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BioMed Research International
Volume 2015, Article ID 263864, 7 pages
Research Article

Ethnic-Specific Genetic Association of Variants in the Corticotropin-Releasing Hormone Receptor 1 Gene with Nicotine Dependence

1State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Zhejiang University School of Medicine, Hangzhou 310009, China
2Department of Public Health Sciences, University of Virginia, Charlottesville, VA 22908, USA
3Department of Otolaryngology and Communicative Sciences, ACT Center for Tobacco Treatment, Education and Research, University of Mississippi Medical Center, Jackson, MS 39213, USA
4Department of Psychiatry and Neurobehavioral Sciences, University of Virginia, Charlottesville, VA 22904, USA

Received 23 September 2014; Accepted 5 January 2015

Academic Editor: Xueyuan Cao

Copyright © 2015 Xiujun Tang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Twin and family studies indicate that smoking addiction is highly influenced by genetic factors. Variants in the corticotropin-releasing hormone receptor 1 (CRHR1) gene have been associated with alcoholism and depression. In this study, we tested five single nucleotide polymorphisms (SNPs) in CRHR1 for their association with ND, which was assessed by smoking quantity (SQ), the Heaviness of Smoking Index (HSI), and the Fagerström test for ND (FTND) in 2,037 subjects from 602 families of either European American (EA) or African American (AA) ancestry. Association analysis of the five SNPs revealed a significant association of rs171440 with SQ in the AA sample and with SQ and FTND in the pooled AA and EA samples. Haplotype-based association analysis indicated significant association of haplotypes C-C (56.9%) and T-C (38.9%), formed by SNPs rs171440 and rs1396862, with SQ in the AA sample, C-C-G (47.6%) with SQ, and T-C-G (42.3%), formed by SNPs rs171440, rs1396862, and rs878886, with SQ and FTND in the pooled AA and EA samples. However, none of these associations remained significant after correction for multiple testing. Together, our results provide suggestive evidence for the involvement of CRHR1 in ND, which warrants further investigation using larger independent samples.