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3 results on '"P. Chiavacci"'

1. Erratum: A genome-wide association study of anorexia nervosa suggests a risk locus implicated in dysregulated leptin signaling

Author

Li, Dong, Chang, Xiao, Connolly, John J, Tian, Lifeng, Liu, Yichuan, Bhoj, Elizabeth J, Robinson, Nora, Abrams, Debra, Li, Yun R, Bradfield, Jonathan P, Kim, Cecilia E, Li, Jin, Wang, Fengxiang, Snyder, James, Lemma, Maria, Hou, Cuiping, Wei, Zhi, Guo, Yiran, Qiu, Haijun, Mentch, Frank D, Thomas, Kelly A, Chiavacci, Rosetta M, Cone, Roger, Li, Bingshan, Sleiman, Patrick A, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Price Foundation Collaborative Group, and Hakonarson, Hakon

Subjects
Biological Sciences, Mathematical Sciences, Genetics, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Price Foundation Collaborative Group
Abstract

A correction to this article has been published and is linked from the HTML version of this paper. The error has been fixed in the paper.

Published
2017

2. A genome-wide association study of anorexia nervosa suggests a risk locus implicated in dysregulated leptin signaling.

Author

Li, Dong, Chang, Xiao, Connolly, John J, Tian, Lifeng, Liu, Yichuan, Bhoj, Elizabeth J, Robinson, Nora, Abrams, Debra, Li, Yun R, Bradfield, Jonathan P, Kim, Cecilia E, Li, Jin, Wang, Fengxiang, Snyder, James, Lemma, Maria, Hou, Cuiping, Wei, Zhi, Guo, Yiran, Qiu, Haijun, Mentch, Frank D, Thomas, Kelly A, Chiavacci, Rosetta M, Cone, Roger, Li, Bingshan, Sleiman, Patrick A, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Price Foundation Collaborative Group, and Hakonarson, Hakon

Subjects
Eating Disorders Working Group of the Psychiatric Genomics Consortium, Price Foundation Collaborative Group
Abstract

We conducted a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently defined phenotype. Analysis of phenotypic variability led to the identification of a specific genetic risk factor that approached genome-wide significance (rs929626 in EBF1 (Early B-Cell Factor 1); P = 2.04 × 10-7; OR = 0.7; 95% confidence interval (CI) = 0.61-0.8) with independent replication (P = 0.04), suggesting a variant-mediated dysregulation of leptin signaling may play a role in AN. Multiple SNPs in LD with the variant support the nominal association. This demonstrates that although the clinical and etiologic heterogeneity of AN is universally recognized, further careful sub-typing of cases may provide more precise genomic signals. In this study, through a refinement of the phenotype spectrum of AN, we present a replicable GWAS signal that is nominally associated with AN, highlighting a potentially important candidate locus for further investigation.

Published
2017

3. A genome-wide association study of anorexia nervosa suggests a risk locus implicated in dysregulated leptin signaling

Author

Li, Dong, Chang, Xiao, Connolly, John J, Tian, Lifeng, Liu, Yichuan, Bhoj, Elizabeth J, Robinson, Nora, Abrams, Debra, Li, Yun R, Bradfield, Jonathan P, Kim, Cecilia E, Li, Jin, Wang, Fengxiang, Snyder, James, Lemma, Maria, Hou, Cuiping, Wei, Zhi, Guo, Yiran, Qiu, Haijun, Mentch, Frank D, Thomas, Kelly A, Chiavacci, Rosetta M, Cone, Roger, Li, Bingshan, Sleiman, Patrick A, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Price Foundation Collaborative Group, and Hakonarson, Hakon

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Prevention, Human Genome, Mental Health, Anorexia, Eating Disorders, Aetiology, 2.1 Biological and endogenous factors, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Price Foundation Collaborative Group
Abstract

We conducted a genome-wide association study (GWAS) of anorexia nervosa (AN) using a stringently defined phenotype. Analysis of phenotypic variability led to the identification of a specific genetic risk factor that approached genome-wide significance (rs929626 in EBF1 (Early B-Cell Factor 1); P = 2.04 × 10-7; OR = 0.7; 95% confidence interval (CI) = 0.61-0.8) with independent replication (P = 0.04), suggesting a variant-mediated dysregulation of leptin signaling may play a role in AN. Multiple SNPs in LD with the variant support the nominal association. This demonstrates that although the clinical and etiologic heterogeneity of AN is universally recognized, further careful sub-typing of cases may provide more precise genomic signals. In this study, through a refinement of the phenotype spectrum of AN, we present a replicable GWAS signal that is nominally associated with AN, highlighting a potentially important candidate locus for further investigation.

Published
2017

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