2021
S63 Genome-wide sex-by-SNP interaction analysis of susceptibility to idiopathic pulmonary fibrosis
Leavy O, Allen R, Oldham J, Guillen-Guio B, Stockwell A, Braybrooke R, Hubbard R, Ma S, Fingerlin T, Kaminski N, Zhang Y, Schwartz D, Yaspan B, Maher T, Molyneaux P, Flores C, Noth I, Jenkins R, Wain L. S63 Genome-wide sex-by-SNP interaction analysis of susceptibility to idiopathic pulmonary fibrosis. Thorax 2021, 76: a42-a42. DOI: 10.1136/thorax-2021-btsabstracts.69.Peer-Reviewed Original ResearchGenome-wide association studiesSNP interaction analysisIPF susceptibilityGenetic determinantsIndependent variantsIPF riskDifferent biological pathwaysGenetic lociSuggestive statistical significancePromoter regionBiological pathwaysAssociation studiesCommon genetic risk factorCase-control data setsGenetic componentIndependent datasetsInteraction analysisSignificant variantsSignificance thresholdBiological mechanismsSNP interactionsGenetic risk factorsEuropean descentFurther insightVariants
2015
Update in Diffuse Parenchymal Lung Disease 2013
Rosas IO, Kaminski N. Update in Diffuse Parenchymal Lung Disease 2013. American Journal Of Respiratory And Critical Care Medicine 2015, 191: 270-274. PMID: 25635490, PMCID: PMC4351573, DOI: 10.1164/rccm.201405-0856up.Peer-Reviewed Original ResearchMeSH KeywordsAnti-Inflammatory Agents, Non-SteroidalClinical Trials, Phase III as TopicDisease ProgressionDrug ApprovalEnzyme InhibitorsGenomicsHumansIdiopathic Pulmonary FibrosisIndolesLung Diseases, InterstitialPolymorphism, GeneticPyridonesTreatment OutcomeUnited StatesUnited States Food and Drug AdministrationConceptsMajority of patientsDistinct clinical presentationsSignificant clinical implicationsClinical presentationPulmonary fibrosis researchDisease progressionClinical implicationsGenetic biomarkersPatientsFibrosis researchGenetic variantsBiological mechanismsIPFNew biological mechanismsNintedanibPirfenidonePeriodHistoric approval