Autologous TCR-engineered T cell therapy (TCR-T) in which a patient’s T cells are transduced with a high-affinity T-cell receptor recognizing KRAS G12V peptide presented by HLA-A*11:01, enabling antigen-specific cytotoxic killing of tumor cells.
Autologous T cells are genetically engineered to express a high‑affinity TCR specific for the KRAS G12V peptide presented by HLA‑A*11:01 on tumor cells; upon infusion they recognize peptide–MHC I, activate via TCR signaling, and execute antigen‑specific cytotoxic killing via perforin/granzyme pathways (with lymphodepletion and IL‑2 support to enhance expansion).
TCR-engineered T cells recognize the KRAS G12V peptide presented by HLA-A*11:01 on tumor cells and directly kill them via cytotoxic T-cell mechanisms (perforin/granzyme-mediated apoptosis, with possible Fas–FasL signaling).
Autologous TCR-engineered T cell therapy (TCR-T) in which a patient’s T cells are transduced with a high-affinity T-cell receptor recognizing KRAS G12D peptide presented by HLA-A*11:01, enabling antigen-specific cytotoxic killing of tumor cells.
Autologous T cells are engineered to express a high-affinity TCR that recognizes the KRAS G12D neoantigen presented by HLA-A*11:01 on tumor cells; TCR engagement triggers antigen-specific activation and cytotoxic killing via perforin/granzyme release, leading to lysis of KRAS-mutant tumor cells.
Engineered TCR T cells recognize the KRAS G12D peptide presented by HLA-A*11:01 on tumor cells, triggering T-cell activation and perforin/granzyme-mediated killing of the target cells.
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
NKG2D CAR-NK cells bind MICA on target cells, triggering NK activation and degranulation to kill via perforin/granzyme-mediated cytotoxicity (with possible death receptor signaling).
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
NKG2D CAR–engineered NK cells bind MICB on target cells, triggering NK activation and cytolysis via perforin/granzyme release (and death-receptor pathways), leading to apoptosis of MICB-expressing cells.
Engineered natural killer cells expressing an NKG2D-based chimeric antigen receptor; administered via endoscopic ultrasound–guided intratumoral injection plus two intravenous infusions to recognize NKG2D ligands (e.g., MICA, MICB, ULBP family) and induce NK-mediated cytotoxicity.
Engineered NK cells expressing an NKG2D-based chimeric antigen receptor bind NKG2D ligands (e.g., MICA, MICB, ULBP family) on tumor cells, triggering NK activation and cytotoxicity (perforin/granzyme release, cytokine production) to kill cancer cells.
NKG2D CAR-NK cells bind ULBP1 on target cells, activating NK degranulation (perforin/granzyme) and inducing target cell lysis/apoptosis.