MET amplification / overexpression in HCC has biological rationale (HGF/MET autocrine loo...
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | BMA-MET-AMP-HCC |
|---|---|
| Type | Actionability |
| Status | reviewed 2026-04-27 | pending_clinical_signoff | actionability review required |
| Diseases | DIS-HCC |
| Sources | SRC-AASLD-HCC-2023 SRC-CIVIC SRC-NCCN-HCC-2025 |
Actionability Facts
| Biomarker | BIO-MET |
|---|---|
| Variant | amplification / overexpression |
| Disease | DIS-HCC |
| ESCAT tier | IIIA |
| Recommended combinations | clinical trial enrollment (basket / MET-targeted) |
| Evidence summary | MET amplification / overexpression in HCC has biological rationale (HGF/MET autocrine loop in subset of HCC). Tivantinib (MET-high IHC) failed phase 3 (METIV-HCC, Rimassa 2018). No approved MET-targeted therapy in HCC; activity in baskets has been modest. |
Notes
ESCAT IIIA (target validated in another tumor, no clinical proof in HCC). OncoKB Level 4 (compelling biological evidence). Standard 1L HCC remains atezolizumab + bevacizumab regardless of MET status.
Used By
No reverse references found in the YAML corpus.