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DDR2 activating mutation — discoidin domain receptor tyrosine kinase 2

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

IDBIO-DDR2
TypeBiomarker
Aliases
DDR2 mutationАктивуюча мутація DDR2 — рецепторна тирозинкіназа 2 дискоїдинового домену
Statusreviewed 2026-05-04 | pending_clinical_signoff
DiseasesNone declared
SourcesSRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025

Biomarker Facts

Biomarker typegene_mutation
Mutation details{"exon": "multiple; hotspots S768R, L239R, I638F, T654M in kinase/extracellular domain", "functional_impact": "gain-of-function (collagen-independent receptor activation → MAPK/SRC signaling)", "gene": "DDR2", "variant_type": "activating missense"}
Measurement
MethodTumor NGS panel (DNA); DDR2 amplification by FISH (rare)
Actionability lookup{"gene": "DDR2", "variant": "activating_mutation"}
Related biomarkersBIO-FGFR1 BIO-KRAS BIO-PIK3CA

Notes

DDR2 (Discoidin Domain Receptor Tyrosine Kinase 2) is a collagen receptor RTK that signals through SRC, MAPK, and PI3K cascades. Activating mutations occur in ~2–4% of squamous cell NSCLC (enriched in squamous histology; rare in adenocarcinoma). Dasatinib inhibits DDR2 kinase in vitro and preclinical models, but clinical responses have been anecdotal (case reports/small series only). No Phase III trial or FDA approval for DDR2-selected therapy. DDR2 mutation in squamous NSCLC co-occurs with FGFR1 amplification (~10–15% of SqCC) and does not exclude standard-of-care chemoimmunotherapy. Clinical significance: investigational target; not used to select therapy outside clinical trials.

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Actionability