Fibroblast growth factor receptor 2 (FGFR2) fusion proteins (FFs) are oncogenic drivers in 10-15% of intrahepatic cholangiocarcinoma (iCCA). FGFR-specific inhibitors provide temporary benefit in FF+ unresectable patients. Recent work with mouse iCCA models has documented the necessary role of RAS-ERK downstream to FFs and provided examples of preclinical experimentation aimed at improving FF targeting in iCCA.
Keywords: FGFR tyrosine kinase inhibitors; FGFR2 fusions; intrahepatic cholangiocarcinoma; mouse models of cholangiocarcinoma; resistance to FGFR tyrosine kinase inhibitors; targeted therapies in cholangiocarcinoma.
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