Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Keywords: CANCER ; LUNG ; MODEL ; MODELS ; FOLLOW-UP ; lung cancer ; LUNG-CANCER ; COHORT ; HISTORY ; RISK ; RISKS ; primary ; RISK-FACTORS ; INTERVENTION ; ASSOCIATION ; BREAST-CANCER ; risk factors ; smoking ; cancer risk ; RISK FACTOR ; DATABASE ; DIETARY ; CANCER-RESEARCH ; FRUIT ; QUESTIONNAIRE ; SMOKERS ; EUROPE ; FOOD ; RELATIVE RISK ; BETA-CAROTENE ; FOOD-FREQUENCY QUESTIONNAIRE ; SUPPLEMENT ; CARDIOVASCULAR-DISEASE ; ASSESSMENT INSTRUMENTS ; COMPOSITION DATABASE ; SERUM MICRONUTRIENTS ; VITAMIN-A ; WOMENS-HEALTH ; YORK-STATE COHORT
    Abstract: Intervention trials with supplemental beta-carotene have observed either no effect or a harmful effect on lung cancer risk. Because food composition databases for specific carotenoids have only become available recently, epidemiological evidence relating usual dietary levels of these carotenoids with lung cancer risk is limited. We analyzed the association between lung cancer risk and intakes of specific carotenoids using the primary data from seven cohort studies in North America and Europe. Carotenoid intakes were estimated from dietary questionnaires administered at baseline in each study. We calculated study-specific multivariate relative risks (RRs) and combined these using a random-effects model. The multivariate models included smoking history and other potential risk factors. During follow-up of up to 7-16 years across studies, 3,155 incident lung cancer cases were diagnosed among 399,765 participants. beta-Carotene intake was not associated with lung cancer risk (pooled multivariate RR = 0.98; 95% confidence interval, 0.87-1.11; highest versus lowest quintile). The RRs for alpha-carotene, lutein/zeaxanthin, and lycopene were also close to unity. beta-Cryptoxanthin intake was inversely associated with lung cancer risk (RR = 0.76; 95% confidence interval, 0.67-0.86; highest versus lowest quintile). These results did not change after adjustment for intakes of vitamin C (with or without supplements), folate (with or without supplements), and other carotenoids and multivitamin use. The associations generally were similar among never, past, or current smokers and by histological type. Although smoking is the strongest risk factor for lung cancer, greater intake of foods high in P-cryptoxanthin, such as citrus fruit, may modestly lower the risk
    Type of Publication: Journal article published
    PubMed ID: 14744731
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: CANCER ; MODEL ; PROSTATE ; DISEASE ; RISK ; GENE ; MARKER ; IMPACT ; BIOMARKERS ; ASSOCIATION ; LINKAGE ; polymorphism ; single nucleotide polymorphism ; SUSCEPTIBILITY ; VARIANTS ; STAGE ; IDENTIFICATION ; HEALTH ; SNP ; PROSTATE-CANCER ; MARKERS ; LINKAGE DISEQUILIBRIUM ; diabetes ; REPLICATION ; FUTURE ; DIABETES-MELLITUS ; ONCOLOGY ; VARIANT ; METAANALYSIS ; biomarker ; methods ; MULTIETHNIC COHORT ; LINKAGE-DISEQUILIBRIUM ; 8Q24 ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; genetic association ; SCAN ; Genetic ; COMMON VARIANTS ; Type ; single nucleotide ; RISK-ASSOCIATED LOCI
    Abstract: Background: Genome-wide association studies have identified multiple genetic variants associated with susceptibility to prostate cancer (PrCa). In the two-stage Cancer Genetic Markers of Susceptibility prostate cancer scan, a single-nucleotide polymorphism (SNP), rs10486567, located within intron 2 of JAZF1 gene on chromosome 7p15.2, showed a promising association with PrCa overall (P = 2.14 x 10(-6)), with a suggestion of stronger association with aggressive disease (P = 1.2 x 10(-7)). Methods: In the third stage of genome-wide association studies, we genotyped 106 JAZF1 SNPs in 10,286 PrCa cases and 9,135 controls of European ancestry. Results: The strongest association was observed with the initial marker rs10486567, which now achieves genome-wide significance [P = 7.79 x 10(-11); ORHET, 1.19 (95% confidence interval, 1.12-1.27); ORHOM, 1.37 (95% confidence interval, 1.20-1.56)]. We did not confirm a previous suggestion of a stronger association of rs10486567 with aggressive disease (P = 1.60 x 10(-4) for aggressive cancer, n = 4,597; P = 3.25 x 10(-8) for non-aggressive cancer, n = 4,514). Based on a multilocus model with adjustment for rs10486567, no additional independent signals were observed at chromosome 7p15.2. There was no association between PrCa risk and SNPs in JAZF1 previously associated with height (rs849140; P = 0.587), body stature (rs849141, tagged by rs849136; P = 0.171), and risk of type 2 diabetes and systemic lupus erythematosus (rs864745, tagged by rs849142; P = 0.657). Conclusion: rs10486567 remains the most significant marker for PrCa risk within JAZF1 in individuals of European ancestry. Impact: Future studies should identify all variants in high linkage disequilibrium with rs10486567 and evaluate their functional significance for PrCa. Cancer Epidemiol Biomarkers Prev; 19(5); 1349-55. (C)2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20406958
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: CANCER ; EXPRESSION ; SURVIVAL ; neoplasms ; PATHWAY ; RISK ; GENE ; ASSOCIATION ; SUSCEPTIBILITY ; BREAST ; BREAST-CANCER ; METASTASIS ; POOR-PROGNOSIS ; HIGH-FREQUENCY ; GENETIC SUSCEPTIBILITY ; OVARIAN ; association study ; CORRELATE ; germline variation ; PIK3CA MUTATIONS ; PTEN LOSS
    Abstract: Background:Somatic mutations in phosphoinositide-3-kinase catalytic subunit alpha (PIK3CA) are frequent in breast tumours and have been associated with oestrogen receptor (ER) expression, human epidermal growth factor receptor-2 overexpression, lymph node metastasis and poor survival. The goal of this study was to evaluate the association between inherited variation in this oncogene and risk of breast cancer.Methods:A single-nucleotide polymorphism from the PIK3CA locus that was associated with breast cancer in a study of Caucasian breast cancer cases and controls from the Mayo Clinic (MCBCS) was genotyped in 5436 cases and 5280 controls from the Cancer Genetic Markers of Susceptibility (CGEMS) study and in 30 949 cases and 29 788 controls from the Breast Cancer Association Consortium (BCAC).Results:Rs1607237 was significantly associated with a decreased risk of breast cancer in MCBCS, CGEMS and all studies of white Europeans combined (odds ratio (OR)=0.97, 95% confidence interval (CI) 0.95-0.99, P=4.6 x 10(-3)), but did not reach significance in the BCAC replication study alone (OR=0.98, 95% CI 0.96-1.01, P=0.139).Conclusion:Common germline variation in PIK3CA does not have a strong influence on the risk of breast cancer.
    Type of Publication: Journal article published
    PubMed ID: 22033276
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    Keywords: CANCER ; COMMON ; DISEASE ; RISK ; RISKS ; GENE ; GENES ; primary ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; SUSCEPTIBILITY ; VARIANTS ; BREAST ; breast cancer ; BREAST-CANCER ; STAGE ; PATTERNS ; OVARIAN-CANCER ; SNP ; DATABASE ; Jun ; POPULATIONS ; familial risk ; BRCA2 MUTATIONS ; SUSCEPTIBILITY GENE ; SINGLE ; AGGREGATION ; VARIANT ; ALLELE ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; CANCER SUSCEPTIBILITY ; ALLELES ; LEVEL ; familial aggregation ; single-nucleotide ; UNIT ; ENGLAND ; LOCI ; CHEK2-ASTERISK-1100DELC ; breast cancer susceptibility ; GENOME-WIDE ASSOCIATION ; association study ; GENETIC-SUSCEPTIBILITY ; GROWTH-FACTOR RECEPTOR-2
    Abstract: Breast cancer exhibits familial aggregation, consistent with variation in genetic susceptibility to the disease. Known susceptibility genes account for less than 25% of the familial risk of breast cancer, and the residual genetic variance is likely to be due to variants conferring more moderate risks. To identify further susceptibility alleles, we conducted a two-stage genome-wide association study in 4,398 breast cancer cases and 4,316 controls, followed by a third stage in which 30 single nucleotide polymorphisms (SNPs) were tested for confirmation in 21,860 cases and 22,578 controls from 22 studies. We used 227,876 SNPs that were estimated to correlate with 77% of known common SNPs in Europeans at r(2) 〉 0.5. SNPs in five novel independent loci exhibited strong and consistent evidence of association with breast cancer (P 〈 10(-7)). Four of these contain plausible causative genes (FGFR2, TNRC9, MAP3K1 and LSP1). At the second stage, 1,792 SNPs were significant at the P 〈 0.05 level compared with an estimated 1,343 that would be expected by chance, indicating that many additional common susceptibility alleles may be identifiable by this approach
    Type of Publication: Journal article published
    PubMed ID: 17529967
    Signatur Availability
    BibTip Others were also interested in ...
  • 7
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: CANCER ; MODEL ; COHORT ; cohort studies ; cohort study ; POPULATION ; RISK ; RISKS ; INDEX ; primary ; RISK-FACTORS ; ASSOCIATION ; BREAST-CANCER ; NO ; HEALTH ; ovarian cancer ; OVARIAN-CANCER ; WOMEN ; PROSPECTIVE COHORT ; cancer risk ; MULTIVARIATE ; NETHERLANDS ; UNITED-STATES ; EUROPE ; RELATIVE RISK ; HETEROGENEITY ; POSTMENOPAUSAL WOMEN ; BODIES ; IGF-I ; ONCOLOGY ; PHYSICAL-ACTIVITY ; HEIGHT ; GROWTH-FACTOR-I ; biomarker ; analysis ; methods ; MASS ; pooled analysis ; USA ; PREMENOPAUSAL ; prospective ; BMI ; cancer research ; CANCER-RISK ; SEX-HORMONES ; postmenopausal ; comparison ; body mass ; POOLED-ANALYSIS ; MENOPAUSAL STATUS ; ANTHROPOMETRIC MEASUREMENTS ; SELF-REPORTED WEIGHT
    Abstract: Background: Although many studies have investigated the association between anthropometry and ovarian cancer risk, results have been inconsistent. Methods: The associations of height, body mass index (BMI), and ovarian cancer risk were examined in a pooled analysis of primary data from 12 prospective cohort studies from North America and Europe. The study population consisted of 531,583 women among whom 2,036 epithelial ovarian cancer cases were identified. To summarize associations, study-specific relative risks (RR) were estimated using the Cox proportional hazards model and then combined using a random-effects model. Results: Women with height 〉= 1.70 m had a pooled multivariate RR of 1.38 [95% confidence interval (95% CI), 1.16-1-65] compared with those with height 〈1.60 m. For the same comparison, multivariate RRs were 1.79 (95% CI, 1.07-3.00) for premenopausal and 1.25 (95% CI, 1.04-1.49) for postmenopausal ovarian cancer (P-interaction = 0.14). The multivariate RR for women with a BMI 〉= 30 kg/m(2) was 1.03 (95% CI, 0.86-1.22) compared with women with a BMI from 18.5 to 23 kg/m(2). For the same comparison, multivariate RRs were 1.72 (95% CI, 1.02-2.89) for premenopausal and 1.07 (95% CI, 0.87-1.33) for postmenopausal women (P-interaction = 0.07). There was no statistically significant heterogeneity between studies with respect to height or BMI. BMI in early adulthood was not associated with ovarian cancer risk. Conclusion: Height was associated with an increased ovarian cancer risk, especially in premenopausal women. BMI was not associated with ovarian cancer risk in postmenopausal women but was positively associated with risk in premenopausal women
    Type of Publication: Journal article published
    PubMed ID: 18381473
    Signatur Availability
    BibTip Others were also interested in ...
  • 10
    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
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...