Onco Wiki / Biomarker

KDR (VEGFR2) Mutation / Verstärkung — vaskuläre endothelielle Wachstumsfaktorrezeptor 2

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

IDBIO-KDR
ArtBiomarker
Aliase
KDR / VEGFR2-MutationМутація / ампліфікація KDR (VEGFR2) — рецептор судинного ендотеліального фактора росту 2
Statusreviewed 2026-05-04 | pending_clinical_signoff
ErkrankungenDIS-NSCLC
QuellenSRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025

Biomarker-Fakten

Biomarker-Typgene_mutation
Angaben zur Mutation{"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)"}
Messung
VerfahrenTumor-NGS-Panel (DNA); IHC (nicht routinemäßig für die Mutationserkennung verwendet); FISH zur Verstärkung
Nachschlagewerk für die Aktionsfähigkeit{"gene": "KDR", "variant": "activating_mutation"}
Verwandte BiomarkerBIO-VEGFA BIO-FGFR1 BIO-PDGFRA

Anmerkungen

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.

Verwendet von

Therapeutische Relevanz