Sameer Agnihotri

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

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.

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

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.

This study shows H3K27M diffuse midline glioma is HRR defective and radiosensitized by PARP inhibitors, with enhanced NK cell-mediated immunity.

This study shows that all-trans retinoic acid (ATRA) improves immune response in IDH-mutant gliomas by restoring the RA pathway, leading to tumor regression in mouse models and a clinical trial for human patients.