Literature DB >> 31294817

Genome-Wide Meta-Analyses of FTND and TTFC Phenotypes.

Jingchun Chen1, Anu Loukola2,3, Nathan A Gillespie4, Roseann Peterson4, Peilin Jia5, Brien Riley4, Hermine Maes4, Daniella M Dick6, Kenneth S Kendler4, M Imad Damaj7, Michael F Miles7, Zhongming Zhao5, Ming D Li8, Jacqueline M Vink9,10, Camelia C Minica9,11,12, Gonneke Willemsen9,11,12, Dorret I Boomsma9,11,12, Beenish Qaiser2,3, Pamela A F Madden13, Tellervo Korhonen2,14, Pekka Jousilahti15, Jenni Hällfors3, Joel Gelernter16, Henry R Kranzler17, Richard Sherva18, Lindsay Farrer18, Brion Maher19, Michael Vanyukov20, Michelle Taylor21, Jenifer J Ware21, Marcus R Munafò21, Sharon M Lutz22, John E Hokanson22, Fangyi Gu23, Maria T Landi23, Neil E Caporaso23, Dana B Hancock24, Nathan C Gaddis25, Timothy B Baker26, Laura J Bierut13, Eric O Johnson24,27, Meghan Chenoweth28, Caryn Lerman29, Rachel Tyndale28, Jaakko Kaprio2,3, Xiangning Chen1,4,30.   

Abstract

INTRODUCTION: FTND (Fagerstrӧm test for nicotine dependence) and TTFC (time to smoke first cigarette in the morning) are common measures of nicotine dependence (ND). However, genome-wide meta-analysis for these phenotypes has not been reported.
METHODS: Genome-wide meta-analyses for FTND (N = 19,431) and TTFC (N = 18,567) phenotypes were conducted for adult smokers of European ancestry from 14 independent cohorts.
RESULTS: We found that SORBS2 on 4q35 (p = 4.05 × 10-8), BG182718 on 11q22 (p = 1.02 × 10-8), and AA333164 on 14q21 (p = 4.11 × 10-9) were associated with TTFC phenotype. We attempted replication of leading candidates with independent samples (FTND, N = 7010 and TTFC, N = 10 061), however, due to limited power of the replication samples, the replication of these new loci did not reach significance. In gene-based analyses, COPB2 was found associated with FTND phenotype, and TFCP2L1, RELN, and INO80C were associated with TTFC phenotype. In pathway and network analyses, we found that the interconnected interactions among the endocytosis, regulation of actin cytoskeleton, axon guidance, MAPK signaling, and chemokine signaling pathways were involved in ND.
CONCLUSIONS: Our analyses identified several promising candidates for both FTND and TTFC phenotypes, and further verification of these candidates was necessary. Candidates supported by both FTND and TTFC (CHRNA4, THSD7B, RBFOX1, and ZNF804A) were associated with addiction to alcohol, cocaine, and heroin, and were associated with autism and schizophrenia. We also identified novel pathways involved in cigarette smoking. The pathway interactions highlighted the importance of receptor recycling and internalization in ND. IMPLICATIONS: Understanding the genetic architecture of cigarette smoking and ND is critical to develop effective prevention and treatment. Our study identified novel candidates and biological pathways involved in FTND and TTFC phenotypes, and this will facilitate further investigation of these candidates and pathways.
© The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved.For permissions, please e-mail: journals.permissions@oup.com.

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Year:  2020        PMID: 31294817      PMCID: PMC7249921          DOI: 10.1093/ntr/ntz099

Source DB:  PubMed          Journal:  Nicotine Tob Res        ISSN: 1462-2203            Impact factor:   4.244


  63 in total

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