Forest plots of the <i>PD-1</i>.<i>3</i>(rs11568821) polymorphism and cancer risk for overall populations (A for AA vs. GG; B for AA vs. AG+GG; C for AA+AG vs. GG; D for AG vs. GG and E for A vs. G).

<p>The squares and horizontal lines correspond to the study-specific ORs and 95% CIs. The areas of the squares reflect the study-specific weights (which was the inverse of the variance). The diamonds represent the pooled ORs and 95% CIs.</p

Flow chart of study selection.

<p>Flow chart of study selection.</p

Forest plots of the <i>PD-1</i>.<i>5</i> (rs2227981) polymorphism and cancer risk for population-based subgroup (A for TT vs. CC; B for TT vs. CT+CC; C for TT+CT vs. CC; D for TC vs. CC and E for T vs. C).

<p>The squares and horizontal lines correspond to the study-specific ORs and 95% CIs. The areas of the squares reflect the study-specific weights (which was the inverse of the variance). The diamonds represent the pooled ORs and 95% CIs.</p

Tamsulosin combined with solifenacin versus tamsulosin monotherapy for male lower urinary tract symptoms: a meta-analysis

<p>To evaluate the efficacy and safety of tamsulosin and solifenacin combination therapy compared with tamsulosin monotherapy for male lower urinary tract symptoms (LUTS).</p> <p>We identified all eligible studies that compared tamsulosin and solifenacin combination therapy with tamsulosin monotherapy for male LUTS (up to January 2015). The fixed- or random-effects model was selected depending on the proportion of heterogeneity.</p> <p>Seven articles were identified as eligible for this meta-analysis, with a total of 3063 participants. Synthetic data showed combination therapy had significant improvements in Storage International Prostate Symptom Score (WMD = −0.60; 95% CI: −0.81 to −0.38, <i>P</i> < 0.0001), quality of life (WMD = −0.23; 95% CI: −0.34 to −0.11, <i>P</i> < 0.0001), micturitions per 24 hours (WMD = −0.70; 95% CI: −0.86 to −0.55, <i>P</i> < 0.0001) and urgency episodes per 24 hours (WMD = −0.26; 95% CI: −0.48 to −0.05, <i>P</i> = 0.018). The incidence of adverse effects in the tamsulosin and solifenacin combined therapy group (30.82%) was similar to the tamsulosin monotherapy group (25.75%). Acute urinary retention was seldom reported in the studies and no clinically significant changes regarding <i>Qmax</i> were showed in our meta-analysis.</p> <p>Tamsulosin and solifenacin combination therapy may be a reasonable option for male LUTS patients, especially for those who have significant storage symptoms. However, PVR should be measured during treatment to assess the increase in PVR or the incidence of AUR.</p

Forest plots of the <i>PD-1</i>.<i>5</i> (rs2227981) polymorphism and cancer risk for overall populations (A for TT vs. CC; B for TT vs. CT+CC; C for TT+CT vs. CC; D for TC vs. CC and E for T vs. C).

<p>The squares and horizontal lines correspond to the study-specific ORs and 95% CIs. The areas of the squares reflect the study-specific weights (which was the inverse of the variance). The diamonds represent the pooled ORs and 95% CIs.</p

Genetic Polymorphisms of <em>GSTM1</em>, <em>GSTT1</em>, and <em>GSTP1</em> with Prostate Cancer Risk: A Meta-Analysis of 57 Studies

<div><h3>Background and Objectives</h3><p>The <em>GSTM1, GSTT1</em> and <em>GSTP1</em> polymorphisms might be involved in inactivation of procarcinogens that contribute to the genesis and progression of cancers. However, studies investigating the association between <em>GSTM1, GSTT1</em> or <em>GSTP1</em> polymorphisms and prostate cancer (PCa) risk report conflicting results, therefore, we conducted a meta-analysis to re-examine the controversy.</p> <h3>Methods</h3><p>Published literature from PubMed, Embase, Google Scholar and China National Knowledge Infrastructure (CNKI) were searched (updated to June 2, 2012). According to our inclusion criteria, studies that observed the association between <em>GSTM1</em>, <em>GSTT1</em> or <em>GSTP1</em> polymorphisms and PCa risk were included. The principal outcome measure was the odds ratio (OR) with 95% confidence interval (CI) for the risk of PCa associated with <em>GSTM1</em>, <em>GSTT1</em> and <em>GSTP1</em> polymorphisms.</p> <h3>Results</h3><p>Fifty-seven studies involving 11313 cases and 12934 controls were recruited. The overall OR, which was 1.2854 (95% CI = 1.1405–1.4487), revealed a significant risk of PCa and <em>GSTM1</em> null genotype, and the similar results were observed when stratified by ethnicity and control source. Further, the more important is that the present study first reported the high risks of PCa for people who with dual null genotype of <em>GSTM1</em> and <em>GSTT1</em> (OR = 1.4353, 95% CI = 1.0345–1.9913), or who with <em>GSTT1</em> null genotype and <em>GSTP1</em> A131G polymorphism (OR = 1.7335, 95% CI = 1.1067–2.7152). But no association was determined between <em>GSTT1</em> null genotype (OR = 1.102, 95% CI = 0.9596–1.2655) or <em>GSTP1</em> A131G polymorphism (OR = 1.0845, 95% CI = 0.96–1.2251) and the PCa risk.</p> <h3>Conclusions</h3><p>Our meta-analysis suggested that the people with <em>GSTM1</em> null genotype, with dual null genotype of <em>GSTM1</em> and <em>GSTT1</em>, or with <em>GSTT1</em> null genotype and <em>GSTP1</em> A131G polymorphism are associated with high risks of PCa, but no association was found between <em>GSTT1</em> null genotype or <em>GSTP1</em> A131G polymorphism and the risk of PCa. Further rigorous analytical studies are highly expected to confirm our conclusions and assess gene-environment interactions with PCa risk.</p> </div

Characteristics of eligible studies in the meta-analysis of <i>PD-1</i> polymorphisms and cancer risk.

<p>Characteristics of eligible studies in the meta-analysis of <i>PD-1</i> polymorphisms and cancer risk.</p

Meta-analysis of <i>GSTM1</i> null genotype and PCa risk.

<p>Meta-analysis of <i>GSTM1</i> null genotype and PCa risk.</p

Programmed Cell Death-1 Polymorphisms Decrease the Cancer Risk: A Meta-Analysis Involving Twelve Case-Control Studies

<div><p>Programmed cell death-1 (<i>PD-1</i>) plays an important inhibitory role in anti-tumor responses, so it is considered as a powerful candidate gene for individual’s genetic susceptibility to cancer. Recently, some epidemiological studies have evaluated the association between <i>PD-1</i> polymorphisms and cancer risk. However, the results of the studies are conflicting. Therefore, a meta-analysis was performed. We identified all studies reporting the relationship between <i>PD-1</i> polymorphisms and cancers by electronically searches. According to the inclusion criteria and the quality assessment of Newcastle-Ottawa Scale (NOS), only high quality studies were included. A total of twelve relevant studies involving 5,206 cases and 5,174 controls were recruited. For <i>PD-1</i>.<i>5</i> (rs2227981) polymorphism, significantly decreased cancer risks were obtained among overall population, Asians subgroup and population-based subgroup both in TT vs. CC and TT vs. CT+CC genetic models. In addition, a similar result was also found in T vs. C allele for overall population. However, there were no significant associations between either <i>PD-1</i>.<i>9</i> (rs2227982) or <i>PD-1</i> rs7421861 polymorphisms and cancer risks in all genetic models and alleles. For <i>PD-1</i>.<i>3</i> (rs11568821) polymorphism, we found different cancer susceptibilities between GA vs. GG and AA vs. AG+GG genetic models, and no associations between AA vs. GG, AA+AG vs. GG genetic models or A vs. G allele and cancer risks. In general, our results firstly indicated that <i>PD-1</i>.<i>5</i> (rs2227981) polymorphism is associated a strongly decreased risk of cancers. Additional epidemiological studies are needed to confirm our findings.</p></div

Summary of meta-analysis of <i>GSTM1, GSTT1</i> and <i>GSTP1</i> polymorphisms and PCa risk.

<p>OR, odds ratio; CI, confidence interval.</p>*<p><i>GSTP1</i> the total result of after excluding three researches deviated from Hardy-Weinberg equilibrium (HWE).</p>a<p><i>GSTM1</i> (−/−) and <i>GSTT1</i> (−/−) vs. <i>GSTM1</i> (+/−) and <i>GSTT1</i> (−/−) with <i>GSTM1</i> (−/−) and <i>GSTT1</i> (+/−).</p>b<p><i>GSTT1</i> (−/−) and <i>GSTP1</i> (AG+GG) vs. <i>GSTT1</i> (+/−) and GSTP1 (AA) with <i>GSTT1</i> (−/−) and GSTP1 (AG+GG).</p>c<p><i>GSTM1</i> (−/−) and <i>GSTP1</i> (AG+GG) vs. <i>GSTM1</i> (+/−) and GSTP1 (AA) with <i>GSTM1</i> (−/−) and GSTP1 (AG+GG).</p>d<p><i>GSTM1</i> (−/−), <i>GSTT1</i> (−/−) and <i>GSTP1</i> (AG+GG) vs. the other combinations of the <i>GSTM1</i>, <i>GSTT1</i> and <i>GSTP1</i> polymorphisms.</p