Lack of association of the iNOS gene polymorphism with risk of cancer: a systematic review and Meta-Analysis.
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ABSTRACT:
SUBMITTER: Jiao J
PROVIDER: S-EPMC4585729 | biostudies-other | 2015
REPOSITORIES: biostudies-other
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Project description:ObjectiveThe TP53BP1 gene may be involved in the development of cancer through disrupting DNA repair. However, studies investigating the relationship between TP53BP1 Glu353Asp (rs560191) polymorphism and cancer yielded contradictory and inconclusive outcomes. In order to realize these ambiguous findings, a meta-analysis was performed to assess the association between the TP53BP1 Glu353Asp (rs560191) polymorphism and susceptibility to cancer.MethodsWe conducted a search of all English reports on studies for the association between the TP53BP1 Asp353Glu (rs560191) polymorphism and susceptibility to cancer using Medline, the Cochrane Library, EMbase, Web of Science, Google (scholar), and all Chinese reports were identified manually and on-line using CBMDisc, Chongqing VIP database, and CNKI database. The strict selection criteria and exclusion criteria were determined, and odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. The fixed or random effect model was selected based on the heterogeneity test among studies. Publication bias was estimated using funnel plots and Egger's regression test.ResultsA total of seven studies were included in the meta-analysis including 3,213 cases and 3,849 controls. The results indicated that the Glu353Asp (rs560191) polymorphism in TP53BP1 gene had no association with cancer risk for all genetic models. In the subgroup analysis, the results suggested that Glu353Asp polymorphism was not associated with the risk of cancer according to ethnicity, cancer type, genotyping method, adjusted with control or not, HWE and quality score.ConclusionsThis meta-analysis suggested that the Glu353Asp (rs560191) polymorphism in TP53BP1 gene was not associated with risk of cancer.
| S-EPMC3946247 | biostudies-literature
Project description:BACKGROUND:Recently, several genome-wide association studies have demonstrated a cumulative association of 17q24 rs1859962 gene variants with prostate cancer (PCa) risk, but conflicting results on this issue have been reported. Hence, we performed a systematic literature review and meta-analysis to assess the association between 17q24 rs1859962 gene and PCa risk. METHODS:Systematic literature searches were conducted with PubMed, EMBASE, Science Direct/Elsevier, CNKI, and the Cochrane Library up to January 2019 for studies focusing on the association of 17q24 rs1859962 gene polymorphism with PCa risk. Meta-analysis was performed with Review Manager and stata software. Combined OR were identified with 95% confidence intervals (95% CI) in a random or fixed effects model. RESULTS:Eight studies were identified, including 7863 cases of PCa patients and 17122 normal controls. Our results revealed significant associations between the 17q24 rs1859962 gene polymorphism and PCa in all genetic models (P < 0.05). The combined odds ratios and 95% confidence intervals were as follows: Additive model (odds ratios [ORs] 1.44, 95%, confidence interval [CI] [1.32, 1.57]); Codominant model (ORs 1.22, 95% CI [1.08, 1.39]); Dominant model (ORs 1.25, 95%, CI [1.17, 1.34]); recessive model (ORs 1.27, 95% CI [1.18, 1.36]); allele model (ORs 1.32, 95% CI [1.12, 1.55]). CONCLUSION:The present study supports the proposed association between the 17q24 gene rs1859962 and PCa progression. Specifically, this polymorphism is suggested to be a risk factor of PCa. However, studies with larger sample sizes are needed to better illuminate the correlation between 17q24 rs1859962 gene polymorphism and PCa.
| S-EPMC7220075 | biostudies-literature
Project description:BackgroundTP53 gene polymorphism could increase risks of several kinds of cancer. But it remained controversial whether TP53 gene codon72 polymorphism was associated with the susceptibility to prostate cancer. Thus, we conducted a meta-analysis that evaluated the association between TP53 gene codon72 polymorphism and prostate cancer risk.MethodA comprehensive research was performed from PubMed, Embase, Web of Science and China National Knowledge Infrastructure (CNKI) up to December 31, 2018. A random effect model was used to evaluate the effect of the outcome. The statistical analyses were performed with Review Manager 5.3.0 and Stata 14.0. The sensitivity analysis and publication bias tests were also performed to confirm the reliability of this meta-analysis.Results22 studies included 3146 cases and 4010 controls were involved in this meta-analysis. Overall, no association was observed between TP53 gene codon72 polymorphism and prostate cancer risk (Arg vs Pro: odds ratio [OR] = 1.12, 95% confidence interval [CI] = 0.98-1.30; ArgArg vs ProPro: OR = 1.26, 95% CI = 0.90-1.75; ProPro vs ArgArg+ ArgPro: OR = 1.17, 95% CI = 0.86-1.57; ArgPro+ ProPro vs ArgArg: OR = 1.21, 95% CI = 0.97-1.51). Subgroup analyses, based on ethnicity, source of control and Hardy-Weinberg equilibrium (HWE) status, showed consistent results.ConclusionThe meta-analysis we performed showed that there was no association of TP53 gene codon72 polymorphism with prostate cancer risk.
| S-EPMC6636943 | biostudies-literature
Project description:BackgroundGenome-wide association studies on Europeans have shown that two polymorphisms (rs17782313, rs12970134) near the melanocortin 4 receptor (MC4R) gene were associated with increased risk of obesity. Subsequently studies among different ethnic populations have shown mixed results with some confirming and others showing inconsistent results, especially among East Asians and Africans. We performed a comprehensive meta-analysis of various studies from different ethnic populations to assess the association of the MC4R polymorphism with obesity risk.MethodsWe retrieved all published literature that investigated association of MC4R variants with obesity from PubMed and Embase. Pooled odds ratio (OR) with 95% confidence interval (CI) was calculated using fixed- or random-effects model.ResultsA total of 61 studies (80,957 cases/220,223 controls) for rs17782313 polymorphism (or proxy) were included in the meta-analysis. The results suggested that rs17782313 polymorphism was significantly associated with obesity risk (OR=1.18, 95%CI=1.15-1.21, p<0.001). Similar trends were observed among subgroups of Europeans and East Asians, adults and children, studies with high quality score, and for each five MC4R polymorphisms independently.ConclusionsThe present meta-analysis confirms the significant association of MC4R polymorphism with risk of obesity. Further studies should be conducted to identify the causal variant and the underlying mechanisms of the identified association.
| S-EPMC3458070 | biostudies-literature
Project description:OBJECTIVE:Studies have assessed the association between aspartic acid (D)-repeat polymorphism in the gene encoding Asporin (ASPN) and knee osteoarthritis (KOA) risk, but the results were inconclusive and contradictory. Therefore, we performed a meta-analysis to investigate the association between ASPN gene D-repeat polymorphism and KOA risk. METHODS:Eligible studies were identified by searching several electronic databases for relevant reports published before September 2016. The pooled odds ratios (ORs) for the association between ASPN polymorphism and KOA and their corresponding 95% confidence intervals (CIs) were estimated using the random- or fixed-effect model. RESULTS:A total of eleven case-control studies in ten publications with 4610 KOA cases and 3621 controls were included for the ASPN D-repeat polymorphism. Overall, no significant association was detected for D14 allele carrier (D14 vs. D13: OR = 1.10, 95% CI = 0.90-1.36, p = 0.32). Meta-analysis of D14 vs. other alleles and D13 vs. other alleles showed the same pattern of KOA association as the D14 vs. D13 (OR = 1.30, 95% CI = 1.00-1.70, p = 0.06; OR = 0.93, 95% CI = 0.82-1.06, p = 0.33, respectively). Also, in the stratified analysis by ethnicity, no significant association of this polymorphism with risk of KOA was found in the European and Asians populations (OR = 1.05, 95% CI = 0.91-1.21, p = 0.49; OR = 0.98, 95% CI = 0.78-1.23, p = 0.88, respectively). CONCLUSIONS:The present meta-analysis suggests that the ASPN D-repeat polymorphism is not associated with an increased KOA risk. However, future large studies with gene-gene and gene-environment interactions are needed to validate these findings. LEVEL OF EVIDENCE:Level III diagnostic study.
| S-EPMC6197333 | biostudies-other
Project description:Interleukin-2 (IL-2) is an important member of the cytokines that play critical roles in carcinogenesis. Many studies have investigated the association between IL-2 rs2069762 polymorphism and cancer risk; however, the results remain controversial. The aim of this study is to assess the correlation between IL-2 rs2069762 polymorphism and cancer risk. All eligible case-control studies accorded with criteria published up to March 30, 2015 were identified by searching Embase and PubMed databases. Association between IL-2 rs2069762 polymorphism and cancer risk was assessed by crude odds ratios (ORs) with 95% confidence intervals (CIs), respectively. Ten case-control studies from nine publications with 3095 cases and 4480 controls were included. Overall, IL-2 rs2069762 polymorphism was not associated with cancer risk in five genetic models (G vs. T: OR = 1.07, 95% CI = 0.95-1.21, P = 0.278; GG vs. TT: OR = 1.16, 95% CI = 0.86-1.57, P = 0.317; GG + TG vs. TT: OR = 1.09, 95% CI = 0.93-1.28, P = 0.273; GG vs. TT + TG: OR = 1.11, 95% CI = 0.85-1.44, P = 0.451; TG vs. TT: OR = 1.08, 95% CI = 0.92-1.28, P = 0.339, respectively). Similar results were also obtained after stratified by ethnicity and cancer type. This meta-analysis indicates that IL-2 rs2069762 T>G polymorphism is not associated with cancer risk. And the same conclusion is drawn after stratified by cancer type and ethnicity.
| S-EPMC4612851 | biostudies-literature
Project description:BackgroundTo investigate the association between sepsis and the vitamin D receptor (VDR) gene polymorphisms.MethodsDatabases including PubMed, Cochrane Library, EMbase, CNKI, Wanfang Data, and VIP Data were systematically searched. The association was assessed using odds ratios (ORs), and 95% confidence intervals (CIs). The statistical tests were performed using Review Manager 5.4.ResultsWe identified a total of 5 studies. The relationship between VDR gene polymorphisms (Apa I, Bsm I, Taq I, and Fok I), and incidence of sepsis was investigated. The results of this meta-analysis showed that the allelic contrast model (F vs f, P = .03, OR = 0.65, 95% CI = 0.44-0.95), dominant genetic model (FF vs Ff + ff, P = .02, OR = 0.53, 95% CI = 0.30-0.91), and codominance genetic model (FF vs ff, P = .03, OR = 0.39, 95% CI = 0.16-0.91) of VDR Fok I locus increased the risk of sepsis, and the lack of association between the VDR Fok I gene polymorphism and the risk assessment of sepsis, based on the ethnic subgroup analysis, might be attributable to the small sample size. The risk of sepsis with Apa I, Bsm I, and Taq I did not appear to be correlated.Conclusion subsectionsThis meta-analysis revealed that the VDR Fok I polymorphism is closely associated with the susceptibility to sepsis, and patients with sepsis have lower 25-hydroxyvitamin D levels. VDR Fok I gene mutations may change the risk of sepsis.
| S-EPMC10519506 | biostudies-literature
Project description:Lung cancer is the leading cause of cancer-related death worldwide and has a high incidence rate. N-Acetyltransferase 2 (NAT2) is a polymorphic xenobiotic enzyme, which can catalyze N-acetylation and O-acetylation of various carcinogens such as aromatic, heterocyclic amines and hydrazines. At present, many studies have explored the effects of NAT2 polymorphism on lung cancer, but we found inconsistent results. We researched 18 published studies, involving 4,016 patients and 5,469 controls, to more accurately assess the effects of NAT2 polymorphism on lung cancer risk and to investigate whether smoking is associated. We used STATA software to analyze the extracted data and used STATA for subgroup analysis, sensitivity analysis, and to perform publication bias tests. To determine the correlation, we used the crude odds ratio (ORs) with 95% confidence interval (CIs). Our study was prospectively registered in PROSPERO (CRD42020159737). The odds ratio was 1.53 (95% CI: 1.21-1.95, I² = 45.2%, P=0.104) for the NAT2 slow + intermediate phenotype versus rapid phenotype. The results suggested that people with NAT2 non-rapid (slow + intermediate) phenotype have a significantly increased risk of lung cancer. In addition, NAT2 rapid phenotype was significantly associated with reduced risk of lung cancer, compared with slow phenotype or intermediate phenotype (slow phenotype vs . rapid phenotype: OR: 1.61, 95% CI: 1.07-2.42, I²= 50%, P= 0.075; intermediate phenotype vs . rapid phenotype: OR: 1.47, 95% CI: 1.15-1.88, I²= 40.3%, P= 0.137).
| S-EPMC7991837 | biostudies-literature
Project description:IntroductionThe present study was conducted to determine the association of transforming growth factor-beta (TGF-β) gene polymorphism and myopia.MethodFour hundred twelve articles were identified, of which 11 articles with 5213 participants in 4 countries were included in the final analysis. Review Manager software (RevMan, version 5.4) was used for data analysis.ResultOdds ratio (OR) value of TGF-β1 rs1800469 is 1.33 (95% confidence interval [CI] = 1.15-1.54) in the allelic model; in the dominant model is 1.76 (95% CI = 1.16-2.67); in homozygous model is 5.98 (95% CI = 4.31-8.06). OR value of TGF-β1 rs4803455 is 0.62 (95% CI = 0.43-0.88) in recessive model. TGF-β2 is not associated with myopia. Relevant study on TGF-β3 is scarce.ConclusionOur systematic review and meta-analysis found that TGF-β1 rs4803455 and rs1800469 were correlated with myopia.
| S-EPMC9333477 | biostudies-literature
Project description:BackgroundTo assess the association of P2RX7 gene rs2230912 polymorphism with mood disorders using a meta-analysis.MethodsData were collected from the following electronic databases: PubMed, Excerpta Medica Database, Elsevier Science Direct, Cochrane Library, and Chinese Biomedical Literature Database, with the last report up to April 1, 2013. Odds ratio (OR) with 95% confidence interval (CI) was used to assess the strength of the association. Dependent on the results of heterogeneity test among individual studies, the fixed effect model (Mantel-Haenszel) or random effect model (DerSimonian-Laird) was selected to summarize the pooled OR.ResultsWe identified 13 separate studies using search (6,962 cases and 9,262 controls). We detected significant between-study heterogeneity. No significant association of this polymorphism with mood disorders was found (P>0.05). We also performed disease-specific meta-analysis in unipolar depression and bipolar disorder. No significant association of this polymorphism with unipolar depression or bipolar disorder was found (P>0.05). Additionally, we performed subgroup analysis by different types of cases. No significant association of this polymorphism with mood disorders in clinical cohorts or population-based cohorts (P>0.05). A significant association of this polymorphism with mood disorders was found for the allele contrast in family-based cohorts (OR = 1.26, 95%CI = 1.05-1.50, P = 0.01).ConclusionsOverall, our meta-analysis suggests that P2RX7 gene rs2230912 polymorphism may not contribute to the risk of developing mood disorders using a case-control design. Given the discordance in the subgroup analysis by different types of cases, further studies based on larger sample size are still needed.
| S-EPMC3922924 | biostudies-literature