Autologous gene-engineered CAR T-cell product expressing a CD70-specific CAR with co-expression of CXCR2 (IL-8 receptor) to enhance trafficking to IL-8–rich glioblastoma, administered as a single IV infusion in dose escalation.
Autologous T cells are gene-engineered to express a CD70-specific chimeric antigen receptor and the IL-8 receptor CXCR2. CXCR2 enhances chemotaxis toward IL-8–rich glioblastoma, improving tumor homing and infiltration. CAR engagement of CD70 on tumor cells activates T-cell effector functions, leading to targeted cytotoxic killing (perforin/granzyme) and cytokine release against CD70-positive glioblastoma cells.
NO
INDIRECT
IL-8 (CXCL8) is only a chemotactic cue for CXCR2 to enhance trafficking; the CAR mediates killing of CD70-positive cells via T-cell cytolysis (perforin/granzyme), not IL-8–expressing cells.
Autologous adoptive T-cell therapy in which patient-derived tumor-reactive T cells are expanded ex vivo and reinfused to recognize peptide-HLA complexes via native T-cell receptors, activating cytotoxic effector functions (perforin/granzyme and cytokines) to kill tumor cells.
Autologous tumor-infiltrating T cells are expanded ex vivo and reinfused to recognize tumor peptide–HLA complexes via their native T‑cell receptors, triggering TCR signaling and cytotoxic effector functions (perforin/granzyme release and cytokine secretion) to kill tumor cells.
YES
DIRECT
TCR recognition of the tumor peptide–HLA-A class I complex activates the reinfused T cells, which kill target cells via perforin/granzyme-mediated lysis and Fas–FasL–induced apoptosis.
Autologous adoptive T-cell therapy in which patient-derived tumor-reactive T cells are expanded ex vivo and reinfused to recognize peptide-HLA complexes via native T-cell receptors, activating cytotoxic effector functions (perforin/granzyme and cytokines) to kill tumor cells.
Autologous tumor-infiltrating T cells are expanded ex vivo and reinfused to recognize tumor peptide–HLA complexes via their native T‑cell receptors, triggering TCR signaling and cytotoxic effector functions (perforin/granzyme release and cytokine secretion) to kill tumor cells.
YES
DIRECT
Adoptively transferred tumor‑reactive T cells recognize the tumor peptide–HLA‑B complex via their native TCR and directly kill the presenting cells through perforin/granzyme-mediated cytolysis and Fas–FasL–induced apoptosis.
Autologous adoptive T-cell therapy in which patient-derived tumor-reactive T cells are expanded ex vivo and reinfused to recognize peptide-HLA complexes via native T-cell receptors, activating cytotoxic effector functions (perforin/granzyme and cytokines) to kill tumor cells.
Autologous tumor-infiltrating T cells are expanded ex vivo and reinfused to recognize tumor peptide–HLA complexes via their native T‑cell receptors, triggering TCR signaling and cytotoxic effector functions (perforin/granzyme release and cytokine secretion) to kill tumor cells.
YES
DIRECT
Tumor-reactive TCR T cells recognize the tumor peptide–HLA-C complex via their TCR and directly induce target-cell death via perforin/granzyme-mediated apoptosis (and Fas–FasL signaling).
Anti-HER2 antibody-drug conjugate that binds HER2, internalizes, and releases the microtubule-disrupting payload MMAE; may exert a bystander effect.
Anti-HER2 monoclonal antibody linked to the microtubule inhibitor MMAE. After binding HER2 on tumor cells, the ADC is internalized and the linker is cleaved to release MMAE, which disrupts microtubules causing cell-cycle arrest and apoptosis; the membrane-permeable payload can produce a bystander effect.
YES
INDIRECT
After HER2 binding and internalization, the ADC releases MMAE, which binds beta‑tubulin to disrupt microtubules, causing mitotic arrest and apoptosis; killing depends on HER2-directed delivery (with possible bystander effect), not on tubulin as a targeting antigen.