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The remaining 5–10% of them (named secondary) arise from lower grade tumors through several genetic mutations, such as retinoblastoma protein (RB), phosphatase and tensin homolog (PTEN), and vascular endothelial growth factor receptor (VEGFR), and other mutations, which finally lead to p53 inhibition, overexpression of platelet-derived growth factor A receptor-α (PDGFA/PDGFRα) and amplified cyclin-dependent kinase 4 (CDK4) ( Although several reports have established the existence of cancer stem cells-like populations within the GBM and several experimental models have demonstrated that transformed neural stem/precursor cells are probably the origin cell of those tumors, conclusive evidence remains missing ( The genesis, development, and progression of GBM and its resistance to standard treatments remains obscure

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doi: 10.1016/j.colsurfb.2020.111263