scholarly journals Meta-analysis of gene-environment interaction exploiting gene-environment independence across multiple case-control studies

2017 ◽  
Vol 36 (24) ◽  
pp. 3895-3909 ◽  
Author(s):  
Jason P. Estes ◽  
John D. Rice ◽  
Shi Li ◽  
Heather M. Stringham ◽  
Michael Boehnke ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Case Control ◽  
Environment Interaction ◽  
Case Control Studies ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Multiple Case

scholarly journals Case-Control Studies of Gene-Environment Interaction: Bayesian Design and Analysis

Biometrics ◽  
2009 ◽  
Vol 66 (3) ◽  
pp. 934-948 ◽  
Author(s):  
Bhramar Mukherjee ◽  
Jaeil Ahn ◽  
Stephen B. Gruber ◽  
Malay Ghosh ◽  
Nilanjan Chatterjee
Keyword(s):  
Case Control ◽  
Environment Interaction ◽  
Case Control Studies ◽  
Bayesian Design ◽  
Gene Environment Interaction ◽  
Gene Environment

scholarly journals Accounting for error due to misclassification of exposures in case–control studies of gene–environment interaction

2008 ◽  
Vol 27 (15) ◽  
pp. 2756-2783 ◽  
Author(s):  
Li Zhang ◽  
Bhramar Mukherjee ◽  
Malay Ghosh ◽  
Stephen Gruber ◽  
Victor Moreno
Keyword(s):  
Case Control ◽  
Environment Interaction ◽  
Case Control Studies ◽  
Gene Environment Interaction ◽  
Gene Environment

scholarly journals Robust Tests for Additive Gene-Environment Interaction in Case-Control Studies Using Gene-Environment Independence

2017 ◽  
Vol 187 (2) ◽  
pp. 366-377 ◽  
Author(s):  
Gang Liu ◽  
Bhramar Mukherjee ◽  
Seunggeun Lee ◽  
Alice W Lee ◽  
Anna H Wu ◽  
...  
Keyword(s):  
Case Control ◽  
Environment Interaction ◽  
Case Control Studies ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Additive Gene ◽  
Robust Tests

Oral Clefts, Maternal Smoking, and TGFA: A Meta-Analysis of Gene-Environment Interaction

2005 ◽  
Vol 42 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Joanna S. Zeiger ◽  
Terri H. Beaty ◽  
Kung-Yee Liang
Keyword(s):  
Logistic Regression ◽  
Maternal Smoking ◽  
Meta Analysis ◽  
Case Control ◽  
Environment Interaction ◽  
Oral Clefts ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Increased Risk ◽  
Polytomous Logistic Regression

Objective A meta-analysis was performed to examine the association among maternal cigarette smoking, infant genotype at the Taq1 site in the transforming growth factor α (TGFA) locus, and risk of nonsyndromic oral clefts, both cleft palate (CP) and cleft lip with or without cleft palate (CL/P). Design Five published case-control studies were included in the meta-analyis. Pooled Mantel-Haenszel odds ratios (OR) and 95% confidence intervals (CIs) were computed. Gene-environment interaction was also assessed by using the pooled data in a case-only analysis and polytomous logistic regression. Results Among nonsmoking mothers, there was no evidence of any increased risk for CP if the infant carried the TGFA Taq1 C2 allele. If the mother reported smoking, however, there was an overall increased risk for CP if the infant carried the C2 allele (ORsmokers = 1.95; 95% CI = 1.22 to 3.10). TGFA genotype did not increase risk to CL/P, regardless of maternal smoking status. Polytomous logistic regression revealed a significant overall smoking effect for CL/P (OR = 1.64, 95% CI = 1.33 to 2.02) and CP (OR = 1.42, 95% CI = 1.06 to 1.90). Conclusions While maternal smoking was a consistent risk factor for both CL/P and CP across all studies, the suggestive evidence for gene-environment interaction between the infant's genotype at the Taq1 marker in TGFA and maternal smoking was limited to CP. Furthermore, evidence for such gene-environment interaction was strongest in a case-control study drawn from a birth defect registry where infants with non-cleft defects served as controls.

Association Between Tfeb Gene Polymorphism, Gene–environment Interaction, and Fatty Liver Disease: a Case–control Study in China

2021 ◽  
Author(s):  
Chunbao Mo ◽  
Tingyu Mai ◽  
Jiansheng Cai ◽  
Haoyu He ◽  
Huaxiang Lu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Case Control Study ◽  
Case Control ◽  
Environment Interaction ◽  
Additive Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Control Study

Abstract Background: Fatty liver disease (FLD) is a serious public health problem that is rapidly increasing. Evidences indicated that the transcription factor EB (TFEB) gene may be involved in the pathophysiology of FLD; however, whether TEFB polymorphism is association with FLD remains unclear.Objectives: To explore the association among TFEB polymorphism, gene–environment interaction, and FLD and provide epidemiological evidence for clarifying the genetic factors of FLD.Methods: This study is a case–control study. Sequenom MassARRAY was applied in genotyping. Logical regression was used to analyze the association between TFEB polymorphism and FLD, and the gene–environment interaction in FLD was evaluated by multiplication and additive interaction models.Results: (1) The alleles and genotypes of each single nucleotide polymorphism of TFEB in the case and control groups were evenly distributed; no statistically substantial difference was observed. (2) Logistic regression analysis indicated that TFEB polymorphism is not remarkably associated with FLD. (3) In the multiplicative interaction model, rs1015149, rs1062966, and rs11754668 had remarkable interaction with smoking amount. Rs1062966 and rs11754668 also had a considerable interaction with body mass index and alcohol intake, respectively. However, no remarkable additive interaction was observed.Conclusion: TFEB polymorphism is not directly associated with FLD susceptibility, but the risk can be changed through gene–environment interaction.

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