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- Ba209d46c7bb0bbbb5da9c8b224d0a92e NCIT_P378 "NCI" @default.
- Ba209d46c7bb0bbbb5da9c8b224d0a92e type Axiom @default.
- Ba209d46c7bb0bbbb5da9c8b224d0a92e annotatedProperty IAO_0000115 @default.
- Ba209d46c7bb0bbbb5da9c8b224d0a92e annotatedSource NCIT_C200041 @default.
- Ba209d46c7bb0bbbb5da9c8b224d0a92e annotatedTarget "A preparation of human allogeneic T-lymphocytes gene-edited with the clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 nuclease complex to disrupt expression of endogenous TCR and major histocompatibility complex (MHC) class I molecules and modified to express a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) human cluster of differentiation 70 (CD70), with potential immunostimulating and antineoplastic activities. Upon introduction into the patient, the allogeneic CRISPR-Cas9 engineered anti-CD70 CAR T-cells CTX131 recognize and bind to CD70-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD70-positive tumor cells. CD70, the ligand for the costimulatory receptor CD27 and a member of the tumor necrosis factor (TNF) family, is found on the surfaces of various types of cancer cells. Disruption of endogenous TCR prevents graft-versus-host disease (GvHD); the disruption of MHC class I molecules increases the persistence of the CAR T-cells." @default.