eligibility_summary
Include: WHO IV malignant brain glioma refractory to standard care, age ≥4, KPS ≥70, adequate marrow/liver/kidney per labs, Ommaya feasible, no coagulopathy, WOCBP: negative test + contraception, consent. Exclude: pregnant/lactating, severe heart/liver/kidney/lung failure or coma, transplant hx, uncontrolled infection (incl HIV), autoimmune/immunodeficiency, systemic steroids or immuno/hormone tx, prior cell therapy, other trial <30 d, PI deems unsuitable.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
manual_review_required
ai_summary
Intervention: Allogeneic Vγ9Vδ2 T cells (biological, adoptive γδ T‑cell therapy) expanded from healthy donors and delivered intraventricularly/intracavitary via an Ommaya reservoir (weekly ×3 per 4‑week course, dose-escalation 1×10^7–3×10^8 cells). Mechanism of action: Vγ9Vδ2 T cells are innate‑like cytotoxic lymphocytes that recognize tumor phosphoantigens generated by dysregulated mevalonate/cholesterol metabolism in gliomas, independent of MHC, chiefly via BTN3A1/BTN2A1, triggering perforin/granzyme killing and cytokine release, they can also respond to stress ligands (e.g., via NKG2D) and mediate ADCC. Targets: Tumor cells in GBM/WHO IV malignant glioma (also DIPG/medulloblastoma), particularly those with phosphoantigen accumulation, key targeted pathways include the mevalonate/cholesterol pathway and stress‑induced ligand signaling. Optional background therapy may include temozolomide/radiation.