odds ratios (ORs) of 1.04 and 1.23, respectively. Among nulliparous women, however, breast cancer risk was elevated for the A1/A2 (OR = 1.31; 95% confidence interval (CI) 0.74 to 2.32) and the A2/A2 genotype (OR = 2.12; 95% CI 1.04 to 4.32) compared with the A1/A1 genotype, with a trend towards increasing risk associated with number of A2 alleles (P = 0.04). Otherwise, the CYP17 polymorphism was found neither to be an effect modifier of breast cancer risks nor to be associated with stage of disease. Conclusion Our results do not indicate a major influence of CYP17 MspA1 polymorphism on the risk of premenopausal breast cancer, but suggest that it may have an impact on breast cancer risk among nulliparous women. The finding, however, needs to be confirmed in further studies
    Type of Publication: Journal article published
    PubMed ID: 15987450
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  • 4
    Keywords: CANCER ; Germany ; RISK ; PATIENT ; ASSOCIATION ; polymorphism ; BREAST-CANCER ; AGE ; CIGARETTE-SMOKING ; smoking ; COLORECTAL-CANCER ; BLADDER-CANCER ; METABOLIC-ACTIVATION ; COLON-CANCER ; case-control studies ; TOBACCO ; INDIVIDUALS ; CONSUMPTION ; RECTAL-CANCER ; case-control study ; population-based case-control study ; RE ; case control studies ; INTERVAL ; RISK-FACTOR ; population-based ; PASSIVE SMOKING ; ARYLAMINE N-ACETYLTRANSFERASE ; INCREASES RISK ; RECOMBINANT HUMAN NAT1
    Abstract: N-Acetyltransferases 1 and 2 (NAT1 and NAT2), both being highly polymorphic, are involved in the metabolism of aromatic and heterocyclic aromatic amines present in cigarette smoke and red meat cooked by high-temperature cooking techniques. We investigated the effect of differences in acetylation capacity, determined by NAT1 and NAT2 genotypes, on colorectal cancer risk associated with exposure to tobacco smoke or red meat consumption. In this population-based case-control study in Germany, 505 patients with incident colorectal cancer and 604 age- and sex-matched control individuals with genotyping data and detailed risk factor information were included. Genotyping of NAT1 and NAT2 genetic polymorphisms was done using a fluorescence-based melting curve analysis method. The association between genotypes, environmental exposures, and colorectal cancer risk was estimated using multivariate logistic regression. Colorectal cancer risk associated with active smoking was elevated after accumulation of 30(+) pack-years of smoking [odds ratio (OR), 1.4; 95% confidence interval (95% CI), 0.9-2.2] but not significantly modified by either NAT1 or NAT2 genotype. Exposure to environmental tobacco smoke was associated with an increased risk for colorectal cancer only among NAT2 fast acetylators (OR, 2.6; 95% CI, 1.1-5.9 for exposure in childhood and adulthood). Frequent consumption of red meat significantly increased colorectal cancer risk for the group comprising all NAT2 fast acetylators or carriers of the NAT1*10 allele (OR, 2.6; 95% Cl, 1.1-6.1) but not among those with "slow" NAT1 and NAT2 genotypes. Our findings indicate that NAT1 and NAT2 genotypes may contribute jointly to individual susceptibility and that heterocyclic aromatic amines may play an important role in colorectal cancer associated with red meat and possibly also exposure to environmental tobacco smoke
    Type of Publication: Journal article published
    PubMed ID: 16434594
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  • 5
    Keywords: CANCER ; MODEL ; LUNG-CANCER ; EXPOSURE ; RISK ; ASSOCIATION ; prevention ; WOMEN ; CIGARETTE-SMOKING ; smoking ; COLORECTAL-CANCER ; case-control studies ; case-control study ; CHILDHOOD ; EPIDEMIOLOGIC EVIDENCE ; PASSIVE SMOKING ; colorectal neoplasm
    Abstract: In a population-based case-control study in Germany, 540 incident cases of colorectal cancer (CRC) aged 〉= 30 years and 614 controls were recruited from January 2003 to June 2004. Information on risk factors of CRC and lifetime history of active smoking and exposure to environmental tobacco smoke (ETS) was obtained by personal interviews. This analysis is limited to never smokers (252 cases and 292 controls). Associations were assessed using conditional logistic regression models adjusting for potential confounders. We found no evidence of an increased risk of CRC following exposure to ETS overall, in childhood or at work. For spousal exposure, we, however, found a significant risk increase for women currently exposed (OR: 3.54; 95% Cl: 1.03-12.15) and for women exposed to 〉 23 pack-years of spousal smoking (OR: 3.02; 95% Cl: 0.99-9.28). Our findings do not indicate a major impact of ETS on CRC risk but suggest that risk may be increased following spousal exposure. European Journal of Cancer Prevention 18:9-12 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins
    Type of Publication: Journal article published
    PubMed ID: 19077559
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  • 6
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    German Medical Science; Düsseldorf, Köln
    In:  50. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 12. Jahrestagung der Deutschen Arbeitsgemeinschaft für Epidemiologie; 20050912-20050915; Freiburg im Breisgau; DOC05gmds198 /20050908/
    Publication Date: 2005-09-09
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 7
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    German Medical Science; Düsseldorf, Köln
    In:  50. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 12. Jahrestagung der Deutschen Arbeitsgemeinschaft für Epidemiologie; 20050912-20050915; Freiburg im Breisgau; DOC05gmds199 /20050908/
    Publication Date: 2005-09-09
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 8
    Keywords: CANCER ; Germany ; human ; POPULATION ; RISK ; PATIENT ; ASSOCIATION ; polymorphism ; ALPHA ; BREAST ; breast cancer ; BREAST-CANCER ; HUMANS ; WOMEN ; cancer risk ; CANCER-PATIENTS ; DIETARY ; CONSUMPTION ; PRECURSORS ; LIGNANS ; urinary estrogen metabolites ; POSTMENOPAUSAL WOMEN ; REGRESSION ; RE ; PHYTO-ESTROGENS ; SERUM ENTEROLACTONE CONCENTRATION ; LEVEL ; ENTEROLACTONE ; CANCER-RISK ; PLASMA ENTEROLACTONE ; TIME-RESOLVED FLUOROIMMUNOASSAY ; isoflavonoids ; cYP17 ; DIETARY PHYTOESTROGEN INTAKE ; GENE CYP17 ; HORMONE CONCENTRATIONS ; MSPA1 POLYMORPHISM ; premenopausal breast cancer
    Abstract: Cytochrome P450c17 alpha (CYP17) has been associated with alterations in steroid hormone levels and premenopausal breast cancer risk and could modify the association between phytoestrogen intake and breast cancer risk. We examined plasma concentrations of enterolactone and genistein, estimated dietary phytoestrogen intake, CYP175'-UTR MspA1 genetic polymorphism, and breast cancer risk in 267 premenopausal breast cancer patients and 573 age-matched population controls from Germany. Multivariate logistic regression was used to estimate breast cancer risk associated with quartiles of phytoestrogen intake by genotype and to investigate gene-nutrient interactions. Premenopausal breast cancer risk was not significantly associated with the CYP17 A2 genotype. We observed a significant modifying effect of CYP17 genotype on plasma enterolactone-associated breast cancer risk (P for interaction 〈 0.01). Plasma enterolactone was significantly inversely related to breast cancer risk only in A2A2 carriers, showing odds ratios and 95% Cl of 0.02 (0.00-0.41) and 0.01 (0.00-0.21) for the third and fourth quartiles vs. the lowest quartile, respectively. This inverse association was also found for the calculated enterolignan production as well as matairesinol intake. Compared with A1A1 carriers with the lowest enterolactone supply, the risk reduction associated with a high enterolactone supply resulted in a comparably decreased breastcancer risk for all genotypes. For genistein, no clear indication for a differential effect by CYP17 genotype was obtained. Our results suggest that CYP17 genotype modifies the protective effect of lignans on premenopausal breast cancer risk. Women homozygous for A2 allele benefit most from high plasma enterolactone concentrations and a high consumption of dietary precursors
    Type of Publication: Journal article published
    PubMed ID: 16702327
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