Personal Research Database Bibliometric

Full Text: 2014\Tum Biol35, 4401.pdf

Abstract: Published literatures on the prognostic value of hypoxia-inducible factor-1 alpha (HIF-1 alpha) overexpression in esophageal squamous cell carcinoma (ESCC) are conflicting and heterogeneous. We performed a meta-analysis to more precisely evaluate the clinicopathological and prognostic value of HIF-1 alpha in patients with ESCC. Searches were applied to MEDLINE, PubMed, Embase, Cochrane Library, Web of Science, and Chinese BioMedical Literature Databases until September 10, 2013, without language restrictions. The pooled hazard ratios (HRs) and odds ratios (ORs) with corresponding 95 % confidence intervals (CIs) were used to estimate the effects. Twelve studies with 942 ESCC patients were selected to evaluate the correlation between HIF-1 alpha and overall survival (OS), disease-free survival (DFS), response to chemoradiation (RC), and clinicopathological features. HIF-1 alpha overexpression was significantly associated with poor OS (HR 1.78, 95 % CI 1.41-2.24), DFS (HR 1.91, 95 % CI 1.15-3.18), and RC (HR 3.56, 95 % CI 1.68-7.53). Besides, HIF-1 alpha overexpression was significantly associated with stage (OR 2.90, 95 % CI 1.97-4.27), lymph node metastasis (OR 1.86, 95 % CI 1.39-2.49), depth of invasion (OR 2.45, 95 % CI 1.24-4.86), lymphatic invasion (OR 2.28, 95 % CI 1.46-3.56), distant metastasis (OR 2.04, 95 % CI 1.19-3.50), and vascular endothelial growth factor (OR 3.67, 95 % CI 1.81-7.46). Our results indicate that HIF-1 alpha overexpression can potently predict the poor prognosis and chemoradiation resistance for ESCC. Large prospective studies with multivariable survival analyses are now needed to confirm the clinical utility of HIF-1 alpha as an independent prognostic marker.

Keywords: Analyses, Angiogenesis, Carcinoma, Cell, Chemoradiation, Chinese, Clinical, Clinical-Trials, Confidence, Confidence Intervals, Correlation, Cyclooxygenase-2 Expression, Databases, Effects, Esophageal Squamous Cell Carcinoma, Factor (Hif)-1-Alpha, Factor 1-Alpha, Gastric-Cancer, Growth, Growth Factor, Growth-Factor-C, Hazard, Hif-1-Alpha, Hypoxia-Inducible Factor-1 Alpha, Intervals, Language, Literature, Lymph-Node Metastasis, Medline, Meta Analysis, Meta-Analysis, Metaanalysis, Metastasis, Patients, Prognosis, Prognostic, Prospective, Prospective Studies, Resistance, Response, Restrictions, Science, Significance, Squamous Cell Carcinoma, Survival, Tumor-Growth, Utility, Value, Vascular Endothelial Growth Factor, Web of Science

? Shi, J., Tong, J.H. and Cai, S. (2014), GH1 T1663A polymorphism and cancer risk: A meta-analysis of case-control studies. Tumor Biology, 35 (5), 4529-4538.

Full Text: 2014\Tum Biol35, 4529.pdf

Abstract: Many studies have demonstrated that the most common polymorphism (T1663A, rs2665802) in the promoter region of growth hormone 1 (GH1) gene might play an important role in cancer development and progression. This meta-analysis aims to investigate a more precise estimation of the relationship between GH1 T1663A polymorphism and cancer risk. We searched CISCOM, CINAHL, Web of Science, PubMed, Google Scholar, EBSCO, Cochrane Library, and CBM databases from inception through October 1st, 2013. Meta-analysis was performed using the STATA 12.0 software. Seven studies were included with a total of 4,018 cancer patients and 5,308 healthy controls. Our meta-analysis results revealed that GH1 T1663A polymorphism was associated with increased cancer risks. Subgroup analysis by cancer type showed significant associations between GH1 T1663A polymorphism and increased colorectal cancer risk, but there was no evidence of any association with breast cancer. Further subgroup analysis based on ethnicity indicated that GH1 T1663A polymorphism might increase cancer risks among Asian populations. However, no statistically significant association was found among Caucasian populations. Meta-regression analyses also suggested that cancer type and ethnicity may be the main sources of heterogeneity. No publication bias was detected in this meta-analysis. The present meta-analysis indicates that GH1 T1663A polymorphism may contribute to the risk of colorectal cancer, especially among Asian populations.

Keywords: Analyses, Analysis, Asian, Association, Bias, Breast Cancer, Breast-Cancer, Cancer, Cancer Risk, Case-Control, Case-Control Studies, Caucasian, Colorectal Cancer, Colorectal-Cancer, Databases, Development, Diseases, Ethnicity, Evidence, Gene, Gene-Environment Interactions, Google, Google Scholar, Growth, Growth Hormone, Growth Hormone 1, Growth-Hormone Receptor, Heterogeneity, Meta Analysis, Meta-Analysis, Meta-Regression, Metaanalysis, Patients, Polymorphism, Populations, Progression, Publication, Publication Bias, PubMed, Region, Risk, Risks, Role, Science, Single Nucleotide Polymorphism, Software, Sources, Susceptibility, Susceptibility, Therapy Response, Web of Science

? Tas, F. (2014), An analysis of the most-cited research papers on oncology: Which journals have they been published in? Tumor Biology, 35 (5), 4645-4649.

Full Text: 2014\Tum Biol35, 4645.pdf

Abstract: The most-cited papers (MCPs) are likely those that impressed researchers and had profound influence on clinical practice or future developments in the related scientific field. This study was conducted to explore a bibliometric approach to assess where the oncology-related MCPs have been published in. The source of the data presented in this study was provided by using the InCitesTM, Web of Science, Thomson Reuters Database (2013). It contained any journal indexed by ISI between 1979 and 2013. The term MCPs arbitrarily defined as equal or more than 100 citations. A total of 565 publications were cited equal or more than 100 times. They were published in 79 different journals (64 oncology, 12 medicine, and 3 science), led by the Journal of Clinical Oncology (n = 76; 13.5 %) and Cancer Research (n = 66; 11.7 %) followed by Oncogene (n = 46; 8.1 %), Nature Reviews Cancer (n = 41; 7.3 %), and Cancer (n = 37; 6.5 %). Moreover, the journal categories with the MCPs were the Oncology with 495 articles (87.6 %), followed by the Medicine with 60 (10.6 %) articles. However, the numbers of journals related to Science (n = 10; 1.8 %) were the least. The MCPs were cited a total of 118,531 times. The citations ranged from 100 to 1,790, and the median number was 149. The total numbers of MCPs were the most prominent for the journals, the New England Journal of Medicine (median 398), Lancet (median 213), and Nature Reviews Cancer (median 210). In other side, the counts of MCPs were the highest for the Science and Medicine-categorized journals (median 212.5 and 192.5 citations, respectively). The MCPs categorized as Oncology were the least cited (median 145). The median number of MCPs per year was 18.7 with range 4.1-858.5. The annual most valuable MCPs were also published in the journal Nature Reviews Cancer (median 42) and the New England Journal of Medicine (median 38.7). Likewise, the numbers of MCPs were the highest for the Science-categorized journals (median 37), whereas the citations per year were significantly lower in Medicine and Oncology-categorized journals (25.8 and 17.8, respectively). In conclusion, most of the MCPs were published in Oncology specialized journals.

Keywords: Analysis, Approach, Articles, Bibliometric, Cancer, Citations, Clinical, Clinical Practice, Data, Database, England, Field, Impact, Influence, Isi, Journal, Journals, Medicine, Most-Cited Papers, Oncology, Papers, Practice, Publication, Publications, Research, Science, Source, Surgical Journals, Term, Thomson Reuters, Thomson-Reuters, Web of Science

? Zhang, L., Jiang, Y.J., Wu, Q.C., Li, Q., Chen, D., Xu, L., Zhang, C., Zhang, M. and Ye, L. (2014), Gene-environment interactions on the risk of esophageal cancer among Asian populations with the G48A polymorphism in the alcohol dehydrogenase-2 gene: A meta-analysis. Tumor Biology, 35 (5), 4705-4717.

Full Text: 2014\Tum Biol35, 4705.pdf

Abstract: The aim of this study is to investigate the gene-environment interactions between the G48A polymorphism in the alcohol dehydrogenase-2 (ADH2) gene and environmental factors in determining the risk of esophageal cancer (EC). A literature search was conducted in the PubMed, Embase, Web of Science, Cochrane Library, and Google Scholar databases to indentify eligible studies published before November 1, 2013. We performed a meta-analysis of 18 case-control studies with a total of 8,906 EC patients and 13,712 controls. The overall analysis suggested that individuals with the GG genotype were associated with a 2.77-fold increased risk of EC, compared with carriers of the GA and AA genotypes. In a stratified analysis by ethnic group, Japanese, Mainland Chinese, and Taiwan Chinese with the GG genotype had a significantly higher risk of EC, compared with Thai and Iranian populations, indicating ethnic variance in EC susceptibility. An analysis of combined effect indicated that GG genotype of ADH2 G48A was associated with the highest risk of EC in heavy drinkers and smokers. A striking difference was found to exist between males and females, showing gender variance for the association between ADH2 G48A and EC risk. This meta-analysis shows that the GG genotype of ADH2 G48A may be associated with an increased risk of EC in Asian populations. In addition, significant gene-environment interactions were found. Heavy drinkers, smokers, and males with the GG genotype may have a higher EC risk. Thus, our results shed new light on the complex gene-environment interactions that exist between environmental factors and ADH2 G48A polymorphism in EC risk.

Keywords: Adenocarcinoma, Adh1b, Alcohol, Alcohol Dehydrogenase-2, Aldehyde Dehydrogenases, Aldh2 Genes, Analysis, Asian, Association, Cancer, Case-Control, Case-Control Studies, Chinese, Chinese Population, Consumption, Databases, Ec, Environmental, Esophageal Cancer, Gender, Gene, Google, Google Scholar, Literature, Literature Search, Meta Analysis, Meta-Analysis, Metaanalysis, Patients, Polymorphism, Populations, PubMed, Risk, S-Transferase M1, Science, Smoking, Squamous-Cell Carcinoma, Susceptibility, Taiwan, Web of Science

? Chang, Z.Q. and Yu, X.C. (2014), Association between p53 codon 72 polymorphism and sarcoma risk among Caucasians. Tumor Biology, 35 (5), 4807-4812.

Full Text: 2014\Tum Biol35, 4807.pdf

Abstract: Many published data on the association between p53 codon 72 polymorphism and sarcoma risk showed inconclusive results. The present study was designed to derive a more precise estimation of this connection among Caucasians. We conducted a literature search in PubMed, EMBASE, Web of Science, and CNKI databases for case-control studies examining the association between p53 codon 72 polymorphism and sarcoma risk. The meta-analysis was performed using STATA 12.0 software. Crude odds ratios (ORs) with corresponding 95 % confidence intervals (CIs) were used to measure the strength of any association. The results of this meta-analysis did not provide statistical evidence for significant sarcoma risk associated with p53 codon 72 polymorphism (ORArg/Arg vs. Pro/Pro = 1.00, 95 % CI = 0.80-1.26, P (heterogeneity) = 0.980; ORArg/Arg + Arg/Pro vs. Pro/Pro = 0.99, 95 % CI = 0.83-1.19, P (heterogeneity) = 0.990; ORArg/Arg vs. Arg/Pro + Pro/Pro = 1.09, 95 % CI = 0.89-1.35, P (heterogeneity) = 0.532; ORallele Arg vs. allele Pro = 1.03, 95 % CI = 0.90-1.18, P (heterogeneity) = 0.883; ORArg/Pro vs. Pro/Pro = 0.95, 95 % CI = 0.71-1.27, P (heterogeneity) = 0.919). We also did not find significant links in further subgroup analyses by ethnicity, control source, and sarcoma type. The present meta-analysis of currently available data suggests that the p53 codon 72 polymorphism may not play a role in sarcoma development in Caucasians.

Keywords: Analyses, Association, Cancer Patients, Case-Control, Case-Control Studies, Confidence, Confidence Intervals, Control, Data, Databases, Development, Embase, Epidemiology, Ethnicity, Evidence, Fusion, Heterogeneity, Intervals, Kaposis-Sarcoma, Literature, Literature Search, Lung-Cancer, Measure, Meta Analysis, Meta-Analysis, Metaanalysis, Osteosarcoma, P, P53, P53 Codon 72, Polymorphism, PubMed, Risk, Role, Sarcoma, Science, Soft-Tissue Sarcomas, Software, Source, Strength, Survival, Tp53 Arg72pro, Translocation, Web of Science

? Liang, J.W., Zhang, J.J., Zhang, T. and Zheng, Z.C. (2014), Clinicopathological and prognostic significance of HER2 overexpression in gastric cancer: A meta-analysis of the literature. Tumor Biology, 35 (5), 4849-4858.

Full Text: 2014\Tum Biol35, 4849.pdf

Abstract: Human epidermal growth factor receptor 2 (HER2) plays an important role in the aggressiveness and progression of gastric cancer. With the publication of trial results, we conducted a meta-analysis to investigate its prognostic significance for patients with gastric cancer. PubMed, Ovid, Web of Science, and Cochrane databases were searched. Statistical analysis was carried out by STATA version 12.0 software. The Newcastle-Ottawa scale was used to assess the quality of evidence. Fifteen studies involving 5,290 patients met the inclusion criteria. The results showed that HER2 overexpression was significantly associated with patients’ overall survival (HR = 1.56, 95 % confidence interval (CI) 1.05-2.07; Z = 6.03; P = 0.000). The results also suggested that HER2 overexpression was associated with Bormann type (odds ratio (OR) = 1.76, 95 % CI 1.19-2.59; Z = 2.85; P = 0.004), tumor differentiation (OR = 3.14, 95 % CI 1.91-5.17; Z = 4.49; P = 0.000), Lauren’s classification (OR = 6.25, 95 % CI 4.29-9.10; Z = 9.54; P = 0.000), lymph node metastasis (OR = 1.43, 95 % CI 1.15-1.77; Z = 3.23; P = 0.001), venous invasion (OR = 1.69, 95 % CI 1.15-2.48; Z = 2.67; P = 0.008), and lymphovascular invasion (OR = 1.57, 95 % CI 1.21-2.04; Z = 3.4; P = 0.001). However, it had no correlation with tumor size, depth of invasion, and tumor stage. This study showed that HER2 overexpression had an unfavorable prognostic role for patients with gastric cancer. HER2-positive expression was associated with Bormann type, Lauren’s classification, tumor differentiation, lymph node status, venous invasion, and lymphovascular invasion.

Keywords: Analysis, C-Erb B-2, C-Erbb-2 Protein, Cancer, Carcinomas, Classification, Confidence, Correlation, Criteria, Databases, Differentiation, Egf Receptor, Epidermal Growth Factor, Evidence, Expression, Gastric, Gastric Cancer, Gene Amplification, Growth, Growth Factor, Her2, Human, In-Situ Hybridization, Interval, Literature, Location, Meta Analysis, Meta-Analysis, Metaanalysis, Metastasis, Odds Ratio, P, Patients, Prognostic, Progression, Protein Expression, Publication, PubMed, Quality, Quality Of, Role, Scale, Science, Significance, Size, Software, Statistical Analysis, Survival, Survival, Trial, Tumor, Version, Web of Science

? Zhu, J., Lu, L., Cheng, X., Xie, R.K., Chen, Z.Q., Li, Y.F., Lin, G.L., Liu, J.M. and Yang, Y. (2014), Association between CD95L polymorphism and cervical cancer risk: Evidence from a meta-analysis. Tumor Biology, 35 (6), 5137-5142.

Full Text: 2014\Tum Biol35, 5137.pdf

Abstract: Several studies have assessed the association of CD95L polymorphism with cervical cancer risk, but the data lack the power to provide compelling evidence. In this study, we aimed to clarify the association through a meta-analysis. A comprehensive search was conducted in PubMed, Embase, and Web of Science. The fixed-effects model was used to calculate odds ratio (OR) with 95 % confidence intervals (CIs). A total of five papers with six case-control studies were derived and finally included in this meta-analysis. The overall estimate did not reveal any significant association between CD95L -844C/T polymorphism and cervical cancer risk. Subgroup analysis in Asian population indicated nonsignificant nevertheless potentially increased risk in CC genotype carriers in comparison with the carriers of CT + TT genotypes (ORCC vs. CT + TT = 1.16, 95 % CI = 0.99-1.36, P for heterogeneity = 0.231). Based on current epidemiological studies, this meta-analysis suggests that CD95L polymorphism may not be a risk factor contributing to cervical cancer development.

Keywords: Analysis, Apoptosis, Asian, Association, Cancer, Cancer Risk, Case-Control, Case-Control Studies, Cd95l, Cell-Death, Cervical Cancer, Comparison, Confidence, Confidence Intervals, Counterattack, Ct, Data, Development, Evidence, Expression, Fas Ligand, Fixed Effects Model, Genes, Heterogeneity, Intervals, Meta Analysis, Meta-Analysis, Metaanalysis, Model, Odds Ratio, P, Pancreatic-Cancer, Papers, Pathogenesis, Polymorphism, Population, Power, Pubmed, Risk, Risk Factor, Science, Susceptibility, Variants, Web Of Science

? Xia, Y., Zhu, Y., Zhou, X.Y. and Chen, Y.J. (2014), Low expression of let-7 predicts poor prognosis in patients with multiple cancers: A meta-analysis. Tumor Biology, 35 (6), 5143-5148.

Full Text: 2014\Tum Biol35, 5143.pdf

Abstract: The connection between microRNA expression and cancers has been identified, and microRNAs may be considered as important prognostic biomarkers. However, it is still inconsistent whether expression of let-7 can predict prognosis in patients with multiple cancers. A meta-analysis was performed by searching PubMed, EMBASE, and ISI Web of Science databases. All data were extracted from articles comparing prognosis in patients with multiple cancers having low expression of let-7 with those having high expression. Pooled hazard ratios (HRs) and corresponding 95 % confidence intervals (CIs) were calculated. Subgroup analyses were conducted for cancer type and ethnicity. A total of 1,757 cases of multiple cancers were involved for this meta-analysis. The HR of low let-7 expression in multiple cancers was 1.80 (95 % CI 1.18-2.76), and that in lung cancer was 1.99 (95 % CI 1.17-3.40). A subgroup analysis was performed on ethnicity; combined HR was 1.61 (95 % CI 0.84-3.11) for Asians and 1.94 (95 % CI 1.11-3.39) for non-Asians. Low expression of let-7 might predict poor prognosis in patients with multiple cancers, especially in lung cancer. Furthermore, let-7 might be a biomarker in non-Asian patients with favorable prognosis.

Keywords: Analyses, Analysis, Articles, Asians, Biomarker, Biomarkers, Breast-Cancer, Cancer, Chemotherapy, Confidence, Confidence Intervals, Data, Databases, Embase, Ethnicity, Expression, Hazard, Intervals, Isi, Isi Web Of Science, Isi Web Of Science Databases, Let-7, Lung, Lung Cancer, Meta Analysis, Meta-Analysis, Metaanalysis, Microrna, Microrna Expression, Multiple Cancers, Pathway, Patients, Prognosis, Prognostic, Pubmed, Science, Squamous-Cell Carcinoma, Web Of Science, Web Of Science Databases

? Zhong, S.L., Chen, Z.Y., Yu, X.N., Chen, W.X., Lv, M.M., Ma, T.F. and Zhao, J.H. (2014), Tea consumption and leukemia risk: A meta-analysis. Tumor Biology, 35 (6), 5205-5212.

Full Text: 2014\Tum Biol35, 5205.pdf

Abstract: Epidemiologic findings concerning the association between tea consumption and leukemia risk yielded mixed results. We aimed to investigate the association by performing a meta-analysis of all available studies. One cohort studies and six case-control studies with 1,019 cases were identified using PubMed, Web of Science, and EMBASE. We computed summary relative risks (RRs) and 95 % confidence intervals (CIs) using random effect model applied to the relative risk associated with ever, moderate, or highest drinkers vs. non/lowest drinkers. Subgroup analyses were performed based on country (China and USA). Compared with non/lowest drinkers, the combined RR for ever drinkers was 0.76 (95 % CI = 0.65-0.89). In subgroup analyses, significant inverse associations were found for both China and USA studies. The summary RR was 0.57 (95 % CI = 0.41-0.78) for highest drinkers. Same results were only found in China studies. No significant associations were found for moderate drinkers in overall analysis or in subgroup analyses. There was some evidence of publication bias. In conclusion, this meta-analysis suggests a significant inverse association of high tea consumption and leukemia risk. Results should be interpreted cautiously given the potential publication bias.

Keywords: (-)-Epigallocatechin Gallate, Acute Myeloid-Leukemia, Analyses, Analysis, Apoptosis, Association, Bias, Cancer Risk, Case-Control, Case-Control Studies, Cell-Death, China, Clinical-Trials, Cohort, Confidence, Confidence Intervals, Consumption, Country, Cumulative Metaanalysis, Diet, Embase, Epidemiologic, Epidemiology, Epigallocatechin-3-Gallate Egcg, Evidence, Green, Hydrogen-Peroxide, Intervals, Leukemia, Meta Analysis, Meta-Analysis, Metaanalysis, Model, Population, Potential, Publication, Publication Bias, Pubmed, Relative Risk, Results, Risk, Risks, Science, Tea, USA, Web Of Science

? Wu, Y.Y. and Yang, Y. (2014), Complex association between ERCC2 gene polymorphisms, gender, smoking and the susceptibility to bladder cancer: A meta-analysis. Tumor Biology, 35 (6), 5245-5257.

Full Text: 2014\Tum Biol35, 5245.pdf

Abstract: Genetic polymorphisms in DNA repair genes may be involved in increasing the risk of bladder cancer. Association studies on the excision repair cross-complementation group 2 (ERCC2) gene polymorphisms and bladder cancer risk have reported conflicting results. The aim of this meta-analysis of eligible cancer case-control studies is to investigate the role of ERCC2 SNPs (Arg156Arg, Asp312Asn, and Lys751Gln), gender and smoking in determining susceptibility to bladder cancer. A literature search was conducted in the PubMed, Embase, Web of Science, Cochrane Library, and Google Scholar databases to indentify eligible studies published before December 1, 2013. We performed a meta-analysis of 23 case-control studies with a total of 7,062 bladder cancer patients and 8,832 controls. The overall analysis suggested that ERCC2 Arg156Arg, Asp312Asn, and Lys751Gln are associated with increased bladder cancer risk. For ERCC2 Arg156Arg, the mutant allele was associated with a 1.36-fold (95 % CI = 1.15-1.61) increased risk of bladder cancer. For ERCC2 Asp312Asn, individuals with the Asn allele were associated with a 1.29-fold (95 % CI = 1.13-1.48) increased risk of bladder cancer. For ERCC2 Lys751Gln, individuals who carried the variant heterozygote Lys/Gln or homozygote Gln/Gln had a significantly increased bladder cancer risk, compared with the wild genotype Lys/Lys (OR = 1.10, 95 % CI = 1.03-1.18). Furthermore, gender and smoking may modify the association between these SNPs and bladder cancer risk. This study provides the strongest evidence to date for the role of common variants of the ERCC2 gene in bladder carcinogenesis. Further studies comprehensively characterizing other DNA repair pathways and accounting for exposure to relevant environmental factors should offer further insight into the role of DNA repair in bladder cancer.

Keywords: Analysis, Asp312asn, Association, Bladder, Bladder Cancer, Breast-Cancer, Cancer, Cancer Risk, Case-Control, Case-Control Studies, Chinese Population, Cigarette-Smoking, Databases, DNA, DNA-Repair Genes, Environmental, ERCC2, Evidence, Exposure, Gender, Gene, Genes, Genetic Polymorphisms, Google, Google Scholar, Heterogeneity, Literature, Literature Search, Lung-Cancer, Meta Analysis, Meta-Analysis, Metaanalysis, Metabolism, Pathways, Patients, Polymorphisms, Pubmed, Risk, Risk-Factors, Role, Science, Smoking, Web Of Science, XPD, XRCC1

? Zhao, W., Bian, Y.S., Zhu, W., Zou, P. and Tang, G.T. (2014), Regulator of telomere elongation helicase 1 (RTEL1) rs6010620 polymorphism contribute to increased risk of glioma. Tumor Biology, 35 (6), 5259-5266.

Full Text: 2014\Tum Biol35, 5259.pdf

Abstract: Regulator of telomere elongation helicase 1 (RTEL1) is critical for genome stability and tumor avoidance. Many studies have reported the associations of RTEL1 rs6010620 with glioma risk, but individually published results were inconclusive. This meta-analysis was performed to quantitatively summarize the evidence for such a relationship. The PubMed, Embase, and Web of Science were systematically searched to identify relevant studies. The odds ratio (OR) and 95 % confidence interval (95 % CI) were computed to estimate the strength of the association using a fixed or random effects model. Ten studies were eligible for meta-analysis including data on glioma with 6,490 cases and 9,288 controls. Overall, there was a significant association between RTEL1 rs6010620 polymorphism and glioma risk in all four genetic models (GG vs. AA: OR = 1.87, 95 % CI = 1.60-2.18, P (heterogeneity) = 0.552; GA vs. AA: OR = 1.30, 95 % CI = 1.16-1.46, P (heterogeneity) = 0.495; dominant model-GG + GA vs. AA: OR = 1.46, 95 % CI = 1.31-1.63, P (heterogeneity) = 0.528; recessive model-GG vs. GA + AA: OR = 1.36, 95 % CI = 1.27-1.46, P (heterogeneity) = 0.093). Subgroup analyses by ethnicity showed that RTEL1 rs6010620 polymorphism resulted in a higher risk of glioma among both Asians and Caucasians. In the stratified analysis by ethnicity and source of controls, significantly increased risk was observed for Asians and Europeans in all genetic models, population-based studies in all genetic models, and hospital-based studies in three genetic models (heterozygote comparison, homozygote comparison, and dominant model). Our meta-analysis suggested that RTEL1 rs6010620 polymorphism is likely to be associated with increased glioma risk, which lends further biological plausibility to these findings.

Keywords: Amplification, Analyses, Analysis, Asians, Association, Biological, Brain, Cancer, Cancer, Comparison, Confidence, Data, Effects, Epidemiology, Ethnicity, Evidence, Genetic, Genetic-Variants, Glioma, Heterogeneity, Homologous Recombination, Interval, Meta Analysis, Meta-Analysis, Metaanalysis, Model, Models, Nervous-System, Odds Ratio, P, Polymorphism, Population Based, Population-Based, Population-Based Studies, Pubmed, Random Effects Model, Risk, Rtel1, Science, Source, Stability, Strength, Susceptibility Loci, Tumor, Tumors, Web Of Science

? Jin, Y. and Hao, Z.P. (2014), Polymorphisms of glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) in ovarian cancer risk. Tumor Biology,