Investigation of ATG16L1 rs2241880 Polymorphism with Cancer Risk: A Meta-Analysis

Background and Objectives: Previous studies have investigated the impact of the ATG16L1 rs2241880 (Thr300Ala) polymorphism on individual susceptibility to cancer, but the conclusions are still controversial. To get a more precise evaluation of the correlation between ATG16L1 rs2241880 polymorphism and cancer susceptibility, we performed a meta-analysis of the association of all eligible studies. Materials and Methods: Searches were performed in the Web of Science, PubMed, Scopus and Google Scholar databases up to November 2018. A total of 12 case-control studies from 9 articles comprising 2254 cases and 4974 controls were included. Statistical analysis was achieved by STATA 14.1 and Review Manager 5.3 software. The odds ratios (ORs) with 95% confidence intervals (95% CIs) under five genetic models were used to determine the strength of association among rs2241880 polymorphism and cancer susceptibility. Results: The findings did not support an association between the rs2241880 variant in either the overall study population or the subgroups, based on cancer types and ethnicity in any of the genetic models. As far as we know, our study is the first meta-analysis of the association between rs2241880 polymorphism and cancer risk. Conclusions: In conclusion, the findings of this meta-analysis proposes that the ATG16L1 rs2241880 polymorphism may not play a role in cancer development. Further well-designed studies are necessary to clarify the precise role of the ATG16L1 rs2241880 polymorphism on cancer risk.

Download Full-text

Association between P2X7 Polymorphisms and Susceptibility to Tuberculosis: An Updated Meta-Analysis of Case-Control Studies

Medicina ◽

10.3390/medicina55060298 ◽

2019 ◽

Vol 55 (6) ◽

pp. 298 ◽

Cited By ~ 1

Author(s):

Taheri ◽

Sarani ◽

Moazeni-Roodi ◽

Naderi ◽

Hashemi

Keyword(s):

Meta Analysis ◽

Extrapulmonary Tuberculosis ◽

Asian Population ◽

Genetic Models ◽

Case Control Studies ◽

Increased Risk ◽

Stratified Analysis ◽

The Impact ◽

Strength Of Association

Background and Objectives: Several studies inspected the impact of P2X7 polymorphisms on individual susceptibility to tuberculosis (TB), but the findings are still controversial and inconclusive. To achieve a more precise estimation, we conducted a meta-analysis of all eligible studies on the association between P2X7 polymorphisms and TB risk. Materials and Methods: Relevant studies were identified by searching the PubMed, Web of Science, Scopus and Google scholar databases up to November 2018. Twenty-four full-text articles were included in our meta-analysis. The strength of association between P2X7 polymorphisms and TB risk was evaluated by odds ratios (ORs) and 95% confidence intervals (95% CIs) under five genetic models. Results: The findings of this meta-analysis revealed that the rs3751143 variant significantly increased the risk of TB in heterozygous codominant (OR = 1.44, 95%CI = 1.17−1.78, p = 0.0006, AC vs. AA), homozygous codominant (OR = 1.87, 95% CI = 1.40−2.49, p = 0.0004, CC vs. AA), dominant (OR = 1.50, 95% CI = 1.22−1.85, p = 0.0002, AC + CC vs. AA), recessive (OR = 1.61, 95% CI = 1.25−2.07, p = 0.001, CC vs. AC + AA), and allele (OR = 1.41, 95% CI = 1.19−1.67, p < 0.0001, C vs. A) genetic models. Stratified analysis showed that rs3751143 increased the risk of pulmonary tuberculosis (PTB) and extrapulmonary tuberculosis (EPTB) in all genetic models. Furthermore, the rs3751143 increased risk of TB in the Asian population. The findings did not support an association between the rs2393799, rs1718119, rs208294, rs7958311, and rs2230911 polymorphisms of P2X7 and TB risk. Conclusions: The findings of this meta-analysis suggest that P2X7 rs3751143 polymorphism may play a role in susceptibility to TB in the Asian population. More well-designed studies are required to elucidate the exact role of P2X7 polymorphisms on TB development.

Download Full-text

Impact of XPF rs2276466 polymorphism on cancer susceptibility: a meta-analysis

Bioscience Reports ◽

10.1042/bsr20181785 ◽

2019 ◽

Vol 39 (5) ◽

Author(s):

Yezhou Liu ◽

Kun Liu ◽

Xueru Zhao ◽

Yidan Sun ◽

Ning Ma ◽

...

Keyword(s):

Cancer Risk ◽

Gastrointestinal Cancer ◽

Cancer Susceptibility ◽

Excision Repair ◽

Meta Analysis ◽

Complementation Group ◽

Current Evidence ◽

Case Control Studies ◽

Summary Estimate ◽

The Impact

Abstract Association between the xeroderma pigmentosum complementation group F (XPF)rs2276466 located in the excision repair cross complementation group 4 (ERCC4) gene and cancer susceptibility has been widely investigated. However, results thus far have remained controversial. A meta-analysis was performed to identify the impact of this polymorphism on cancer susceptibility. PubMed, Embase and Science-Web databases were searched systematically up to May 20, 2018, to obtain all the records evaluating the association between the rs2276466 polymorphism and the risk of all types of cancers. We used the odds ratio (OR) as a measure of effect, and pooled the data in a Mantel-Haenszel weighed random-effects meta-analysis to provide a summary estimate of the impact of this polymorphism on gastrointestinal cancer, neurogenic cancer and other cancers (breast cancer and SCCHN). All the analyses were carried out in STATA 14.1.11 case–control studies that consisted of 5730 cases and 6756 controls, were eventually included in our meta-analysis. The significant association was observed between the XPFrs2276466 polymorphism and neurogenic cancer susceptibility (recessive model: OR = 1.648, 95% CI = 1.294–2.098, P<0.001). Furthermore, no significant impact of this polymorphism was detected on decreased gastrointestinal cancer risk (dominant model: OR = 1.064, 95%CI = 0.961–1.177, P = 0.233). The rs2276466 polymorphism might play different roles in carcinogenesis of various cancer types. Current evidence did not suggest that this polymorphism was directly associated with gastrointestinal susceptibility. However, this polymorphism might contribute to increased neurogenic cancer risk. More preclinical and epidemiological studies are still imperative for further evaluation

Download Full-text

Association between PD-1 and PD-L1 Polymorphisms and the Risk of Cancer: A Meta-Analysis of Case-Control Studies

Cancers ◽

10.3390/cancers11081150 ◽

2019 ◽

Vol 11 (8) ◽

pp. 1150 ◽

Cited By ~ 11

Author(s):

Mohammad Hashemi ◽

Shima Karami ◽

Sahel Sarabandi ◽

Abdolkarim Moazeni-Roodi ◽

Andrzej Małecki ◽

...

Keyword(s):

Cell Death ◽

Cancer Risk ◽

Programmed Cell Death ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Case Control ◽

Case Control Studies ◽

Programmed Cell Death 1 ◽

Risk Of Cancer ◽

The Impact

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.

Download Full-text

Lack of Association between miR-605 rs2043556 Polymorphism and Overall Cancer Risk: A Meta-analysis of Case-control Studies

MicroRNA ◽

10.2174/2211536608666181204110508 ◽

2019 ◽

Vol 8 (2) ◽

pp. 94-100 ◽

Cited By ~ 3

Author(s):

Abdolkarim Moazeni-Roodi ◽

Saeid Ghavami ◽

Mohammad Hashemi

Keyword(s):

Cancer Risk ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Random Effect ◽

Random Effect Model ◽

Cancer Type ◽

Case Control Studies ◽

Tract Cancer ◽

Cancer Breast ◽

The Impact

Growing evidence propose an association between miRNA polymorphisms and cancer susceptibility. This study aimed to examine the impact of miR-605 rs2043556 polymorphism on cancer risk through a meta-analysis based on 3198 cancer cases and 4943 controls. Eligible studies were retrieved by searching Web of Science, PubMed, Scopus, and Google Scholar databases up to August 27, 2018. The pooled Odds Ratios (ORs) with 95% Confidence Intervals (CIs) were calculated using a random-effect model to estimate the strength of association between rs2043556 variant of miR-605 and cancer risk. Overall, no significant association was found between miR-605 rs2043556 polymorphism and cancer risk in heterozygous codominant (OR=0.93, 95% CI=0.76-1.13, p=0.44, AG vs. AA), homozygous codominant (OR=1.01, 95%CI=0.78-1.30, p=0.94, GG vs. AA), dominant (OR=0.95, 95% CI=0.79-1.13, p=0.55, AG+GG vs. AA), recessive (OR=1.07, 95%CI=0.84-1.38, p=0.57, GG vs. AG+AA), overdominant (OR=0.93, 95% CI=0.76-1.12, p=0.43, AG vs. GG+AA), and allele (OR=0.98, 95% CI=0.87-1.10, p=0.73, G vs. A) genetic models tested. Stratified analysis by cancer type revealed that the rs2043556 variant was not associated with digestive tract cancer, breast cancer, gastric cancer as well as lung cancer. </P><P> Taken together, the findings of this meta-analysis did not support an association between miR-605 rs2043556 polymorphism and cancer susceptibility.

Download Full-text

Association of miRNA biosynthesis genes DROSHA and DGCR8 polymorphisms with cancer susceptibility: a systematic review and meta-analysis

Bioscience Reports ◽

10.1042/bsr20180072 ◽

2018 ◽

Vol 38 (3) ◽

Cited By ~ 4

Author(s):

Jing Wen ◽

Zhi Lv ◽

Hanxi Ding ◽

Xinxin Fang ◽

Mingjun Sun

Keyword(s):

Cancer Risk ◽

Genetic Model ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Population Based ◽

Nucleotide Polymorphisms ◽

Case Control Studies ◽

Exclusion Criteria ◽

Single Nucleotide ◽

Stratified Analysis

Single nucleotide polymorphisms (SNPs) in miRNA biosynthesis genes DROSHA and DGCR8 were indicated to be correlated with cancer risk. We comprehensively reviewed and analyzed the effect of DROSHA and DGCR8 polymorphisms on cancer risk. Eligible articles were selected according to a series of inclusion and exclusion criteria. Consequently, ten case–control studies (from nine citations) with 4265 cancer cases and 4349 controls were involved in a meta-analysis of seven most prevalent SNPs (rs10719 T/C, rs6877842 G/C, rs2291109 A/T, rs642321 C/T, rs3757 G/A, rs417309 G/A, rs1640299 T/G). Our findings demonstrated that the rs417309 SNP in DGCR8 was significantly associated with an elevated risk of overall cancer in every genetic model. In stratified analysis, correlations of DROSHA rs10719 and rs6877842 SNPs were observed in Asian and laryngeal cancer subgroups, respectively. Moreover, associations of the rs417309 SNP could also be found in numerous subgroups including: Asian and Caucasian population subgroups; laryngeal and breast cancer subgroups; population-based (PB) and hospital-based (HB) subgroups. In conclusion, the DROSHA rs10719, rs6877842 SNPs, and DGCR8 rs417309 SNP play pivotal roles in cancerogenesis and may be potential biomarkers for cancer-forewarning.

Download Full-text

The association of FOXP3 gene polymorphisms with cancer susceptibility: a comprehensive systemic review and meta-analysis

Bioscience Reports ◽

10.1042/bsr20181809 ◽

2019 ◽

Vol 39 (3) ◽

Author(s):

Yan Chen ◽

Xiaoxue Qi ◽

Ce Bian ◽

Chen Ling ◽

Tao Yi ◽

...

Keyword(s):

Gene Polymorphisms ◽

Chinese Population ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Systemic Review ◽

Cancer Type ◽

Case Control Studies ◽

Foxp3 Gene ◽

Cancer Types ◽

Risk Of Cancer

Abstract The role of forkhead box P3 (FOXP3) protein in tumorigenesis has long been controversial and existing data on the association between FOXP3 gene polymorphisms and cancer susceptibility were inconsistent. Here, we conducted a meta-analysis to better clarify the relationship. A comprehensive search of studies published from July 2008 to June 2018 was conducted. The statistical analyses of the pooled odds ratios (ORs) and the corresponding 95% confidence intervals (95% CIs) were performed using the Revman 5.2 software. A total of 12 articles with 19 case–control studies and 10389 participants were included. Three FOXP3 polymorphisms and six cancer types were evaluated. While no significant results were observed in overall and breast cancer groups for rs3761548 (A/C) polymorphisms, the pooled data showed an elevated risk of cancer in variant AA genotypes and A allele for Chinese population (AA vs. AC+CC: OR = 1.61, 95% CI = 1.09, 2.39; AA vs. CC: OR = 1.74, 95% CI = 1.05, 2.89; A vs. C: OR = 1.34, 95% CI = 1.00, 1.78). Neither the overall group analyses nor the subgroup analyses stratified by cancer type and ethnicity proposed any significant association of rs2280883 (C/T) and rs3761549 (T/C) polymorphisms with cancer susceptibility. This meta-analysis suggested that FOXP3 rs3761548 (A/C) polymorphisms were associated with increased cancer risk in Chinese population while rs2280883 (C/T) and rs3761549 (T/C) polymorphisms were not. More large-sample researches with diverse ethnicities and cancer types are needed to draw a concrete conclusion.

Download Full-text

ASSOCIATION OF INTERLEUKIN-10 -1082 A/G (RS1800896) POLYMORPHISM WITH SUSCEPTIBILITY TO GASTRIC CANCER: META-ANALYSIS OF 6,101 CASES AND 8,557 CONTROLS

Arquivos de Gastroenterologia ◽

10.1590/s0004-2803.201800000-18 ◽

2018 ◽

Vol 55 (1) ◽

pp. 33-40 ◽

Cited By ~ 13

Author(s):

Abolfazl NAMAZI ◽

Mohammad FORAT-YAZDI ◽

Mohammadali JAFARI ◽

Soudabeh FARAHNAK ◽

Rezvan NASIRI ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Risk ◽

Web Of Science ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Interleukin 10 ◽

Dominant Model ◽

Gastric Cancer Risk ◽

Case Control Studies ◽

Allele Model

ABSTRACT BACKGROUND: The promoter -1082 A/G (rs1800896) polymorphism of Interleukin-10 (IL-10) gene have been widely reported and considered to have a significant role on gastric cancer risk, but the results are inconsistent. OBJECTIVE: To clarify the association, we conducted a meta-analysis to investigate the associations IL-10 -1082 A/G polymorphism with gastric cancer. METHODS: Eligible articles were identified by searching databases including PubMed, Web of Science, and Google Scholar up to August 03, 2017. Odds ratios (OR) with corresponding 95% confidence intervals (CIs) were used to assess the association. RESULTS: A total of 30 case-control studies with 6,101 cases and 8,557 controls were included in this meta-analysis. Overall, a significant association between IL-10 -1082 A/G polymorphism and gastric cancer risk was observed under the allele model (G vs A: OR=1.305, 95% CI=1.076-1.584; P=0.007), heterozygote model and (GA vs AA: OR=1.252, 95% CI=1.252-1.054; P=0.011) and dominant model (GG+GA vs AA: OR=1.264, 95% CI=1.053-1.516; P=0.012). In the subgroup analysis by ethnicity, increased gastric cancer risk were found in Asians under the allele model (G vs A: OR=1.520, 95% CI=1.172-1.973; P=0.002), homozygote model (GG+GA vs AA: OR=1.571, 95% CI=1.023-2.414; P= 0.039), heterozygote model (GA vs AA: OR=1.465, 95% CI=1.192-1.801; P≤0.001) and dominant model (GG+GA vs AA: OR=1.448, 95% CI=1.152-1.821; P=0.002), but not among Caucasian and Latinos populations. CONCLUSION: These results suggested that the IL-10 -1082 A/G (rs1800896) polymorphism might contribute to the gastric cancer susceptibility, especially among Asians.

Download Full-text

Does miR-618 rs2682818 variant affect cancer susceptibility? Evidence from 10 case–control studies

Bioscience Reports ◽

10.1042/bsr20190741 ◽

2019 ◽

Vol 39 (8) ◽

Cited By ~ 1

Author(s):

Xingliang Feng ◽

Dan Ji ◽

Chaozhao Liang ◽

Song Fan

Keyword(s):

Breast Cancer ◽

Cancer Risk ◽

Structure Prediction ◽

Genetic Model ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Case Control Studies ◽

Stem Loop ◽

Contrast Model ◽

Pooled Data

Abstract Piles of evidence have supported the relationship between miR-618 rs2682818 polymorphism and tumorigenesis, but the conclusion remains inconsistent. In the present study, we conducted a meta-analysis to sniff out the potential risk between miR-618 rs2682818 and overall cancers. Crude odds ratios (ORs) and 95% confidence intervals (CIs) analyzed by Z-test were employed to estimate the potential interrelation in five genetic models. We also prospected how the rs2682818 affects the second structure of miR-618. Finally, 10 independent studies meet the enrolled criteria, along with 4099 cancer cases and 5057 healthy controls. Overall, no exceeding interrelation was sniffed out in the pooled data among five inherited models, as well as stratified analyses. Whereas, the enhanced cancer risk of miR-618 rs2682818 variant stratified by breast cancer was revealed, in heterozygote genetic model (AC vs. CC: OR = 1.291, 95%CI = 1.012–1.648, P = 0.040) and dominant contrast model (AA + AC vs. CC: OR = 1.280, 95%CI = 1.009–1.623, P = 0.042). The second structure prediction result shown that the mutant A allele might change the first stem-loop of miR-618, and the free energy of it would turn from –39.1 to –35.1 kcal/mol. All in all, our meta-analysis had successfully chased down that miR-618 rs2682818 polymorphism is not linked with overall cancer risk, but in the dominant genotype of breast cancer.

Download Full-text

Association between apurinic/apyrimidinic endonuclease 1 rs1760944 T>G polymorphism and susceptibility of cancer: a meta-analysis involving 21764 subjects

Bioscience Reports ◽

10.1042/bsr20190866 ◽

2019 ◽

Vol 39 (12) ◽

Cited By ~ 1

Author(s):

Guowen Ding ◽

Yu Chen ◽

Huiwen Pan ◽

Hao Qiu ◽

Weifeng Tang ◽

...

Keyword(s):

Cancer Risk ◽

Publication Bias ◽

Protective Factor ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Pooled Analysis ◽

Case Control ◽

Current Evidence ◽

Case Control Studies ◽

Risk Of Cancer

Abstract Background: Previous case–control studies have suggested that apurinic/apyrimidinic endonuclease 1 (APE1) rs1760944 T>G polymorphism may be associated with cancer risk. Here, we carried out an updated meta-analysis to focus on the correlation between APE1 rs1760944 T>G locus and the risk of cancer. Methods: We used the crude odds ratios (ORs) with their 95% confidence intervals (CIs) to evaluate the possible relationship between the APE1 rs1760944 T>G polymorphism and cancer risk. Heterogeneity, publication bias and sensitivity analysis were also harnessed to check the potential bias of the present study. Results: Twenty-three independent studies involving 10166 cancer cases and 11598 controls were eligible for this pooled analysis. We found that APE1 rs1760944 T>G polymorphism decreased the risk of cancer in four genetic models (G vs. T: OR, 0.87; 95% CI, 0.83–0.92; P<0.001; GG vs. TT: OR, 0.77; 95% CI, 0.69–0.86; P<0.001; GG/TG vs. TT: OR, 0.83; 95% CI, 0.77–0.89, P<0.001 and GG vs. TT/TG: OR, 0.85; 95% CI, 0.80–0.92, P<0.001). Results of subgroup analyses also demonstrated that this single-nucleotide polymorphism (SNP) modified the risk among lung cancer, breast cancer, osteosarcoma, and Asians. Evidence of publication bias was found in the present study. When we treated the publication bias with ‘trim-and-fill’ method, the adjusted ORs and CIs were not significantly changed. Conclusion: In conclusion, current evidence highlights that the APE1 rs1760944 T>G polymorphism is a protective factor for cancer susceptibility. In the future, case–control studies with detailed risk factors are needed to confirm or refute our findings.

Download Full-text

Association between interleukin-10 -592 A/C polymorphism and gastrointestinal tract cancer risk: A meta-analysis

The International Journal of Biological Markers ◽

10.1177/1724600817747525 ◽

2018 ◽

Vol 33 (3) ◽

pp. 244-253 ◽

Cited By ~ 1

Author(s):

Mohammad Hossein Sahami-Fard

Keyword(s):

Gastrointestinal Tract ◽

Cancer Risk ◽

Cancer Susceptibility ◽

Meta Analysis ◽

Interleukin 10 ◽

Cancer Type ◽

Case Control Studies ◽

China National Knowledge Infrastructure ◽

Tract Cancer ◽

Gastrointestinal Tract Cancer

Background: Recent evidence suggests that -592 A/C polymorphism in the interleukin-10 (IL-10) gene may influence risk of gastrointestinal tract cancer; however, individual studies have provided conflicting and inconclusive results. Therefore, this meta-analysis was conducted to assess the association between IL-10 -592 A/C polymorphism and gastrointestinal tract cancer susceptibility. Methods: EMBASE, PubMed, Web of Science, and China National Knowledge Infrastructure databases were searched for case-control studies published before 1 May 2017. A total of 36 studies involving 8069 cases and 13,089 controls were included in the present meta-analysis according to the inclusion criteria. The random- or fixed-effect model was utilized to calculate pooled odds ratio (OR) with 95% confidence interval (CI), and to survey the association. Results: By and large IL-10 -592 A/C (rs1800872) polymorphism was not associated with gastrointestinal cancer risk in five genetic models (A vs. C: OR 1.00; 95% CI 0.93, 1.08; POR = 0.960; AA vs. CC: OR 0.98; 95% CI 0.85, 1.14; POR = 0.835; CA vs. CC: OR 1.01; 95% CI 0.94, 1.08; POR = 0.776; AA+CA vs. CC: OR 1.03; 95% CI 0.94, 1.12; POR = 0.592; AA vs. CA+CC: OR 0.98; 95% CI 0.87, 1.10; POR = 0.666). Similar results were also achieved after stratification by the Hardy–Weinberg equilibrium, ethnicity, source of controls, and cancer type. Conclusion: The results of this meta-analysis indicated that there is no association between the IL-10 -592 A/C promoter polymorphism and gastrointestinal tract cancer susceptibility.

Download Full-text