The GSTP1 Ile105Val polymorphism is not associated with susceptibility to colorectal cancer

The glutathione S transferase (GST) family is a major part of cellular defense mechanisms against endogenous and exogenous substances, many of which have carcinogenic potential. Alteration in the expression level or structure of the glutathione-S-transferase (GST) enzymes may lead to inadequate detoxification of potential carcinogens and consequently contribute to cancer development. A member of the glutathione-S-transferase (GST) family, GSTP1, is an attractive candidate for involvement in susceptibility to carcinogen-associated colorectal cancer. An A>G transition in exon 5 resulting in an Ile105Val amino acid substitution has been identified which alters catalytic efficiency. The present study investigated the possible impact of Ile105Val GSTP1 polymorphism on susceptibility to colorectal cancer. in Jordan We examined 90 tissue samples previously diagnosed with colorectal carcinoma, and 56 non-cancerous colon tissues. DNA was extracted from paraffin embedded tissues and the status of the GSTP1 polymorphism was determined using a polymerase chain reaction restriction fragment length polymorphism (RFLP) method. No statistically significant differences were found between colorectal cancer cases and controls for the GSTP1 Ile/Ile, Ile/Val and Val/Val genotypes. The glutathione S-transferase polymorphism was not associated with risk in colorectal cancer cases in Jordan stratified by age, sex, site, grade or tumor stage. In conclusion, the GSTP1 Ile105Val polymorphism is unlikely to affect the risk of colorectal cancer.     

Quantitative assessment of the association between glutathione S-transferase P1 Ile105Val polymorphism and bladder cancer risk

Previous studies investigating the association between glutathione S-transferase P1 (GSTP1) Ile105Val polymorphism and bladder cancer risk reported controversial results. This study aimed to quantify the strength of the association between GSTP1 Ile105Val polymorphism and bladder cancer risk by performing a meta-analysis. We searched the PubMed, Embase, and Wanfang databases for publications on the association between GSTP1 Ile105Val polymorphism and bladder cancer risk. We estimated the pooled odds ratios (ORs) with their confidence intervals (95 %CIs) to assess the association. Twenty-five individual studies with a total of 12,360 subjects were finally included. Meta-analysis of all 25 studies showed that GSTP1 Ile105Val polymorphism was associated with increased risk of bladder cancer risk under four genetic comparison models (for G versus A, random-effect OR?=?1.19, 95 %CI 1.05–1.35; for GG versus AA, random-effect OR?=?1.49, 95 %CI 1.12–1.97; for GG/GA versus AA, random-effect OR?=?1.20, 95 %CI 1.03–1.39; for GG versus GA/AA, random-effect OR?=?1.41, 95 %CI 1.10–1.80). Sensitivity analysis showed that GSTP1 Ile105Val polymorphism was still associated with bladder cancer risk under three genetic comparison models (for G versus A, random-effects OR?=?1.13, 95 %CI 1.01–1.26; for GG versus AA, random-effects OR?=?1.29, 95 %CI 1.01–1.65; for GG versus GA/AA, random-effects OR?=?1.19, 95 %CI 1.04–1.35). No evidence of publication bias was observed. This meta-analysis shows that there is an obvious association between GSTP1 Ile105ValIle105Val polymorphism and bladder cancer risk, and GSTP1 ILE105VAL polymorphism contributes to bladder cancer risk.     

Association between GSTP1 Ile105Val polymorphism and oxaliplatin-induced neuropathy: a systematic review and meta-analysis

Background and aims

The association between glutathione-S-transferase P1 (GSTP1) Ile105Val polymorphism and oxaliplatin-induced neuropathy has been investigated in a number of published studies. However, most of these studies were based on small sample sizes and the results remained inconsistent. To assess the relationship between GSTP1 gene Ile105Val polymorphism and its susceptibility to oxaliplatin-induced neuropathy, a meta-analysis of previous studies was conducted.

Methods

Two investigators independently searched studies published up to December 2012 from the databases of PubMed, EMBASE and The Cochrane Library. The pooled effect was calculated as odds ratio (OR) and corresponding 95 % confidence intervals (CIs) using fixed-effect or random-effect model.

Results

Twelve prospective trials and two retrospective clinical trials involving 2,191 participants met the inclusion criteria. Combined analyses of these studies showed no significant associations between GSTP1 Ile105Val polymorphism and oxaliplatin-induced neuropathy, yielding OR of 1.08 (95 %CI 0.67–1.74, P = 0.754) in dominant model. Similar results were also obtained in recessive model (OR = 1.67, 95 %CI 0.56–4.93, P = 0.357) and allelic analysis (OR = 1.22, 95 %CI 0.67–2.24, P = 0.513). Since significant heterogeneity across studies, the pooled effects were calculated by random-effect model. No evidence of publication biases was identified in this meta-analysis.

Conclusion

This meta-analysis did not support the hypothesis that GSTP1 Ile105Val polymorphism was related to the occurrence of neurotoxicity in oxaliplatin-treated patients. Given the limited number of studies and potential bias, large-scale and well-designed clinical trials should be needed to confirm these hypotheses.     

Association between GSTP1 Ile105Val polymorphism and glioma risk: A systematic review and meta-analysis

Glutathione S-transferase P1 (GSTP1) gene Ile105Val polymorphism has been suggested to be involved in the development of glioma. However, the results from the studies regarding the association between GSTP1 Ile105Val polymorphism and glioma risk have been inconsistent. Thus, we performed a meta-analysis to investigate this association. Pooled odds ratios (ORs) with 95 % confidence intervals (95 %CIs) were calculated using random or fixed effects model. Nine studies with 2,078 cases and 3,970 controls were finally included into this meta-analysis. The results suggested there was no association between GSTP1 Ile105Val polymorphism and glioma risk under recessive model (OR?=?1.138, 95 %CI?=?0.966–1.341, P _{heterogeneity}?=?0.088, P?=?0.123). Subgroup analyses by ethnicity showed there was also no association between GSTP1 Ile105Val polymorphism and glioma risk in mixed populations under recessive model (OR?=?1.199, 95 %CI?=?0.928–1.549, P _{heterogeneity}?=?0.060, P?=?0.166) and Caucasian populations(OR?=?1.097, 95 %CI?=?0.885–1.360, P _{heterogeneity}?=?0.186, P?=?0.398). In conclusion, the meta-analysis suggests that there is no association between GSTP1 Ile105Val polymorphism and glioma risk. However, more well-designed and larger studies are needed to further assess this association.     

Association between the GSTP1 Ile105Val polymorphism and prostate cancer risk: a systematic review and meta-analysis

Many studies have reported the role of glutathione S-transferase P1 (GSTP1) Ile105Val polymorphism with prostate cancer (PCa) risk. However, these studies have yielded conflicting results. Hence, we performed this meta-analysis to investigate the association between GSTP1 Ile105Val polymorphism and PCa in different inheritance models. A total of 13 eligible studies were pooled into this meta-analysis. There was significant association between the GSTP1 Ile158Val variant genotypes and PCa for Ile/Ile vs Val/Val comparison [odds ratio (OR)?=?0.705; I ²?=?63.7 %; 95 % confidence interval (95 % CI)?=?0.508–0.977], Ile/Val vs Val/Val comparison (OR?=?0.736; I ²?=?8.0 %; 95 % CI?=?0.613–0.883), and dominant model (OR?=?0.712; I ²?=?45.5 %; 95 % CI?=?0.555–0.913). However, no associations were detected for other genetic models. In the stratified analysis by ethnicity, significant associations between GSTP1 Ile105Val polymorphism and PCa risk were also found among Caucasians (Ile/Ile vs Val/Val comparison OR?=?0.818, I ²?=?0.0 %, 95 % CI?=?0.681–0.982; Ile/Val vs Val/Val comparison OR?=?0.779, I ²?=?0.0 %, 95 % CI?=?0.651–0.933; and dominant model OR?=?0.794, I ²?=?0.0 %, 95 % CI?=?0.670–0.941), while there were no associations found for other genetic models. However, no associations were found in Asians and African-Americans for all genetic models when stratified by ethnicity. In conclusion, our meta-analysis indicates that GSTP1 Ile105Val polymorphisms contributed to the PCa susceptibility. However, a study with the larger sample size is needed to further evaluate gene–environment interaction on GSTP1 Ile105Val polymorphisms and PCa risk.     

Association of the GSTP1 gene (Ile105Val) Polymorphism withChronic Myeloid Leukemia

The GSTP1 enzyme plays a key role in biotransformation and bioactivation of certain environmentalpollutants such as benzo[a]pyrene-7, 8-diol-9,10-epoxide (BPDE) and other diol epoxides of polycyclic aromatichydrocarbons. It catalyses the detoxification of base propanols that arise from DNA oxidation thus offering cellularprotection against oxidative stress. A single nucleotide polymorphism at codon 105 results in the substitutionof isoleucine (Ile) to valine (Val) causing a metabolically less active variant of the enzyme. We here assessed theimpact of the GSTP1 codon 105 polymorphism in chronic myeloid leukemia (CML) development and therapyresponse. The Ile105Val polymorphism was analyzed using a PCR-RFLP technique. Two hundred and sixtypatients with CML and 248 healthy, age and sex matched controls were included in the study of associations withpatient characteristics and treatment outcome. The GSTP1 Ile105Val polymorphism was significantly associatedwith CML development (χ2 = 9.57; df = 2; p = 0.0084). With respect to clinical phase, CML patients in advancedphase (accelerated and blast crisis) had higher frequency of heterozygous (Ile/Val) genotype (47.62%) comparedto chronic phase (36.5%). Further 54.5% of patients in blast crisis carried valine allele as compared to thosein chronic phase (36.5%). The frequency of combined genotypes (Ile/Val, Val/Val) was elevated in cytogeneticpoor (41.6%) and minor (53.57%) responders as compared to major (38.51%) responders. Hence the presentstudy suggests that GSTP1 Ile105Val polymorphism with reduced GSTP1 enzyme activity might influence CMLdevelopment, progression and response rates.     

Prostate cancer risk from occupational exposure to polycyclic aromatic hydrocarbons interacting with the GSTP1 Ile105Val polymorphism

BACKGROUND: Variation in the glutathione S-transferase (GSTP1) gene and occupational polycyclic aromatic hydrocarbons (PAH) exposure are putative prostate cancer risk factors. An Ile/Val polymorphism in codon 105 of GSTP1 affects its enzymatic activity toward PAH detoxification, a possible mechanism in prostate carcinogenesis. METHODS: To determine whether the GSTP1 Ile105Val polymorphism modifies prostate cancer risk associated with occupational PAH exposure, we studied 637 prostate cancer cases and 244 controls of White and African-American race from the Henry Ford Health System in Detroit, Michigan. Occupational exposure to PAH from wood, petroleum, coal or other sources through respiratory and cutaneous routes was retrospectively assessed by expert review of job histories. The association of occupational PAH exposure and GSTP1 Ile105Val polymorphism with prostate cancer was tested in multiple logistic regression models adjusting for potential confounders. Cases were over sampled compared with controls to evaluate gene-environment interaction with the statistically efficient case-only analytic approach. RESULTS: Neither carriage of the GSTP1 Val(105) variant allele nor occupational PAH exposure was significantly associated with prostate cancer. However, case-only analyses revealed that carriage of the GSTP1 Val(105) variant allele was associated with increasing levels of occupational respiratory PAH exposures from any source and from petroleum (trend test p=0.01 for both). The GSTP1 Val(105) allele was observed most frequently in cases in the highest quartile of occupational respiratory PAH exposures from petroleum (OR=1.74; 95% CI=1.11-2.72) or from any source (OR=1.85; 95% CI=1.19-2.89). The gene-environment risk estimate in the highest PAH petroleum exposure quartile was greatest in men under age 60 (OR=4.52; 95% CI=1.96-10.41) or with a positive family history of prostate cancer (OR=3.02; 95% CI=1.15-7.92). CONCLUSIONS: Our results suggest men who carry the GSTP1 Val(105) variant and are exposed at high levels to occupational PAH have increased risk for prostate cancer. This increased risk is more pronounced in men under age 60 or with a family history of prostate cancer.     

谷胱甘肽S转移酶P1 Ile105Val多态性与肺癌易感性关系的Meta分析

 目的用Meta分析的方法综合评价谷胱甘肽S转移酶P1基因(GSTP1)105氨基酸位点Ile/Val多态性与肺癌易感性 的关系。方法检索公开发表的关于谷胱甘肽S转移酶P1基因105氨基酸位点Ile/Val多态性与肺癌易感性关系的文献 ,把研究人群分为高加索人群及东亚人群,以病例组及对照组比值比(OR值)为效应指标,应用Meta分析软件RevMan 4.2分别计算两种人群及其亚组的合并OR值及95% CI,进行敏感度分析和发表偏倚评估,给出Meta分析森林图和漏 斗图。结果共纳入文献24篇,其中高加索人群15篇,纳入病例6 601例,对照6 821例,东亚人群9篇,纳入病例1 822例,对照2 017例,分别计算两组人群及其各亚组的GG+AG/AA合并OR值,两种人群总体OR值及各亚组OR值均未提 示有相关性,敏感度分析表明结果稳定,高加索人群研究有发表偏倚,东亚人群研究未见发表偏倚。结论谷胱甘肽 S转移酶P1基因(GSTP1)105氨基酸位点Ile/Val多态性与高加索人群和东亚人群肺癌易感性均不具有相关性,但是没 有根据吸烟量进行亚组分析。     

Quantitative synthesis of the association between the cytochrome P450 1A1 Ile462Val polymorphism and prostate cancer risk

The association between the cytochrome P450 1A1 (CYP1A1) Ile462Val polymorphism and prostate cancer risk remains inconclusive owing to the conflicting findings from previous studies. To get a more precise estimate of the possible association, we performed the present meta-analysis. We searched the PUBMED, EMBASE, and Wanfang databases for the studies which met the inclusion criteria. The pooled odds ratio (OR) with corresponding 95 % confidence interval (95 % CI) was used to estimate the association between CYP1A1 Ile462Val polymorphism and prostate cancer risk. A total of 13 studies with 2,350 cases and 2,992 controls were included in the meta-analysis. The results indicated that there was an obvious association between CYP1A1 Ile462Val polymorphism and increased risk of prostate cancer (for Val versus Ile: OR?=?1.27, 95 % CI 1.13–1.43, P?<?0.001; for ValVal versus IleIle: OR?=?1.51, 95 % CI 1.14–2.01, P?=?0.004; for ValVal?+?ValIle versus IleIle: OR?=?1.31, 95 % CI 1.14–1.51, P?<?0.001; for ValVal versus IleIle + ValIle: OR?=?1.38, 95 % CI 1.05–1.81, P?=?0.020). Subgroup analyses by ethnicity suggested that CYP1A1 Ile462Val polymorphism was associated with prostate cancer risk in Asians but not in Caucasians. This meta-analysis suggests that there is an association between CYP1A1 Ile462Val polymorphism and increased risk of prostate cancer. More studies with large sample are needed to further assess the association in Caucasians.     

Relationship between GSTP1 Ile105Val polymorphism and docetaxel-induced peripheral neuropathy: clinical evidence of a role of oxidative stress in taxane toxicity

BackgroundGlutathione-S-transferases (GST) regulate the cellular response to oxidative stress. We previously highlighted the importance of oxidative stress in taxane toxicity and therefore investigated the relationship between the GST isoforms M1, T1 and P1 gene polymorphisms and docetaxel (Taxotere)-induced peripheral neuropathy (DIPN).Patients and methodsThe GSTM1 (null), GSTT1 (null) and GSTP1 (Ile¹⁰⁵Val and Ala¹¹⁴Val) polymorphisms were determined in a cohort of cancer patients treated with docetaxel and entered in a clinical trial database. The relationship between GST polymorphisms and grade ≥2 DIPN as primary end point was studied.ResultsFifty-eight patients (median age 61 years) received a total of 261 cycles of docetaxel given as single agent. Patients with GSTP1¹⁰⁵Ile/¹⁰⁵Ile genotype had a higher risk of developing a grade ≥2 DIPN than did those with other GSTP1 genotypes (8 of 27 versus 2 of 31, respectively, odds ratio 6.11; 95% confidence interval 1.17–31.94; P = 0.03). In multivariate analysis, grade ≥2 DIPN was strongly correlated with GSTP1¹⁰⁵Ile/¹⁰⁵Ile genotype (P = 0.01) and the number of cycles (P = 0.03).ConclusionWe found a significant correlation between GSTP1¹⁰⁵Ile/¹⁰⁵Ile genotype and the development of grade ≥2 DIPN. This finding strongly suggests a role of oxidative stress in the pathophysiology of DIPN.     

GSTP1 Gene Ile105Val Polymorphism Causes an Elevated Risk for Bladder Carcinogenesis in Smokers

Background: The glutathione S transferase (GST) family of enzymes plays a vital role in the phase IIbiotransformation of environmental carcinogens, pollutants, drugs and other xenobiotics. GSTs are polymorphicand polymorphisms in GST genes have been associated with cancer susceptibility and prognosis. GSTP1 isassociated with risk of various cancers including bladder cancer. A case control study was conducted to determinethe genotype distribution of GSTP1 A>G SNP, to elucidate the possible role of this SNP as a risk factor in urinarybladder cancer (UBC) development and to examine its correlation with clinico-pathologic variables inUBC cases.Materials and Methods: Using the polymerase chain reaction-restriction fragment length polymorphism (PCRRFLP)approach, we tested the genotype distribution of 180 bladder cancer patients in comparison with 210cancer-free controls from the same geographical region with matched frequency in age and gender. Results: Wedid not observe significant genotype differences between the control and bladder cancer patients overall with anodds ratio (OR)=1.23 (p>0.05). The rare allele (AG+GG) was found to be present more in cases (28.3%) than incontrols (24%), though the association was not significant (p<0.05). However, a significant risk of more than 2-foldwas found for the variant allele (AG+GG) with smokers in cases as compared to controls (p>0.05). Conclusions:Thus, it is evident from our study that GSTP1 SNP is not implicated overall in bladder cancer, but that the rare,valine-related allele is connected with higher susceptibility to bladder cancer in smokers and also males.     

Association between survival after treatment for breast cancer and glutathione S-transferase P1 Ile105Val polymorphism

A glutathione S-transferase (GST) P1 polymorphism results in an amino acid substitution, Ile105Val; the Val-containing enzyme has reduced activity toward alkylating agents. Cancer patients with the variant enzyme may differ in removal of treatment agents and in outcomes of therapy. We evaluated survival according to GSTP1 genotype among women (n = 240) treated for breast cancer. Women with the low-activity Val/Val genotype had better survival. Compared with Ile/Ile, hazard ratios for overall survival were 0.8 (95% confidence interval, 0.5-1.3) for Ile/Val and 0.3 (95% confidence interval, 0.1-1.0) for Val/Val (P for trend = 0.04). Inherited metabolic variability may influence treatment outcomes.     

Glutathione S-transferase P1 Ile105Val polymorphism, cigarette smoking and prostate cancer

The enzyme glutathione S-transferase P1 (GSTP1) detoxifies carcinogenic products of tobacco smoke. This exploratory case-control study evaluates the possible effect modification by the GSTP1 Ile105Val polymorphism (replacement of isoleucine by valine at codon 105) on smoking and prostate cancer. Because the Val variant possesses up to a five-fold greater enzymatic activity towards the carcinogenic metabolites of tobacco smoke, the Ile allele is expected to be related to an increase in the risk of prostate cancer among smokers. GSTP1 genotype and epidemiological data were obtained from 122 cases of prostate cancer and 135 healthy males as controls. A logistic regression model was used to estimate odds ratios and 95% confidence intervals. The adjusted OR of homozygous Ile compared to other genotypes for prostate cancer was 1.21 (95% CI: 0.61-2.83). Smoking was not significantly associated with prostate cancer with an adjusted OR of 1.56 (95% CI: 0.78-3.12). However, among individuals with the Ile/Ile genotype, smoking was strongly associated with an increased risk of prostate cancer with an adjusted odds ratio of 4.09 (95% CI: 1.25-13.35). A potential multiplicative interaction was suggested between GSTP1 and smoking on the risk of prostate cancer with the adjusted OR for the interaction of 4.52 (95% CI: 1.07-19.17). To our knowledge, this is the first time that a potential effect modification by the GSTP1 Ile/Ile genotype on smoking and the risk of prostate cancer is suggested.     

亚甲基四氢叶酸还原酶A1298C基因多态性与肝细胞性肝癌遗传易感性的Meta分析

目的探讨亚甲基四氢叶酸还原酶（methylenetetrahy drofolate reductase,MTHFR）A1298C基因多态性与肝细胞性肝癌（hepatocellular carcinoma,HCC）遗传易感性的关系。方法计算机检索PubMed、EMbase和中国学术期刊全文数据库等,收集有关MTHFR基因多态性与HCC遗传易感性的病例一对照研究资料,按照纳入标准选择文献,提取相关数据进行Mcta分析。以病例组和对照组基凶型分布的比值比（OR）为效应指标,对纳入文献进行异质性检验,应用Stata12．0软件对各研究原始数据进行Meta合并,计算合并效应量OR值及95％可信区间（95％CI）。结果共纳入6项病例一对照研究,病例组为1708例,对照组为2911名。等位基因比较模型（C vs A）：OR（95％CI）=0．95（0．85～1．06）,P=0．342;纯合子比较模型（CC vs AA）：OR（95％CI）=0．55（0．38～0．79）,P=0．001;隐性模型（CC vs AC／AA）：OR（95％CI）=0．54（0．38～0．78）,P=0．001。结论MTHFR A1298C基因多态位点CC基因型能够降低HCC遗传易感性,为保护基因型。     

IGF-1R基因多态性与原发性肝癌易感性的相关性研究

目的 探讨广西肝癌高发区肝癌相关基因IGF-1R基因多态性与原发性肝癌易感性的关系.方法 采用病例对照研究方法,在广西肝癌高发现场人群中选取113例原发性肝癌及113名健康对照人群.以筛选IGF-1R基因SNP rs 61740868位点为遗传标志,采用聚合酶链式反应-限制性片段长度多态性方法(PCR-RFLP法)检测IGF-1R基因rs 61740868多态性及其基因分布的频率.结果 肝癌病例组与对照组IGF-I R基因rs 61740868位点均未发生基因突变,其基因型均为CC型,两组比较差异无统计学意义(P＞0.05).结论 IGF-1R基因rs 61740868位点多态性与肝癌发生无关,可能不是肝癌的危险因素之一.     

miRNA-146a rs2910164基因多态性与肝癌易感性的Meta分析

目的系统评价miRNA-146ars2910164基因多态性与肝癌易感性之间的相关性。方法全面检索PubMed、Excerpta Medica Database（Embase）、中国生物医学文献数据库（Chinese Biomedical Literature Database,CBM）、the Cochrane Library、维普、谷歌学术和万方数据库,文献检索起止时间均为从建库至2013-11。搜集研究miRNA-146a rs2910164基因多态性与肝癌相关性的文献。对miRNA-146ars2910164G/C各基因型比较模型,包括G与C、GG与CC、GG与GC、GC与CC、GG＋GC与CC以及GG与GC＋CC,在病例组和对照组的分布情况进行定量综合分析。结果共纳入9篇文献,共有2 951例肝癌及3 217名健康对照。miRNA-146ars2910164基因多态性与肝癌易感性之间具有相关性,GG与CC比较的OR=1.21,95%CI为1.04～1.42,P=0.02;GC与CC比较的OR=1.15,95%CI为1.02～1.29,P=0.02;GG＋GC与CC比较的OR=1.16,95%CI为1.04～1.29,P=0.009。亚组分析结果发现,在亚洲人群中也有相似的结论,GC与CC比较的OR=1.15,95%CI为1.02～1.29,P=0.02;GG＋GC与CC比较的OR=1.16,95%CI为1.04～1.30,P=0.009。结论 miRNA-146ars2910164基因多态性与肝癌易感性之间具有相关性,并且miRNA-146a rs2910164基因多态性的CC基因型可能是肝癌的保护因素。     

Glutathione S-transferase P1 Ile105Val polymorphism contributes to increased risk of gastric cancer in East Asians

Glutathione S-transferase P1 (GSTP1) is an important enzyme playing critical roles in the phase II detoxification pathway. There were many studies investigating the association between GSTP1 gene Ile105Val polymorphism and gastric cancer risk, but studies from East Asians reported inconsistent findings. We performed a meta-analysis to investigate the association in East Asians. Published literature from PubMed and Chinese Biomedical Literature databases were searched for eligible publications. Pooled odds ratios (ORs) with 95 % confidence intervals (95 %CIs) were calculated using random or fixed-effect model according the between-study heterogeneity. A total of 12 studies with 2,552 cases and 5,474 controls were finally included into the meta-analysis. Meta-analysis of those 12 studies showed that there was an obvious association between GSTP1 Ile105Val polymorphism and gastric cancer risk in East Asians under three genetic models (for valine vs. isoleucine, OR?=?1.32, 95 %CI 1.05–1.66, P?=?0.015; for ValVal vs. IleIle, OR?=?2.00, 95 %CI 1.34–2.98, P?=?0.001; for the recessive model, OR?=?1.96, 95 %CI 1.35–2.83, P?<?0.001). Sensitivity analysis by removing one study at a time suggested the pooled results were stable under the three genetic models above. There was no risk of publication bias. In conclusion, the meta-analysis suggests that there is a strong evidence for the association between GSTP1 Ile105Val polymorphism and increased risk of gastric cancer in East Asians and contributes to increased risk of gastric cancer in East Asians.     

Glutathione S-transferase P1 gene Ile105Val polymorphism might be associated with lung cancer risk in the Chinese Han population

Genetic variations in glutathione S-transferase P1 (GSTP1) gene have been suggested to be involved in the development of cancer. However, the results from the studies regarding the association between GSTP1 Ile105Val polymorphism and lung cancer risk in the Chinese population have been inconsistent. Thus, we conducted a meta-analysis to investigate the association. Published literature from PubMed, Chinese Biomedical Literature Database, Chinese Wanfang Data, and Chinese National Knowledge Infrastructure databases were searched for eligible publications. Pooled odds ratios (ORs) with 95?% confidence intervals (CIs) were calculated using random or fixed effect model. Ten studies (1,506 cases/1,714 controls) were included in the meta-analysis. The results suggested that GSTP1 Ile105Val polymorphism was marginally associated with lung cancer risk in the Chinese Han population under a multiplicative model (G vs. A, odds ratio (OR)?=?1.22, 95?% confidence interval?=?1.02?C1.46), under a homogeneous codominant model (GG vs. AA, OR?=?1.67, 95?% CI?=?1.14?C2.45), under a heterogeneous codominant model (GA vs. AA, OR?=?1.15, 95?% CI?=?0.98?C1.35), under a dominant model (GG + GA vs. AA, OR?=?1.21, 95?% CI?=?1.04?C1.39), and under a recessive model (GG vs. GA + AA, OR?=?1.59, 95?% CI?=?1.09?C2.31), respectively. Moreover, after adjusted for age, gender, and smoking status, the significant association under dominant model remained (OR?=?1.27, 95?% CI?=?1.07?C1.51). This meta-analysis suggested that there might be an association between GSTP1 Ile105Val polymorphism and lung cancer in the Chinese Han population.     

Quantitative assessment of the association between +61A>G polymorphism of epidermal growth factor gene and susceptibility to glioma

Numerous studies have investigated the risk of cancer associated with the polymorphism of epidermal growth factor (EGF) 61A>G, but results have been inconsistent. We performed this meta-analysis to drive a more precise estimation of the association between this polymorphism and risk of glioma. A comprehensive search was conducted to identify all case–control studies on the EGF +61A>G polymorphism and glioma risk. Odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were calculated to assess the strength of the association. Statistical analysis was performed with the software program Stata (version 12.0). A total of ten eligible studies, including 1,888 cases and 2,836 controls were included in this work. Overall, there was a significant association between EGF +61A>G polymorphism and glioma risk in the allele model (OR?=?1.419, 95 % CI?=?1.144–1.759, P?=?0.001). In the subgroup analysis by ethnicity, significant associations were also found in Asian populations under all different genetic models (homozygote model: OR?=?1.727, 95 % CI?=?1.310–2.275, P?=?0.000; heterozygote model: OR?=?1.202, 95 % CI?=?1.023–1.413, P?=?0.025; dominant model: OR?=?1.279, 95 % CI?=?1.096–1.491, P?=?0.002; recessive model: OR?=?1.590, 95 % CI?=?1.221–2.070, P?=?0.001; and A-allele versus G-allele OR?=?1.600, 95 % CI?=?1.145–2.236, P?=?0.006). However, no significant associations were found among Caucasians in all comparison models. In conclusion, the results suggest that there is a significant association between EGF +61A>G polymorphism and glioma risk among Asians.