scholarly journals Genetic variants in matrix metalloproteinase genes as disposition factors for ovarian cancer risk, survival, and clinical outcome

2013 ◽  
Vol 54 (6) ◽  
pp. 430-439 ◽  
Author(s):  
Yan Wang ◽  
Yuanqing Ye ◽  
Jie Lin ◽  
Larissa Meyer ◽  
Xifeng Wu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Clinical Outcome ◽  
Matrix Metalloproteinase ◽  
Genetic Variants ◽  
Ovarian Cancer Risk

scholarly journals Genetic variants within the cancer susceptibility region 8q24 and ovarian cancer risk in Han Chinese women

Oncotarget ◽  
2017 ◽  
Vol 8 (22) ◽  
pp. 36462-36468 ◽  
Author(s):  
Jing Han ◽  
Jing Zhou ◽  
Hua Yuan ◽  
Longbiao Zhu ◽  
Hongxia Ma ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Genetic Variants ◽  
Cancer Susceptibility ◽  
Chinese Women ◽  
Han Chinese ◽  
Ovarian Cancer Risk ◽  
Susceptibility Region

scholarly journals Genetic Variants in TGF-β Pathway Are Associated with Ovarian Cancer Risk

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e25559 ◽  
Author(s):  
Jikai Yin ◽  
Karen Lu ◽  
Jie Lin ◽  
Lei Wu ◽  
Michelle A. T. Hildebrandt ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Genetic Variants ◽  
Ovarian Cancer Risk

Abstract 3593: Genetic variants in NER pathway genes and ovarian cancer risk and outcomes

2010 ◽  
Author(s):  
Yilei Gong ◽  
Jie Lin ◽  
Yuanqing Ye ◽  
Lei Wu ◽  
Xia Pu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Genetic Variants ◽  
Ovarian Cancer Risk

scholarly journals Evaluating causal associations between previously reported risk factors and epithelial ovarian cancer: a Mendelian randomization analysis

2018 ◽  
Author(s):  
James Yarmolinsky ◽  
Caroline L Relton ◽  
Artitaya Lophatananon ◽  
Kenneth Muir ◽  
Usha Menon ◽  
...  
Keyword(s):  
Risk Factors ◽  
Ovarian Cancer ◽  
Cancer Risk ◽  
Epithelial Ovarian Cancer ◽  
Genetic Variants ◽  
Mendelian Randomization ◽  
Modifiable Risk Factors ◽  
Ovarian Cancer Risk ◽  
Genetic Liability ◽  
Suggestive Evidence

AbstractBackgroundVarious modifiable risk factors have been associated with epithelial ovarian cancer risk in observational epidemiological studies. However, the causal nature of the risk factors reported, and thus their suitability as effective intervention targets, is unclear given the susceptibility of conventional observational designs to residual confounding and reverse causation. Mendelian randomization uses genetic variants as proxies for modifiable risk factors to strengthen causal inference in observational studies. We used Mendelian randomization to evaluate the causal role of 13 previously reported risk factors (reproductive, anthropometric, clinical, lifestyle, and molecular factors) in overall and histotype-specific epithelial ovarian cancer in up to 25,509 case subjects and 40,941 controls in the Ovarian Cancer Association Consortium.Methods and FindingsGenetic instruments to proxy 13 risk factors were constructed by identifying single nucleotide polymorphisms (SNPs) robustly (P<5×10−8) and independently associated with each respective risk factor in previously reported genome-wide association studies. SNPs were combined into multi-allelic inverse-variance weighted fixed or random-effects models to generate causal estimates. Three complementary sensitivity analyses were performed to examine violations of Mendelian randomization assumptions: MR-Egger regression and weighted median and mode estimators. A Bonferroni-corrected P-value threshold was used to establish “strong evidence” (P<0.0038) and “suggestive evidence” (0.0038<P<0.05) for associations.In Mendelian randomization analyses, there was strong or suggestive evidence that 9 of 13 risk factors had a causal effect on overall or histotype-specific epithelial ovarian cancer. There was strong evidence that genetic liability to endometriosis increased risk of epithelial ovarian cancer (OR per log odds higher liability:1.27, 95% CI: 1.16-1.40; P=6.94×10−7) and suggestive evidence that lifetime smoking exposure increased risk of epithelial ovarian cancer (OR per unit increase in smoking score:1.36, 95% CI: 1.04-1.78; P=0.02). In histotype-stratified analyses, the strongest associations found were between: height and clear cell carcinoma (OR per SD increase:1.36, 95% CI: 1.15-1.61; P=0.0003); age at natural menopause and endometrioid carcinoma (OR per year later onset:1.09, 95% CI: 1.02-1.16; P=0.007); and genetic liability to polycystic ovary syndrome and endometrioid carcinoma (OR per log odds higher liability:0.74, 95% CI:0.62-0.90; P=0.002). There was little evidence for an effect of genetic liability to type 2 diabetes, parity, or circulating levels of 25-hydroxyvitamin D and sex hormone-binding globulin on ovarian cancer or its subtypes. The primary limitations of this analysis include: modest statistical power for analyses of risk factors in relation to some less common ovarian cancer histotypes (low grade serous, mucinous, and clear cell carcinomas), the inability to directly examine the causal effects of some ovarian cancer risk factors that did not have robust genetic variants available to serve as proxies (e.g., oral contraceptives, hormone replacement therapy), and the assumption of linear relationships between risk factors and ovarian cancer risk.ConclusionsOur comprehensive examination of possible etiological drivers of ovarian carcinogenesis using germline genetic variants to proxy risk factors supports a causal role for few of these factors in epithelial ovarian cancer and suggests distinct etiologies across histotypes. The identification of novel modifiable risk factors remains an important priority for the control of epithelial ovarian cancer.

Abstract 2835: Mitochondrial genetic variants influence ovarian cancer risk

2010 ◽  
Author(s):  
Jennifer Permuth-Wey ◽  
Ya-Yu Tsai ◽  
Y. Ann Chen ◽  
Zhihua Chen ◽  
Johnathan M. Lancaster ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Genetic Variants ◽  
Ovarian Cancer Risk

scholarly journals Genetic Variants in the Fibroblast Growth Factor Pathway as Potential Markers of Ovarian Cancer Risk, Therapeutic Response, and Clinical Outcome

2014 ◽  
Vol 60 (1) ◽  
pp. 222-232 ◽  
Author(s):  
Qing H Meng ◽  
Enping Xu ◽  
Michelle A T Hildebrandt ◽  
Dong Liang ◽  
Karen Lu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Overall Survival ◽  
Growth Factor ◽  
Cancer Risk ◽  
Fibroblast Growth Factor ◽  
Genetic Variants ◽  
Therapeutic Response ◽  
Ovarian Cancer Risk ◽  
Fibroblast Growth ◽  
Multiple Snps

AbstractBACKGROUNDThe fibroblast growth factor (FGF) and FGF receptor (FGFR) axis plays a critical role in tumorigenesis, but little is known of its influence in ovarian cancer. We sought to determine the association of genetic variants in the FGF pathway with risk, therapeutic response, and survival of patients with ovarian cancer.METHODSWe matched 339 non-Hispanic white ovarian cancer cases with 349 healthy controls and genotyped them for 183 single-nucleotide polymorphisms (SNPs) from 24 FGF (fibroblast growth factor) and FGFR (fibroblast growth factor receptor) genes. Genetic associations for the main effect, gene–gene interactions, and the cumulative effect were determined.RESULTSMultiple SNPs in the FGF–FGFR axis were associated with an increased risk of ovarian cancer. In particular, FGF1 [fibroblast growth factor 1 (acidic)] SNP rs7727832 showed the most significant association with ovarian cancer (odds ratio, 2.27; 95% CI, 1.31–3.95). Ten SNPs were associated with a reduced risk of ovarian cancer. FGF18 (fibroblast growth factor 18) SNP rs3806929, FGF7 (fibroblast growth factor 7) SNP rs9920722, FGF23 (fibroblast growth factor 23) SNP rs12812339, and FGF5 (fibroblast growth factor 5) SNP rs3733336 were significantly associated with a favorable treatment response, with a reduction of risk of nonresponse of 40% to 60%. Eleven SNPs were significantly associated with overall survival. Of these SNPs, FGF23 rs7961824 was the most significantly associated with improved prognosis (hazard ratio, 0.55; 95% CI, 0.39–0.78) and was associated with significantly longer survival durations, compared with individuals with the common genotype at this locus (58.1 months vs. 38.0 months, P = 0.005). Survival tree analysis revealed FGF2 rs167428 as the primary factor contributing to overall survival.CONCLUSIONSSignificant associations of genetic variants in the FGF pathway were associated with ovarian cancer risk, therapeutic response, and survival. The discovery of multiple SNPs in the FGF–FGFR pathway provides a molecular approach for risk assessment, monitoring therapeutic response, and prognosis.

scholarly journals Genetic variants in telomere-maintenance genes are associated with ovarian cancer risk and outcome

2016 ◽  
Vol 21 (3) ◽  
pp. 510-518 ◽  
Author(s):  
Yuhui Sun ◽  
Wade Tao ◽  
Maosheng Huang ◽  
Xifeng Wu ◽  
Jian Gu
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Genetic Variants ◽  
Telomere Maintenance ◽  
Ovarian Cancer Risk

scholarly journals Genetic Variants in MicroRNA Biosynthesis Pathways and Binding Sites Modify Ovarian Cancer Risk, Survival, and Treatment Response

2010 ◽  
Vol 70 (23) ◽  
pp. 9765-9776 ◽  
Author(s):  
Dong Liang ◽  
Larissa Meyer ◽  
David W. Chang ◽  
Jie Lin ◽  
Xia Pu ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Treatment Response ◽  
Genetic Variants ◽  
Binding Sites ◽  
Ovarian Cancer Risk
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