Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
  • 1
    Keywords: CANCER ; MODEL ; POPULATION ; RISK ; SITE ; SITES ; GENE ; GENES ; BIOMARKERS ; ASSOCIATION ; polymorphism ; POLYMORPHISMS ; single nucleotide polymorphism ; SUSCEPTIBILITY ; VARIANTS ; HEALTH ; ovarian cancer ; OVARIAN-CANCER ; WOMEN ; REPLICATION ; glycosylation ; ONCOLOGY ; SINGLE NUCLEOTIDE POLYMORPHISMS ; biomarker ; CANCER-RISK ; Genetic ; single nucleotide
    Abstract: Aberrant glycosylation is a well-described hallmark of cancer. In a previous ovarian cancer case control study that examined polymorphisms in 26 glycosylation-associated genes, we found strong statistical evidence (P = 0.00017) that women who inherited two copies of a single-nucleotide polymorphism in the UDP-N-acetylgalactosamine:polypeptide N-acetylgalactosaminyltransferase, GALNT1, had decreased ovarian cancer risk. The current study attempted to replicate this observation. The GALNT1 single-nucleotide polymorphism rs17647532 was genotyped in 6,965 cases and 8,377 controls from 14 studies forming the Ovarian Cancer Association Consortium. The fixed effects estimate per rs17647532 allele was null (odds ratio, 0.99; 95% confidence interval, 0.92-1.07). When a recessive model was fit, the results were unchanged. Test for hetero geneity of the odds ratios revealed consistency across the 14 replication sites but significant differences compared with the original study population (P = 0.03). This study underscores the need for replication of putative findings in genetic association studies. Cancer Epidemiol Biomarkers Prev; 19(2); 600-4. (C) 2010 AACR
    Type of Publication: Journal article published
    PubMed ID: 20142253
    Signatur Availability
    BibTip Others were also interested in ...
  • 2
    Keywords: TUMORS ; polymorphism ; VARIANTS ; BREAST-CANCER ; BRCA1 ; WOMEN ; HETEROZYGOSITY ; MUTATIONS ; SINGLE-NUCLEOTIDE POLYMORPHISMS ; LOCUS ; GENOME-WIDE ASSOCIATION ; association studies ; Meiosis ; risk of ovarian cancer
    Abstract: Common germline genetic variation in the population is associated with susceptibility to epithelial ovarian cancer. Microcell-mediated chromosome transfer and expression microarray analysis identified nine genes associated with functional suppression of tumorogenicity in ovarian cancer cell lines; AIFM2, AKTIP, AXIN2, CASP5, FILIP1L, RBBP8, RGC32, RUVBL1 and STAG3. Sixty-three tagging single nucleotide polymorphisms (tSNPs) in these genes were genotyped in 1,799 invasive ovarian cancer cases and 3,045 controls to look for associations with disease risk. Two SNPs in RUVBL1, rs13063604 and rs7650365, were associated with increased risk of serous ovarian cancer [HetOR = 1.42 (1.15-1.74) and the HomOR = 1.63 (1.10-1.42), p-trend = 0.0002] and [HetOR = 0.97 (0.80-1.17), HomOR = 0.74 (0.58-0.93), p-trend = 0.009], respectively. We genotyped rs13063604 and rs7650365 in an additional 4,590 cases and 6,031 controls from ten sites from the United States, Europe and Australia; however, neither SNP was significant in Stage 2. We also evaluated the potential role of tSNPs in these nine genes in ovarian cancer development by testing for allele-specific loss of heterozygosity (LOH) in 286 primary ovarian tumours. We found frequent LOH for tSNPs in AXIN2, AKTIP and RGC32 (64, 46 and 34%, respectively) and one SNP, rs1637001, in STAG3 showed significant allele-specific LOH with loss of the common allele in 94% of informative tumours (p = 0.015). Array comparative genomic hybridisation indicated that this nonrandom allelic imbalance was due to amplification of the rare allele. In conclusion, we show evidence for the involvement of a common allele of STAG3 in the development of epithelial ovarian cancer
    Type of Publication: Journal article published
    PubMed ID: 20635389
    Signatur Availability
    BibTip Others were also interested in ...
  • 3
    Keywords: TUMORS ; ASSOCIATION ; WOMEN ; ORAL-CONTRACEPTIVES ; HISTOLOGIC TYPE ; LIFE-STYLE FACTORS ; inflammation ; TOBACCO USE ; HORMONE-THERAPY ; BORDERLINE
    Abstract: PURPOSE: The majority of previous studies have observed an increased risk of mucinous ovarian tumors associated with cigarette smoking, but the association with other histological types is unclear. In a large pooled analysis, we examined the risk of epithelial ovarian cancer associated with multiple measures of cigarette smoking with a focus on characterizing risks according to tumor behavior and histology. METHODS: We used data from 21 case-control studies of ovarian cancer (19,066 controls, 11,972 invasive and 2,752 borderline cases). Study-specific odds ratios (OR) and 95 % confidence intervals (CI) were obtained from logistic regression models and combined into a pooled odds ratio using a random effects model. RESULTS: Current cigarette smoking increased the risk of invasive mucinous (OR = 1.31; 95 % CI: 1.03-1.65) and borderline mucinous ovarian tumors (OR = 1.83; 95 % CI: 1.39-2.41), while former smoking increased the risk of borderline serous ovarian tumors (OR = 1.30; 95 % CI: 1.12-1.50). For these histological types, consistent dose-response associations were observed. No convincing associations between smoking and risk of invasive serous and endometrioid ovarian cancer were observed, while our results provided some evidence of a decreased risk of invasive clear cell ovarian cancer. CONCLUSIONS: Our results revealed marked differences in the risk profiles of histological types of ovarian cancer with regard to cigarette smoking, although the magnitude of the observed associations was modest. Our findings, which may reflect different etiologies of the histological types, add to the fact that ovarian cancer is a heterogeneous disease.
    Type of Publication: Journal article published
    PubMed ID: 23456270
    Signatur Availability
    BibTip Others were also interested in ...
  • 4
    Keywords: THERAPY ; HEALTH ; WOMEN
    Abstract: BACKGROUND: Half the epidemiological studies with information about menopausal hormone therapy and ovarian cancer risk remain unpublished, and some retrospective studies could have been biased by selective participation or recall. We aimed to assess with minimal bias the effects of hormone therapy on ovarian cancer risk. METHODS: Individual participant datasets from 52 epidemiological studies were analysed centrally. The principal analyses involved the prospective studies (with last hormone therapy use extrapolated forwards for up to 4 years). Sensitivity analyses included the retrospective studies. Adjusted Poisson regressions yielded relative risks (RRs) versus never-use. FINDINGS: During prospective follow-up, 12 110 postmenopausal women, 55% (6601) of whom had used hormone therapy, developed ovarian cancer. Among women last recorded as current users, risk was increased even with 〈5 years of use (RR 1.43, 95% CI 1.31-1.56; p〈0.0001). Combining current-or-recent use (any duration, but stopped 〈5 years before diagnosis) resulted in an RR of 1.37 (95% CI 1.29-1.46; p〈0.0001); this risk was similar in European and American prospective studies and for oestrogen-only and oestrogen-progestagen preparations, but differed across the four main tumour types (heterogeneity p〈0.0001), being definitely increased only for the two most common types, serous (RR 1.53, 95% CI 1.40-1.66; p〈0.0001) and endometrioid (1.42, 1.20-1.67; p〈0.0001). Risk declined the longer ago use had ceased, although about 10 years after stopping long-duration hormone therapy use there was still an excess of serous or endometrioid tumours (RR 1.25, 95% CI 1.07-1.46, p=0.005). INTERPRETATION: The increased risk may well be largely or wholly causal; if it is, women who use hormone therapy for 5 years from around age 50 years have about one extra ovarian cancer per 1000 users and, if its prognosis is typical, about one extra ovarian cancer death per 1700 users. FUNDING: Medical Research Council, Cancer Research UK.
    Type of Publication: Journal article published
    PubMed ID: 25684585
    Signatur Availability
    BibTip Others were also interested in ...
  • 5
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 6
    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
    Signatur Availability
    BibTip Others were also interested in ...
  • 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
    Signatur Availability
    BibTip Others were also interested in ...
  • 8
    Keywords: SUSCEPTIBILITY ; WOMEN ; ORAL-CONTRACEPTIVES ; HISTOLOGIC TYPE ; inflammation ; GENOME-WIDE ASSOCIATION
    Abstract: BACKGROUND: There are several well-established environmental risk factors for ovarian cancer, and recent genome-wide association studies have also identified six variants that influence disease risk. However, the interplay between such risk factors and susceptibility loci has not been studied. METHODS: Data from 14 ovarian cancer case-control studies were pooled, and stratified analyses by each environmental risk factor with tests for heterogeneity were conducted to determine the presence of interactions for all histologic subtypes. A genetic "risk score" was created to consider the effects of all six variants simultaneously. A multivariate model was fit to examine the association between all environmental risk factors and genetic risk score on ovarian cancer risk. RESULTS: Among 7,374 controls and 5,566 cases, there was no statistical evidence of interaction between the six SNPs or genetic risk score and the environmental risk factors on ovarian cancer risk. In a main effects model, women in the highest genetic risk score quartile had a 65% increased risk of ovarian cancer compared with women in the lowest [95% confidence interval (CI), 1.48-1.84]. Analyses by histologic subtype yielded risk differences across subtype for endometriosis (Phet 〈 0.001), parity (Phet 〈 0.01), and tubal ligation (Phet = 0.041). CONCLUSIONS: The lack of interactions suggests that a multiplicative model is the best fit for these data. Under such a model, we provide a robust estimate of the effect of each risk factor that sets the stage for absolute risk prediction modeling that considers both environmental and genetic risk factors. Further research into the observed differences in risk across histologic subtype is warranted. Cancer Epidemiol Biomarkers Prev; 22(5); 880-90. (c)2013 AACR.
    Type of Publication: Journal article published
    PubMed ID: 23462924
    Signatur Availability
    BibTip Others were also interested in ...
  • 9
    Keywords: CLASSIFICATION ; TUMORS ; WOMEN ; HEIGHT ; METAANALYSIS ; BODY-MASS INDEX ; PREMENOPAUSAL ; SEX-HORMONES ; SELF-REPORTED WEIGHT ; HORMONE-THERAPY
    Abstract: Whilst previous studies have reported that higher BMI increases a woman's risk of developing ovarian cancer, associations for the different histological subtypes have not been well defined. As the prevalence of obesity has increased dramatically, and classification of ovarian histology has improved in the last decade, we sought to examine the association in a pooled analysis of recent studies participating in the Ovarian Cancer Association Consortium. We evaluated the association between BMI (recent, maximum and in young adulthood) and ovarian cancer risk using original data from 15 case-control studies (13 548 cases and 17 913 controls). We combined study-specific adjusted odds ratios (ORs) using a random-effects model. We further examined the associations by histological subtype, menopausal status and post-menopausal hormone use. High BMI (all time-points) was associated with increased risk. This was most pronounced for borderline serous (recent BMI: pooled OR=1.24 per 5 kg/m(2); 95% CI 1.18-1.30), invasive endometrioid (1.17; 1.11-1.23) and invasive mucinous (1.19; 1.06-1.32) tumours. There was no association with serous invasive cancer overall (0.98; 0.94-1.02), but increased risks for low-grade serous invasive tumours (1.13, 1.03-1.25) and in pre-menopausal women (1.11; 1.04-1.18). Among post-menopausal women, the associations did not differ between hormone replacement therapy users and non-users. Whilst obesity appears to increase risk of the less common histological subtypes of ovarian cancer, it does not increase risk of high-grade invasive serous cancers, and reducing BMI is therefore unlikely to prevent the majority of ovarian cancer deaths. Other modifiable factors must be identified to control this disease.
    Type of Publication: Journal article published
    PubMed ID: 23404857
    Signatur Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...