Preferred Label : Autologous Anti-EGFRvIII synNotch Receptor-induced Anti-EphA2/IL-13Ralpha2 CAR-T Cells;
NCIt synonyms : Autologous Anti-EGFRvIII synNotch Receptor Induced Anti-EphA2/IL-13Ra2 CAR T Cells; Autologous Anti-EGFRvIII synNotch Receptor Induced Anti-EphA2/IL-13R alpha2 CAR T
Cells; E-SYNC T Cells;
NCIt definition : A preparation of autologous T-lymphocytes engineered to express a synthetic Notch
(synNotch) receptor targeting epidermal growth factor receptor variant III (EGFRvIII)
that induces the expression of a chimeric antigen receptor (CAR) specific for Ephrin
receptor A2 (EphA2) and interleukin-13 receptor alpha 2 (IL13Ra2) upon antigen binding,
with potential immunostimulating and antineoplastic activities. After isolation, transduction,
expansion and reintroduction into the patient, autologous anti-EGFRvIII synNotch receptor-induced
anti-EphA2/IL-13Ralpha2 CAR-T cells target and bind to EGFRvIII-expressing tumor cells,
which induces the expression of CAR specific for EphA2 and IL13Ra2. This induces selective
toxicity in EphA2-expressing and IL13Ra2-expressing tumor cells locally. EGFRvIII,
an in-frame deletion of exons 2-7 in the EGFR gene, is overexpressed by a variety
of cancer cell types but absent in normal, healthy cells. It plays a key role in tumor
cell proliferation, tumor angiogenesis and resistance to both radio- and chemotherapy.
IL13Ra2, a cancer-associated receptor, is overexpressed by a variety of tumor cell
types; it is associated with increased invasiveness of tumor cells. EphA2, a member
of the ephrin family of receptor tyrosine kinases (RTKs) involved in mammalian development,
is overexpressed by a variety of different cancer cell types. EphA2 expression is
associated with poor prognosis.;
Origin ID : C203620;
chemical_or_drug_affects_cell_type_or_tissue
- chemical_or_drug_has_mechanism_of_action
- chemical_or_drug_has_physiologic_effect
- concept_is_in_subset
- has_target
