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357 Addressing these mechanisms is crucial for improving GBM therapy, highlighting the need for novel approaches such as combination therapies, MGMT inhibitors, and alternative drug delivery systems to increase TMZ efficacy

1 Introduction 1.1 BRAF V600E mutation in central nervous system tumors have diverse prognosis and are candidates for molecular targeted therapy The MEK-ERK signaling pathway is activated by growth factor-stimulated RAS binding to BRAF, which, when dysregulated, can initiate tumorigenesis by promoting uncontrolled cell growth ( V600E and KIAA1549::BRAF fusion being significant drivers of cellular transformation in pediatric CNS tumors, with high occurrences in low-grade gliomas (LGGs, up to 35%), and low occurrences in high-grade gliomas (HGGs, ~5% for BRAF V600E ) ( V600E is a class I mutation, the most common class of mutations in glioma