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Diffuse‐type gastric carcinomas ( DGC ) exhibit more aggressive progression and poorer prognosis than intestinal‐type and other gastric carcinomas. To identify potential therapeutic targets, we examined protein tyrosine phosphorylation in a panel of  DGC  and other gastric cancer cell lines. Protein tyrosine phosphorylation was significantly enhanced or altered in  DGC  cell lines compared with that in other gastric cancer cell lines. Affinity purification and mass spectrometry analysis of tyrosine‐phosphorylated proteins identified  M et as a protein that is preferentially expressed and phosphorylated in  DGC  cell lines. Unexpectedly,  M et inhibitors blocked cell growth,  M et downstream signaling and peritoneal dissemination  in vivo  in only a subset of cell lines that exhibited remarkable overexpression of  M et. Likewise, only cell lines with overexpression of fibroblast growth factor receptor 2 ( FGFR 2) or phosphorylation of  FRS 2 were sensitive to an  FGFR 2 inhibitor. A  S rc inhibitor saracatinib impaired growth in cell lines that are insensitive to both  M et and  FGFR 2 inhibitors. Saracatinib also effectively impaired peritoneal dissemination of  M et‐independent and  FGFR 2‐independent  SGC  cells. Moreover,  DGC  cell lines exhibited nearly mutually exclusive susceptibility to  M et,  FGFR  and  S rc inhibitors. These results suggest that  DGC  have distinct sensitivities to molecular target drugs and that targeting  S rc is beneficial in the treatment of  DGC  insensitive to  M et and  FGFR  inhibition.

cancer science

Saracatinib impairs the peritoneal dissemination of diffuse‐type gastric carcinoma cells resistant to  M et and fibroblast growth factor receptor inhibitors