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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 ; METABOLISM ; polymorphism ; BREAST ; breast cancer ; BREAST-CANCER ; AGE ; WOMEN ; cancer risk ; Jun ; gene-environment interaction ; CARRIERS ; alcohol dehydrogenase ; ALCOHOL-CONSUMPTION ; case-control study ; case control studies ; INTERVAL ; GENETIC-POLYMORPHISM ; CARRIER ; EUROPEANS ; alcohol consumption
    Abstract: In a population-based study of 613 cases and 1082 controls, alcohol dehydrogenase 1B (ADH1B) genotype was not an independent risk factor for breast cancer, athough the possibility was raised that it modifies risk associated with high levels of alcohol consumption ( OR 1.1, 95% confidence interval (CI) 0.8 - 1.6 for ADH1B*1/*1 genotype vs 0.2, 95% CI 0.1 - 1.0 for ADH1B*2 carriers)
    Type of Publication: Journal article published
    PubMed ID: 15886702
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  • 3
    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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  • 4
    Keywords: CANCER ; IRRADIATION ; radiotherapy ; Germany ; TOXICITY ; FOLLOW-UP ; INFORMATION ; COHORT ; LONG-TERM ; NEW-YORK ; RISK ; TISSUE ; SURGERY ; radiation ; TIME ; PATIENT ; RISK-FACTORS ; SKIN ; treatment ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; DIFFERENCE ; AGE ; risk factors ; smoking ; RECURRENCE ; PROGNOSTIC-FACTORS ; MULTIVARIATE ; CANCER-PATIENTS ; PROGNOSTIC FACTORS ; NORMAL TISSUE ; side effects ; CANCER PATIENTS ; PROGNOSTIC FACTOR ; COMPLICATIONS ; TELANGIECTASIA ; fibrosis ; ONCOLOGY ; REGRESSION ; RE ; INCREASE ; prospective studies ; CARCINOGEN-DNA ADDUCTS ; PROGNOSTIC-FACTOR ; development ; INTERVAL ; analysis ; USA ; prospective ; prospective study ; odds ratio ; RISK-FACTOR ; LOGISTIC-REGRESSION ; nonsmokers ; REPAIR GENES ; CLINICAL RADIOSENSITIVITY ; CONSERVATION THERAPY ; CONSERVING THERAPY ; cosmesis ; EORTC BOOST ; late side effects ; NO BOOST TRIAL ; POSTMASTECTOMY RADIOTHERAPY ; RADIATION-INJURY
    Abstract: Radiotherapy after breast-conserving surgery is commonly applied to reduce recurrence of breast cancer but may cause acute and late side effects. To identify prognostic factors for the development of late toxicity after radiotherapy, we conducted a prospective study of breast cancer patients. We assessed late complications of radiotherapy and collected information on epidemiologic factors in a cohort of breast cancer patients who had received radiotherapy after breast-conserving surgery. Among 416 patients with complete follow-up data, the association between possible risk factors and development of late complications was evaluated using multivariate logistic regression analysis. After a median follow-up time of 51 months, 131 (31.4%) patients presented with telangiectasia and 28 (6.7%) patients with fibrosis. We observed a strong association between development of telangiectasia and fibrosis (p 〈 0.01). Increasing age of the patient was a risk factor for both telangiectasia and fibrosis (p-value for trend 〈 0.01 and 0.03, respectively). Patients with acute skin toxicity (odds ratio (OR) 1.8, 95% confidence interval (CI) 1.0-3.1) were at higher risk to develop telangiectasia. Long-term smoking was associated with a significant increase in risk of telangiectasia compared to non-smokers (OR 2.3, 95% CI 1.2-4.6). Our study revealed several factors other than radiation dose that may predispose to late complications following radiotherapy. Further understanding of differences in response to irradiation may advance individualized treatment and improve cosmetic outcome
    Type of Publication: Journal article published
    PubMed ID: 17221151
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  • 5
    Keywords: CANCER ; EXPRESSION ; tumor ; BLOOD ; CELL LUNG-CANCER ; Germany ; PROSTATE ; THERAPY ; SUPPORT ; RISK ; DISTINCT ; GENE ; GENE-EXPRESSION ; GENES ; RNA ; transcription ; PATIENT ; DNA ; MESSENGER-RNA ; MARKER ; IMPACT ; primary ; prognosis ; RISK-FACTORS ; CARCINOGENESIS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; VARIANTS ; lifestyle ; DIFFERENCE ; PLASMA ; REPAIR ; risk factors ; COLORECTAL-CANCER ; prostate cancer ; PROSTATE-CANCER ; MARKERS ; LYMPHOCYTES ; MDM2 ; CANCER-PATIENTS ; POLYMERASE-CHAIN-REACTION ; PREDICTION ; CANCER PATIENTS ; PERIPHERAL-BLOOD ; POLYMERASE CHAIN-REACTION ; NUCLEOTIDE EXCISION-REPAIR ; DNA repair ; TP53 ; BETA-CAROTENE ; molecular ; CHAIN ; ONCOLOGY ; REGRESSION ; RE ; TUMOR-SUPPRESSOR ; VARIANT ; THERAPIES ; mRNA ; LEVEL ; SUPPRESSOR ; GENOTYPE ; HAPLOTYPE ; OXIDATIVE DNA-DAMAGE ; RISK-FACTOR ; ENGLAND ; COEFFICIENTS ; quantitative ; outcome ; VALUES ; tumor suppressor ; MDM2 SNP309 ; genetic variants ; treatment outcome
    Abstract: Both genetic variants and messenger RNA (mRNA) expression of DNA repair and tumor suppressor genes have been investigated as molecular markers for therapy outcome. However, the phenotypic impact of genetic variants often remained unclear, thus the rationale of their use in risk prediction may be limited. We therefore analyzed genetic variants together with anthropometric and lifestyle factors to see how these affect mRNA levels of ERCC1, MDM2 and TP53 in primary blood lymphocytes. mRNA expression was measured in 376 prostate cancer patients by quantitative real-time polymerase chain reaction after reverse transcription, and ERCC1 rs11615 T 〉 C, ERCC1 rs3212986 C 〉 A, MDM2 rs2279744 T 〉 G and TP53 rs17878362 (p53PIN3) polymorphisms were determined. Considerable interindividual differences in mRNA expression were found (coefficients of variation: ERCC1, 45%; MDM2, 43% and TP53, 35%). ERCC1 expression was positively correlated with plasma levels of beta-carotene (P = 0.03) and negatively correlated with canthaxanthin (P = 0.02) and lutein (P = 0.02). Overall, the polymorphisms affected mRNA expression only weakly. Carriers of a distinct ERCC1 haplotype (CC) showed, however, significantly lower expression values than non-carriers (P = 0.001). Applying logistic regression, we found that CC haplotype carriers had a 1.69-fold increased odds ratio (95% confidence interval: 1.06-2.71) for reduced ERCC1 mRNA levels. This low ERCC1 expression might be associated with reduced DNA repair and better therapy response. In summary, the association we have found between ERCC1 genotype and mRNA expression supports recent clinical observations that genetic variation in ERCC1 can affect treatment outcome and prognosis. Our study further revealed a modulating effect by nutritional factors
    Type of Publication: Journal article published
    PubMed ID: 18332046
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  • 6
    Keywords: CANCER ; COMBINATION ; Germany ; EXPOSURE ; HISTORY ; RISK ; METABOLISM ; PATIENT ; GENETIC POLYMORPHISMS ; HETEROCYCLIC AMINES ; HUMAN CYTOSOLIC SULFOTRANSFERASES ; PHENOL SULFOTRANSFERASES ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; AGE ; WOMEN ; CIGARETTE-SMOKING ; smoking ; cancer risk ; EPITHELIAL-CELLS ; CARRIERS ; POSTMENOPAUSAL WOMEN ; case-control study ; RE ; CANCER SUSCEPTIBILITY ; case control studies ; INTERVAL ; GENETIC-POLYMORPHISM ; CARRIER ; sulfotransferase ; MEAT INTAKE
    Abstract: Introduction Sulfotransferase 1A1 (encoded by SULT1A1) is involved in the metabolism of procarcinogens such as heterocyclic amines and polycyclic aromatic hydrocarbons, both of which are present in tobacco smoke. We recently reported a differential effect of N-acetyltransferase (NAT) 2 genotype on the association between active and passive smoking and breast cancer. Additional investigation of a common SULT1A1 genetic polymorphism associated with reduced enzyme activity and stability might therefore provide deeper insight into the modification of breast cancer susceptibility. Methods We conducted a population-based case-control study in Germany. A total of 419 patients who had developed breast cancer by age 50 years and 884 age-matched control individuals, for whom risk factor information and detailed smoking history were available, were included in the analysis. Genotyping was performed using a fluorescence-based melting curve analysis method. Multivariate logistic regression analysis was used to estimate breast cancer risk associated with the SULT1A1 Arg(213)His polymorphism alone and in combination with NAT2 genotype in relation to smoking. Results The overall risk for breast cancer in women who were carriers of at least one SULT1A1*2 allele was not significantly different from that for women with the SULT1A1*1/*1 genotype (adjusted odds ratio 0.83, 95% confidence interval 0.66-1.06). Risk for breast cancer with respect to several smoking variables did not differ substantially between carriers of the *2 allele and noncarriers. However, among NAT2 fast acetylators, the odds ratio associated with passive smoking only (3.23, 95% confidence interval 1.05-9.92) was elevated in homozygous carriers of the SULT1A1*1 allele but not in carriers of the SULT1A1*2 allele (odds ratio 1.28, 95% confidence interval 0.50-3.31). Conclusion We found no evidence that the SULT1A1 genotype in itself modifies breast cancer risk associated with smoking in women up to age 50 years. In combination with NAT2 fast acetylator status, however, the SULT1A1*1/*1 genotype might increase breast cancer risk in women exposed to tobacco smoke
    Type of Publication: Journal article published
    PubMed ID: 15743503
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  • 7
    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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  • 8
    Keywords: EXPRESSION ; radiotherapy ; DNA ; IMPACT ; GENE ; GENE-EXPRESSION ; gene expression ; genetics ; REPAIR ; DNA-REPAIR ; heredity ; DNA repair ; side effects ; USA ; TOXICOLOGY ; PREDICT ; LEVEL ; mutagen
    Type of Publication: Meeting abstract published
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  • 9
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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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  • 10
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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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