Michael D. Taylor

This study identifies AHCY as a key driver of epigenetic and metabolic reprogramming in ZFTA-RELA ependymomas, revealing its role in promoting tumor growth through pyrimidine synthesis and asparagine dependency.

This study identifies metabolic partnerships between medulloblastoma and macrophages that drive leptomeningeal metastases and suggests targeting the CXCL12-SCARB1-cholesterol axis as a therapeutic strategy.

The paper identifies ependymomas as originating from the pre-neural crest/roof plate lineage using single-cell transcriptomics and lineage tracing.

The paper shows that H3K27me3 spreading regulates chromatin architecture and gene repression, with implications for cell fate and tumor development.

This study examines hTERT expression and its prognostic impact in pediatric medulloblastoma, finding higher expression correlates with worse survival outcomes.

This study investigates EZHIP mutations in pediatric brain tumors, showing their presence in new tumor types and revealing their role in neuronal-like gene programs and polyamine metabolism repression.

The paper constructs a transcriptomic landscape for medulloblastoma and ependymoma, revealing subtype-specific biology through clustering and molecular signatures.

This study identifies RREB1 as a key driver of Group 3 medulloblastoma, showing its role in tumor growth and survival through the c-MET signaling pathway.

This paper introduces RECODR, a computational pipeline that tracks transcriptome changes in cancer development and treatment to predict resistance mechanisms and design effective therapies.

The paper validates the existence of transitional cerebellar progenitors using multimodal approaches across multiple datasets and stages.

The paper shows BRCA1 correlates with proliferation in human neural progenitor cells and medulloblastoma, particularly in Group 3 and 4 tumors, and is linked to worse prognosis.

This paper identifies how PVT1 rearrangements in MYC+ cancers generate oncogenic peptides that synergistically activate MYC, AKT, and RAS-MAPK pathways, enhancing tumor aggressiveness.

This study shows that valproic acid reduces medulloblastoma cell viability and affects stemness, differentiation, and gene expression through histone acetylation changes.

This study uses scRNA-seq data to identify developmental-like cell states in brain tumors, suggesting potential cells of origin for medulloblastoma, glioma, and diffuse midline glioma.

This study shows Ezh2 suppresses differentiation gene activation in cerebellar granule neurons and medulloblastoma cells, and its inhibition combined with cell cycle exit promotes differentiation.

DeepVelo estimates cell-specific transcriptional kinetics in scRNA-seq data using GCNs, enabling analysis of complex differentiation processes with time-varying rates.

The paper investigates synapse-specific diversity of GluN2 subunits in spinal lamina I neurons and shows how they differentially tune depolarization events.

The paper uses single-cell transcriptomics to show childhood cerebellar tumors mirror fetal cerebellar cell lineages, linking tumor subtypes to specific developmental stages.