eligibility_summary
Include: age 15–79, recurrent/unresectable solid tumor, KPS≥50/ECOG≤2, survival >3 mo, systemic therapy washout ≥2 wks or ≥5 half-lives before apheresis (ICIs excepted), adequate counts/organ function, EF≥45, SpO2≥92, not pregnant+contraception, consent. Exclude: rapid/short survival, active infection (incl HIV/HBV/HCV), CNS disease, major cardiac events ≤12 mo, anticoagulation/coagulopathy, conflicting meds, biologic allergy, pregnancy/lactation, recent systemic steroids, poor T-cell transduction/expansion, other trials or PI concern.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
manual_review_required
ai_summary
Intervention: CAR-T/CAR-NK cell injection (biologic, gene‑modified cellular immunotherapy). Patients receive fludarabine/cyclophosphamide lymphodepletion, then a single IV infusion (~1–2×10^6 cells/kg). Mechanisms: CAR-T—autologous T cells engineered with chimeric antigen receptors (scFv linked to CD3ζ ± costimulatory domains) for MHC‑independent recognition of tumor‑associated antigens, triggering T-cell activation, cytokine release, and cytotoxic killing. CAR‑NK—engineered NK cells with CARs to augment antigen‑specific killing while leveraging innate NK cytotoxicity. Cells/pathways targeted: tumor cells in solid tumors (pancreatic, prostate, breast, glioma, etc.) expressing the study’s selected antigen(s), downstream effector pathways include CAR signaling and perforin/granzyme‑mediated lysis and apoptosis (Fas/TRAIL). Lymphodepletion targets host lymphocytes to promote CAR expansion and persistence. Primary outcomes: safety and antitumor activity (RECIST).