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  • 1
    Keywords: CANCER ; SURVIVAL ; RISK ; FAMILY ; ASSOCIATION ; SUSCEPTIBILITY ; BREAST-CANCER ; MUTATIONS ; MUTATION CARRIERS ; susceptibility loci ; GENOME-WIDE ASSOCIATION ; CONSORTIUM
    Abstract: Purpose: An assay for the single-nucleotide polymorphism (SNP), rs61764370, has recently been commercially marketed as a clinical test to aid ovarian cancer risk evaluation in women with family histories of the disease. rs67164370 is in a 3'-UTR miRNA binding site of the KRAS oncogene and is a candidate for epithelial ovarian cancer (EOC) susceptibility. However, only one published article, analyzing fewer than 1,000 subjects in total, has examined this association. Experimental Design: Risk association was evaluated in 8,669 cases of invasive EOC and 10,012 controls from 19 studies participating in the Ovarian Cancer Association Consortium, and in 683 cases and 2,044 controls carrying BRCA1 mutations from studies in the Consortium of Investigators of Modifiers of BRCA1/2. Prognosis association was also examined in a subset of five studies with progression-free survival (PFS) data and 18 studies with all-cause mortality data. Results: No evidence of association was observed between genotype and risk of unselected EOC (OR = 1.02, 95% CI: 0.95-1.10), serous EOC (OR = 1.08, 95% CI: 0.98-1.18), familial EOC (OR = 1.09, 95% CI: 0.78-1.54), or among women carrying deleterious mutations in BRCA1 (OR = 1.09, 95% CI: 0.88-1.36). There was little evidence for association with survival time among unselected cases (HR = 1.10, 95% CI: 0.99-1.22), among serous cases (HR = 1.12, 95% CI = 0.99-1.28), or with PFS in 540 cases treated with carboplatin and paclitaxel (HR = 1.18, 95% CI: 0.93-1.52). Conclusions: These data exclude the possibility of an association between rs61764370 and a clinically significant risk of ovarian cancer or of familial ovarian cancer. Use of this SNP for ovarian cancer clinical risk prediction, therefore, seems unwarranted.
    Type of Publication: Journal article published
    PubMed ID: 21385923
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  • 2
    Keywords: CANCER ; RISK ; GENE ; BIOMARKERS ; ASSOCIATION ; polymorphism ; SUSCEPTIBILITY LOCUS ; BREAST ; HEALTH ; MUTATIONS ; ENVELOPE ; GENOME-WIDE ASSOCIATION ; SYNE-1 ; CANDIDATE SNPS ; single nucleotide
    Abstract: We genotyped 13 single nucleotide polymorphisms (SNPs) in the estrogen receptor alpha gene (ESR1) region in three population-based case-control studies of epithelial ovarian cancer conducted in the United States, comprising a total of 1,128 and 1,866 non-Hispanic white invasive cases and controls, respectively. A SNP 19 kb downstream of ESR1. (rs2295190, G-to-T change) was associated with invasive ovarian cancer risk, with a per-T-allele odds ratio (OR) of 1.24 [95% confidence interval (CI), 1.06-1.44, P = 0.0061. rs2295190 is a nonsynonymous coding SNP in a neighboring gene called spectrin repeat containing, nuclear envelope I (SYNE1), which is involved in nuclear organization and structural integrity, function of the Golgi apparatus, and cytokinesis. An isoform encoded by SYNE1 has been reported to be down-regulated in ovarian and other cancers. rs2295190 was genotyped in an additional 12 Studies through the Ovarian Cancer Association Consortium, with 5,279 invasive epithelial cases and 7,450 controls. The per-T-allele OR for this 12-study set was 1.09 (95% CI, 1.02-1.17; P = 0.017). Results for the serous subtype in the 15 combined studies were similar to those overall (n = 3,545; OR, 1.09; 95% Cl, 1.01-1.18; P = 0.025), and our findings were strongest for the mucinous subtype (n = 447; OR, 1.32; 95% CI, 1.11-1.58; P = 0.002). No association was observed for the endometrioid Subtype. In an additional analysis of 1,459 borderline ovarian cancer cases and 7,370 controls, rs2295190 was not associated with risk. These data provide suggestive evidence that the rs2295190 T allele, or another allele in linkage disequilibrium with it, may be associated with increased risk of invasive ovarian cancer. Cancer Epidemiol Biomarkers Prev; 190); 245-50. (C) 2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20056644
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  • 3
    Abstract: Epithelial ovarian cancer (EOC) is the leading cause of death from gynecological malignancy in the developed world, accounting for 4% of the deaths from cancer in women(1). We performed a three-phase genome-wide association study of EOC survival in 8,951 individuals with EOC (cases) with available survival time data and a parallel association analysis of EOC susceptibility. Two SNPs at 19p13.11, rs8170 and rs2363956, showed evidence of association with survival (overall P = 5 x 10(-4) and P = 6 x 10(-4), respectively), but they did not replicate in phase 3. However, the same two SNPs demonstrated genome-wide significance for risk of serous EOC (P = 3 x 10(-9) and P = 4 x 10(-11), respectively). Expression analysis of candidate genes at this locus in ovarian tumors supported a role for the BRCA1-interacting gene C19orf62, also known as MERIT40, which contains rs8170, in EOC development
    Type of Publication: Journal article published
    PubMed ID: 20852633
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  • 4
    Abstract: Ovarian cancer accounts for more deaths than all other gynecological cancers combined. To identify common low-penetrance ovarian cancer susceptibility genes, we conducted a genome-wide association study of 507,094 SNPs in 1,768 individuals with ovarian cancer (cases) and 2,354 controls, with follow up of 21,955 SNPs in 4,162 cases and 4,810 controls, leading to the identification of a confirmed susceptibility locus at 9p22 (in BNC2)(1). Here, we report on nine additional candidate loci (defined as having P 〈= 10(-4)) identified after stratifying cases by histology, which we genotyped in an additional 4,353 cases and 6,021 controls. We confirmed two new susceptibility loci with P 〈= 5 x 10(-8) (8q24, P = 8.0 x 10(-15) and 2q31, P = 3.8 x 10(-14)) and identified two additional loci that approached genome-wide significance (3q25, P = 7.1 x 10(-8) and 17q21, P = 1.4 x 10(-7)). The associations of these loci with serous ovarian cancer were generally stronger than with other cancer subtypes. Analysis of HOXD1, MYC, TIPARP and SKAP1 at these loci and of BNC2 at 9p22 supports a functional role for these genes in ovarian cancer development
    Type of Publication: Journal article published
    PubMed ID: 20852632
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  • 5
    Keywords: CANCER ; MODEL ; PATHWAY ; PATHWAYS ; ALGORITHM ; RISK ; GENE ; GENES ; SAMPLE ; DNA ; FAMILY ; BIOMARKERS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; VARIANTS ; STAGE ; HEALTH ; BRCA1 ; ovarian cancer ; OVARIAN-CANCER ; WOMEN ; MUTATION ; SNP ; cancer risk ; MUTATIONS ; MULTIVARIATE ; UNITED-STATES ; REPLICATION ; VALIDITY ; inflammation ; STATES ; ONCOLOGY ; FAMILIES ; VARIANT ; SINGLE NUCLEOTIDE POLYMORPHISMS ; SNPs ; ARRAY ; METAANALYSIS ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; biomarker ; analysis ; HAPLOTYPE ; USA ; CANDIDATE ; cancer research ; CANCER-RISK ; COMMUNITY ; REPAIR GENES ; RATIO ; CONSORTIUM ; NUCLEOTIDE ; STATE ; genetic variants ; COLLABORATIVE ANALYSIS ; HORMONAL FACTORS ; STATES CASE-CONTROL
    Abstract: Over 22,000 cases of ovarian cancer were diagnosed in 2007 in the United States, but only a fraction of them can be attributed to mutations in highly penetrant genes such as BRCA1. To determine whether low-penetrance genetic variants contribute to ovarian cancer risk, we genotyped 1,536 single nucleotide polymorphisms (SNP) in several candidate gene pathways in 848 epithelial ovarian cancer cases and 798 controls in the North Carolina Ovarian Cancer Study (NCO) using a customized Illumina array. The inflammation gene interleukin-18 (IL18) showed the strongest evidence for association with epithelial ovarian cancer in a gene-by-gene analysis (P = 0.002) with a 〈 25% chance of being a false-positive finding (q value = 0.240). Using a multivariate model search algorithm over 11 IL18 tagging SNPs, we found that the association was best modeled by rs1834481. Further, this SNP uniquely tagged a significantly associated IL18 haplotype and there was an increased risk of epithelial ovarian cancer per rs1834481 allele (odds ratio, 1.24; 95% confidence interval, 1.06-1.45). In a replication stage, 12 independent studies from the Ovarian Cancer Association Consortium (OCAC) genotyped rs1834481 in an additional 5,877 cases and 7,791 controls. The fixed effects estimate per rs1834481 allele was null (odds ratio, 0.99; 95% confidence interval, 0.94-1.05) when data from the 12 OCAC studies were combined. The effect estimate remained unchanged with the addition of the initial North Carolina Ovarian Cancer Study data. This analysis shows the importance of consortia, like the OCAC, in either confirming or refuting the validity of putative findings in studies with smaller sample sizes. (Cancer Epidemiol Biomarkers Prev 20081-17(12):3567-72)
    Type of Publication: Journal article published
    PubMed ID: 19064572
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  • 6
    Keywords: ALLELES, ASSOCIATION, BASAL-CELL CARCINOMA, BREAST-CANCER, CANCER, CANCERS, CANDIDATE SNPS, COLORECT
    Abstract: Epithelial ovarian cancer has a major heritable component, but the known susceptibility genes explain less than half the excess familial risk(1). We performed a genome-wide association study (GWAS) to identify common ovarian cancer susceptibility alleles. We evaluated 507,094 SNPs genotyped in 1,817 cases and 2,353 controls from the UK and similar to 2 million imputed SNPs. We genotyped the 22,790 top ranked SNPs in 4,274 cases and 4,809 controls of European ancestry from Europe, USA and Australia. We identified 12 SNPs at 9p22 associated with disease risk (P 〈 10(-8)). The most significant SNP (rs3814113; P = 2.5 x 10(-17)) was genotyped in a further 2,670 ovarian cancer cases and 4,668 controls, confirming its association (combined data odds ratio (OR) - 0.82, 95% confidence interval (CI) 0.79-0.86, P-trend = 5.1 x 10(-19)). The association differs by histological subtype, being strongest for serous ovarian cancers (OR 0.77, 95% CI 0.73-0.81, Ptrend 4.1 x 10(-21))
    Type of Publication: Journal article published
    PubMed ID: 19648919
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  • 7
    Keywords: carcinoma ; GENES ; SUSCEPTIBILITY ; WOMEN ; PATHOGENESIS ; inflammation ; infertility ; ORIGIN ; HOSPITAL DISCHARGE DIAGNOSIS ; FERTILITY DRUGS
    Abstract: BACKGROUND: Endometriosis is a risk factor for epithelial ovarian cancer; however, whether this risk extends to all invasive histological subtypes or borderline tumours is not clear. We undertook an international collaborative study to assess the association between endometriosis and histological subtypes of ovarian cancer. METHODS: Data from 13 ovarian cancer case-control studies, which were part of the Ovarian Cancer Association Consortium, were pooled and logistic regression analyses were undertaken to assess the association between self-reported endometriosis and risk of ovarian cancer. Analyses of invasive cases were done with respect to histological subtypes, grade, and stage, and analyses of borderline tumours by histological subtype. Age, ethnic origin, study site, parity, and duration of oral contraceptive use were included in all analytical models. FINDINGS: 13 226 controls and 7911 women with invasive ovarian cancer were included in this analysis. 818 and 738, respectively, reported a history of endometriosis. 1907 women with borderline ovarian cancer were also included in the analysis, and 168 of these reported a history of endometriosis. Self-reported endometriosis was associated with a significantly increased risk of clear-cell (136 [20.2%] of 674 cases vs 818 [6.2%] of 13 226 controls, odds ratio 3.05, 95% CI 2.43-3.84, p〈0.0001), low-grade serous (31 [9.2%] of 336 cases, 2.11, 1.39-3.20, p〈0.0001), and endometrioid invasive ovarian cancers (169 [13.9%] of 1220 cases, 2.04, 1.67-2.48, p〈0.0001). No association was noted between endometriosis and risk of mucinous (31 [6.0%] of 516 cases, 1.02, 0.69-1.50, p=0.93) or high-grade serous invasive ovarian cancer (261 [7.1%] of 3659 cases, 1.13, 0.97-1.32, p=0.13), or borderline tumours of either subtype (serous 103 [9.0%] of 1140 cases, 1.20, 0.95-1.52, p=0.12, and mucinous 65 [8.5%] of 767 cases, 1.12, 0.84-1.48, p=0.45). INTERPRETATION: Clinicians should be aware of the increased risk of specific subtypes of ovarian cancer in women with endometriosis. Future efforts should focus on understanding the mechanisms that might lead to malignant transformation of endometriosis so as to help identify subsets of women at increased risk of ovarian cancer. FUNDING: Ovarian Cancer Research Fund, National Institutes of Health, California Cancer Research Program, California Department of Health Services, Lon V Smith Foundation, European Community's Seventh Framework Programme, German Federal Ministry of Education and Research of Germany, Programme of Clinical Biomedical Research, German Cancer Research Centre, Eve Appeal, Oak Foundation, UK National Institute of Health Research, National Health and Medical Research Council of Australia, US Army Medical Research and Materiel Command, Cancer Council Tasmania, Cancer Foundation of Western Australia, Mermaid 1, Danish Cancer Society, and Roswell Park Alliance Foundation.
    Type of Publication: Journal article published
    PubMed ID: 22361336
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