eligibility_summary
Eligible: age 2–60, consent, WHO 2008 diagnosis, refractory/relapsed with >5% blasts, CD7 or CD5 ≥70%, ECOG ≤2, expected survival >12 wks, Hgb ≥70 g/L, bilirubin ≤3×ULN, AST/ALT ≤5×ULN. Exclude: no consent, prior solid-organ transplant, cardiac disease (AF, MI <12 mo, long QT, pericardial effusion, NYHA III–IV), severe pulmonary disease, uncontrolled infection, severe autoimmune/immunodeficiency, active hepatitis, HIV, significant/uncontrolled viral infections incl EBV.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Intervention: Sequential CD5- and CD7-directed CAR-T cells (genetically engineered T‑cell immunotherapy) following lymphodepleting chemotherapy. Mechanisms: Patient T cells are modified to express chimeric antigen receptors that bind CD5 or CD7 on target cells, antigen engagement triggers T‑cell activation (via CD3ζ/co-stimulatory domains), proliferation, and cytotoxic killing of malignant T cells. Preconditioning uses fludarabine (purine analog causing lymphodepletion) and cyclophosphamide (alkylating agent, immunodepletion) to enhance CAR-T expansion and persistence. Targets: CD5+ and/or CD7+ T‑lymphoblasts in relapsed/refractory T‑ALL, ETP‑ALL, and TLBL, pathways include CAR-mediated immune synapse formation and depletion of CD5/CD7-expressing T‑cell compartments, with expected on-target effects such as T‑cell aplasia and risk of cytokine release. Trial: open-label, single-arm Phase 1/2.