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ALK-Umstellung (meist NPM1-ALK t(2;5))

Deterministische Ansicht der Quelle YAML Entität. Klinische Autorität bleibt mit den zitierten Quell-IDs und Rezensenten Sign-off Zustand.

IDBIO-ALK-REARRANGEMENT
ArtBiomarker
Aliase
ALK-FusionALK-UmstellungALK rearrangement (найчастіше NPM1-ALK t(2;5))ALK+NPM1-ALK
Statusreviewed 2026-04-25 | pending_clinical_signoff
ErkrankungenDIS-ALCL DIS-IMT
QuellenSRC-NCCN-BCELL-2025

Biomarker-Fakten

Biomarker-Typgene_fusion
Angaben zur Mutation{"functional_impact": "constitutive ALK kinase activation", "gene": "ALK", "variant_type": "fusion — multiple partners: NPM1 (most common t(2;5)), TPM3, ATIC, CLTC, MSN, others"}
Messung
VerfahrenFISH-Break-Apart-Sonde oder ALK IHC (D5F3-Klon) auf FFPE-Biopsie; molekularer RT-PCR bestätigt Partner
Einheitencategorical (positive | negative)
Verwandte BiomarkerNone declared

Anmerkungen

Defining stratification within systemic ALCL: - **ALCL ALK+** (~70% of systemic ALCL): younger patients (median ~30-40), favorable prognosis (~70-80% 5y OS), responds well to CHP-Bv. Brentuximab + crizotinib emerging in r/r. - **ALCL ALK-** (~30%): older (median ~60), adverse prognosis (~30-40% 5y OS), benefits more from autoSCT consolidation in CR1. Both ALK+ and ALK- treated with same 1L (CHP-Bv per ECHELON-2). Status drives **consolidation strategy** (autoSCT for fit younger ALK- in CR1) and **r/r therapy choice** (crizotinib for ALK+ vs brentuximab/clinical trial for ALK-). Outside ALCL: ALK rearrangements in NSCLC drive crizotinib/alectinib (different therapeutic context); inflammatory myofibroblastic tumor (IMT). Lymphoma scope: ALCL only.

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