Ji-Heui Seo

Histone modifications define distinct nucleosome positions in cell-free DNA

This paper identifies histone modification-associated nucleosome positions in cfDNA that correlate with tumor fraction and cancer state across multiple cancers.

Transcription Factor Subtype Governs Response and Resistance to DLL3-Directed T-Cell Engagement in Small Cell Lung Cancer

This study investigates how transcription factor subtypes in small cell lung cancer influence response and resistance to DLL3-targeted therapy, revealing subtype-specific mechanisms of resistance.

Integrated inference of cancer gene expression from cell-free plasma chromatin

APEX infers cancer gene expression from plasma cfChIP-seq data, outperforming existing methods and enabling subtype classification and biomarker identification.

Detection and monitoring of translocation renal cell carcinoma via plasma cell-free epigenomic profiling

This paper detects and monitors translocation renal cell carcinoma (tRCC) using plasma cell-free epigenomic profiling, achieving high accuracy in distinguishing tRCC from other cancers and healthy controls.

SNAP: Streamlined Nextflow Analysis Pipeline for Immunoprecipitation-Based Epigenomic Profiling of Circulating Chromatin

SNAP improves classification performance for cell-free chromatin data while maintaining data retention through optimized quality filters and modular design.

Decoding the Epigenetics and Chromatin Loop Dynamics of Androgen Receptor-Mediated Transcription

The paper investigates how AR-bound CREs influence gene expression through epigenetic changes and chromatin looping, finding that contact frequency with promoters drives expression.

Epigenomic signatures as circulating and predictive biomarkers in sarcomatoid renal cell carcinoma

The paper identifies epigenomic signatures in sarcomatoid renal cell carcinoma (sRCC) that predict response to immune checkpoint inhibitors and are detectable in plasma, enabling non-invasive diagnosis.

Genetic determinants of chromatin reveal prostate cancer risk mediated by context-dependent gene regulation

The paper introduces CWAS, a method linking genetic variation to chromatin states, identifying novel prostate cancer risk loci and regulatory mechanisms not detectable by eQTLs.

MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets

This study shows MYC overexpression disrupts AR transcriptional pause release, promoting aggressive prostate cancer progression.

A genome-scale CRISPR screen reveals PRMT1 as a critical regulator of androgen receptor signaling in prostate cancer

This study identifies PRMT1 as a critical regulator of AR signaling in prostate cancer through genome-scale CRISPR screening and shows its potential as a therapeutic target.

H3k27ac-HiChIP in prostate cell lines identifies risk genes for prostate cancer susceptibility

The paper uses HiChIP to link prostate cancer GWAS risk variants to target genes, finding new associations not detected by eQTL methods and validating them with CRISPRi.

Transcriptome and interactome analyses identify the TP53 interacting gene RCCD1 as a candidate susceptibility gene at the 15p26.1 breast and ovarian cancer risk locus

The paper identifies RCCD1 as a susceptibility gene for breast and ovarian cancer by fine-mapping a risk locus and showing its expression and interaction patterns are associated with cancer risk.

Ovarian Cancer Risk Variants are Enriched in Histotype-Specific Enhancers that Disrupt Transcription Factor Binding Sites

Allelic imbalance reveals widespread germline-somatic regulatory differences and prioritizes risk loci in Renal Cell Carcinoma

The paper identifies allele-specific quantitative trait loci (asQTLs) in RCC, showing their enrichment in GWAS risk loci and linking them to hypoxia pathway interactions.

Integrated Molecular Profiling Studies to Characterize the Cellular Origins of High-Grade Serous Ovarian Cancer

The paper uses transcriptomic and epigenomic profiling to show that high-grade serous ovarian cancers predominantly originate from fallopian tube secretory epithelial cells, with distinct transcription factors driving tumorigenesis based on cell-of-origin.