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. Author manuscript; available in PMC: 2019 Sep 16.
Published in final edited form as: Curr Pharm Des. 2017 Nov 16;23(29):4226–4246. doi: 10.2174/1381612823666170616082125

Figure 1. Schematic representation of the RTK signaling network and nodes of therapeutic blockade.

Figure 1.

Activation of RTKs can result in signaling via two pathways: PI3/AKT and RAS/RAF/MEK/ERK. PI3K/AKT signaling induces cell survival, increases protein synthesis, activates glucose metabolism, and decreases apoptosis. RAS/RAF/MEK/ERK increases cellular proliferation, angiogenesis, migration, and differentiation by activating transcriptional factors in a cascade. Each ligand binds to RTK and transfers the extracellular signal to the cytosol and then, ultimately, to the nucleus. Targeted therapy using monoclonal antibody (-MAB or -IB) or TKI can block the extracellular signals which enter the cell through the RTK pathway.