scholarly journals Meta-analysis of gene-environment interaction: joint estimation of SNP and SNP × environment regression coefficients

2010 ◽  
Vol 35 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Alisa K. Manning ◽  
Michael LaValley ◽  
Ching-Ti Liu ◽  
Kenneth Rice ◽  
Ping An ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Joint Estimation ◽  
Regression Coefficients ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment

scholarly journals Effect of polygenic risk scores on depression in childhood trauma

2014 ◽  
Vol 205 (2) ◽  
pp. 113-119 ◽  
Author(s):  
Wouter J. Peyrot ◽  
Yuri Milaneschi ◽  
Abdel Abdellaoui ◽  
Patrick F. Sullivan ◽  
Jouke J. Hottenga ◽  
...  
Keyword(s):  
Childhood Trauma ◽  
Meta Analysis ◽  
Genetic Effect ◽  
Risk Scores ◽  
Environment Interaction ◽  
Polygenic Risk ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Genome Wide ◽  
Direct Genetic Effect

BackgroundResearch on gene×environment interaction in major depressive disorder (MDD) has thus far primarily focused on candidate genes, although genetic effects are known to be polygenic.AimsTo test whether the effect of polygenic risk scores on MDD is moderated by childhood trauma.MethodThe study sample consisted of 1645 participants with a DSM-IV diagnosis of MDD and 340 screened controls from The Netherlands. Chronic or remitted episodes (severe MDD) were present in 956 participants. The occurrence of childhood trauma was assessed with the Childhood Trauma Interview and the polygenic risk scores were based on genome-wide meta-analysis results from the Psychiatric Genomics Consortium.ResultsThe polygenic risk scores and childhood trauma independently affected MDD risk, and evidence was found for interaction as departure from both multiplicativity and additivity, indicating that the effect of polygenic risk scores on depression is increased in the presence of childhood trauma. The interaction effects were similar in predicting all MDD risk and severe MDD risk, and explained a proportion of variation in MDD risk comparable to the polygenic risk scores themselves.ConclusionsThe interaction effect found between polygenic risk scores and childhood trauma implies that (1) studies on direct genetic effect on MDD gain power by focusing on individuals exposed to childhood trauma, and that (2) individuals with both high polygenic risk scores and exposure to childhood trauma are particularly at risk for developing MDD.

scholarly journals Characterization of 9p24 Risk Locus and Colorectal Adenoma and Cancer: Gene–Environment Interaction and Meta-Analysis

2010 ◽  
Vol 19 (12) ◽  
pp. 3131-3139 ◽  
Author(s):  
Jonathan D. Kocarnik ◽  
Carolyn M. Hutter ◽  
Martha L. Slattery ◽  
Sonja I. Berndt ◽  
Li Hsu ◽  
...  
Keyword(s):  
Colorectal Adenoma ◽  
Meta Analysis ◽  
Environment Interaction ◽  
Cancer Gene ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Risk Locus

scholarly journals Role of the Common PRSS1-PRSS2 Haplotype in Alcoholic and Non-Alcoholic Chronic Pancreatitis: Meta- and Re-Analyses

Genes ◽  
2020 ◽  
Vol 11 (11) ◽  
pp. 1349
Author(s):  
Anthony F. Herzig ◽  
Emmanuelle Génin ◽  
David N. Cooper ◽  
Emmanuelle Masson ◽  
Claude Férec ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Risk Allele ◽  
Genetic Model ◽  
Meta Analysis ◽  
Risk Haplotype ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Alcoholic Chronic Pancreatitis ◽  
Gene Environment ◽  
Association Data

The association between a common PRSS1-PRSS2 haplotype and alcoholic chronic pancreatitis (ACP), which was revealed by the first genome-wide association study of chronic pancreatitis (CP), has been consistently replicated. However, the association with non-ACP (NACP) has been controversial. Herein, we sought to clarify this basic issue by means of an allele-based meta-analysis of currently available studies. We then used studies informative for genotype distribution to explore the biological mechanisms underlying the association data and to test for gene-environment interaction between the risk haplotype and alcohol consumption by means of a re-analysis. A literature search was conducted to identify eligible studies. A meta-analysis was performed using the Review Manager software. The association between the risk genotypes and NACP or ACP was tested for the best-fitting genetic model. Gene-environment interaction was estimated by both case-only and multinomial approaches. Five and eight studies were employed for the meta-analysis of ACP and NACP findings, respectively. The risk allele was significantly associated with both ACP (pooled odds ratio (OR) 1.67, 95% confidence interval (CI) 1.56–1.78; p < 0.00001) and NACP (pooled OR 1.28, 95% CI 1.17–1.40; p < 0.00001). Consistent with a dosage effect of the risk allele on PRSS1/PRSS2 mRNA expression in human pancreatic tissue, both ACP and NACP association data were best explained by an additive genetic model. Finally, the risk haplotype was found to interact synergistically with alcohol consumption.

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.

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 Role of the common PRSS1-PRSS2 haplotype in alcoholic and non-alcoholic chronic pancreatitis: meta- and re-analyses

2020 ◽  
Author(s):  
Anthony F. Herzig ◽  
Emmanuelle Génin ◽  
David N. Cooper ◽  
Emmanuelle Masson ◽  
Claude Férec ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Risk Allele ◽  
Genetic Model ◽  
Meta Analysis ◽  
Risk Haplotype ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Alcoholic Chronic Pancreatitis ◽  
Gene Environment ◽  
Association Data

AbstractThe association between a common PRSS1-PRSS2 haplotype and alcoholic chronic pancreatitis (ACP), which was revealed by the first genome-wide association study of chronic pancreatitis (CP), has been consistently replicated. However, the association with non-ACP (NACP) has been controversial. Herein, we sought to clarify this basic issue by means of an allele-based meta-analysis of currently available studies. We then used studies informative for genotype distribution to explore the biological mechanisms underlying the association data and to test for gene-environment interaction between the risk haplotype and alcohol consumption by means of a re-analysis. A literature search was conducted to identify eligible studies. Meta-analysis was performed using the Review Manager software. The association between the risk genotypes and NACP or ACP was tested for the best-fitting genetic model. Gene-environment interaction was estimated by both case-only and multinomial approaches. Five and eight studies were employed for the meta-analysis of ACP and NACP findings, respectively. The risk allele was significantly associated with both ACP (pooled OR 1.67, 95% CI 1.56–1.78; P<0.00001) and NACP (pooled OR 1.28, 95% CI 1.17–1.40; P<0.00001). Consistent with a dosage effect of the risk allele on PRSS1/PRSS2 mRNA expression in human pancreatic tissue, both ACP and NACP association data were best explained by an additive genetic model. Finally, the risk haplotype was found to interact synergistically with ACP.

scholarly journals Gene Expression Meta-Analysis of Cerebellum Samples Supports the FKBP5 Gene-Environment Interaction Model for Schizophrenia

Life ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 190
Author(s):  
Libi Hertzberg ◽  
Ada H Zohar ◽  
Assif Yitzhaky
Keyword(s):  
Gene Expression ◽  
Differential Expression ◽  
Meta Analysis ◽  
Expression Patterns ◽  
Interaction Model ◽  
Childhood Adversity ◽  
Brain Regions ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment

Background: One of the most studied molecular models of gene-environment interactions is that of FKBP5, which has been shown to interact with childhood adversity to increase the risk of psychiatric disorders, and has been implicated in schizophrenia. While the model predicts up-regulation of FKBP5, previous brain samples gene expression studies yielded inconsistent results. Methods: We performed a systematic gene expression meta-analysis of FKBP5 and NR3C1, a glucocorticoid receptor inhibited by FKBP5, in cerebellum samples of patients with schizophrenia. The gene expression databases GEO, SMRI and those of NIMH were searched, and out of six screened datasets, three were eligible for the meta-analysis (overall 69 with schizophrenia and 78 controls). Results: We detected up-regulation of FKBP5 and down-regulation of NR3C1 in schizophrenia, and a negative correlation between their expression patterns. Correlation analysis suggested that the detected differential expression did not result from potential confounding factors. Conclusions: Our results give significant support to the FKBP5 gene-environment interaction model for schizophrenia, which provides a molecular mechanism by which childhood adversity is involved in the development of the disorder. To explore FKBP5’s potential as a therapeutic target, a mapping of its differential expression patterns in different brain regions of schizophrenia patients is needed.

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