Samuel K. McBrayer

This study identifies GAA accumulation in gliomas as a driver of neuronal activity and tumor growth, linking cancer metabolism to neuroscience through GABAA receptor activation.

The paper develops a biosensor to monitor α-ketoglutarate in human cells and identifies a mitochondrial-to-nuclear pathway regulating chromatin methylation.

The paper develops a platform to trace 30 nitrogen isotope-labeled metabolites, revealing cell state-specific pyrimidine synthesis pathway preferences in primitive and differentiated cells.

This study identifies KDM6 enzymes as targets of R2HG from mutant IDH, linking them to replication stress sensitivity in gliomas and introduces a DHODH inhibitor, GLIO-1, with potential clinical applications.

This study identifies specific developmental epigenomic states that enable ZFTA-RELA-driven ependymoma formation and reveals how these states shape tumor progression.

This study shows that L-2HG accumulation due to L2HGDH deficiency impairs neuronal differentiation by epigenetically activating MYC, leading to stem cell self-renewal and reduced neuron formation.

This study shows that doxycycline induces mitochondrial stress and selectively kills glioblastoma stem-like cells, offering a drug repurposing strategy for therapy-resistant gliomas.

This study shows mutant IDH reprograms neural progenitor cell fate by silencing Gsx2, promoting gliomagenesis through lineage switching.

This study develops matched patient-derived organoids and cell lines from melanoma brain metastases to evaluate responses to targeted therapies, finding both models respond to BRAF and MEK inhibitors.

This paper develops a method to assess cancer organoid viability using rapid imaging and a fragmentation algorithm, finding significant correlations between SSD scores and traditional viability markers.

The paper shows that KDM6A, an H3K27 histone demethylase, is oxygen-sensitive and its inactivation under hypoxia affects chromatin and cell fate.