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  • 1
    Keywords: RECEPTOR ; CANCER ; Germany ; PROSTATE ; COMMON ; COHORT ; RISK ; GENE ; GENES ; SAMPLE ; RELEASE ; RISK-FACTORS ; GENETIC POLYMORPHISMS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; prevention ; HEALTH ; WOMEN ; SNP ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; RISK FACTOR ; POPULATIONS ; genetic polymorphism ; EPIC ; nutrition ; CODE ; SINGLE ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; LEVEL ; HAPLOTYPE ; HORMONES ; TESTOSTERONE ; prospective ; RISK-FACTOR ; CANCER-RISK ; CIRCULATING LEVELS ; MULTIETHNIC COHORT ; BASE-LINE CHARACTERISTICS ; COMMON VARIANT ; LUTEINIZING-HORMONE ; androgens ; ESTROGENS ; CONSORTIUM ; androstenedione ; Genetic ; COMMON VARIANTS
    Abstract: Background: Gonadotropin releasing hormone (GNRH1) triggers the release of follicle stimulating hormone and luteinizing hormone from the pituitary. Genetic variants in the gene encoding GNRH1 or its receptor may influence breast cancer risk by modulating production of ovarian steroid hormones. We studied the association between breast cancer risk and polymorphisms in genes that code for GNRH1 and its receptor (GNRHR) in the large National Cancer Institute Breast and Prostate Cancer Cohort Consortium (NCI-BPC3). Methods: We sequenced exons of GNRH1 and GNRHR in 95 invasive breast cancer cases. Resulting single nucleotide polymorphisms ( SNPs) were genotyped and used to identify haplotype-tagging SNPs (htSNPS) in a panel of 349 healthy women. The htSNPs were genotyped in 5,603 invasive breast cancer cases and 7,480 controls from the Cancer Prevention Study-II (CPS-II), European Prospective Investigation on Cancer and Nutrition ( EPIC), Multiethnic Cohort (MEC), Nurses' Health Study ( NHS), and Women's Health Study (WHS). Circulating levels of sex steroids ( androstenedione, estradiol, estrone and testosterone) were also measured in 4713 study subjects. Results: Breast cancer risk was not associated with any polymorphism or haplotype in the GNRH1 and GNRHR genes, nor were there any statistically significant interactions with known breast cancer risk factors. Polymorphisms in these two genes were not strongly associated with circulating hormone levels. Conclusion: Common variants of the GNRH1 and GNRHR genes are not associated with risk of invasive breast cancer in Caucasians
    Type of Publication: Journal article published
    PubMed ID: 19640273
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  • 2
    Keywords: RECEPTOR ; CANCER ; COHORT ; RISK ; GENE ; MECHANISM ; MARKER ; RISK-FACTORS ; mechanisms ; BINDING ; CELL-LINES ; ASSOCIATION ; LINKAGE ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; prevention ; HEALTH ; WOMEN ; SNP ; risk factors ; prostate cancer ; PROSTATE-CANCER ; MARKERS ; cancer risk ; DATABASE ; REGION ; REGIONS ; LINKAGE DISEQUILIBRIUM ; nutrition ; POSTMENOPAUSAL WOMEN ; PROGRAM ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; LOCUS ; single-nucleotide ; BLOCKS ; DEHYDROEPIANDROSTERONE-SULFATE ; SEX-HORMONE LEVELS ; prospective ; RISK-FACTOR ; CANCER-RISK ; MULTIETHNIC COHORT ; ANDROGEN ; BASE-LINE CHARACTERISTICS ; CAG REPEAT POLYMORPHISM ; COMMON VARIANT ; LINKAGE-DISEQUILIBRIUM ; NURSES HEALTH ; POLYGLUTAMINE TRACTS ; POSSIBLE MECHANISMS ; RECEPTOR GENE ; SET ; VITAMIN-D-RECEPTOR
    Abstract: Introduction Androgens have been hypothesised to influence risk of breast cancer through several possible mechanisms, including their conversion to estradiol or their binding to the oestrogen receptor and/ or androgen receptor ( AR) in the breast. Here, we report on the results of a large and comprehensive study of the association between genetic variation in the AR gene and risk of breast cancer in the National Cancer Institute Breast and Prostate Cancer Cohort Consortium ( BPC3). Methods The underlying genetic variation was determined by first sequencing the coding regions of the AR gene in a panel of 95 advanced breast cancer cases. Second, a dense set of markers from the public database was genotyped in a panel of 349 healthy women. The linkage disequilibrium relationships ( blocks) across the gene were then identified, and haplotypetagging single nucleotide polymorphisms ( htSNPs) were selected to capture the common genetic variation across the locus. The htSNPs were then genotyped in the nested breast cancer cases and controls from the Cancer Prevention Study II, European Prospective Investigation into Cancer and Nutrition, Multiethnic Cohort, Nurses' Health Study, and Women's Health Study cohorts ( 5,603 breast cancer cases and 7,480 controls). Results We found no association between any genetic variation ( SNP, haplotype, or the exon 1 CAG repeat) in the AR gene and risk of breast cancer, nor were any statistical interactions with known breast cancer risk factors observed. Conclusion Among postmenopausal Caucasian women, common variants of the AR gene are not associated with risk of breast cancer
    Type of Publication: Journal article published
    PubMed ID: 16987421
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  • 3
    Keywords: CANCER ; tumor ; carcinoma ; PROSTATE ; COMMON ; DIAGNOSIS ; COHORT ; MORTALITY ; RISK ; GENE ; GENES ; SAMPLE ; SAMPLES ; TUMORS ; validation ; MARKER ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; BREAST ; breast cancer ; BREAST-CANCER ; NO ; STAGE ; COMPARATIVE GENOMIC HYBRIDIZATION ; HEALTH ; DIFFERENCE ; AGE ; WOMEN ; MEN ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; REGION ; POPULATIONS ; CARRIERS ; case-control studies ; PREDICTORS ; LIFE-STYLE ; NESTED CASE-CONTROL ; SINGLE ; ONCOLOGY ; case control study ; case-control study ; RE ; VARIANT ; ALLELE ; GROWTH-FACTOR-I ; case control studies ; INTERVAL ; CARRIER ; GENOTYPE ; single-nucleotide ; USA ; NO ASSOCIATION ; cancer research ; CANCER-RISK ; MULTIETHNIC COHORT ; BASE-LINE CHARACTERISTICS ; nested case-control study ; case control ; case-control ; AFRICAN-AMERICAN
    Abstract: Two recent studies independently identified polymorphisms in the 8q24 region, including a single nucleotide polymorphism (rsl447295), strongly associated with prostate cancer risk. Here, we replicate the overall association in a large nested case-control study from the National Cancer Institute Breast and Prostate Cancer Cohort Consortium using 6,637 prostate cancer cases and 7,361 matched controls. We also examine whether this polymorphism is associated with breast cancer among 2,604 Caucasian breast cancer cases and 3,118 matched controls. The rs1447295 marker was strongly associated with prostate cancer among Caucasians (P = 1.23 x 10(-13)). When we exclude the Multiethnic Cohort samples, previously reported by Freedman et al., the association remains highly significant (P = 8.64 X 10(-13)). Compared with wild-type homozygotes, carriers with one copy of the minor allele had an ORAC = 1.34 (99% confidence intervals, 1.19-1.50) and carriers with two copies of the minor allele had an ORAA = 1.86 (99% confidence intervals, 1.30-2.67). Among African Americans, the genotype association was statistically significant in men diagnosed with prostate cancer at an early age (P = 0.011) and nonsignificant for those diagnosed at a later age (P = 0.924). This difference in risk by age at diagnosis was not present among Caucasians. We found no statistically significant difference in risk when tumors were classified by Gleason score, stage, or mortality. We found no association between rs1447295 and breast cancer risk (P = 0.590). Although the gene responsible has yet to be identified, the validation of this marker in this large sample of prostate cancer cases leaves little room for the possibility of a false-positive result
    Type of Publication: Journal article published
    PubMed ID: 17409400
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  • 4
    Keywords: CANCER ; PROSTATE ; COMMON ; CT ; SUPPORT ; COHORT ; POPULATION ; RISK ; GENE ; ASSOCIATION ; LINKAGE ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; SUSCEPTIBILITY ; ALPHA ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; ENCODES ; HEALTH ; WOMEN ; SNP ; MEN ; prostate cancer ; PROSTATE-CANCER ; LINE ; REGION ; LINKAGE DISEQUILIBRIUM ; POPULATIONS ; POSTMENOPAUSAL WOMEN ; SINGLE ; DEFICIENCY ; ONCOLOGY ; ASSOCIATIONS ; SNPs ; CANCER SUSCEPTIBILITY ; METAANALYSIS ; biomarker ; INTERVAL ; HAPLOTYPE ; HAPLOTYPES ; single-nucleotide ; USA ; HORMONES ; STEROID-HORMONES ; odds ratio ; cancer research ; MULTIETHNIC COHORT ; PREDICT ; steroids ; postmenopausal ; block ; HORMONE-LEVELS ; EXONS ; GENETIC-VARIATION ; ANDROGEN RECEPTOR GENE ; BRAZILIAN PATIENTS ; SERUM ANDROGENS
    Abstract: CYP17 encodes cytochrome p450c17 alpha, which mediates activities essential for the production of sex steroids. Common germ line variation in the CYP17 gene has been related to inconsistent results in breast and prostate cancer, with most studies focusing on the nonsynonymous single nucleotide polymorphism (SNP) T27C (rs743572). We comprehensively characterized variation in CYP17 by direct sequencing of exons followed by dense genotyping across the 58 kb region around CYP17 in five racial/ethnic populations. Two blocks of strong linkage disequilibrium were identified and nine haplotype-tagging SNPs, including T27C, were chosen to predict common haplotypes (R-h(2) 〉= 0.85). These haplotype-tagging SNPs were genotyped in 8,138 prostate cancer cases and 9,033 controls, and 5,333 breast cancer cases and 7,069 controls from the Breast and Prostate Cancer Cohort Consortium. We observed borderline significant associations with prostate cancer for rs2486758 [TC versus TT, odds ratios (OR), 1.07; 95% confidence intervals (95% Cl), 1.00-1.14; CC versus TT, OR, 1.09; 95% CI, 0.95-1.26; P trend = 0.04] and rs6892 (AG versus AA, OR, 1.08; 95% CI, 1.00-1.15; GG versus AA, OR, 1.11; 95% CI, 0.95-1.30; P trend = 0.03). We also observed marginally significant associations with breast cancer for rs4919687 (GA versus GG, OR, 1.04; 95% CI, 0.97-1.12, AA versus GG, OR, 1.17; 95% CI, 1.03-1.34; P trend = 0.03) and rs4919682 (CT versus CC, OR, 1.04; 95% CI, 0.97-1.12; TT versus CC, OR, 1.16; 95% CI, 1.01-1.33; P trend = 0.04). Common variation at CYP17 was not associated with circulating sex steroid hormones in men or postmenopausal women. Our findings do not support the hypothesis that common germ line variation in CYP17 makes a substantial contribution to postmenopausal breast or prostate cancer susceptibility
    Type of Publication: Journal article published
    PubMed ID: 18006912
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  • 5
    Keywords: CANCER ; EXPRESSION ; DISEASE ; RISK ; GENE ; GENES ; ASSOCIATION ; SUSCEPTIBILITY ; BREAST ; breast cancer ; BREAST-CANCER ; genetics ; familial risk ; USA ; LOCI ; GENOME-WIDE ASSOCIATION ; CONFER SUSCEPTIBILITY ; Genetic ; 33 ; COMMON VARIANTS ; Genome-wide association studies
    Abstract: Genome-wide association studies (GWAS) have identified seven breast cancer susceptibility loci, but these explain only a small fraction of the familial risk of the disease. Five of these loci were identified through a two-stage GWAS involving 390 familial cases and 364 controls in the first stage, and 3,990 cases and 3,916 controls in the second stage(1). To identify additional loci, we tested over 800 promising associations from this GWAS in a further two stages involving 37,012 cases and 40,069 controls from 33 studies in the CGEMS collaboration and Breast Cancer Association Consortium. We found strong evidence for additional susceptibility loci on 3p (rs4973768: per-allele OR 1.11, 95% CI = 1.08-1.13, P = 4.1 x 10(-23)) and 17q (rs6504950: per-allele OR 0.95, 95% CI = 0.92-0.97, P = 1.4 x 10(-8)). Potential causative genes include SLC4A7 and NEK10 on 3p and COX11 on 17q
    Type of Publication: Journal article published
    PubMed ID: 19330027
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  • 6
    Keywords: CANCER ; THERAPY ; INFORMATION ; COHORT ; DISEASE ; incidence ; RISK ; RISK-FACTORS ; BREAST ; BREAST-CANCER ; DESIGN ; AGE ; WOMEN ; PROSPECTIVE COHORT ; smoking ; cancer risk ; UNITED-STATES ; ALCOHOL ; ALCOHOL-CONSUMPTION ; CONSUMPTION ; BIRTH COHORT ; POSTMENOPAUSAL WOMEN ; MASS INDEX ; ORAL-CONTRACEPTIVE USE ; REQUIRING PROLONGED OBSERVATION ; METAANALYSIS ; HORMONAL FACTORS ; ANTHROPOMETRIC MEASURES ; EPITHELIAL OVARIAN
    Abstract: BACKGROUND: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. METHODS AND FINDINGS: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p〈0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p〈0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p〈0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. CONCLUSIONS: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with a 3% increase in ovarian cancer incidence per decade. Please see later in the article for the Editors' Summary.
    Type of Publication: Journal article published
    PubMed ID: 22606070
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  • 7
    Keywords: RECEPTOR ; CANCER ; tumor ; COHORT ; DISEASE ; EPIDEMIOLOGY ; RISK ; GENE ; METABOLISM ; TUMORS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; BREAST ; breast cancer ; BREAST-CANCER ; PROSTATE-CANCER ; INDIVIDUALS ; POSTMENOPAUSAL WOMEN ; SUBSET ; RE ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; ESTROGEN ; single-nucleotide ; haplotype-tagging ; MULTIETHNIC COHORT ; BASE-LINE CHARACTERISTICS ; 17-BETA-HYDROXYSTEROID-DEHYDROGENASE TYPE-1 ; HORMONE-RECEPTOR
    Abstract: The 17 beta-hydroxysteroid dehydrogenase 1 gene (HSD17B1) encodes 17HSD1, which catalyzes the final step of estradiol biosynthesis. Despite the important role of HSD17B1 in hormone metabolism, few epidemiologic studies of HSD17B1 and breast cancer have been conducted. This study includes 5,370 breast cancer cases and 7,480 matched controls from five large cohorts in the Breast and Prostate Cancer Cohort Consortium. We characterized variation in HSD17B1 by resequencing and dense genotyping a multiethnic sample and identified haplotype-tagging single nucleotide polymorphisms (htSNP) that capture common variation within a 33.3-kb region around HSD17B1. Four htSNPs, including the previously studied SNP rs605059 (S312G), were genotyped to tag five common haplotypes in all cases and controls. Conditional logistic regression was used to estimate odds ratios (OR) for disease. We found no evidence of association between common HSD17B1 haplotypes or htSNPs and overall risk of breast cancer. The OR for each haplotype relative to the most common haplotype ranged from 0.98 to 1.07 (omnibus test for association: X-2 = 3.77, P = 0.58, 5 degrees of freedom). When cases were subdivided by estrogen receptor (ER) status, two common haplotypes were associated with ER-negative tumors (test for trend, Ps = 0.0009 and 0.0076; n = 353 cases). HSD17B1 variants that are common in Caucasians are not associated with overall risk of breast cancer; however, there was an association among the subset of ER-negative tumors. Although the probability that these ER-negative findings are false-positive results is high, these findings were consistent across each cohort examined and warrant further study
    Type of Publication: Journal article published
    PubMed ID: 16489054
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  • 8
    Keywords: CANCER ; COHORT ; RISK ; GENE ; ASSOCIATION ; FREQUENCY ; LINKAGE ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; FREQUENCIES ; BREAST ; breast cancer ; BREAST-CANCER ; hormone ; PATTERNS ; HEALTH ; WOMEN ; SNP ; PROSPECTIVE COHORT ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; HUMAN GENOME ; REGION ; LINKAGE DISEQUILIBRIUM ; nutrition ; POSTMENOPAUSAL WOMEN ; ONCOLOGY ; ASSOCIATIONS ; RE ; INCREASE ; SNPs ; ESTROGEN ; LEVEL ; ENZYME ; analysis ; HAPLOTYPE ; HAPLOTYPES ; LOCUS ; single-nucleotide ; single-nucleotide polymorphism ; HORMONES ; prospective ; cancer research ; CANCER-RISK ; MULTIETHNIC COHORT ; BASE-LINE CHARACTERISTICS ; PREDICT ; NONCARRIERS ; AROMATASE
    Abstract: The CYP19A1 gene encodes the enzyme aromatase, which is responsible for the final step in the biosynthesis of estrogens. In this study, we used a systematic two-step approach that included gene resequencing and a haplotype-based analysis to comprehensively survey common genetic variation across the CYP19A1 locus in relation to circulating postmenopausal steroid hormone levels and breast cancer risk. This study was conducted among 5,356 invasive breast cancer cases and 7,129 controls comprised primarily of White women of European descent drawn from five large prospective cohorts within the National Cancer Institute Breast and Prostate Cancer Cohort Consortium. A high-density single-nucleotide polymorphism (SNP) map of 103 common SNPs (〉= 5% frequency) was used to identify the linkage disequilibrium and haplotype patterns across the CYP19A1 locus, and 19 haplotype-tagging SNPs were selected to provide high predictability of the common haplotype patterns. We found haplotype-tagging SNPs and common haplotypes spanning the coding and proximal 5' region of CYP-19A1 to be significantly associated with a 10% to 20% increase in endogenous estrogen levels in postmenopausal women [effect per copy of the two-SNP haplotype rs749292-rs727479 (A-A) versus noncarriers; P = 4.4 X 10(-15)]. No significant associations were observed, however, with these SNPs or common haplotypes and breast cancer risk. Thus, although genetic variation in CM19A1 produces measurable differences in estrogen levels among postmenopausal women, the magnitude of the change was insufficient to contribute detectably to breast cancer
    Type of Publication: Journal article published
    PubMed ID: 17325027
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  • 9
    Keywords: CANCER ; PROSTATE ; COHORT ; RISK ; polymorphism ; POLYMORPHISMS ; BREAST ; breast cancer ; BREAST-CANCER ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; LEVEL ; IGFBP3 ; CANCER-RISK ; IGFBP-3 ; PREDICT ; IGF1 ; breast cancer risk ; CONSORTIUM
    Type of Publication: Journal article published
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  • 10
    Keywords: CANCER ; GROWTH ; PROSTATE ; COMMON ; COHORT ; RISK ; GENE ; CARCINOGENESIS ; BIOMARKERS ; LINKAGE ; polymorphism ; POLYMORPHISMS ; VARIANTS ; BREAST ; hormone ; HEALTH ; AGE ; MEN ; prostate cancer ; PROSTATE-CANCER ; cancer risk ; LINKAGE DISEQUILIBRIUM ; GERMLINE ; POSTMENOPAUSAL WOMEN ; SINGLE ; VARIANT ; DETERMINANTS ; prospective studies ; GROWTH-FACTOR-I ; LEVEL ; biomarker ; EPIDEMIOLOGIC EVIDENCE ; HAPLOTYPE ; HAPLOTYPES ; LOCUS ; USA ; HORMONES ; HORMONE LEVELS ; TESTOSTERONE ; prospective ; prospective study ; STEROID-HORMONES ; JAPANESE ; UNIT ; cancer research ; CANCER-RISK ; ESTROGEN-LEVELS ; MULTIETHNIC COHORT ; ANDROGEN ; COMMON VARIANT ; SEX-HORMONES ; JAPANESE POPULATION ; androgens ; NONCARRIERS ; FREE TESTOSTERONE ; SERUM ANDROGENS ; CONSORTIUM ; 3 ; Genetic ; genetic variation ; COMMON VARIANTS ; GENE VARIANT ; ALLELIC VARIANTS ; ANDROGEN BIOSYNTHESIS ; UNRELATED INDIVIDUALS
    Abstract: Sex hormones, particularly the androgens, are important for the growth of the prostate gland and have been implicated in prostate cancer carcinogenesis, yet the determinants of endogenous steroid hormone levels remain poorly understood. Twin studies suggest a heritable component for circulating concentrations of sex hormones, although epidemiologic evidence linking steroid hormone gene variants to prostate cancer is limited. Here we report on findings from a comprehensive study of genetic variation at the CYP19A1 locus in relation to prostate cancer risk and to circulating steroid hormone concentrations in men by the Breast and Prostate Cancer Cohort Consortium (BPC3), a large collaborative prospective study. The BPC3 systematically characterized variation in CYP19A1 by targeted resequencing and dense genotyping; selected haplotype-tagging single nuclecitide polymorphisms (htSNP) that efficiently predict common variants in U.S. and Europe-an whites, Latinos, Japanese Americans, and Native Hawaiians; and genotyped these htSNPs; in 8,166 prostate cancer cases and 9,079 study-, age-, and ethnicity-matched controls. CYP19A1 htSNPs, two common missense variants and common haplotypes were not significantly associated with risk of prostate cancer. However, several htSNPs in linkage disequilibrium blocks 3 and 4 were significantly associated with a 5% to 10% difference in estradiol concentrations in men [association per copy of the two-SNP haplotype rs749292-rs727479 (A-A) versus noncarriers; P = 1 x 10(-5)], and with inverse, although less marked changes, in free testosterone concentrations. These results suggest that although germline variation in CYP19A1 characterized by the htSNPs produces measurable differences in sex hormone concentrations in men, they do not substantially influence risk of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2734-44)
    Type of Publication: Journal article published
    PubMed ID: 19789370
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