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  • 1
    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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  • 2
    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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  • 3
    Keywords: tumor ; THERAPY ; RISK ; mechanisms ; LIGHT ; SUBTYPES ; NURSES HEALTH ; CIRCADIAN DISRUPTION ; MELATONIN ; SHIFT-WORK
    Abstract: Objectives The potential mechanisms that link night-shift work with breast cancer have been extensively discussed. Exposure to light at night (LAN) depletes melatonin that has oncostatic and anti-estrogenic properties and may lead to a modified expression of estrogen receptor (ER) alpha. Here, we explored the association between shift work and breast cancer in subgroups of patients with ER-positive and -negative tumors. Methods GENICA (Gene-ENvironment Interaction and breast CAncer) is a population-based case control study on breast cancer with detailed information on shift work from 857 breast cancer cases and 892 controls. ER status was assessed by immunohistochemical staining. Associations between night-shift work and ER-positive and -negative breast cancer were analyzed with conditional logistic regression models, adjusted for potential confounders. Results ER status was assessed for 827 cases and was positive in 653 and negative in 174 breast tumors. Overall, 49 cases and 54 controls were "ever employed" in shift work including night shifts for year. In total, "ever shift work" and "ever night work" were not associated with an elevated risk of ER-positive or -negative breast tumors. Night work for 〉= 20 years was associated with a significantly elevated risk of ER-negative breast cancer [odds ratio (OR) 4.73, 95% confidence interval (95% CI) 1.22-18.36]. Conclusions Our case-control study suggests that long-term night-shift work is associated with an increased risk of ER-negative breast cancers. Further studies on histological subtypes and the analysis of other potentially relevant factors are crucial for discovering putative mechanisms.
    Type of Publication: Journal article published
    PubMed ID: 23543199
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  • 4
    Keywords: RECEPTOR ; CANCER ; tumor ; Germany ; INFORMATION ; POPULATION ; RISK ; TUMORS ; COMPLEX ; COMPLEXES ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; BREAST ; breast cancer ; BREAST-CANCER ; prevention ; PATTERNS ; HEALTH ; AGE ; CIGARETTE-SMOKING ; PROSPECTIVE COHORT ; smoking ; CONSUMPTION ; ESTROGEN-RECEPTOR ; POSTMENOPAUSAL WOMEN ; ONCOLOGY ; case-control study ; PATTERN ; MUTATION CARRIERS ; ALLELES ; HAPLOTYPE ; MOLECULAR-GENETICS ; estrogen receptor ; HAPLOTYPE RECONSTRUCTION ; STEROID-HORMONE RECEPTORS ; HYDROCARBON RECEPTOR ; COFFEE CONSUMPTION ; aromatic and heterocyclic amines ; CAFFEINE CONSUMPTION ; N-acetyltransferase 2 ; N-ACETYLTRANSFERASE-2 GENE
    Abstract: The role of N-acetyltransferase 2 (NAT2) polymorphism in breast cancer is still unclear. We explored the associations between potential sources of exposure to aromatic and heterocyclic amines (AHA), acetylation status and receptor-defined breast cancer in 1020 incident cases and 1047 population controls of the German GENICA study. Acetylation status was assessed as slow or fast. Therefore, NAT2 haplotypes were estimated using genotype information from six NAT2 polymorphisms. Most probable haplotypes served as alleles for the deduction of NAT2 acetylation status. The risks of developing estrogen receptor alpha (ER) and progesterone receptor (PR)-positive or negative tumors were estimated for tobacco smoking, consumption of red meat, grilled food, coffee, and tea, as well as expert-rated occupational exposure to AHA with logistic regression conditional on age and adjusted for potential confounders. Joint effects of these factors and NAT2 acetylation status were investigated. Frequent consumption of grilled food and coffee showed higher risks in slow acetylators for receptor-negative tumors [grilled food: ER-: odds ratio (OR) 2.57, 95% confidence interval (CI) 1.07-6.14 for regular vs. rare; coffee: ER-: OR 2.55, 95% CI 1.22-5.33 for 〉= 4 vs. 0 cups/day]. We observed slightly higher risks for never smokers that are fast acetylators for receptor-positive tumors compared with slow acetylators (ER-: OR 1.32, 95% CI 1.00-1.73). Our results support differing risk patterns for receptor-defined breast cancer. However, the modifying role of NAT2 for receptor-defined breast cancer is difficult to interpret in the light of complex mixtures of exposure to AHA. European Journal of Cancer Prevention 19: 100-109 (C) 2010 Wolters Kluwer Health Lippincott Williams & Wilkins
    Type of Publication: Journal article published
    PubMed ID: 19996973
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  • 5
    Keywords: case-control studies ; case control study ; case-control study ; population-based case-control study ; OCCUPATIONAL-EXPOSURE ; THERAPIES ; hormone ; breast cancer ; BREAST-CANCER ; HORMONE REPLACEMENT THERAPY ; THERAPY ; EXPOSURE ; NEW-YORK ; RISK
    Type of Publication: Meeting abstract published
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