ALK rearrangement (most commonly NPM1-ALK t(2;5))

Deterministic view of the source YAML entity. Clinical authority remains with the cited source IDs and reviewer sign-off state.

ID	`BIO-ALK-REARRANGEMENT`
Type	Biomarker
Aliases	ALK fusionALK rearrangementALK rearrangement (найчастіше NPM1-ALK t(2;5))ALK+NPM1-ALK
Status	reviewed 2026-04-25 \| pending_clinical_signoff
Diseases	None declared
Sources	`SRC-NCCN-BCELL-2025`

Biomarker Facts

Biomarker type	gene_fusion
Mutation details	{"functional_impact": "constitutive ALK kinase activation", "gene": "ALK", "variant_type": "fusion — multiple partners: NPM1 (most common t(2;5)), TPM3, ATIC, CLTC, MSN, others"}
Measurement	MethodFISH break-apart probe OR ALK IHC (D5F3 clone) on FFPE biopsy; molecular RT-PCR confirms partner Unitscategorical (positive \| negative)
Related biomarkers	None declared

Notes

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.

Used By

Biomarker

BIO-ALK-G1202R - ALK G1202R resistance mutation
BIO-ALK-L1196M - ALK L1196M gatekeeper resistance mutation

Indications

IND-ALCL-2L-CRIZOTINIB-ALKPOS - IND-ALCL-2L-CRIZOTINIB-ALKPOS

Questionnaires

QUEST-ALCL-1L-STUB - Anaplastic Large Cell Lymphoma, Systemic — first line

Red flag

RF-IMT-HIGH-RISK-BIOLOGY - Inflammatory myofibroblastic tumor with actionable fusion driver: ALK fusion (TPM3-ALK, T...