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

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1150 ◽  
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.

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

PLoS ONE ◽  
2016 ◽  
Vol 11 (3) ◽  
pp. e0152448 ◽  
Author(s):  
Wenjing Dong ◽  
Mancheng Gong ◽  
Zhirong Shi ◽  
Jianjun Xiao ◽  
Junkai Zhang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Risk ◽  
Programmed Cell Death ◽  
Meta Analysis ◽  
Case Control ◽  
Case Control Studies ◽  
Programmed Cell Death 1

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

2019 ◽  
Vol 39 (12) ◽  
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.

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

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

scholarly journals Association between TP53 codon 72 G>C Polymorphism and Thyroid Carcinoma Risk: An Up-to-Date Meta-Analysis

2016 ◽  
Vol 1 (4) ◽  
pp. 89-95
Author(s):  
Jamal Jafari Nedooshan ◽  
Mohammad Forat Yazdi ◽  
Hossein Neamatzadeh ◽  
Masoud Zare Shehneh ◽  
Saeed Kargar ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cancer Risk ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Case Control ◽  
Case Control Studies ◽  
P53 Codon 72 ◽  
Codon 72 ◽  
Thyroid Cancer Risk ◽  
Carcinoma Risk

Objective: Many published data on the association between p53 codon 72 G>C polymorphism and thyroid carcinoma risk showed inconclusive results. The aim this study was to assess the association between p53 codon 72 G>C polymorphism and thyroid cancer risk. Methods: A literature search of PubMed, EMBASE, Google scholar and Web of Science databases for case–control studies examining the association between p53 codon 72 G>C polymorphism and thyroid cancer susceptibility up October 2016 was performed. Odds ratios (OR) with 95 % confidence intervals (95 % CI) were used to assess the strength of the association. Results: A total of 12 case–control studies involving 2,062 thyroid cancer patients and 3,027 controls were included. There was a significant association between the p53 codon 72 G>C polymorphism and thyroid cancer susceptibility in the overall populations under homozygote (CC vs. GG: OR = 1.18, 95% CI 1.12-3.05, P = 0.01) and recessive model (CC vs. GC+GG: OR = 1.73, 95% CI 1.16-2.59, P = 0.007). Subgroup analysis by ethnicity showed that there was no significant association between p53 codon 72 G>C polymorphism and thyroid cancer risk in Caucasians, Asians and mixed Brazilian. No significant publication bias was observed by using Begg’s funnel plot and Egger’s test. Conclusion: Present meta-analysis indicated that the p53 codon 72 G>C polymorphism may be associated with thyroid cancer risk. However, more studies with large sample size are needed to further assess the associations.

Analysis of the Association of Matrix Metalloproteinase-1 Gene Promoter (rs1799750) Polymorphism and Risk of Ovarian Cancer

2015 ◽  
Vol 25 (6) ◽  
pp. 961-967 ◽  
Author(s):  
Lijie Wang ◽  
Beihua Kong
Keyword(s):  
Ovarian Cancer ◽  
Cancer Risk ◽  
Matrix Metalloproteinase ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Gene Promoter ◽  
Case Control ◽  
Ovarian Cancer Risk ◽  
Case Control Studies ◽  
Matrix Metalloproteinase 1

ObjectiveStudies investigating the association betweenmatrix metalloproteinase-1(MMP1) gene promoter 1607–base pair (bp) polymorphism and ovarian cancer risk have yielded conflicting results.MethodsWe therefore carried out a meta-analysis of 754 ovarian cancer cases and 1184 controls from 5 published case-control studies. The strength of the association betweenMMP11607-bp polymorphism and ovarian cancer susceptibility was calculated using pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs).ResultsThe results suggest that no statistically significant associations exist betweenMMP11607-bp polymorphisms and ovarian cancer risk in all 4 genetic models (2G2G vs 1G1G: OR, 1.08; 95% CI, 0.81–1.43;P= 0.23; 1G2G vs 1G1G: OR, 1.06; 95% CI, 0.82–1.36;P= 0.15; 1G2G + 2G2G vs 1G1G: OR, 1.05; 95% CI, 0.83–1.34;P= 0.16; 2G2G vs 1G1G + 1G2G: OR, 0.98; 95% CI, 0.80–1.20;P= 0.84).ConclusionsIn summary, this meta-analysis showed that theMMP11607-bp polymorphism is not associated with ovarian cancer risk.

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

Medicina ◽  
2019 ◽  
Vol 55 (8) ◽  
pp. 425 ◽  
Author(s):  
Moazeni-Roodi ◽  
Tabasi ◽  
Ghavami ◽  
Hashemi
Keyword(s):  
Cancer Risk ◽  
Cancer Susceptibility ◽  
Meta Analysis ◽  
Genetic Models ◽  
Case Control Studies ◽  
Study Population ◽  
Cancer Types ◽  
The Impact ◽  
Strength Of Association

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.

scholarly journals Exposure to Secondhand Smoke and Risk of Cancer in Never Smokers: A Meta-Analysis of Epidemiologic Studies

2018 ◽  
Vol 15 (9) ◽  
pp. 1981 ◽  
Author(s):  
A-Sol Kim ◽  
Hae-Jin Ko ◽  
Jin-Hyun Kwon ◽  
Jong-Myung Lee
Keyword(s):  
Breast Cancer ◽  
Cancer Risk ◽  
Secondhand Smoke ◽  
Meta Analysis ◽  
Case Control ◽  
Case Control Studies ◽  
Prospective Cohort Studies ◽  
Never Smokers ◽  
Risk Of Cancer ◽  
Exposure To Secondhand Smoke

This is first meta-analysis to evaluate cancer risk associated with secondhand smoking across all cancers. A literature search was conducted for articles published before June 2014 on Pubmed, SCOPUS, Cochrane library, and CINAHL, and 40 articles on secondhand smoke and the prevalence of cancer among never smokers were selected for final analysis as per the inclusion criteria. Of the 40 articles, 27 were case-control studies and 13 were prospective cohort studies. With respect to overall cancer risk, odds ratio (OR) involving never smokers with significant exposure to secondhand smoke compared to never smokers without such exposure was 1.163 (95%CI 1.058–1.279). Subgroup meta-analyses by study design showed significant positive associations for both case-control studies and prospective cohort studies (OR 1.165, 95%CI 1.029–1.320; and OR 1.160, 95%CI 1.002–1.343, respectively). The association was stronger in the case of females (OR 1.253, 95%CI 1.142–1.374), lung cancer (OR 1.245, 95%CI 1.026–1.511), and breast cancer (OR 1.235, 95%CI 1.102–1.385). Secondhand smoking may increase the overall risk of cancer for never smokers, particularly lung and breast cancer, and especially in women. Strict implementation of smoking cessation programs should be encouraged, not only to reduce active smoking but also to limit exposure to secondhand smoke.

scholarly journals The Association between PON1 (Q192R and L55M) Gene Polymorphisms and Risk of Cancer: A Meta-Analysis Based on 43 Studies

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Xiaolan Pan ◽  
Lei Huang ◽  
Meiqin Li ◽  
Dan Mo ◽  
Yihua Liang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Risk ◽  
Gene Polymorphisms ◽  
Meta Analysis ◽  
Population Based ◽  
Case Control ◽  
Cancer Type ◽  
Case Control Studies ◽  
Increased Risk ◽  
Risk Of Cancer

Q192R and L55M polymorphism were considered to be associated with the development of multiple cancers. Nevertheless, the results of these researches were inconclusive and controversial. Therefore, we conducted a meta-analysis of all eligible case-control studies to assess the association between PON1 (Q192R and L55M) gene polymorphisms and risk of cancer. With the STATA 14.0 software, we evaluated the strength of the association by using the odds ratios (ORs) and 95% confidence intervals (CIs). A total of 43 case-control publications 19887 cases and 23842 controls were employed in our study. In all genetic models, a significant association between PON1-L55M polymorphisms and overall cancer risk was observed. Moreover, in the stratified analyses by cancer type, polymorphism of PON1-L55M played a risk factor in the occurrence of breast cancer, hematologic cancer, and prostate cancer. Similarly, an increased risk was observed in the Caucasian and Asian population as well as hospital-based group and population-based group. For PON1-Q192R polymorphisms, in the stratified analyses by cancer type, PON1-Q192R allele was associated with reduced cancer risks in breast cancer. Furthermore, for racial stratification, there was a reduced risk of cancer in recession model in Caucasian population. Similarly, in the stratification analysis of control source, the overall risk of cancer was reduced in the heterozygote comparison and dominant model in the population-based group. In conclusion, PON1-Q192R allele decreased the cancer risk especially breast cancer; there was an association between PON1-L55M allele and increased overall cancer risk. However, we need a larger sample size, well-designed in future and at protein levels to confirm these findings.

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

MicroRNA ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 94-100 ◽  
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.

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