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Glioma-related targets refer to a diverse group of molecular entities, including receptors, enzymes, and signaling proteins, that drive the pathogenesis, progression, and treatment resistance of gliomas, particularly glioblastoma multiforme (GBM) [1, 5]. Key targets include receptor tyrosine kinases such as the epidermal growth factor receptor (EGFR) and platelet-derived growth factor receptor (PDGFR), which promote uncontrolled cell growth, and vascular endothelial growth factor (VEGF), which stimulates tumor angiogenesis [2, 3]. Intracellular signaling pathways like PI3K/Akt/mTOR and MAPK/ERK are also frequently dysregulated and serve as focal points for small-molecule inhibitors [6, 13]. Additionally, metabolic and epigenetic factors like isocitrate dehydrogenase (IDH) and O6-methylguanine-DNA methyltransferase (MGMT) play dual roles as therapeutic targets and essential biomarkers for patient stratification [5, 11]. While numerous drugs have been developed to interact with these targets, including temozolomide and bevacizumab, clinical efficacy is often hampered by the blood-brain barrier and high intratumoral heterogeneity [5, 8]. Understanding these targets is crucial for developing personalized treatment strategies and overcoming the inherent resistance of high-grade gliomas [6, 10].
Therapeutic mechanisms include DNA alkylation and cross-linking (Temozolomide, Nitrosoureas), inhibition of vascular endothelial growth factor (VEGF) to suppress angiogenesis (Bevacizumab), inhibition of epidermal growth factor receptor (EGFR) tyrosine kinase activity (Erlotinib), and inhibition of the mammalian target of rapamycin (mTOR) pathway (Everolimus) [1, 2, 5, 6].
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