ALK rearrangement in advanced NSCLC: alectinib (ALEX, Peters 2017) and lorlatinib (CROWN,...
Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.
| ID | BMA-ALK-FUSION-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-ALK-FUSION |
|---|---|
| Variant | fusion (gene-level, TKI-naive) |
| Disease | DIS-NSCLC |
| ESCAT tier | IA |
| Recommended combinations | alectinib monotherapy (1L), lorlatinib monotherapy (1L, preferred for CNS disease), brigatinib monotherapy (1L) |
| Contraindicated monotherapy | crizotinib (inferior to 2nd/3rd-gen ALK-TKIs, no longer 1L) |
| Evidence summary | ALK rearrangement in advanced NSCLC: alectinib (ALEX, Peters 2017) and lorlatinib (CROWN, Solomon 2024 — 5-yr PFS 60%) outperform crizotinib 1L. Lorlatinib has the highest CNS activity. Adjuvant alectinib improves DFS post-resection (ALINA, Solomon 2024). |
Notes
ESCAT IA. OncoKB Level 1. ~5% NSCLC adenocarcinoma. Detection by RNA-NGS / FISH / IHC (D5F3). EML4-ALK most common partner; variant type (v1 vs v3) influences resistance pattern and TKI selection.
Used By
No reverse references found in the YAML corpus.