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Gene Expression Profiling in Patients with Idiopathic Pulmonary Fibrosis (IPF) in the INMARK Trial
( Jin Woo Song ),( Moisés Selman ),( R Gisli Jenkins ),( Eric S White ),( Vincent Cottin ),( Yasuhiko Nishioka ),( Imre Noth ),( Antje Prasse ),( Benjamin Strobel ),( German Leparc ),( Carina Ittrich 대한결핵 및 호흡기학회 2020 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.128 No.-
Background The INMARK trial investigated blood biomarkers as predictors of disease progression in patients with IPF and preserved lung function. In this study, we investigated changes in gene expression levels in patients treated with nintedanib and placebo. Methods Subjects with IPF and FVC ≥80% predicted were randomized 1:2 to receive nintedanib or placebo for 12 weeks followed by open-label nintedanib for 40 weeks. Total RNA was extracted from whole blood samples taken at baseline and week 12. Changes in gene expression levels from baseline to week 12 were analyzed. Data were log2 transformed prior to analysis. Changes in gene expression levels were considered significant if p≤0.05 and |log2fold change|≥0.5. Results Of 116 and 230 subjects randomized to receive nintedanib and placebo, respectively, data from 110 and 217 patients were included in the analysis. Of 60,675 genes evaluated, 14,799 had counts per million ≥1 in at least half the samples from either treatment group per time point and were included in the analysis. In adjusted analyses, compared with baseline levels, no genes were downregulated after 12 weeks’ treatment with placebo, while nine genes were downregulated after 12 weeks’ treatment with nintedanib (Table). No genes were upregulated. In unadjusted analyses, the change from baseline in expression level at week 12 was significantly different between nintedanib and placebo for five genes (SHISA4, LTF, CTSG, OLFM4, DEFA4) (Table). Pathways analysis suggested that the genes downregulated in patients treated with nintedanib were related to neutrophil function and extracellular matrix organization. Conclusions These analyses of the INMARK trial, based on genome-wide transcriptome profiling, identified a small number of genes that were downregulated after 12 weeks of nintedanib treatment in subjects with IPF and preserved lung function. The potential of gene expression profiling as a marker of treatment response in patients with IPF requires further study.