Autologous peripheral blood T cells engineered with the Sleeping Beauty transposon/transposase to express patient-specific TCRs recognizing mutated neoantigens; adoptive cellular gene therapy mediating HLA-restricted tumor cell killing.
Autologous peripheral blood T cells are genetically modified using the Sleeping Beauty transposon/transposase system to express patient-specific TCRs that recognize mutated neoantigen peptides presented by HLA on tumor cells. Upon infusion, TCR–HLA engagement activates the T cells to mediate targeted, HLA-restricted tumor cell killing via cytotoxic effector mechanisms (perforin/granzyme) and cytokine release.
NO
INDIRECT
Engineered TCR T cells kill only cells presenting the specific mutated peptide bound to the patient’s HLA allele via TCR recognition and perforin/granzyme cytotoxicity; expression of the HLA molecule alone does not trigger killing.
TROP2-directed antibody–drug conjugate; the monoclonal antibody binds TROP2 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I–inhibiting payload causing DNA replication stress, single-strand breaks, and apoptosis (with potential bystander effect).
TROP2-targeted monoclonal antibody that is internalized and releases a camptothecin-class topoisomerase I–inhibiting payload, inducing DNA replication stress and single-strand breaks that trigger apoptosis, with potential bystander killing of neighboring tumor cells.
YES
DIRECT
An anti-TROP2 antibody–drug conjugate binds TROP2, is internalized, and releases a camptothecin-class topoisomerase I inhibitor that induces DNA damage/replication stress, leading to apoptosis (with potential bystander effect).
TROP2-directed antibody–drug conjugate; the monoclonal antibody binds TROP2 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I–inhibiting payload causing DNA replication stress, single-strand breaks, and apoptosis (with potential bystander effect).
TROP2-targeted monoclonal antibody that is internalized and releases a camptothecin-class topoisomerase I–inhibiting payload, inducing DNA replication stress and single-strand breaks that trigger apoptosis, with potential bystander killing of neighboring tumor cells.
NO
INDIRECT
The ADC binds TROP2 (not topoisomerase I), is internalized, and releases a camptothecin-class topoisomerase I inhibitor that induces DNA damage and apoptosis in targeted (and nearby) cells; topoisomerase I is the intracellular enzyme inhibited by the payload, not the surface target of the drug.
Autologous gene-modified T-cell therapy: patient T cells are collected, transduced ex vivo with a lentiviral vector encoding the EB103 transgene, then reinfused to redirect and activate T cells against malignant B-cell non-Hodgkin lymphoma (CAR-like signaling) leading to antigen-specific proliferation and cytotoxic killing.
Autologous T cells are transduced ex vivo with a lentiviral vector to express an anti‑CD19 antibody‑TCR (AbTCR) and a costimulatory molecule, enabling MHC‑independent recognition of CD19 on B‑cell malignancies. Upon reinfusion, engagement of CD19 triggers CAR‑like activation, proliferation, and T‑cell–mediated cytotoxic killing of tumor cells.
YES
DIRECT
Engineered autologous T cells recognize CD19 in an MHC-independent, CAR-like manner and kill CD19+ cells via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and apoptosis).
An intrathecal, autologous dendritic cell (DC1) vaccine loaded with HER2 and HER3 peptides to present tumor antigens and prime/activate tumor-specific T cells (Th1/CTL) within the cerebrospinal fluid for immune-mediated killing of cancer cells in leptomeningeal disease from TNBC or HER2+ breast cancer.
Autologous DC1 dendritic cells pulsed with HER2/HER3 peptides are administered intrathecally to present these antigens via MHC to T cells in the CSF, inducing Th1 polarization and priming/activating tumor‑specific CD4+ and CD8+ cytotoxic T cells to recognize and kill HER2/HER3‑expressing leptomeningeal tumor cells.
YES
INDIRECT
DC1 vaccine primes/activates HER2/HER3-specific T cells that recognize HER2 peptide–MHC on tumor cells and kill them via perforin/granzyme (and Fas–FasL) cytotoxicity.