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A broken-and-rejoined FGFR2 gene that drives about one in eight intrahepatic bile duct cancers and can be switched off with pills.
Detected by RNA or DNA sequencing; partners are diverse (BICC1 most common). Pemigatinib (ORR 37%) and futibatinib (ORR 42%) are approved; acquired resistance arises through FGFR2 kinase-domain mutations (N550, V565 gatekeeper) that next-generation inhibitors (tinengotinib, RLY-4008 lirafugratinib) target. Hyperphosphataemia is the class effect.
In plain words · FGFR2 is a growth receptor fused in bile-duct cancer and overproduced in gastric cancer.
Showing the target this term concerns: FGFR2.
The glossary entry explains the word; the readout page carries the scoring rule, the thresholds approvals use, the companion diagnostics and the tests.
Shares Tinengotinib, ctDNA-guided switching among FGFR inhibitors, FGFR2, Intrahepatic cholangiocarcinoma.
Shares ctDNA-guided switching among FGFR inhibitors, Pemigatinib, FGFR2, Intrahepatic cholangiocarcinoma.
Shares Tinengotinib, ctDNA-guided switching among FGFR inhibitors, Biliary tract cancer (cholangiocarcinoma).
Shares FGFR2 fusion or rearrangement, Futibatinib, Pemigatinib, FGFR2.
Shares ctDNA-guided switching among FGFR inhibitors, Pemigatinib, Intrahepatic cholangiocarcinoma, Biliary tract cancer (cholangiocarcinoma).
Shares Futibatinib, FGFR2, Intrahepatic cholangiocarcinoma, Biliary tract cancer (cholangiocarcinoma).
Shares Pemigatinib, Intrahepatic cholangiocarcinoma, Biliary tract cancer (cholangiocarcinoma).
Shares ctDNA-guided switching among FGFR inhibitors, Futibatinib, Biliary tract cancer (cholangiocarcinoma).