Peter B. Dirks

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 SAT1 as a key driver of quiescence in glioblastoma stem cells through metabolic rewiring and viral mimicry, showing it can induce reversible growth arrest.

This study develops a mouse model of pediatric gliomas and identifies BRAF and MAPK signaling as critical drivers of tumor progression and therapeutic resistance.

The paper presents a chemical-genetic interaction matrix derived from CRISPR/Cas9 screens, revealing drug mechanisms and genetic architecture in human cells.

The paper shows that glioblastoma stem cells form spatial patterns correlated with their transcriptional state, using image analysis to link morphology and gene expression.

This study identifies DNA-PK as a synthetic lethal target in TP53-deficient SHH medulloblastoma, showing that inhibiting DNA-PK enhances radiosensitivity and improves survival in preclinical models.

This study identifies EP300 as a regulator of the Injury-Response state in Glioblastoma Stem Cells through a CRISPR-Cas9 screen, showing its role in maintaining IR state features and tumor aggressiveness.

This paper identifies PRMT5 as a regulator of HTT mRNA splicing and alternative polyadenylation, showing that its inhibition reduces full-length HTT protein levels by promoting premature termination and cleavage.

This study differentiates human hindbrain neuroepithelial stem cells into cerebellar granule neurons in vitro, recapitulating key progenitor states and showing SHH's role in lineage specification and maturation.

The paper constructs a molecular atlas of the human brain vasculature using single-cell RNA sequencing, revealing molecular heterogeneity and disease-related alterations in vascular cells.

This study compares five data integration methods for single-cell RNA sequencing of cancer samples, finding STACAS and fastMNN most effective in correcting batch effects while preserving biological variability.

This study uses CRISPR-Cas9 screens in patient-derived glioblastoma stem cells to identify essential genes and pathways for stemness and drug resistance, revealing new therapeutic targets.