Fig. 3

Signalling pathway and targeted therapy in gastric cancer. Percentages signify the overall molecular characteristics in the disease: FGFR2 amplification (9 %), VEGF/VEGFR overexpression (36–40 %), EGFR amplification and overexpression (27–44 %), HER2 amplification and overexpression (7–34 %), c-MET amplification (10–15 %), kRAS mutation (2–20 %), Raf mutation (0–3 %), PI3K mutation (4–36 %), phospho-Akt expression (29–86 %), phospho-mTOR expression (60–88 %), PTCH1 overexpression (16%), SMO overexpression (12%), and HER3 mutations (10%, not shown). *No clinical trials of these agents have yet been reported in gastric cancer. ^‡No known numbers or percentages for these genes and pathways. Abbreviations: EGFR epidermal growth factor receptor, FGFR fibroblast growth factor receptor, GLI glioma-associated oncogene family zinc finger 1, HDAC histone deacetylase, HER human epidermal growth factor receptor, HGF hepatocyte growth factor, Hh Hedgehog, IGFR insulin-like growth factor receptor, MMP matrix metalloproteinase, mTOR mammalian target of rapamycin, PDGFR platelet-derived growth factor receptor, Ptch-1 protein patched homolog 1, Smo smoothened, VEGF vascular endothelial growth factor, VEGFR vascular endothelial growth factor receptor (reproduced with permission from Wadhwa, R. et al. Nat. Rev. Clin. Oncol. 10, 643–655 (2013) [181])