Jeong Hyun Yun

The paper introduces FICTURE2, a statistical model that infers transcriptional programs from individual RNA molecules in spatial transcriptomics data, revealing spatial organization and cellular identity without segmentation.

This study investigates the association between mosaic loss of Y chromosome (mLOY) and lung function, emphysema, and epigenetic aging in men across multiple cohorts.

The paper identifies HHIP protein interactions in lung cells, revealing new connections to COPD GWAS genes and providing insights into COPD pathogenesis.

This study identifies LIFR as a master amplifier of fibroblast activation in IPF, showing that blocking LIFR reduces fibrosis in ex vivo tissue.

FICTURE provides a scalable segmentation-free method for analyzing high-resolution spatial transcriptomics data, revealing detailed tissue architecture in complex regions.

The paper develops a method to quantify somatic mutation burden in whole-genome sequencing data without paired-tissue samples and identifies genetic and phenotypic correlates of clonal hematopoiesis without known driver mutations.

The paper estimates mCA fitness in the NHLBI TOPMed cohort and identifies genetic variants associated with clonal expansion rates.

The paper develops PACER to infer clonal expansion rates from single timepoint data and identifies TCL1A activation as a mediator of clonal hematopoiesis fitness.

The paper finds that somatic mutations in diseased lung tissue correlate with reduced lung function and cell type proportions in COPD and IPF.

This study uses whole-genome sequencing to analyze mosaic chromosomal alterations across diverse ancestries, finding higher rates in certain populations and associations with germline variants.

This study analyzes clonal hematopoiesis in over a million diverse individuals, identifying 72 genome-wide significant loci and linking CHIP to various phenotypes.

This study identifies peripheral blood microbial signatures associated with COPD and exacerbation phenotypes in smokers.

The paper identifies FBXO38 as a novel COPD susceptibility gene by analyzing genetically driven alternative splicing and finding a protective exon associated with COPD risk.

The paper examines immune cell changes in COPD patients and finds associations between cell counts and lung function decline, suggesting immune response roles in disease progression.