eligibility_summary
Adults 18–75 with advanced gastric cancer post-standard therapy and no options, measurable lesion (imRECIST), ECOG 0–2, adequate labs/organs, prior therapy/surgery washed out, toxicities ≤G1, PD-1 6w, CTLA-4 4w. Exclude HBV/HCV/HIV/syphilis/TB, uncontrolled cardiac/respiratory/cerebrovascular disease, transplant or coagulopathy, immune disorder on immunosuppressants, CNS mets/meningitis, immunotherapy allergy, drug abuse, pregnant/lactating, in other trials, investigator concern.
trial_source
clinical_trials.gov from Dec 2, 2025
annotation_status
manual_review_required
ai_summary
Interventions and mechanisms: • Neoantigen Reactive T cells (NRTs) – autologous adoptive cell therapy (biologic). Patient-derived CD8+/CD4+ T cells are expanded ex vivo to recognize tumor-specific neoantigen peptides from somatic mutations. Mechanism: TCR recognition of neoantigen–HLA on tumor cells triggers cytotoxic killing (perforin/granzyme) and IFN-γ–mediated effects, boosts tumor-specific cellular immunity. • Preconditioning chemo: nab‑paclitaxel (albumin‑bound paclitaxel, microtubule‑stabilizing cytotoxic taxane) and cyclophosphamide (alkylating agent) used for lymphodepletion/tumor debulking and to reduce Tregs, enhancing NRT engraftment and function. • Support: Interleukin‑2 (cytokine) continuous infusion to promote proliferation and persistence of infused T cells. Targeted cells/pathways: Tumor cells presenting patient-specific neoantigens on MHC I/II, transferred T cells via TCR signaling, downstream cytotoxic pathways, immune milieu modulation via lymphodepletion and Treg reduction.