Acute myeloid leukemia manages to cleverly evade the surface markers that the immune system recognizes in order to attack malignant cells. But Mount Sinai researchers have successfully deciphered the biological mechanisms of that resistance and proposed a novel combination treatment, which has shown considerable promise in mouse and human models.
Patients with acute myeloid leukemia (AML) have not benefited from the use of T-cell checkpoint blockade immunotherapy, to date. AML manages to cleverly evade the surface markers that the immune system recognizes in order to attack malignant cells.
But researchers at the Icahn School of Medicine at Mount Sinai have successfully deciphered the biological mechanisms of that resistance and proposed a novel combination treatment that has shown considerable promise in mouse and human models. The regimen consists of antibody-mediated inhibition of the shedding of the proteins MICA and MICB expressed by cancer cells, which, in turn, promotes macrophage-driven destruction of leukemia cells. The process is described in a research article currently in press in the journal Blood.
