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. 2021 Jun 2;13(11):2765. doi: 10.3390/cancers13112765

Figure 1.

Figure 1

Schematic representation of tyrosine kinase receptor activation and the major downstream signaling pathways involved in the pathogenesis of glioblastoma multiforme. Receptor tyrosine kinase are activated by ligand binding causing receptor dimerization and auto phosphorylation of the tyrosine kinase domain. This results in activation of two main downstream signaling pathways: Ras/ERK and PI3K/AKT. These receptors activate downstream signaling cascade that participates in cell survival, proliferation, angiogenesis. Legend: EGF—endothelial growth factor; EGFR—epidermal growth factor receptor; PDGF—platelet derived growth factor; PDGFR—platelet derived growth factor receptor; VEGF—vascular endothelial growth factor; VEGFR—vascular endothelial growth factor receptor; mTOR 1—mammalian target of rapamycin 1; HIF1α—hypoxia-inducible factor 1α; HSF—Heat shock protein; PTEN—phosphatase tensin homolog; MMP-2—matrix metallopeptidase 2; PI3K—Phosphoinositide 3-kinases; NFκB—nuclear factor κB; MAPK: Mitogen—activated protein kinase; MEK—MAPK extracellular signaling-regulated kinase; FOXO—Forkhead box O; FGFR—fibroblast growth factor receptor; BAX—BCL2-associated X protein; MDM2—murine double minute 2 ERK Extracellular regulated kinase; p53—tumor protein.