Yeon Bi Han
Seoul National University · Medicine
About the Lab
Professor Yeon Bi Han's research lab specializes in respiratory and immune system pathophysiology, with a focus on lung diseases, including chronic respiratory disorders, lung cancer subtypes such as pulmonary sarcomatoid carcinoma and adenocarcinoma, and inflammatory conditions like chronic rhinosinusitis with nasal polyps. The lab employs advanced single-cell genomics, multi-omics integration, and functional immunology to dissect disease mechanisms, immune microenvironment dynamics, and viral responses in human airway epithelium and tumor tissues. A central theme is understanding the role of mitochondrial dsRNA and innate immune sensors like MDA5 and SLIRP in driving aberrant inflammation and autoimmunity.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
15We present an in-depth single-cell atlas of in vitro multiculture systems on human primary airway epithelium derived from normal and diseased lungs of 27 individual donors. Our large-scale single-cell profiling identified new cell states and differentiation trajectories of rare airway epithelial cell types in human distal lungs. By integrating single-cell datasets of human lung tissues, we discovered immune-primed subsets enriched in lungs and organoids derived from patients with chronic respira
Many studies support a stepwise continuum of morphologic changes between atypical adenomatous hyperplasia (AAH) and lung adenocarcinoma (ADC). Here we characterized gene expression patterns and the association of differentially expressed genes and immune tumor microenvironment behaviors in AAH to ADC during ADC development. Tumor tissues from nine patients with ADC and synchronous multiple ground glass nodules/lesions (GGN/Ls) were analyzed using RNA sequencing. Using clustering, we identified g
PURPOSE: Pulmonary sarcomatoid carcinoma (PSC) is a rare aggressive subtype of non-small cell lung cancer (NSCLC) with limited therapeutic strategies. We attempted to elucidate the evolutionary trajectories of PSC using multiregional and longitudinal tumor samples. MATERIALS AND METHODS: A total of 31 patients were enrolled in this study and 11 longitudinal samples were available from them. Using whole exome sequencing data, we analyzed the mutational signatures in both carcinomatous and sarcoma
OBJECTIVES: Several criteria exist for classifying chronic rhinosinusitis with nasal polyps (CRSwNP) as eosinophilic or non-eosinophilic. This study attempted to evaluate several criteria for defining eosinophilic CRSwNP from clinical and immunological perspectives. METHODS: A cohort of 84 patients (73 patients with CRSwNP and 11 control patients) was retrospectively analyzed. Patients were divided into eosinophilic and non-eosinophilic CRSwNP based on four different criteria: eosinophils (EOS)
BACKGROUND: Activating mutations in the tyrosine kinase domain of epidermal growth factor receptor (EGFR) are predictive biomarkers for response to EGFR-tyrosine kinase inhibitor (TKI) therapy in lung adenocarcinoma (LUAD). Here, we characterized the clinicopathologic features associated with EGFR mutations via peptide nucleic acid clamping-assisted fluorescence melting curve analysis (PANAMutyper) and evaluated the feasibility of targeted deep sequencing for detecting the mutations. METHODS: We
BTK expression may be utilized to stratify risk in patients with DLBCL.
Abnormal innate immune response is a prominent feature underlying autoimmune diseases. One emerging factor driving dysregulated immune activation is cytosolic mitochondrial double-stranded RNAs (mt-dsRNAs). However, the mechanism by which mt-dsRNAs stimulate immune responses remains poorly understood. Here, we discover SRA stem-loop-interacting RNA-binding protein (SLIRP) as an amplifier of mt-dsRNA-triggered antiviral signals. In autoimmune diseases, SLIRP is commonly upregulated, and the targe
Lung adenocarcinoma with coexpression of HLA class I and PD-L1 was associated with poor prognosis. This subgroup may evade immune attack by expressing PD-L1 protein despite HLA expression.
PURPOSE: Despite advances in treatment, lung cancer remains the leading cause of cancer mortality. This study aimed to characterise genome-wide tumorigenesis events and to understand the hypothesis of the multistep carcinogenesis of lung adenocarcinoma (LUAD). MATERIALS AND METHODS: We conducted multiregion whole-exome sequencing of LUAD with synchronous atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ, or minimally invasive adenocarcinoma of 19 samples from three patients to chara
Research Areas
Dive deeper into Yeon Bi Han's research on Nubint
Open this lab's papers in the app to read with AI, summarize, and cite in your writing.