The CCND1 G870A Gene Polymorphism and Leukemia or Non-Hodgkin Lymphoma Risk: a Meta-analysis

In recent years, mounting evidence has indicated that the CCND1 G870A gene polymorphism, which impacts the mitotic cell cycle, may influence leukemia or non-Hodgkin lymphoma risk. Unfortunately, the previous results were inconsistent. Therefore, a meta-analysis was performed to obtain a more precise estimation of any association. We conducted a search in PubMed, Embase and CNKI covering all published papers up to March, 2014. A total of 9 publications including 10 case-control studies met the inclusion criteria. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assess association. The pooled ORs showed significant association in non-Hodgkin lymphoma (comparison A vs G: OR= 1.114, 95%CI=1.053-1.179, p=0.000; homozygote comparison AA vs GG: OR=1.245, 95%CI=1.110-1.396, p=0.000; heterozygote comparison AG vs GG: OR=1.095, 95%CI=1.000-1.199, p=0.05; dominant model AA/GA vs GG: OR=1.137, 95%CI=1.043-1.239, p=0.003; and recessive model AA vs GA/GG: OR=1.177, 95%CI=1.066-1.301, p=0.001). However, there was no association between the CCND1 G870A polymorphism and leukemia risk. In conclusion, the CCND1 G870A polymorphism may increase risk of non-Hodgkin lymphoma, but not leukemia. However, more primary large scale and well-designed studies are still required to evaluate the interaction of CCND1 G870A polymorphism with leukemia and non-Hodgkin lymphoma risk.     

The 2518 A/G Polymorphism in the MCP-1 Gene and Cancer Risk: A Meta-analysis

Background: The 2518 A/G polymorphism in the MCP-1 gene has been extensively studied for associationswith cancer; however, results from replication studies have been inconsistent. The aim of this investigationwas to determine links with risk of cancer by meta-analysis. Methods: We searched Pubmed, Embase, CNKI,Weipu and Wanfang databases, covering all case-control studies until March, 2013. Statistical analyses wereperformed using the Revman 5.0 software. Results: A total of 11 case-control studies met our inclusion criteria,including 1,422 cases and 2,237 controls. The results indicated that the MCP-1 2518 gene polymorphism had noassociation with cancer risk overall (GG vs.GA+ AA: OR = 0.89, 95%CI = 0.61–1.28, P = 0.52). However, in thesubgroup analysis by ethnicity, a decrease of cancer risk was found in Asian populations (GG vs.GA+ AA: OR =0.79, 95%CI = 0.63–0.99, P = 0.04). Conclusion: This meta-analysis suggested that the 2518A/G polymorphismof MCP-1 gene is associated with risk of cancer among Asian, but not in Caucasian populations.     

The Cyclin D1 G870A Polymorphism and Colorectal Cancer Susceptibility: A Meta-analysis of 20 Populations

Purpose: Studies of the association between the cyclin D1 (CCND1) G870A genetic polymorphism and riskof colorectal cancer (CRC) have generated conflicting results. In order to derive a more precise estimation, ameta-analysis was here performed. Materials and methods: An extensive search of relevant studies was carriedout as a meta-analysis of twenty studies with 5,975 cases and 8,333 controls. Results: Overall, a significantlyelevated colorectal cancer risk was associated with variant allele 870A when all studies were pooled (AA vs.GG: OR = 1.23, 95%CI = 1.04-1.44; GA vs. GG: OR = 1.13, 95%CI = 1.01-1.26; dominant model: OR = 1.16,95%CI = 1.03-1.31). In the subgroup analysis by ethnicity, significantly increased risks were detected amongCaucasians (AA vs. GG: OR = 1.27, 95%CI = 1.04-1.44; and dominant model: OR = 1.17, 95%CI = 1.02-1.34).With stratification into sporadic CRC and hereditary nonpolyposis colorectal cancer (HNPCC), the formerdemonstrated increased cancer susceptibility (AA vs. GG: OR = 1.24, 95%CI = 1.04-1.48; dominant model:OR = 1.17, 95%CI = 1.04-1.33). However, no significant associations were found in either Asians or HNPCCpatients for any genetic model. Conclusion: The results suggest that the cyclin D1 870A allele is a low-penetrantrisk factor for development of sporadic colorectal cancer, especially among Caucasians.     

CCND1 G/A位点基因多态性与肝细胞癌发生风险相关性的Meta分析

目的探讨细胞周期蛋白D1(CCND1)G/A位点基因多态性与肝细胞癌(HCC)发生风险的相关性。方法利用Pub Med、CNKI和EMbase数据库系统检索:CCND1 G/A位点基因多态性与肝细胞癌发生风险相关性的病例-对照研究。以病例组与对照组CCND1 G/A位点各种基因模型的比值比(OR)及95%可信区间(CI)为效应指标,并用Egger检验和Begg检验进行发表偏倚评价。结果有7项研究符合纳入标准。共纳入1108例肝癌患者和1477例对照。Meta分析结果表明:CCND1 G/A位点基因多态性与肝细胞癌发生风险无明显相关性,其中(AA vs GG:OR=1.33,95%CI:0.98~1.82,P=0.07;GA vs GG:OR=1.07,95%CI:0.92~1.24,P=0.37;GA+AA vs GG:OR=0.93,95%CI:0.82~1.05,P=0.23;AA vs GG+GA:OR=1.08,95%CI:0.95~1.22,P=0.24)。结论基于目前研究结果,尚不能认为CCND1 G/A位点基因多态性与肝细胞癌发生风险有显著相关性。     

A Cyclin D1 (CCND1) Gene Polymorphism Contributes to Susceptibility to Papillary Thyroid Cancer in the Turkish Population

Cyclin D1 is an important positive regulator of the G1/S phase of the cell cycle. We investigated the association between the CCND1 G870A polymorphism and susceptibility to papillary thyroid cancer in Turkish people. This study covered 102 patients with papillary thyroid cancer and 174 healthy controls. CCND1 genotypingwas determined by the PCR-RFLP method. We found that the A allele frequency was higher in the cases than in the controls (p=0.042). On stratification analysis, papillary thyroid cancer risk was significantly elevated in individuals older than 45 years with the A allele (OR=1.91, 95% CI, 1.09-3.35, p=0.024) and in females with the A allele (OR=1.73, 95% CI, 1.06-2.84, p=0.029), compared to the G allele. According to the subject age, there was an increased papillary thyroid cancer risk for the individuals older than 45 years with the AA genotype (OR=2.28, 95% CI, 1.02-5.13, p=0.046) compared to the AG+GG combined genotypes. In conclusion, it is suggested that the CCND1 G870A polymorphism may contribute to the susceptibility to papillary thyroid cancer, especially in those who were older subjects (45≤ years old) and female, in the Turkish population.     

The RTEL1 rs6010620 Polymorphism and Glioma Risk: a Meta-analysis Based on 12 Case-control Studies

Background: The association between the RTEL1 rs6010620 single nucleotide polymorphism (SNP) and gliomarisk has been extensively studied. However, the results remain inconclusive. To further examine this association,we performed a meta-analysis. Materials and Methods: A computerized search of the PubMed and Embasedatabases for publications regarding the RTEL1 rs6010620 polymorphism and glioma cancer risk was performed.Genotype data were analyzed in a meta-analysis. Odds ratios (ORs) with 95% confidence intervals (CIs) wereestimated to assess the association. Sensitivity analyses, tests of heterogeneity, cumulative meta-analyses, andassessments of bias were performed in our meta-analysis. Results: Our meta-analysis confirmed that risk withallele A is lower than with allele G for glioma. The A allele of rs6010620 in RTEL1 decreased the risk of developingglioma in the 12 case-control studies for all genetic models: the allele model (OR=0.752, 95%CI: 0.715-0.792),the dominant model (OR=0.729, 95%CI: 0.685-0.776), the recessive model (OR=0.647, 95%CI: 0.569-0.734), thehomozygote comparison (OR=0.528, 95%CI: 0.456-0.612), and the heterozygote comparison (OR=0.761, 95%CI:0.713-0.812). Conclusions: In all genetic models, the association between the RTEL1 rs6010620 polymorphismand glioma risk was significant. This meta-analysis suggests that the RTEL1 rs6010620 polymorphism may be arisk factor for glioma. Further functional studies evaluating this polymorphism and glioma risk are warranted.     

No Association Between the CYP1B1 C4326G Polymorphism and Endometrial Cancer Risk: a Meta-analysis

Purpose: Any association between the CYP1B1 C4326G polymorphism and endometrial cancer risk remains inconclusive. In order to provide a more precise estimate, we performed the present meta-analysis. Methods: We used fixed effect or random effect models to estimate pooled odds ratios (ORs) with 95% confidence intervals (CIs) for endometrial cancer risk, with the Chi-square-based Q-test used to test for heterogeneity. Begg’s and Egger’s tests were adopted to check publication bias. Results: Six published case-control studies of association between the CYP1B1 C4326G polymorphism and endometrial cancer risk covering 6,577 subjects were included in the meta-analysis, but the results indicated no significant correlation with allele contrast and genotype comparisons (G vs C: OR 1.01, 95% CI 0.93-1.09; GG vs CC: OR 1.04, 95% CI 0.88-1.23; CG + GG vs CC: OR 1.08, 95% CI 0.97-1.21; GG vs CC + CG: OR 1.01, 95% CI 0.87-1.17). Heterogeneity hypothesis test did not reveal any heterogeneity and Begg’s and Egger’s tests did not detect obvious publication bias. Conclusions: There is no association between the CYP1B1 C4326G polymorphism and endometrial cancer risk.     

Specific CCND1 G870A Alleles Associated with Breast Cancer Susceptibility: a Meta-analysis of 5,528 Cases and 5,353 Controls

Background: The Cyclin D1(CCND1) G870A polymorphism may be associated with breast cancer, but theevidence from individual studies is inconclusive. The aim of this study was to investigate the correlation betweenthe CCND1 G870A polymorphism and breast cancer risk in a meta-analysis. Materials and Methods: Wesearched Pubmed and analysed 11 articles on 5,528 cases and 5,353 controls before February 1, 2012. Results:we found there are significant association for AA versus GG and AA versus GA/GG. No significant associationswere found for GA versus GG, GA/AA versus GG. There are significant association for AA versus GG ,and AAversus GA/GG in Caucasians. We didn’t find any significant main effects for G870A polymorphism on breastcancer risk either in recessive or dominant models in Asians. Conclusion: This meta-analysis suggests that AAof the CCND1 G870A polymorphism is associated with breast cancer susceptibility.     

The 870G>A Polymorphism of the Cyclin D1 Gene is not Associated with Breast Cancer

A common 870G > A polymorphism in the gene for cyclin D1, CCND1, has been linked to alternative splicing and cancer susceptibility. To analyze its role for breast cancer, we determined the CCND1 genotype in 500 breast cancer patients and 500 controls. CCND1 genotype frequencies were similar among patients and controls. The CCND1 genotype was furthermore not associated with tumor characteristics. We conclude that the CCND1 870G > A polymorphism is not associated with breast cancer.     

The NAD(P)H: Quinine Oxidoreductase 1 (NQO1) Gene 609 C>T Polymorphism is Associated with Gastric Cancer Risk: Evidence from a Case-control Study and a Meta-analysis

The association between the NAD(P)H:quinone oxidoreductase 1 (NQO1) gene C609T polymorphism(rs1800566) and gastric cancer has been widely evaluated, but a definitive answer is so far lacking. We firstconducted a case-control study to assess this association in a large Han Chinese population, and then performeda meta-analysis to further address this issue. Although our case-control association study indicated no significantdifference in the genotype and allele distributions of C609T polymorphism between gastric cancer patientsand controls, in the meta analysis involving 4,000 subjects, comparison of alleles 609T and 609C indicated asignificantly increased risk (46%) for gastric cancer (95% confidence interval (95%CI) for odds ratio (OR)=1.20-1.79) in individuals with the T allele. The tendency was similar to the homozygote (OR=1.81, 95%CI: 1.16-2.84),dominant models (OR=1.41, 95%CI: 1.12-1.79), as well as recessive model (OR=1.58, 95%CI: 1.06-2.35). Stratifiedanalysis by study design demonstrated stronger associations in population-based than in hospital-based studies.And ethnicity-based analysis demonstrated a significant association in Asians. We conclude that the NQO1 geneC609T polymorphism increases the risk for gastric cancer, especially in Asian populations.     

Association Between the (GT)n Polymorphism of the HO-1 Gene Promoter Region and Cancer Risk: a Meta-analysis

Background: Several studies have previously focused on associations between the (GT)n repeat polymorphismof the heme oxygenase-1 (HO-1) gene promoter region and risk of cancers, but results are complex. We conductedthe present meta-analysis to integrate relevant findings and evaluate the association between HO-1 (GT)nrepeat polymorphism and cancer susceptibility. Materials and Methods: Published literature was retrievedfrom the PubMed/MEDLINE, EMBASE and ISI Web of Science databases before November 2013. For allalleles and genotypes, odds ratios were pooled to assess the strength of the associations using either fixed-effectsor random-effects models according to heterogeneity. Subgroup analysis was conducted according to ethnicityand histopathology. Results: A total of 10 studies involving 2,367 cases and 2,870 controls were identified. Theresults showed there was no association between HO-1 (GT)n repeat polymorphism and the cancer risk both atthe allelic and genotypic level. However, in the stratified analysis, we observed an increased risk of squamouscell carcinoma in persons carrying the LL genotype and the LL+LS genotype as compared with those carryingthe SS genotype. When the LS and SS genotypes were combined, the odds ratio for squamous cell carcinoma inLL-genotype carriers, were also significantly increased. No publication bias was observed. Conclusions: The LLgenotype and L-allele carrying genotypes (LL+LS) of HO-1 (GT)n repeat polymorphism are potential geneticfactors for developing squamous cell carcinoma. More large and well-designed studies are required for furthervalidations.     

The XRCC1 Arg280His Gene Polymorphism and HepatocellularCarcinoma Risk: A Meta-analysis

Many studies have suggested that the XRCC1 Arg280His gene polymorphism might be involved in thedevelopment of hepatocellular carcinoma (HCC). However, the results have been inconsistent. In this study, theauthors performed a meta-analysis to assess the association between XRCC1 Arg280His and HCC susceptibility.Published literature from PubMed, EMBASE and CNKI Data was searched. Pooled odds ratios (ORs) and 95%confidence intervals (CIs) were calculated using fixed- or random- effects models when appropriate. Begg’stest was used to measure publication bias. A total of 7 case-control studies covering 1,448 HCC cases and 1,544controls were included. No significant variation in HCC risk was detected in any of the genetic models overall.In the stratified analysis, four studies with sample sizes over 300 produced similar results. The correspondingpooled ORs were not substantially altered after the exclusion of three studies deviating from Hardy-Weinbergequilibrium in the control group, which indicated reliability for our meta-analysis results.     

CCND1基因G870A位点多态性与宫颈癌易感性的Meta分析

目的:运用Meta分析方法研究CCND1基因G870A位点多态性与宫颈癌易感性的发生风险。方法:检索PubMed和CNKI数据库中有关CCND1基因G870A位点多态性与宫颈癌易感性的相关性研究,根据纳入标准提取文献数据,应用STATA 11.0软件以OR值和95%可信区间为效应指标,进行Meta统计分析,并对发表偏倚及检测敏感性进行检测。结果:纳入9篇对照研究,共计2638例宫颈癌患者和3651例健康对照人群,Meta分析结果显示,总人群中,CCND1基因G870A位点多态性与宫颈癌风险之间没有显著关联(GA vs GG:OR=1.07,95%CI=0.86-1.34,P=0.53,I2=57.6%;AA vs GG:OR=1.09,95%CI=0.79-1.51,P=0.59,I2=75.0%;(GA+AA) vs GG:OR=1.08,95%CI=0.86-1.36,P=0.49,I2=64.6%;AA vs (GG+GA):OR=1.07,95%CI=0.83-1.36,P=0.61,I2=73.3%)。在针对种族和对照人群来源设计的亚组分析中,仍没有发现CCND1基因G870A位点多态性和宫颈癌的发生风险具有相关性。结论:CCND1基因G870A位点多态性可能与宫颈癌的发生无关。     

Lack of Association Between the CYP1A1 Ile462Val Polymorphism and Endometrial Cancer Risk: a Meta-analysis

Purpose: Any association between the CYP1A1 Ile462Val polymorphism and endometrial cancer risk remainsinconclusive. For a more precise estimate, we performed the present meta-analysis. Methods: PUBMED, OVIDand EMBASE were searched for the studies which met inclusion criteria. Data in all eligible studies wereevaluated and extracted by two authors independently. The meta-analysis estimated pooled odds ratio (OR) with95% confidence interval (CI) for endometrial cancer risk attributable to the CYP1A1 Ile462Val polymorphism.Results: A total of 7 studies were included in this meta-analysis. The results indicated no association betweenendometrial cancer risk and the CYP1A1 Ile462Val polymorphism (for Val vs Ile allele model [OR 1.09, 95%CI 0.73-1.62]; for Val.Val vs Ile.Ile genotype model [OR 1.54, 95% CI 0.56-4.23]; for (Ile.Val + Val.Val) vs Ile.Ilegenotpye model [OR 1.08, 95% CI 0.71-1.63]; for Val.Val vs (Ile.Ile + Ile.Val) genotype model [OR 1.46, 95% CI0.53-4.04]). Conclusions: This meta-analysis suggests that there is no association between endometrial cancerrisk and the CYP1A1 Ile462Val polymorphism.     

Cyclin D1 G870A Polymorphism: Relation to the Risk of ALL Development,Prognosis Impact,and Methotrexate Cytotoxicity

Background: Cyclin D1 (CCND1) regulates cell cycle progression during the late G1 and S phase and takes part in methotrexate metabolism. It was hypothesized that CCND1 gene polymorphism affects acute lymphoblastic leukemia (ALL) development, prognosis and may relate to methotrexate cytotoxicity. Subjects and methods: This study included 50 ALL patients and 50 healthy controls, CCND1 G870A polymorphism was studied in all items using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and evaluated methotrexate cytotoxicity for ALL patients using liver function tests before and after methotrexate treatment. We followed up patients for one year to determine disease-free survival (DFS) and overall survival (OS) and its relation to the CCND1 genotype. Results: We found that AA genotype and A allele have a higher risk of developing ALL compared to the control group. Additionally, we found no notable association between CCND1 variant and methotrexate cytotoxicity and no role of CCND1 polymorphism in ALL prognosis. Conclusion: Our results suggested that CCND1 G870A polymorphism is associated with a high risk of ALL development. However, it has no role in ALL prognosis or methotrexate cytotoxicity.     

CTLA-4 +49 A/G Polymorphism and the Risk of Lung Cancer: a Meta-analysis

Background and objectiveLung cancer is one of the malignant tumors. Gene mutations associated with cellular immune function and regulating the activation and proliferation of immune cells. Several publications have explored the relationship between cytotoxic T lymphocyte antigen-4 (CTLA-4) +49 adenine (A)/guanine (G) polymorphism and susceptibility of lung cancer, but the results remain controversial. Thus, we performed this meta-analysis to derive a more comprehensive estimation of the relationship.MethodsAll articles addressed lung cancer and polymorphisms of CTLA-4 were searched from the PubMed, EMBASE databases published up to June 29, 2019. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association. Publication bias of relevant studies was examined via Begg''s test and funnel plots.ResultsThe meta-analysis included 8 case-control studies covering 4, 430 lung cancer patients and 5, 198 healthy controls from September 2008 to April 2020. The overall eligible data indicated that CTLA-4 +49A/G polymorphisms did not correlate with the elevated lung cancer risk in all genetic comparison models (dominant model: OR=1.037, 95%CI: 0.925-1.161; recessive model: OR=0.968, 95%CI: 0.888-1.055; allele model: OR=0.992, 95%CI: 0.933-1.054; homozygous model: OR=0.980, 95%CI: 0.857-1.121; heterozygous model: OR=1.023, 95%CI: 0.906-1.154). In further stratified analyses, CTLA-4 +49A/G polymorphism was found to be significantly associated with susceptibility to NSCLC in these models (dominant model: OR=1.404, 95%CI: 1.074-1.836; allele model: OR=1.273, 95%CI: 1.034-1.565; homozygous model: OR=1.553, 95%CI: 1.044-2.310; heterozygous model: OR=1.308, 95%CI: 1.062-1.611).ConclusionCTLA-4 +49A/G polymorphism were not associated with the risk of lung cancer but might be a risk factor only in NSCLC.     

Association between the MDM2 T309G Polymorphism and Leukemia Risk: a Meta-analysis

Several studies have suggested associations between MDM2 (mouse double minute 2 homolog) polymorphisms and leukemia risk, but they reported contradictory results. For better understanding of the effect of MDM2 T309G polymorphism on leukemia risk, we performed a meta-analysis. All eligible studies were identified through a search of PubMed, Web of Science, EMBASE, and Chinese Biomedical Literature (CBM) databases before May 2014. Assessment of associations between the MDM2 T309G polymorphism and leukemia risk was conducted by odds ratios (ORs) and 95% confidence intervals (95% CIs). Finally, a total of 11 publications covering 12 case-control studies with 2, 362 cases and 5, 562 controls concerning MDM2 T309G polymorphism with respect to leukemia were included in the meta-analysis. Significant associations were found between MDM2 T309G polymorphism and leukemia risk in four models in overall populations (G vs T: OR=1.29, 95% CI=1.11-1.49, p=0.001; GG vs TT: OR=1.67, 95% CI=1.21-2.30, p=0.002; GG vs TG/TT: OR=1.56, 95% CI=1.21-2.00,p=0.001; GG/TG vs TT: OR=1.28, 95% CI=1.05-1.57, p=0.015). In the sub-group analysis according to ethnicity, increased leukemia risks were observed in three genetic models among Asians but not Caucasians. In conclusion, the results of our meta-analysis suggest that the MDM2 T309G polymorphism can increase the risk of leukemia, especially among Asian populations.     

TERT rs2736098 Polymorphism and Cancer Risk: Results of a Meta-analysis

Objective: Several studies have demonstrated associations between the TERT rs2736098 single nucleotidepolymorphisms (SNPs) and susceptibility to cancer development. However, there are conflicting results. Asystematic meta-analysis was therefore performed to establish the cancer risk associated with the polymorphism.Methods: In this meta-analysis, a total of 6 case-control studies, including 5,567 cases and 6,191 controls, wereincluded. Crude odds ratios with 95% confidence intervals were used to assess the strength of associations inseveral genetic models. Results: Our results showed no association reaching the level of statistical significancefor overall risk. Interestingly, in the stratified analyses (subdivided by ethnicity), significantly increased riskswere found in the Asian subgroup which indicates the TERT rs2736098 polymorphism may have controversialinvolvement in cancer susceptibility. Conclusions: Overall, this meta-analysis indicates that the TERT rs2736098polymorphism may have little involvement in cancer susceptibility.     

The Exonuclease 1 Glu589Lys Gene Polymorphism and Cancer Susceptibility: Evidence Based on a Meta-analysis

Background: Published studies on the association between the exonuclease 1 (EXO1) Glu589Lys polymorphismand cancer susceptibility have yielded conflicting results. Thus, a meta-analysis of published studies was performedto assess the possible association. Materials and Methods: All eligible case-control studies published up to January2013 on the association between the EXO1 Glu589Lys polymorphism and cancer susceptibility were identified bysearching PubMed, Web of Science, Science Direct and hand search. Either fixed-effect or random-effect modelswere used to calculate pooled odds ratios (ORs) with 95% confidence intervals (CIs) using the ComprehensiveMeta-Analysis software version 2.2. Results: A total of 4,391 cancer cases and 4,339 controls from 10 studieswere included. Overall, no significant association between the EXO1 Glu589Lys polymorphism and cancersusceptibility was observed in either genetic model. However; in subgroup analyses by cancer type, a significantassociation between EXO1 Glu589Lys and lung cancer risk was found (Lys vs Glu: OR=1.23, 95%CI=1.07-1.41, pheterogeneity=0.05). Further, subgroup analysis by ethnicity indicated that there was a statistically increasedcancer risk in Asians (Lys vs Glu: OR=1.42, 95%CI=1.30-1.55, pheterogeneity=0.07; Lys/Lys vs Glu/Glu: OR=1.93,95%CI=1.20-3.12, pheterogeneity=0.01; Lys/Lys+Glu/Lys vs Glu/Glu: OR=1.52, 95%CI=1.37-1.68, pheterogeneity=0.42;Lys/Lys vs Glu/Lys+Glu/Glu: OR=1.68, 95%CI=1.07-2.65, pheterogeneity=0.02). However, significant association wasabsent in Caucasians. Conclusions: This meta-analysis suggests, for the first time, that the EXO1 Glu589Lyspolymorphism is not associated with overall cancer susceptibility, although marginal associations were found forlung cancer and Asian subgroups. Additional well-designed studies with larger sample size focusing on differentethnicities and cancer types are needed to confirm these findings.     

The P275A Polymorphism in the Macrophage Scavenger Receptor 1 Gene and Prostate Cancer Risk: a Meta-Analysis

Background: Published data regarding associations between the P275A polymorphism in the macrophagescavenger receptor 1 (MSR1) gene and prostate cancer (PCa) risk are inconclusive. The aim of this study wasto comprehensively evaluate the genetic risk of P275A polymorphism in MSR1 gene for PCa. Materials andMethods: A systematic literature search was carried out in Pubmed, Medline (Ovid), Embase, CBM, CNKI,Weipu, and Wanfang databases, covering all available publications (last search was performed on Apr 27, 2015).Statistical analysis was performed using Revman 5.2 and STATA 10.1 software. Results: A total of 5,017 casesand 4,869 controls in 12 case-control studies were included in this meta-analysis. When all groups were pooled,there was no evidence that the P275A polymorphism had a significant association with PCa under dominant(OR=0.93, 95%CI=0.81-1.06, and p=0.28), co-dominant (homogeneous OR=0.97, 95%CI=0.56-1.68, and p=0.92;heterogeneous OR=0.93, 95%CI=0.74-1.15, and p=0.49), recessive (OR=1.10, 95%CI=0.65-1.87, and p=0.73),over-dominant (OR=0.93, 95%CI=0.75-1.15, and p=0.50), and allelic (OR=0.95, 95%CI=0.77-1.16, and p=0.61)genetic models. For stratified analyses by ethnicity and study design, no significant associations were found in thewhite race, the yellow race, the black race and mixed ethnicity, and the population-based case-control (PCC) andhospital-based case-control (HCC) studies under all genetic models. Conclusions: Based on our meta-analysis,the P275A polymorphism in the MSR1 gene is unlikely to be a risk factor for PCa.