Figure 1: Effect of inhibitors on EGFR and c-Met signaling pathways in cancer: The binding of ligands EGF/HGF to their corresponding receptors, EGFR/c-Met, leads to phosphorylation of specific tyrosine residues and activation of these receptors. Overexpression of EGFR and c-Met RTKs results in activation of downstream signaling pathways, PI3K/Akt and MAPK (RAS-RAF-MEK-ERK/MAPK), in several cancers. The induction of these signaling cascades results in the stimulation of cancer cell survival through dysregulation of cell death pathways. Several inhibitors are in clinical trials that inhibit these pathways, by binding to tyrosine kinase domains or to ligands, resulting in receptor inactivation. TKIs and MAbs of the EGFR/c-Met signaling pathways are shown in gray boxes, with their targets marked by inhibitory arrows.