EGFR amplification (~40%) and EGFRvIII variant (~25%) are common in glioblastoma but no t...
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | BMA-EGFR-MUTATION-GBM |
|---|---|
| Type | Actionability |
| Status | reviewed 2026-04-27 | pending_clinical_signoff | actionability review required |
| Diseases | DIS-GBM |
| Sources | SRC-CIVIC SRC-EANO-GBM-2024 SRC-NCCN-CNS-2025 |
Actionability Facts
| Biomarker | BIO-EGFR-MUTATION |
|---|---|
| Variant | EGFRvIII / amplification |
| Disease | DIS-GBM |
| ESCAT tier | X |
| Contraindicated monotherapy | erlotinib (negative trials in GBM), gefitinib (negative trials in GBM), osimertinib (insufficient CNS activity for EGFRvIII) |
| Evidence summary | EGFR amplification (~40%) and EGFRvIII variant (~25%) are common in glioblastoma but no targeted therapy has shown OS benefit. Erlotinib, gefitinib, lapatinib trials negative. Depatuxizumab-mafodotin (ADC) failed phase III INTELLANCE-1. Currently no actionable EGFR-targeted therapy in GBM. |
Notes
ESCAT X — no actionable evidence in GBM despite high alteration frequency. EGFRvIII vaccines (rindopepimut) failed phase III. EGFR CAR-T trials ongoing but investigational.
Used By
No reverse references found in the YAML corpus.