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  • 1
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The homozygous deletion allele (DD) of the angiotensin-I converting enzyme (ACE) gene and the T235 homozygote of the angiotensinogen (AGT) gene have been reported to be correlated with an increased prevalence of coronary artery disease (CAD) and myocardial infarction (MI). The importance of the DD genotype and T235 homozygote as genetic risk factors for CAD in Chinese remains uncertain. This study included 426 patients who underwent coronary angiography and 180 healthy subjects without clinical evidence of CAD. Coronary angiography identified 268 patients with CAD (CAD group) and 158 patients without CAD. The healthy subjects and patients without angiographic evidence of CAD constituted the control group. Three polymorphisms were studied: an insertion/deletion (I/D) polymorphism of the ACE gene and the T174 M and M235T polymorphisms of the AGT gene. No association was found between any of the three studied polymorphisms and the risk of CAD or MI in Chinese using univariate or multivariate analysis. In multivariate analysis, the relative risks were 1.20 (95% confidence interval = 0.91–1.61, P = 0.20) for the DD genotype, 1.05 (95% CI = 0.82–1.35, P = 0.69) for the T174 homozygote, and 1.19 (95% CI = 0.91–1.55, P = 0.20) for the T235 homozygote. Similarly, no significant difference was found in the frequencies of the DD genotype and the T174 and T235 homozygotes between the control group, the CAD group, the non-MI group, and the MI group when analyzed according to sex, age, or degree of risk. Our data suggest that neither the DD genotype of the ACE I/D polymorphism nor the T174 and T235 homozygotes of the AGT gene confer significant risk for CAD or MI in Chinese.
    Type of Medium: Electronic Resource
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    Keywords: CANCER ; Germany ; DISEASE ; POPULATION ; RISK ; GENOME ; PATIENT ; ASSOCIATION ; FREQUENCY ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; BRCA1 ; WOMEN ; MUTATION ; REPAIR ; cancer risk ; MUTATIONS ; DNA-DAMAGE ; case-control studies ; RISK ASSESSMENT ; PREVALENCE ; BRCA1/2 ; EUROPE ; ONCOLOGY ; case control study ; case-control study ; ASSOCIATIONS ; RE ; ALLELE ; case control studies ; NEED ; EUROPEAN POPULATIONS ; breast cancer patients selected for family history and age ; CHEK2 GENE ; CHEK2*1100delC variant ; population-based study
    Abstract: CHEK2*1100delC is associated with a twofold increased breast cancer risk. This was shown in a collaborative analysis of European populations, but not in other populations from Europe and the US. Accordingly, there is a need to clarify the role of CHEK2*1100delC in breast cancer. We established its prevalence in two German populations GENICA (Northrhine-Westphalia, it = 724) and KORA (Bavaria, n = 600) and in women with breast cancer. The latter included cases (n = 688) from the GENICA breast cancer case-control study, patients with early-onset breast cancer (n = 86) and patients with familial breast cancer (n = 71). The latter patient groups were previously investigated for BRCA1/2-mutations and tested negative. Mutation analysis was performed by combined PCR/DHPLC methodology. CHEK2*1100delC was found in 0.9% of GENICA controls and was absent in the KORA controls indicating a significant difference between the two populations (P = 0.03). The frequency of CHEK2*1100delC in age-matched cases of the GENICA collection was 0.8% and thus not different from controls (OR 0.88, 95% CI 0.21-3.50). In patients with early-onset disease CHEK2*1100delC was found at a frequency of 2.3% referring to an increased breast cancer risk of 2.56 (95% Cl 0.25-14.58). In patients with familial disease the frequency was 1.4% referring to an increased risk of 1.53 (95% CI 0.03-12.93). Our data showed variations in CHEK2*1100delC prevalence within German populations suggesting possible inaccuracies in breast cancer risk assessments from non population-based studies. In patients with a high-risk profile however, CHEK2*1100delC was indicative for this risk and highest for early-onset breast cancer. (c) 2005 Elsevier Ltd. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 16239104
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    Keywords: CANCER ; Germany ; THERAPY ; DENSITY ; COHORT ; HISTORY ; RISK ; FAMILY ; ASSOCIATION ; BREAST ; breast cancer ; BREAST-CANCER ; TRIAL ; family history ; WOMEN ; HORMONE REPLACEMENT THERAPY ; cancer risk ; MAMMOGRAPHY ; case-control studies ; case-control study ; population-based case-control study ; HORMONE-REPLACEMENT THERAPY ; case control studies ; INTERVAL ; SCREEN ; FAMILY-HISTORY ; ESTROGEN PLUS PROGESTIN ; HEALTHY POSTMENOPAUSAL WOMEN ; breast cancer risks ; family history of cancer ; HRT USE ; risk-modifying factors
    Abstract: Objectives: Hormone-replacement therapy (HRT) is an established risk factor for breast cancer. HRT users are different from non-users with respect to socio-economic and other characteristics. There may be women where the HRT-related risk could be modulated by other factors. Methods: We conducted a population-based case-control study with 688 breast cancer cases and 724 controls to characterize HRT users and to estimate odds ratios (OR) and 95% confidence intervals (CI) for HRT use and potentially risk modifying factors. Results: In women aged 50 years and older, 58% of controls and 61% of cases ever used HRT. Among women in natural menopause, HRT use for 10 years and more years was associated with an increased breast cancer risk (OR 1.79, 95% CI, 1.12-2.87), but not among women in surgical menopause (OR 0.61, 95% CI, 0.09-4.17). In the subgroup of women with a positive family history of breast cancer, each year of HRT use increased the risk by 1.22 (95% CI, 1.02-1.47). Another subgroup comprised women with at least 10 diagnostic mammograms (OR 4.04, 95% CI, 1.10-14.81 for using HRT 10 or more years). Conclusions: Long-term HRT use was associated with a breast cancer risk in women with natural menopause. Our findings suggest that this risk may be increased in women with a positive family history of breast cancer and in women who received frequent diagnostic mammographic screens
    Type of Publication: Journal article published
    PubMed ID: 16151884
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  • 5
    Keywords: RECEPTOR ; CANCER ; EXPRESSION ; GROWTH ; IN-VITRO ; tumor ; carcinoma ; Germany ; human ; INFORMATION ; ENZYMES ; PROTEIN ; DRUG ; METABOLISM ; DIFFERENTIATION ; TISSUE ; TUMORS ; PATIENT ; prognosis ; ASSOCIATION ; ALPHA ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; PROGRESSION ; immunohistochemistry ; TUMOR PROGRESSION ; METASTASIS ; cancer risk ; CARCINOMAS ; HUMAN LIVER ; CARCINOGENS ; GST ; ESTROGEN-RECEPTOR ; glutathione-S-transferase ; GLUTATHIONE S-TRANSFERASE ; cytochrome P450 ; FEATURES ; ASSOCIATIONS ; TUMOR-GROWTH ; CARCINOGEN ; ESTROGEN ; ENZYME ; CANCER DEVELOPMENT ; estrogen receptor ; breast carcinoma ; HORMONES ; lymph node ; LYMPH-NODE ; GLUTATHIONE S-TRANSFERASES ; CYP ; CYP1B1 ; CYP3A5 ; CYTOCHROME-P450 ENZYMES ; IMMUNOHISTOCHEMICAL-DEMONSTRATION ; NONTUMOR TISSUES ; progesterone receptor
    Abstract: The potential to metabolize endogenous and exogenous substances may influence breast cancer development and tumor growth. Therefore, the authors investigated the protein expression of Glutathione S-transferase (GST) isoforms and cytochrome P450 (CYP) known to be involved in the metabolism of steroid hormones and endogenous as well as exogenous carcinogens in breast cancer tissue to obtain new information on their possible role in tumor progression. Expression of GST pi, mu, alpha and CYP1A1/2, 1A2, 3A4/5, 1B1, 2E1 was assessed by immunnhistochemistry for primary breast carcinomas of 393 patients from the German GENICA breast cancer collection. The percentages of positive tumors were 50.1 and 44.5% for GST mu and CYP2E1, and ranged from 13 to 24.7% for CYP1A2, GST pi, CYP1A1/2, CYP3A4/5, CYP1B1. GST alpha was expressed in 1.8% of tumors. The authors observed the following associations between strong protein expression and histopathological characteristics: GST expression was associated with a better tumor differentiation (GST mu, p = 0.018) and with reduced lymph node metastasis (GST pi, p = 0.02). In addition, GST mu expression was associated with a positive estrogen receptor and progesterone receptor status (p 〈 0.001). CYP3A4/5 expression was associated with a positive nodal status (p = 0.018). Expression of CYP1B1 was associated with poor tumor differentiation (p = 0.049). Our results demonstrate that the majority of breast carcinomas expressed xenobiotic and drug metabolizing enzymes. They particularly suggest that GST mu and pi expression may indicate a better prognosis and that strong CYP3A4/5 and CYP1B1 expression may be key features of nonfavourable prognosis. (c) 2006 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 16721811
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    Keywords: RISK ; ASSOCIATION ; METAANALYSIS ; CHINESE WOMEN ; RECEPTOR STATUS ; MELATONIN ; SHIFT-WORK ; GERMAN GENICA ; CLOCK GENES ; IJAZ S
    Abstract: Objectives: The role of genetic variants and environmental factors in breast cancer etiology has been intensively studied in the last decades. Gene-environment interactions are now increasingly being investigated to gain more insights into the development of breast cancer, specific subtypes, and therapeutics. Recently, night shift work that involves circadian disruption has gained rising interest as a potential non-genetic breast cancer risk factor. Here, we analyzed genetic polymorphisms in genes of cellular clocks, melatonin biosynthesis and signaling and their association with breast cancer as well as gene-gene and gene-night work interactions in a German case-control study on breast cancer. Methods: GENICA is a population-based case-control study on breast cancer conducted in the Greater Region of Bonn. Associations between seven polymorphisms in circadian genes (CLOCK, NPAS2, ARTNL, PER2 and CRY2), genes of melatonin biosynthesis and signaling (AANAT and MTNR1B) and breast cancer were analyzed with conditional logistic regression models, adjusted for potential confounders for 1022 cases and 1014 controls. Detailed shift-work information was documented for 857 breast cancer cases and 892 controls. Gene-gene and gene-shiftwork interactions were analyzed using model-based multifactor dimensionality reduction (mbMDR). Results: For combined heterozygotes and rare homozygotes a slightly elevated breast cancer risk was found for rs8150 in gene AANAT (OR 1.17; 95% CI 1.01-1.36), and a reduced risk for rs3816358 in gene ARNTL (OR 0.82; 95% CI 0.69-0.97) in the complete study population. In the subgroup of shift workers, rare homozygotes for rs10462028 in the CLOCK gene had an elevated risk of breast cancer (OR for AA vs. GG: 3.53; 95% CI 1.09-11.42). Shift work and CLOCK gene interactions were observed in the two-way interaction analysis. In addition, gene-shiftwork interactions were detected for MTNR1B with NPAS2 and ARNTL. Conclusions: In conclusion, the results of our population-based case-control study support a putative role of the CLOCK gene in the development of breast cancer in shift workers. In addition, higher order interaction analyses suggest a potential relevance of MTNR1B with the key transcriptional factor NPAS2 with ARNTL. Hence, in the context of circadian disruption, multivariable models should be preferred that consider a wide range of polymorphisms, e.g. that may influence chronotype or light sensitivity. The investigation of these interactions in larger studies is needed.
    Type of Publication: Journal article published
    PubMed ID: 25229211
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    Keywords: CANCER ; carcinoma ; CELL ; Germany ; LUNG ; PATHWAYS ; EXPOSURE ; RISK ; TISSUE ; radiation ; CIGARETTE-SMOKING ; SIGNAL-TRANSDUCTION ; adenocarcinoma ; squamous cell carcinoma ; PREVALENCE ; LUNG-CARCINOMA ; MATRIX ; radon ; INCREASE ; LEVEL ; lung carcinoma ; HISTOLOGY ; RADIATION EXPOSURE ; HEDGEHOG ; DAUGHTERS ; silicosis ; uranium mining
    Abstract: BACKGROUND. In East Germany, uranium mining was undertaken on a large scale from 1946 to 1990. Poor working conditions led to a high level of exposure to ionizing radiation and quartz dust. This analysis evaluates the histopathology of lung carcinoma ill uranium miners in relation to radon exposure and silicosis. METHODS. A database developed for autopsy cases ascertained in a pathological tissue repository, of German uranium miners was used to estimate odds ratios for developing lung carcinoma by major cell type with regard to radon exposure and silicosis. Silicosis information was extracted from autopsy protocols. Working level months (WLM) were calculated with a job-exposure matrix to assess lifetime radon exposure. Risk estimates were based oil 3414 male miners who died from small cell lung carcinoma (SCLC, n = 1446), squamous cell carcinoma (SqCC, n = 1006), or adenocarcinoma (AC, n = 962) between 1957 and 1990. RESULTS. SCLC and SqCC seem more likely to be associated with high radon exposure than AC. Mean Cumulative radon exposure was 868 (SD 631) WLM in SCLC, 871 (SD 652) WLM in SqCC, and 743 (SD 598) WLM in AC. Silicosis prevalence was 26% in SCLC 38% in SqCC, and 30% in AC. In silicotics, AC and SqCC had a relatively higher frequency at the expense of SCLC. SCLC occurred earlier than AC and SqCC. CONCLUSION. High radon exposure was associated with a higher relative frequency of SCLC and SqCC than AC. Silicosis tended to increase the appearance of SqCC and AC
    Type of Publication: Journal article published
    PubMed ID: 16411224
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  • 10
    Keywords: CANCER ; EXPRESSION ; RISK ; GENE ; SAMPLE ; SAMPLES ; transcription ; DNA ; REDUCTION ; CARCINOGENESIS ; GENETIC POLYMORPHISMS ; BINDING ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; NO ; PATTERNS ; PROMOTER ; WOMEN ; inactivation ; cancer risk ; genetic polymorphism ; METHYLATION ; German population ; ONCOLOGY ; RE ; PATTERN ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; ARRAY ; CATECHOL-O-METHYLTRANSFERASE ; SUBSTRATE ; ENZYME ; analysis ; FUNCTIONAL GENOMIC ANALYSIS ; HAPLOTYPE ; USA ; PREMENOPAUSAL ; cancer research ; CANCER-RISK ; GENOME-WIDE ASSOCIATION ; ESTROGENS ; NUCLEOTIDE ; COMT ; MENOPAUSAL STATUS
    Abstract: Catechol O-methyltransferase (COMT)-catalyzed methylation of catecholestrogens has been proposed to play a protective role in estrogen-induced genotoxic carcinogenesis. We have taken a comprehensive approach to test the hypothesis that genetic variation in COMT might influence breast cancer risk. Fifteen COMT single nucleotide polymorphisms (SNPs) selected on the basis of in-depth resequencing of the COMT gene were genotyped in 1,482 DNA samples from a Mayo Clinic breast cancer case control study. Two common SNPs in the distal promoter for membrane-bound (MB) COMT, rs2020917 and rs737865, were associated with breast cancer risk reduction in premenopausal women in the Mayo Clinic study, with allele-specific odds ratios (OR) of 0.70 [95% confidence interval (CI), 0.52-0.95] and 0.68 (95% CI, 0.51-0.92), respectively. These two SNPs were then subjected to functional genomic analysis and were genotyped in an additional 3,683 DNA samples from two independent case control studies (GENICA and GESBC). Functional genomic experiments showed that these SNPs could up-regulate transcription and that they altered DNA-protein binding patterns. Furthermore, substrate kinetic and exon array analyses suggested a role for MB-COMT in catecholestrogen inactivation. The GENICA results were similar to the Mayo case control observations, with ORs of 0.85 (95% CI, 0.72-1.00) and 0.85 (95% CI, 0.721.01) for the two SN-Ps. No significant effect was observed in the GESBC study. These studies showed that two SNPs in the COMT distal promoter were associated with breast cancer risk reduction in two of three case control studies, compatible with the results of functional genomic experiments, suggesting a role for MB-COMT in breast cancer risk
    Type of Publication: Journal article published
    PubMed ID: 18632656
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