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- B7ce40ab0dae8de401465595dac0f6946 NCIT_P378 "NCI" @default.
- B7ce40ab0dae8de401465595dac0f6946 type Axiom @default.
- B7ce40ab0dae8de401465595dac0f6946 annotatedProperty IAO_0000115 @default.
- B7ce40ab0dae8de401465595dac0f6946 annotatedSource NCIT_C178434 @default.
- B7ce40ab0dae8de401465595dac0f6946 annotatedTarget "A preparation of allogeneic T-lymphocytes transduced with a lentiviral vector encoding a chimeric antigen receptor (CAR) specific for the tumor-associated antigen (TAA) CD19, with genetic modification of CD52 and T-cell receptor alpha constant (TRAC) loci via clustered regularly interspaced short palindromic repeats (CRISPR), with potential immunostimulating and antineoplastic activities. Upon administration, the allogeneic CRISPR-edited anti-CD19 CAR T cells PBLTT52CAR19 recognize and bind to CD19-overexpressing tumor cells. This may result in a specific cytotoxic T-lymphocyte (CTL)-mediated killing of CD19-positive tumor cells. CD19 antigen is a B-cell specific cell surface antigen expressed in all B-cell lineage malignancies. The editing of the CD52 gene may make the modified donor T-cells resistant to the anti-CD52 monoclonal antibody alemtuzumab, which is used during lymphodepletion. The editing of the TRAC may eliminate TCR expression, which may abrogate the potential induction of graft-versus-host disease (GvHD) by the donor T-cells, and may also result in uniform CAR expression and enhanced T-cell potency." @default.