EGFR T790M is the dominant acquired-resistance mechanism after 1st/2nd-gen EGFR-TKI (gefi...
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | BMA-EGFR-T790M-NSCLC |
|---|---|
| Type | Actionability |
| Status | reviewed 2026-04-27 | pending_clinical_signoff | actionability review required |
| Diseases | DIS-NSCLC |
| Sources | SRC-CIVIC SRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025 |
Actionability Facts
| Biomarker | BIO-EGFR-MUTATION |
|---|---|
| Variant | T790M |
| Disease | DIS-NSCLC |
| ESCAT tier | IA |
| Recommended combinations | osimertinib monotherapy |
| Contraindicated monotherapy | gefitinib (T790M-resistant), erlotinib (T790M-resistant), afatinib (T790M-resistant) |
| Evidence summary | EGFR T790M is the dominant acquired-resistance mechanism after 1st/2nd-gen EGFR-TKI (gefitinib/erlotinib/afatinib). Osimertinib (3rd-gen) is active against T790M and is standard 2L (AURA3, Mok et al. 2017). In the modern era T790M is rarely encountered de novo since osimertinib has moved to 1L; remains relevant after legacy 1L-TKI use. |
Notes
ESCAT IA. OncoKB Level 1. ctDNA testing at progression on 1st/2nd-gen TKI is standard; tissue rebiopsy if plasma negative. Companion diagnostic: cobas EGFR Mutation Test v2.
Used By
No reverse references found in the YAML corpus.