Analysis of the Association of Matrix Metalloproteinase-1 Gene Promoter (rs1799750) Polymorphism and Risk of Ovarian Cancer

2015 ◽  
Vol 25 (6) ◽  
pp. 961-967 ◽  
Author(s):  
Lijie Wang ◽  
Beihua Kong

ObjectiveStudies investigating the association betweenmatrix metalloproteinase-1(MMP1) gene promoter 1607–base pair (bp) polymorphism and ovarian cancer risk have yielded conflicting results.MethodsWe therefore carried out a meta-analysis of 754 ovarian cancer cases and 1184 controls from 5 published case-control studies. The strength of the association betweenMMP11607-bp polymorphism and ovarian cancer susceptibility was calculated using pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs).ResultsThe results suggest that no statistically significant associations exist betweenMMP11607-bp polymorphisms and ovarian cancer risk in all 4 genetic models (2G2G vs 1G1G: OR, 1.08; 95% CI, 0.81–1.43;P= 0.23; 1G2G vs 1G1G: OR, 1.06; 95% CI, 0.82–1.36;P= 0.15; 1G2G + 2G2G vs 1G1G: OR, 1.05; 95% CI, 0.83–1.34;P= 0.16; 2G2G vs 1G1G + 1G2G: OR, 0.98; 95% CI, 0.80–1.20;P= 0.84).ConclusionsIn summary, this meta-analysis showed that theMMP11607-bp polymorphism is not associated with ovarian cancer risk.

Author(s):  
Veronika S. Biller ◽  
Michael F. Leitzmann ◽  
Anja M. Sedlmeier ◽  
Felix F. Berger ◽  
Olaf Ortmann ◽  
...  

AbstractSedentary behaviour is an emerging risk factor for several site-specific cancers. Ovarian cancers are often detected at late disease stages and the role of sedentary behaviour as a modifiable risk factor potentially contributing to ovarian cancer risk has not been extensively examined. We systematically searched relevant databases from inception to February 2020 for eligible publications dealing with sedentary behaviour in relation to ovarian cancer risk. We conducted a systematic review and meta-analysis, calculating summary relative risks (RR) and 95% confidence intervals (CI) using a random-effects model. We calculated the E-Value, a sensitivity analysis for unmeasured confounding. We tested for publication bias and heterogeneity. Seven studies (three prospective cohort studies and four case–control studies) including 2060 ovarian cancer cases were analysed. Comparing highest versus lowest levels of sedentary behaviour, the data indicated a statistically significant increase in the risk of ovarian cancer in relation to prolonged sitting time (RR = 1.29, 95% CI = 1.07–1.57). Sub-analyses of prospective cohort studies (RR = 1.33, 95% CI = 0.92–1.93) and case–control studies (RR = 1.28, 95% CI = 0.98–1.68) showed statistically non-significant results. Sensitivity analysis showed that an unmeasured confounder would need to be related to sedentary behaviour and ovarian cancer with a RR of 1.90 to fully explain away the observed RR of 1.29. Our analyses showed a statistically significant positive association between sedentary behaviour and ovarian cancer risk.


2010 ◽  
Vol 91 (6) ◽  
pp. 1752-1763 ◽  
Author(s):  
Fariba Kolahdooz ◽  
Jolieke C van der Pols ◽  
Christopher J Bain ◽  
Geoffrey C Marks ◽  
Maria Celia Hughes ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Cunzhong Yuan ◽  
Xiaoyan Liu ◽  
Shi Yan ◽  
Cunfang Wang ◽  
Beihua Kong

This meta-analysis aims to examine whether theXRCC3polymorphisms are associated with ovarian cancer risk. Eligible case-control studies were identified through search in PubMed. Pooled odds ratios (ORs) were appropriately derived from fixed effects models. We therefore performed a meta-analysis of 5,302 ovarian cancer cases and 8,075 controls from 4 published articles and 8 case-control studies for 3 SNPs ofXRCC3. No statistically significant associations betweenXRCC3rs861539 polymorphisms and ovarian cancer risk were observed in any genetic models. ForXRCC3rs1799794 polymorphisms, we observed a statistically significant correlation with ovarian cancer risk using the homozygote comparison (T2T2 versus T1T1: OR = 0.70, 95% CI = 0.54–0.90,P=0.005), heterozygote comparison (T1T2 versus T1T1: OR = 1.10, 95% CI = 1.00–1.21,P=0.04), and the recessive genetic model (T2T2 versus T1T1+T1T2: OR = 0.67, 95% CI = 0.52–0.87,P=0.002). ForXRCC3rs1799796 polymorphisms, we also observed a statistically significant correlation with ovarian cancer risk using the heterozygote comparison (T1T2 versus T1T1: OR = 0.91, 95% CI = 0.83–0.99,P=0.04). In conclusion, this meta-analysis shows that theXRCC3were associated with ovarian cancer risk overall for Caucasians. Asian and African populations should be further studied.


Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1150 ◽  
Author(s):  
Mohammad Hashemi ◽  
Shima Karami ◽  
Sahel Sarabandi ◽  
Abdolkarim Moazeni-Roodi ◽  
Andrzej Małecki ◽  
...  

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.


2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Guowen Ding ◽  
Yu Chen ◽  
Huiwen Pan ◽  
Hao Qiu ◽  
Weifeng Tang ◽  
...  

Abstract Background: Previous case–control studies have suggested that apurinic/apyrimidinic endonuclease 1 (APE1) rs1760944 T>G polymorphism may be associated with cancer risk. Here, we carried out an updated meta-analysis to focus on the correlation between APE1 rs1760944 T>G locus and the risk of cancer. Methods: We used the crude odds ratios (ORs) with their 95% confidence intervals (CIs) to evaluate the possible relationship between the APE1 rs1760944 T>G polymorphism and cancer risk. Heterogeneity, publication bias and sensitivity analysis were also harnessed to check the potential bias of the present study. Results: Twenty-three independent studies involving 10166 cancer cases and 11598 controls were eligible for this pooled analysis. We found that APE1 rs1760944 T>G polymorphism decreased the risk of cancer in four genetic models (G vs. T: OR, 0.87; 95% CI, 0.83–0.92; P<0.001; GG vs. TT: OR, 0.77; 95% CI, 0.69–0.86; P<0.001; GG/TG vs. TT: OR, 0.83; 95% CI, 0.77–0.89, P<0.001 and GG vs. TT/TG: OR, 0.85; 95% CI, 0.80–0.92, P<0.001). Results of subgroup analyses also demonstrated that this single-nucleotide polymorphism (SNP) modified the risk among lung cancer, breast cancer, osteosarcoma, and Asians. Evidence of publication bias was found in the present study. When we treated the publication bias with ‘trim-and-fill’ method, the adjusted ORs and CIs were not significantly changed. Conclusion: In conclusion, current evidence highlights that the APE1 rs1760944 T>G polymorphism is a protective factor for cancer susceptibility. In the future, case–control studies with detailed risk factors are needed to confirm or refute our findings.


2021 ◽  
Author(s):  
Mario Giuseppe Mirisola ◽  
Antonio Galvano ◽  
Valerio Gristina ◽  
Maria La Mantia ◽  
Sofia Cutaia ◽  
...  

Abstract Background Breast cancer susceptibility gene 1 and 2 (BRCA 1/2) pathogenic germline variants (gPV) are involved in an increased cumulative risk for cancers (above all breast and ovarian cancers). Overweight/obesity is a well-known systemic condition conferring higher cancer risk too. Methods We performed a systematic review collecting data on Medline, Scopus, and Cochrane-Library database until August 2020. We included four case-control studies (Fu et al, Bissonauth et al, Khachatryan et al, Nkondjoc et al) assessing the risk for cancer according to different BMI strata in BRCA-positive healthy individuals. Results Four studies for a total of 1148 patients evaluated breast and ovarian cancer risk in a healthy BRCA1/2 population. No other tumor histotypes risk has been observed within the selected population. Pooled results demonstrated that different BMI conditions (lower or upper 25 kg/m2) were not associated with increased cancer risk (OR 1.15, 95% CI 0.92–1.44 and OR 1.48, 95% CI 0.84–2.62 respectively). Additionally, no differences were reported according to menopausal status. Conclusion Despite the need for other prospective investigations in larger cohorts, our results suggest no BMI contribution in cancer risk in this special population, determining a new important point of view and a new potential field of investigation.


2019 ◽  
Author(s):  
Yuhang Long ◽  
Hui Fei ◽  
Sumei Xu ◽  
Jianzhen Wen ◽  
Lihua Ye ◽  
...  

Abstract Background: Changes in dietary vitamin C intake have been related to the risks of various cancers. However, the association between dietary vitamin C intake and the risk of ovarian cancer has not been fully determined. A meta-analysis was performed to evaluate the relationship between vitamin C intake and ovarian cancer risk. Methods: Observational studies that evaluated the association between vitamin C intake and ovarian cancer risk were identified via systematic search of PubMed and Embase databases. A random effect model was used to combine relative risk (RR) with corresponding 95% confidence intervals (CI). Results: Sixteen studies (5 cohort studies and 11 case-control studies) with 4,553 cases and 439,741 participants were included. Pooled results showed that dietary vitamin C intake had non-significant association on the risk of ovarian cancer (RR=0.95, 95%CI= 0.81-1.11, I2= 52.1%, P for heterogeneity= 0.008). Subgroup analyses according to characteristics including geographic location and study design showed consistent results with the overall result. Conclusions: In summary, findings from this study indicated that dietary vitamin C intake is not associated with the risk of ovarian cancer.


Sign in / Sign up

Export Citation Format

Share Document