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KDR (VEGFR2) mutaciones somáticas activantes ocurren en ~2–3% de NSCLC a través de histologías. KDR...

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IDBMA-KDR-NSCLC
TipoRelevancia terapéutica
Situaciónreviewed 2026-05-04 | pending_clinical_signoff | actionability review required
EnfermedadesDIS-NSCLC
FuentesSRC-ESMO-NSCLC-METASTATIC-2024 SRC-NCCN-NSCLC-2025

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BiomarcadorBIO-KDR
VarianteKDR (VEGFR2) mutación somática activante en NSCLC (~2–3%); no se ha seleccionado tratamiento aprobado con mutación KDR; ramucirumab aprobado para NSCCL independientemente del estado de KDR
EnfermedadDIS-NSCLC
El nivel de ESCATIIIB
Combinaciones recomendadasPembrolizumab 200 mg q3w ± quimioterapia de platino — 1L NSCLC por PD-L1 e histología (KEYNOTE-189/407; no específico de KDR), Ramucirumab 10 mg/kg IV + docetaxel 75 mg/m2 q3W — 2L NscLC después de la progresión del platino (REVEL; FDA 2014; aprobado independientemente del estado de mutación de KRD)
Resumen de las pruebasKDR (VEGFR2) somatic activating mutations occur in ~2–3% of NSCLC across histologies. KDR is the primary signal transducer for VEGF-driven tumor angiogenesis; multiple approved anti-angiogenic agents target KDR/VEGFR2 (ramucirumab, cabozantinib, lenvatinib, sunitinib). Clinical evidence for KDR mutation-selected therapy in NSCLC: (1) Ramucirumab + docetaxel (REVEL, FDA 2014): approved 2L NSCLC (regardless of KDR status); ramucirumab is an anti-VEGFR2 antibody but approval is biomarker-unselected. (2) Bevacizumab + chemotherapy: VEGF-A targeted, not KDR-mutation selected; contraindicated in squamous histology (central tumor, hemorrhage risk). (3) Cabozantinib, lenvatinib: multi-RTK inhibitors with VEGFR2 activity; no KDR mutation- selected NSCLC approval; under investigation in basket trials. (4) Hypothesized predictive value: KDR activating mutation may confer intrinsic VEGFR2 activation independent of VEGF-A — theoretically higher VEGFR2 dependence. No prospective evidence that KDR mutation predicts better response to ramucirumab vs. KDR wild-type. Standard of care: chemoimmunother...

Notas

ESCAT IIIB: KDR mutation in NSCLC is an investigational marker. Practical notes: (1) KDR mutation is detectable on comprehensive NGS panels; not in NCCN's required biomarker panel (EGFR, ALK, ROS1, BRAF, KRAS, MET, RET, NTRK, PD-L1, TMB for NSCLC). (2) Anti-angiogenic treatment decisions use VEGF/VEGFR2 protein expression (PD-L1 analogue reasoning) or histology (bevacizumab contraindicated in squamous), not KDR mutation. (3) For KDR-mutant NSCLC patients who have progressed on standard therapy, basket trial enrollment with a VEGFR2/multi-TKI arm is appropriate. (4) KDR mutation in other tumor types (e.g., angiosarcoma, renal cell carcinoma) may have different clinical significance — those contexts are outside this BMA scope.

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