Henry W. Long

This study profiles B cell activation states using multi-omics data to identify genetic mechanisms underlying immune-mediated diseases.

This study identifies a tumor-cell MHC-II program linked to immunotherapy outcomes in bladder cancer across different stages and treatment settings.

This study identifies epigenetic subtypes of high-grade T1 bladder cancer using integrated chromatin and transcriptomic data, revealing intra-tumor heterogeneity and distinct tumor microenvironment interactions.

scATAnno automatically annotates scATAC-seq data using reference atlases, outperforming existing methods across multiple datasets.

This paper identifies the EZH2-TTP-mTORC1 axis as a driver of phenotypic plasticity and therapeutic vulnerability in prostate cancer, showing that combined inhibition of EZH2 and PI3K/mTORC1 improves anti-tumor activity.

This study shows EED inactivation impairs SCLC tumorigenesis and drives LUAD-to-SCLC transformation, highlighting its role in maintaining SCLC neuroendocrine identity.

This study shows that EZH2 influences the evolution of aggressive prostate cancer subtypes but is not essential for neuroendocrine prostate cancer development.

This study reprograms AR-active prostate cancer to NEPC using ASCL1 and NeuroD1, revealing their role in silencing AR and altering chromatin structure.

This study shows that ARv7 drives AR activity in castration-resistant prostate cancer through increased chromatin accessibility mediated by NFI factors.

This study identifies mSWI/SNF complex activity as a targetable dependency in POU2F3-positive small cell lung cancer, showing that inhibiting mSWI/SNF or BRD9 reduces tumor growth and improves survival.

This study investigates transcription factor dynamics during human enteroendocrine cell differentiation, finding that oscillations of ASCL1 and NEUROD1 enable accurate cell type diversification.

This study identifies a targetable dependency on noncanonical PI3Kγ signaling in acute leukemias, showing that PI3Kγ inhibition with eganelisib improves survival when combined with cytarabine.

This study shows that breast cancer cells respond differently to low and high levels of progestins, with low levels promoting proliferation through specific molecular mechanisms.

This study investigates Thio-2's mechanism of action in inhibiting AR signaling in CRPC, showing it acts independently of BAG-1 isoforms and with potential AR NTD binding.

MIRA jointly models gene expression and chromatin accessibility in single cells to infer regulatory circuits and lineage trees during development.

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

This study identifies thyroid hormone receptor THRB as a key regulator of hepatocyte maturation from human PSCs, showing that T3 treatment enhances gene expression and epigenetic features of mature hepatocytes.

CoBRA provides a reproducible pipeline for ChIP/ATAC-seq analysis, including peak calling, clustering, and pathway analysis, with code available at the given URL.

CHIPS is a Snakemake pipeline for processing chromatin profiling data, providing quality control metrics and reproducible analysis workflows for ChIP-seq, ATAC-seq, and DNase-seq experiments.

The paper introduces UniNicE-seq, a method for high-resolution accessible chromatin profiling in formaldehyde-fixed and FFPE tissues without optimization steps.

The paper identifies DNA methylation as a key mechanism for maintaining monoallelic expression on autosomes and reveals its tunable control of allele-specific expression.