FGFR2 fusion in intrahepatic cholangiocarcinoma (~10-15%): pemigatinib (FIGHT-202, Abou-A...
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | BMA-FGFR2-FUSION-CHOLANGIO |
|---|---|
| Type | Actionability |
| Status | reviewed 2026-04-27 | pending_clinical_signoff | actionability review required |
| Diseases | DIS-CHOLANGIOCARCINOMA |
| Sources | SRC-CIVIC SRC-FDA-CDS-2026 |
Actionability Facts
| Biomarker | BIO-FGFR2 |
|---|---|
| Variant | fusion / rearrangement (BICC1-FGFR2 most common; ~10-15% intrahepatic cholangio) |
| Disease | DIS-CHOLANGIOCARCINOMA |
| ESCAT tier | IA |
| Recommended combinations | pemigatinib monotherapy (2L+ post-gemcitabine/cisplatin), futibatinib monotherapy (2L+; preferred after pemigatinib resistance) |
| Evidence summary | FGFR2 fusion in intrahepatic cholangiocarcinoma (~10-15%): pemigatinib (FIGHT-202, Abou-Alfa Lancet Oncol 2020 — ORR 36%, mDOR 9.1 mo) and futibatinib (FOENIX-CCA2, Goyal NEJM 2023 — ORR 42%, mPFS 9.0 mo) are FDA-approved for previously-treated FGFR2-fusion cholangio. Futibatinib is irreversible and has activity against pemigatinib-resistance gatekeeper mutations. |
Notes
ESCAT IA. OncoKB Level 1. 1L remains gemcitabine + cisplatin ± durvalumab (TOPAZ-1). FGFR2-fusion testing recommended at diagnosis by NCCN to plan 2L. Detection: RNA-NGS preferred (intronic breakpoints commonly missed by DNA panels). Resistance: gatekeeper V564F, molecular brake L617M, kinase-domain N549K — futibatinib retains activity vs many of these. Source-gap: SRC-NCCN-HEPATOBILIARY / SRC-FIGHT-202 / SRC-FOENIX-CCA2 not yet ingested.
Used By
No reverse references found in the YAML corpus.