2017
DOI: 10.1038/mp.2017.193
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Genome-wide association study across European and African American ancestries identifies a SNP in DNMT3B contributing to nicotine dependence

Abstract: Cigarette smoking is a leading cause of preventable mortality worldwide. Nicotine dependence, which reduces the likelihood of quitting smoking, is a heritable trait with firmly established associations with sequence variants in nicotine acetylcholine receptor genes and at other loci. To search for additional loci, we conducted a genome-wide association study (GWAS) meta-analysis of nicotine dependence, totaling 38,602 smokers (28,677 Europeans/European Americans and 9,925 African Americans) across 15 studies. … Show more

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Cited by 83 publications
(105 citation statements)
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“…One approach to recover the so‐called “missing heritability” is to increase the sample size in order to obtain greater statistical power for the discovery of additional SNPs. The largest GWAS meta‐analysis of nicotine dependence reported so far (Hancock et al ., ) included 15 studies (38 602 smokers of both European and African descent), in which FTND scores were available for each study. In addition to confirming the well‐known associations of CHRNA5‐CHRNA3‐CHRNB4 genes and nicotine dependence, a novel association with the DNA methyltransferase, DNMT3B, was reported.…”
Section: Withdrawal and Dependencementioning
confidence: 99%
“…One approach to recover the so‐called “missing heritability” is to increase the sample size in order to obtain greater statistical power for the discovery of additional SNPs. The largest GWAS meta‐analysis of nicotine dependence reported so far (Hancock et al ., ) included 15 studies (38 602 smokers of both European and African descent), in which FTND scores were available for each study. In addition to confirming the well‐known associations of CHRNA5‐CHRNA3‐CHRNB4 genes and nicotine dependence, a novel association with the DNA methyltransferase, DNMT3B, was reported.…”
Section: Withdrawal and Dependencementioning
confidence: 99%
“…Conversion of h 2 g estimates from observed to 325 liability scale was performed assuming population prevalences of 0.159 and 0.111 for 326 AD in alcohol-exposed EU and AA individuals, respectively 3 . 327 328 Genetic correlation between AD and 42 traits from LD Hub 33 and other published 329 studies [34][35][36][37][38][39][40][41][42][43][44] was examined with the same unrelated EU meta-analysis (10,206 cases 330 and 28,480 controls) and precomputed European LD scores using LDSR. To avoid 331 increasing the multiple testing burden, redundant or highly-correlated phenotypes were 332 reduced by manually selecting the version of the phenotype with the greatest predicted 333 relevance to AD, largest sample size, or highest heritability (Supplementary 334 Information).…”
mentioning
confidence: 99%
“…Overall, the pattern of gene x gene interactions we evidenced in the AAO of daily smoking is supported by the biological function of the SNPs that are involved -considered both individually and under their interaction. It also highlighted gene expression regulation in the cerebellum, the role of which is increasingly recognized in addiction, to nicotine [49,50].…”
Section: Discussionmentioning
confidence: 99%