Targeted
cancer therapy acts on targeted molecules, is less toxic to normal cells, and acts more specifically on
cancer cells. The two primary strategies for preventing
malignancy growth are the blocking of T-cell repression signals or forwarding of T-cell to
tumor target with both T and
tumor-specific
antibodies. The CAR comprises three domains, the extracellular
antigen recognition domain and the intracellular T-cell signaling domain, which participate in activating T-cells. The two most common adverse effects of CAR T-cell treatment are
cytokine release syndrome (CRS) and
cell-associated neurotoxicity syndrome (CANS). The adaptability of intracellular signaling domains inside CARs allows the cell to counterbalance the downregulation of costimulatory molecules produced by
tumor cells, either indirectly or directly. The major disadvantage of CAR-T cell therapy is off-target toxicity. Treatment with CARs expressing CD3, CD123, Lewis Y, CLL-1, CD44v6, FLT3, and
folate receptors showed promising results in preclinical models of
acute myeloid leukemia (AML). A recent study has revealed that B7-H3 CART cells exhibit significant anticancer efficacy in a variety of solid
tumor preclinical models, including PDAC,
ovarian cancer,
neuroblastoma, and various pediatric
malignancies. The notion of SUPRA CAR, with its unique capacity to alter targets without the need to re-engineer, is a recent innovation in CAR. Given the importance of NK cells in
tumor development and metastatic defence, NK cell-based
immunotherapies, including adoptive transfer of NK cells, have garnered a lot of interest. With the advancement of improved cellular manufacturing methods, novel cellular engineering strategies, precision genome editing technologies, and combination
therapy approaches, we firmly believe that CAR-T cells will soon become an off-the-shelf, cost-effective, and potentially curative
therapy for
oncogenesis.