El adenocarcinoma gástrico positivo al VEB es un subtipo molecular definido por el TCGA (~9% de la...
Vista determinista de la entidad fuente YAML. La autoridad clínica sigue con los ID de fuente citados y estado de firma del revisor.
| ID | BMA-EBV-POSITIVE-GASTRIC |
|---|---|
| Tipo | Relevancia terapéutica |
| Situación | reviewed 2026-05-07 | pending_clinical_signoff | actionability review required |
| Enfermedades | DIS-GASTRIC |
| Fuentes | SRC-ESMO-GASTRIC-2024 SRC-KEYNOTE-061-SHITARA-2018 SRC-KIM-PEMBRO-EBV-NATMED-2018 SRC-NCCN-GASTRIC-2025 SRC-TCGA-GASTRIC-BASS-2014 |
Hechos relativos a la posibilidad de adoptar medidas
| Biomarcador | BIO-EBV-STATUS |
|---|---|
| Variante | Adenocarcinoma gástrico positivo a VEB por hibridación in situ de EBER en tejido tumoral (subtipo molecular de VEB de TCGA; ~9% de adenocarcinoma gástrica) |
| Enfermedad | DIS-GASTRIC |
| El nivel de ESCAT | IIIA |
| Combinaciones recomendadas | Selección del tratamiento impulsada por HER2 / MSI / CLDN18.2 / PD-L1 CPS (hierarquía existente de 1L); el estado de EBV+ refuerza la lógica de la ICI y genera hipótesis para la ICC en la SPC<5 (desprovisto de etiquetado / ensayo) |
| Resumen de las pruebas | EBV-positive gastric adenocarcinoma is a TCGA-defined molecular subtype (~9% of gastric adenocarcinoma; Cancer Genome Atlas Research Network, Nature 2014) characterized by recurrent PIK3CA mutations (~80%), ARID1A mutations (~55%), CDKN2A silencing, JAK2 / PD-L1 / PD-L2 amplification at 9p24.1, and elevated tumor PD-L1 expression. Clinically, EBV+ gastric tumors show high PD-L1 expression (CPS ≥1 in >90%) and exceptional response signals to immune-checkpoint inhibitors (pembrolizumab single-agent ORR ~33% in EBV+ vs ~12% in EBV-negative in small cohorts: Kim et al. Nature Medicine 2018; Janjigian KEYNOTE-061 EBV+ subset analysis). Functions primarily as a SUBTYPE ROUTER / EXPLANATORY biomarker in the current KB — it identifies a population highly likely to derive ICI benefit independent of CPS thresholding. Standard 1L treatment selection remains driven by HER2 / MSI / CLDN18.2 / PD-L1 CPS hierarchy; EBV+ status reinforces ICI rationale where CPS-driven indications already apply, and is hypothesis-generating for ICI consideration in CPS<5 patients (off-label / trial). Routine EBV te... |
Notas
ESCAT IIIA — explanatory / subtype-routing biomarker; not treatment-selecting on its own. Primary citations now include the TCGA gastric classification paper (Bass et al., Nature 2014) and Kim et al. Nature Medicine 2018 (pembrolizumab response in EBV+ metastatic gastric). NCCN gastric v2025 and ESMO gastric 2024 retained as guideline corroboration. KEYNOTE-061 EBV+ subset analysis (Janjigian) is still pending source-ingestion; the parent trial KN-061 is now cited as Shitara 2018 Lancet (PMID 29880231) for context, but no EBV-specific subset claim is asserted on the basis of that citation. Co-positivity with MSI-H, PD-L1 CPS+, HER2+ is mostly mutually exclusive (EBV+ rarely overlaps with MSI-H — both confer immunogenicity through different mechanisms); HER2+ and EBV+ cooccur in <2% of cases. NOT a 1L-routing biomarker in current OpenOnco algorithm; documented for clinician context and for future ICI-prioritization rule when phase 3 EBV-stratified data emerges. Engine routing intentionally does not fire on this BMA alone; it is consumed by the render layer for explanatory display.
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