Association between XRCC2 Arg188His Polymorphism and Breast Cancer Susceptibility: A Systematic Review and Meta-Analysis
Seyed Alireza DastgheibSoheila SayadSepideh AziziNazanin HajizadehFatemeh AsadianMojgan Karimi‐ZarchiMaedeh BarahmanAmirmasoud ShiriMohammad ManzourolhojehKazem AghiliHossein Neámatzadeh
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Breast cancer is one of the most common cancers in the world and leading cause of cancer-related death among women. Several studies indicated that Arg188His (rs3218536) polymorphism of X-ray repair cross-complementing 2 (XRCC2) may be associated with breast cancer risk. However, this association remains ambiguous. Thus, we performed a meta-analysis to provide more precise conclusion on this issue. A comprehensive search in PubMed, Google Scholar and ISI Web of Science was performed to select all relevant studies. Odds ratios (OR) with corresponding 95% confidence intervals (CI) were applied to assess the strength of the relationships. A total of 17 studies with 5694 breast cancer cases and 6450 healthy subjects were identified. The pooled data revealed that XRCC2 Arg188His polymorphism was marginally with susceptibility to breast cancer globally under the heterozygote contrast (OR = 0.929, 95% CI = 0.873-0.987, p=0.018). Moreover, subgroup analysis by ethnicity revealed that this polymorphism was associated with breast cancer risk among Caucasians. On the whole, the present study demonstrates that the XRCC2 Arg188His polymorphism may contribute to an increased risk of breast cancer.Keywords:
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Publication bias is a substantial problem for the credibility of research in general and of meta-analyses in particular, as it yields overestimated effects and may suggest the existence of non-existing effects. Although there is consensus that publication bias exists, how strongly it affects different scientific literatures is currently less well-known. We examined evidence of publication bias in a large-scale data set of primary studies that were included in 83 meta-analyses published in Psychological Bulletin (representing meta-analyses from psychology) and 499 systematic reviews from the Cochrane Database of Systematic Reviews (CDSR; representing meta-analyses from medicine). Publication bias was assessed on all homogeneous subsets (3.8% of all subsets of meta-analyses published in Psychological Bulletin) of primary studies included in meta-analyses, because publication bias methods do not have good statistical properties if the true effect size is heterogeneous. The Monte-Carlo simulation study revealed that the creation of homogeneous subsets resulted in challenging conditions for publication bias methods since the number of effect sizes in a subset was rather small (median number of effect sizes equaled 6). No evidence of bias was obtained using the publication bias tests. Overestimation was minimal but statistically significant, providing evidence of publication bias that appeared to be similar in both fields. These and other findings, in combination with the small percentages of statistically significant primary effect sizes (28.9% and 18.9% for subsets published in Psychological Bulletin and CDSR), led to the conclusion that evidence for publication bias in the studied homogeneous subsets is weak, but suggestive of mild publication bias in both psychology and medicine.
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Effective obesity interventions in adolescent populations have been identified as an immediate priority action to stem the increasing prevalence of adult obesity. The purpose of this meta-analysis was to make a quantitative analysis of the impact of school-based interventions on body mass index during adolescence. Studies were retrieved from PubMed, Scopus, Science Direct and Web of Science databases. Results were pooled using a random-effects model with 95% confidence interval considered statistically significant. Of the 18 798 possible relevant articles identified, 12 articles were included in this meta-analysis. The global result showed a low magnitude effect, though it was statistically significant (N = 14 428), global e.s. = -0.055, P = 0.004 (95% CI = -0.092, -0.017). Heterogeneity was low among the studies (I2 = 9.017%). The funnel plot showed no evidence of publication bias. The rank-correlation test of Begg (P = 0.45641) and Egger's regression (P = 0.19459) confirmed the absence of bias. This meta-analysis reported a significant effect favoring the interventions; however, future research are needed since the reported the evidence was of low magnitude, with the studies following a substantial range of approaches and mostly had a modest methodological quality.
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Objective: To explore the relationship between daily tea intake and cardiovascular disease (CVD) mortality. Methods: PubMed, EMbase, The Cochrane, Chinese Biomedical Literature Database, CNKI, and Wanfang Database were searched to collect research on tea intake and CVD mortality. The search period was from the establishment of the database to June 2020. Two researchers independently screened and extracted literature. The risk of bias was evaluated in the included studies, a dose-response meta-analysis was conducted, sensitivity analysis and publication bias analysis of the research results, and quality evaluation of the included literature and GRADE classification of the evidence body were performed. Results: A total of 21 cohort or case-control studies were included, including 1 304 978 subjects. Among them, 38 222 deaths from CVD were reported. The quality scores of the included studies were all ≥ 6 points. The dose-response meta-analysis showed that for every additional cup of tea intake per day, the mortality rate of CVD decreased by about 3% (95%CI 0.95-0.98, P<0.05), and there was a non-linear dose-response relationship (P<0.05). Compared with people who do not drink tea, people who drink 1 to 8 cups of tea a day have 8% lower CVD mortality (RR=0.92, 95%CI 0.89-0.95), 13% (RR=0.87, 95 %CI 0.84-0.91), 15% (RR=0.85, 95%CI 0.82-0.89), 15% (RR=0.85, 95%CI 0.81-0.89), 16% (RR=0.84, 95%CI 0.80-0.89), 16% (RR=0.84, 95%CI 0.81-0.88), 16% (RR=0.84, 95%CI 0.81-0.87), 16% (RR=0.84, 95%CI 0.80-0.88), respectively. The results of traditional meta-analysis showed that compared with people who do not drink tea, people who drink more than 1 cup of tea a day are associated with 14% lower CVD mortality rate (RR=0.86, 95%CI 0.81-0.91, I2=73.2%, P<0.05). The results of subgroup analysis showed that compared with the corresponding people who did not drink tea, men who drank more than 1 cup of tea a day reduced the CVD mortality rate by 24%, women by 14%, European and American populations by 12%, and Asian populations by 15%. The population who consumed green tea decreased CVD mortality by 15%, and the population of non-smokers decreased CVD mortality by 20% (all P<0.05). The population who consumed black tea decreased CVD mortality by 8%, and the smoking population who consumed black tea decreased CVD mortality by 3%, and the difference was not statistically significant (all P>0.05). The results of the bias analysis showed that Begg=0.42 and Egger=0.62, indicating that the distribution on both sides of the funnel chart is symmetrical, suggesting that there is no publication bias. The results of sensitivity analysis showed that the effect size of the outcome index did not change significantly after excluding any article, indicating that the results are robust and credible. The GRADE evaluation showed that the evidence grades of the outcome indicators were all low grade. Conclusions: Daily tea consumption is related to reduced CVD mortality. It is therefore recommended to drink an appropriate amount of tea daily.目的： 探讨茶每日摄入量与心血管疾病（CVD）死亡率的关系。 方法： 检索PubMed、EMbase、The Cochrane、中国生物医学文献数据库、中国知网和万方数据库，搜集有关茶摄入量与CVD死亡率的相关研究，检索时限均从建库至2020年6月。由2名研究者独立筛选、提取文献。评价纳入研究的偏倚风险，进行剂量-反应荟萃分析，对研究结果进行敏感性分析和发表偏倚分析，并对结局指标进行证据体的GRADE分级。 结果： 共纳入21篇队列或病例对照研究，包括1 304 978名受试者，其中CVD死亡人数为38 222例，纳入研究质量评分均≥6分。剂量-反应荟萃分析结果显示，茶摄入量每天每增加1杯CVD死亡率下降约3%（95%CI 0.95~0.98，P<0.05），且存在一种非线性剂量反应关系（P<0.05）；与不喝茶的人群相比较，每天喝1~8杯茶的人群的CVD死亡率分别降低8%（RR=0.92，95%CI 0.89~0.95），13%（RR=0.87，95%CI 0.84~0.91），15%（RR=0.85，95%CI 0.82~0.89），15%（RR=0.85，95%CI 0.81~0.89），16%（RR=0.84，95%CI 0.80~0.89），16%（RR=0.84，95%CI 0.81~0.88），16%（RR=0.84，95%CI 0.81~0.87），16%（RR=0.84，95%CI 0.80~0.88）。传统荟萃分析结果显示，与不喝茶的人群相比，每天喝茶大于1杯的人群CVD死亡率可以降低14%（RR=0.86，95%CI 0.81~0.91，I2=73.2%，P<0.05）。亚组分析结果显示，与相对应的不喝茶的人群相比，每天喝茶大于1杯的男性CVD死亡率降低24%，女性降低14%，欧美人群降低12%，亚洲人群降低15%，饮用绿茶的人群降低15%，不吸烟人群降低20%，差异均具有统计学意义（P均<0.05）；饮用红茶的人群降低8%，吸烟人群降低3%，差异无统计学意义（P均>0.05）。偏倚分析结果显示Begg=0.42，Egger=0.62，表明漏斗图两侧分布对称，提示不存在发表偏倚。敏感性分析结果显示排除任何一篇文献结局指标效应量未发生明显变化，表明结果稳健可信。GRADE评价显示结局指标的证据分级均为低等级别。 结论： 每日饮用茶水能够降低CVD死亡率，推荐每天饮用适量茶水。.
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Publication bias is a substantial problem for the credibility of research in general and of meta-analyses in particular, as it yields overestimated effects and may suggest the existence of non-existing effects. Although there is consensus that publication bias exists, how strongly it affects different scientific literatures is currently less well-known. We examined evidence of publication bias in a large-scale data set of primary studies that were included in 83 meta-analyses published in Psychological Bulletin (representing meta-analyses from psychology) and 499 systematic reviews from the Cochrane Database of Systematic Reviews (CDSR; representing meta-analyses from medicine). Publication bias was assessed on all homogeneous subsets (3.8% of all subsets of meta-analyses published in Psychological Bulletin) of primary studies included in meta-analyses, because publication bias methods do not have good statistical properties if the true effect size is heterogeneous. Publication bias tests did not reveal evidence for bias in the homogeneous subsets. Overestimation was minimal but statistically significant, providing evidence of publication bias that appeared to be similar in both fields. However, a Monte-Carlo simulation study revealed that the creation of homogeneous subsets resulted in challenging conditions for publication bias methods since the number of effect sizes in a subset was rather small (median number of effect sizes equaled 6). Our findings are in line with, in its most extreme case, publication bias ranging from no bias until only 5% statistically nonsignificant effect sizes being published. These and other findings, in combination with the small percentages of statistically significant primary effect sizes (28.9% and 18.9% for subsets published in Psychological Bulletin and CDSR), led to the conclusion that evidence for publication bias in the studied homogeneous subsets is weak, but suggestive of mild publication bias in both psychology and medicine.
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Abstract Visfatin levels have been reported to be abnormal in many types of cancers. However, epidemiological studies yielded inconsistent results. Therefore, a meta‐analysis was performed to assess the association between circulating visfatin levels and cancer risk. A systematic search was conducted for relevant studies in health‐related electronic databases up to March 2018. Data related to standard mean difference (SMD) and overall odds ratio (ORS) were collected and analyzed. Summary SMD and pooled OR with 95% CIs were calculated using a random‐effect model. Funnel plot and Egger's linear regression test were conducted to examine the risk of publication bias. A total of 27 studies with 2,693 cases and 3,040 healthy controls were included in meta‐analysis for pooling SMD analysis. The results of the meta‐analysis showed a significant higher visfatin levels in patients with various cancers than in controls, with a pooled SMD of 0.88, 95% CI = 0.56–1.20, p = 0.000. In subgroup, metaregression, Galbraith plot, and sensitivity analysis showed no substantial difference among all the analyzed factors. Data from 14 studies were also used for pooling ORs analysis. Metaresults revealed that high visfatin levels were associated with cancer risk (OR = 1.24, 95% CI: 1.14–1.34, p = 0.000). No evidence of publication bias was observed for pooling ORs and SMD analysis. This meta‐analysis indicated a significant association between high circulating visfatin levels and increased risk of various cancers. Visfatin may represent a potential biomarker for early detection of cancers who may benefit from preventive treatment.Note.
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Selective publication and reporting in individual papers compromise the scientific record, but are meta-analyses as compromised as their constituent studies? We systematically sampled 63 meta-analyses (each comprising at least 40 studies) in PLOS One, top medical journals, top psychology journals, and Metalab, an online, open-data database of developmental psychology meta-analyses. We empirically estimated publication bias in each. Across all meta-analyses, “statistically significant” results in the expected direction were only 1.17 times more likely to be published than “nonsignificant” results or those in the unexpected direction (95%CI: [0.94, 1.47]), with a confidence interval substantially overlapping the null. Comparable estimates were 0.83 for meta-analyses in PLOS One, 1.02 for top medical journals, 1.54 for top psychology journals, and 4.70 for Metalab. The severity of publication bias did differ across individual meta-analyses; in a small minority (10%; 95% CI: [2%, 21%]), publication bias appeared to favor "significant" results in the expected direction by more than 3-fold. We estimated that for 89% of meta-analyses, the amount of publication bias that would be required to attenuate the point estimate to the null exceeded the amount of publication estimated to be actually present in the vast majority of meta-analyses from the relevant scientific discipline (exceeding the 95th percentile of publication bias). Study-level measures (“statistical significance” with a point estimate in the expected direction and point estimate size) did not indicate more publication bias in higher-tier versus lower-tier journals, nor in the earliest studies published on a topic versus later studies. Overall, the mere act of performing a meta-analysis with a large number of studies (at least 40) and that includes non-headline results may largely mitigate publication bias in meta-analyses, suggesting optimism about the validity of meta-analytic results.
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Objective The aim of this analysis was to perform a meta-analysis evaluating gender difference of delayed healing risk in patients with venous leg ulcers. Methods We searched the PubMed and Web of Knowledge from their inception to 4 July 2015. The meta-analysis of pooled odds ratio and 95% confidence interval for venous leg ulcers healing risk were calculated. Results Twelve studies with 4453 patients were included in the meta-analysis. The pooled odds ratio for healing rate stratified by gender was 1.055 (95% CI 0.955–1.165; Z = 1.05, p = 0.292) by fix-effects model. The Begg's test (z = 2.67, p = 0.007), the Egger's test (t = 4.00, p = 0.003), and asymmetric funnel plot suggested there was significant publication bias. Subgroup analysis showed the pooled odds ratios were 1.048 (95% CI 0.945–1.162; Z = 0.88, p = 0.376) in prospective studies and 1.439 (95% CI 0.757–2.736; Z = 1.11, p = 0.266) in retrospective studies. Sensitivity analyses by only pooled adjusted odds ratios showed the pooled odds ratio was 1.049 (95% CI 0.946–1.163; Z = 0.91, p = 0.365), which indicated the results of meta-analysis were robust. Meta-regression analysis showed the healing rate odds ratio stratified by gender was not related with healing rate (t = 0.73, p = 0.484). Conclusion Our meta-analysis indicates that no gender difference existed for delayed healing in venous leg ulcers. Our results may be also useful in developing a risk score for failure of venous leg ulcers to heal.
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Background The evidence for association between Epstein-Barr virus (EBV) infection and risk of oral squamous cell carcinoma (OSCC) is inconsistent in the literature. Therefore, this meta-analysis was conducted to clarify this association. Methods A literature search was conducted in electronic databases for English- and Chinese-language publications until March 31, 2017 to include eligible case-control studies. The pooled odds ratio (OR) and 95% confidence interval (95% CI) were estimated to determine the association between EBV infection and OSCC risk using a fixed- or random-effects model based on heterogeneity. Publication bias was assessed using funnel plot analysis. Results A total of 13 case-control studies with 686 OSCC patients and 433 controls were included based on predetermined inclusion and exclusion criteria. The pooled OR with 95% CI between EBV infection and OSCC risk was 5.03 (1.80–14.01) with significant heterogeneity observed (I2 = 87%). The subgroup analysis indicates that the year of publication, study location, economic level, sample size, tissue type, detection method and marker, control type, and language might explain potential sources of heterogeneity. Publication bias was not observed, and sensitivity analysis showed stable results. Conclusions The results of the current meta-analysis suggest that EBV infection is statistically associated with increased risk of OSCC. However, additional high-quality studies with larger sample sizes are needed to further confirm the relationship between EBV and OSCC.
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