Autologous adoptive T-cell therapy derived from tumor-draining lymph node T cells, ex vivo activated and expanded with patient-specific neoantigen proteins, then infused intravenously to provide polyclonal, neoantigen-specific T-cell immunity against colorectal cancer.
Autologous T cells from tumor‑draining lymph nodes are activated and expanded ex vivo with patient‑specific neoantigen proteins to enrich polyclonal, neoantigen‑specific TCRs. Following lymphodepletion, the infused cells recognize neoantigen peptides presented on MHC I/II on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine‑driven immune responses, boosting tumor‑specific immunity and overcoming tolerance in colorectal cancer.
Neoantigen-specific TCRs recognize the mutant peptide–HLA class I complex on tumor cells, activating cytotoxic T cells to kill via perforin/granzyme-mediated apoptosis (± Fas–FasL), with supportive cytokine effects.
Autologous, gene-modified CAR T-cell therapy in which a patient’s T cells are transduced to express a CD19-directed KIR-based chimeric antigen receptor; upon binding CD19 on malignant B cells, the KIR-derived signaling domain activates the T cell to mediate cytokine release and cytotoxic killing of CD19+ cells.
Autologous T cells are genetically modified to express a CD19-directed KIR-based chimeric antigen receptor; binding to CD19 on malignant B cells triggers KIR-derived signaling that activates the T cells, inducing cytokine release and cytotoxic killing of CD19+ cells.
CAR T cells expressing a CD19-directed KIR-based receptor bind CD19 and are activated to kill CD19+ cells via perforin/granzyme-mediated cytolysis (and Fas/FasL), with cytokine release.
Autologous adoptive T-cell therapy derived from tumor-draining lymph node T cells, ex vivo activated and expanded with patient-specific neoantigen proteins, then infused intravenously to provide polyclonal, neoantigen-specific T-cell immunity against colorectal cancer.
Autologous T cells from tumor‑draining lymph nodes are activated and expanded ex vivo with patient‑specific neoantigen proteins to enrich polyclonal, neoantigen‑specific TCRs. Following lymphodepletion, the infused cells recognize neoantigen peptides presented on MHC I/II on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine‑driven immune responses, boosting tumor‑specific immunity and overcoming tolerance in colorectal cancer.
TCR recognition of the personalized neoantigen peptide–HLA class II complex on tumor cells activates infused neoantigen-specific T cells, which kill targets via perforin/granzyme release (and potentially Fas–FasL).
Anti-HER2 antibody–drug conjugate delivering a topoisomerase I inhibitor payload to induce DNA damage.
Anti-HER2 antibody–drug conjugate (trastuzumab linked to the topoisomerase I inhibitor deruxtecan). After HER2 binding and internalization, deruxtecan is released to inhibit topoisomerase I, inducing DNA damage, replication arrest, and apoptosis; also elicits ADCC and a bystander killing effect.
HER2-targeted ADC binds HER2 and is internalized; the deruxtecan payload (topoisomerase I inhibitor) is released intracellularly, causing DNA damage and apoptosis; can also trigger ADCC and a bystander effect.
Anti-HER2 monoclonal antibody (trastuzumab) conjugated to the microtubule inhibitor DM1 via a nonreducible linker. The antibody binds HER2 on tumor cells and is internalized; intracellular DM1 binds tubulin, disrupting microtubule dynamics to cause mitotic arrest and cell death. The trastuzumab component also inhibits HER2 signaling and can mediate ADCC.
An ADC: trastuzumab binds HER2 and is internalized; lysosomal processing releases DM1, which binds tubulin to disrupt microtubules, causing mitotic arrest and apoptosis. The antibody can also mediate ADCC.