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Wan, Emily

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Wan

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Emily

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Wan, Emily

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Author's Publications: search.filters.isAuthorOfPublication.010cde33-a4b4-4587-8392-5ffe58d7d25d

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    A Genome-wide analysis of the response to inhaled beta2-agonists in Chronic Obstructive Pulmonary Disease
    (2015) Hardin, Megan; Cho, Michael; McDonald, Merry-Lynn N; Wan, Emily; Lomas, David A.; Coxson, Harvey O.; MacNee, William; Vestbo, Jørgen; Yates, Julie C.; Agusti, Alvar; Calverley, Peter MA; Celli, Bartolome; Crim, Courtney; Rennard, Stephen; Wouters, Emiel; Bakke, Per; Bhatt, Surya P; Kim, Victor; Ramsdell, Joe; Regan, Elizabeth A.; Make, Barry J.; Hokanson, John E.; Crapo, James D.; Beaty, Terri H.; Hersh, Craig
    Short-acting β2-agonist bronchodilators are the most common medications used in treating chronic obstructive pulmonary disease (COPD). Genetic variants determining bronchodilator responsiveness (BDR) in COPD have not been identified. We performed a genome-wide association study (GWAS) of BDR in 5789 current or former smokers with COPD in one African American and four white populations. BDR was defined as the quantitative spirometric response to inhaled β2-agonists. We combined results in a meta-analysis. In the meta-analysis, SNPs in the genes KCNK1 (P=2.02×10−7) and KCNJ2 (P=1.79×10−7) were the top associations with BDR. Among African Americans, SNPs in CDH13 were significantly associated with BDR (P=5.1×10−9). A nominal association with CDH13 was identified in a gene-based analysis in all subjects. We identified suggestive association with BDR among COPD subjects for variants near two potassium channel genes (KCNK1 and KCNJ2). SNPs in CDH13 were significantly associated with BDR in African Americans.
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    The metabolomics of asthma control: a promising link between genetics and disease
    (John Wiley & Sons, Ltd, 2015) McGeachie, Michael; Dahlin, Amber; Qiu, Weiliang; Croteau-Chonka, Damien; Savage, Jessica; Wu, Ann; Wan, Emily; Sordillo, Joanne; Al-Garawi, Amal; Martinez, Fernando D; Strunk, Robert C; Lemanske, Robert F; Liu, Andrew H; Raby, Benjamin; Weiss, Scott; Clish, Clary B; Lasky-Su, Jessica
    Short-acting β agonists (e.g., albuterol) are the most commonly used medications for asthma, a disease that affects over 300 million people in the world. Metabolomic profiling of asthmatics taking β agonists presents a new and promising resource for identifying the molecular determinants of asthma control. The objective is to identify novel genetic and biochemical predictors of asthma control using an integrative “omics” approach. We generated lipidomic data by liquid chromatography tandem mass spectrometry (LC-MS), ­ using plasma samples from 20 individuals with asthma. The outcome of interest was a binary indicator of asthma control defined by the use of albuterol inhalers in the preceding week. We integrated metabolomic data with genome-wide genotype, gene expression, and methylation data of this cohort to identify genomic and molecular indicators of asthma control. A Conditional Gaussian Bayesian Network (CGBN) was generated using the strongest predictors from each of these analyses. Integrative and metabolic pathway over-representation analyses (ORA) identified enrichment of known biological pathways within the strongest molecular determinants. Of the 64 metabolites measured, 32 had known identities. The CGBN model based on four SNPs (rs9522789, rs7147228, rs2701423, rs759582) and two metabolites—monoHETE_0863 and sphingosine-1-phosphate (S1P) could predict asthma control with an AUC of 95%. Integrative ORA identified 17 significantly enriched pathways related to cellular immune response, interferon signaling, and cytokine-related signaling, for which arachidonic acid, PGE2 and S1P, in addition to six genes (CHN1, PRKCE, GNA12, OASL, OAS1, and IFIT3) appeared to drive the pathway results. Of these predictors, S1P, GNA12, and PRKCE were enriched in the results from integrative and metabolic ORAs. Through an integrative analysis of metabolomic, genomic, and methylation data from a small cohort of asthmatics, we implicate altered metabolic pathways, related to sphingolipid metabolism, in asthma control. These results provide insight into the pathophysiology of asthma control.