CD56-targeted

Acute myeloid leukemia (AML) is a heterogeneous hematological malignancy that starts from bone marrow and spreads to other organs. At the time of diagnosis, both innate and defective natural killer (NK) cells are present in AML patients. The dysfunction of the NK cells is due to the absence of NK cell receptors such as NKG2D on tumor cells that help with tumor immune escape, and also the polycomb protein, EzH2, which plays an important role in the commitment and differentiation of NK cells. The inhibition of EzH2 activates NK cells towards enhanced lytic activity. However, the adoptive transfer of NK cells for cancer treatment is still under scrutiny due to limitations like production cost, vein-to-vein time, and complicated experimental procedures. In order to circumvent these issues, here,