Figure 1

The growth factor signaling pathways and their inhibition in malignant gliomas (MGs). Growth-factor binding stimulates receptor tyrosine kinase activity, leading to the activation of multiple downstream signaling cascades. These signaling pathways regulate processes such as cell survival, proliferation, and angiogenesis. Moreover, various intra-and extracellular proteins of these signaling pathways are also potential therapeutic targets for the treatment of malignant gliomas. X indicates the site of inhibition of targeted molecular agents; R, receptor; K, kinase; EGFR, epidermal growth factor receptor; EGF, epidermal growth factor; PDGFR, platelet-derived growth factor receptor; PDGF, platelet-derived growth factor; mTOR, mammalian target of rapamycin; PTEN, tumor-suppressor phosphatase and tensin homolog; PKC, protein kinase C; PI3K, phosphatidylinositol-3-kinase; PLC, phospholipase C; Akt, protein kinase B; MEK-1/2, mitogen-activated protein kinase and extracellular signal-regulated protein kinase-1/2 kinase; MAPK/ERK-1/2, mitogen-activated protein kinase/extracellular signal-regulated protein kinase-1/2.