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KDR (VEGFR2) mutation / amplification — vascular endothelial growth factor receptor 2

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

IDBIO-KDR
TypeBiomarker
Aliases
KDR / VEGFR2 mutationМутація / ампліфікація KDR (VEGFR2) — рецептор судинного ендотеліального фактора росту 2
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; kinase domain (V297I, T771A, Q472H) and extracellular domain", "functional_impact": "gain-of-function (autonomous VEGFR2 activation → PI3K/AKT, MAPK, PLCγ → angiogenesis, survival)", "gene": "KDR", "variant_type": "activating missense; amplification (rare)"}
Measurement
MethodTumor NGS panel (DNA); IHC (not routinely used for mutation detection); FISH for amplification
Actionability lookup{"gene": "KDR", "variant": "activating_mutation"}
Related biomarkersBIO-VEGFA BIO-FGFR1 BIO-PDGFRA

Notes

KDR encodes VEGFR2 (Vascular Endothelial Growth Factor Receptor 2), the primary mediator of VEGF-driven tumor angiogenesis. Somatic KDR activating mutations occur in ~2–3% of NSCLC (mixed histologies) and ~1–2% across multiple other solid tumors. Multiple approved multi-target TKIs inhibit VEGFR2 (ramucirumab, lenvatinib, cabozantinib, regorafenib, sunitinib, sorafenib), but none are approved in a KDR mutation-selected indication. In NSCLC, ramucirumab + docetaxel (REVEL, FDA 2014) is approved for 2L regardless of KDR status. KDR mutation has been hypothesized to predict response to VEGFR-targeted agents, but prospective evidence is lacking; no companion diagnostic exists. Clinical significance: investigational target; KDR mutation is reported on NGS panels but does not currently change standard therapy selection in NSCLC.

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Actionability