eligibility_summary
Include: women ≥18 with HLA‑A2+, NY‑ESO‑1–overexpressing, measurable metastatic TNBC after ≥2 (<4) prior SOC lines (incl ICI, chemo, T‑DXd, PARPi if indicated), ECOG 0–1, life ≥6 mo, adequate marrow/renal/hepatic (AST/ALT <2×ULN, ≤5× if liver mets), bilirubin <2×ULN, EF ≥50%, consent, contraception, biopsies. Exclude: recent therapy, cyclophosphamide <4 mo, serious cardiac/QT, CNS mets, pregnancy, liver/GI disease, uncontrolled illness/infection, immunosuppression, HBV/HCV/HIV, recent surgery.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
ai
ai_summary
Phase Ib, single-arm dose-escalation in relapsed/refractory HLA-A2+ TNBC overexpressing NY-ESO-1. Interventions: A2-ESO-1 TCR-engineered autologous T cells (cell therapy, genetically modified T lymphocytes expressing an HLA-A2–restricted TCR specific for NY-ESO-1 peptide), lymphodepleting chemotherapy—cyclophosphamide (alkylating agent) and fludarabine (purine analog antimetabolite), and aldesleukin/IL-2 (recombinant cytokine). Mechanisms: TCR-T cells recognize the NY-ESO-1 peptide–HLA-A2 complex on tumor cells and execute cytotoxic killing, cyclophosphamide/fludarabine deplete lymphocytes (including Tregs) to enhance engraftment and reduce cytokine sinks, IL-2 drives expansion and persistence of infused T cells. Targets/pathways: NY-ESO-1 cancer-testis antigen on tumor cells, TCR signaling, IL-2/IL-2R pathway, exploratory immune markers include PD-L1, Tregs, and tumor-associated macrophages.