New research may provide a new avenue for the treatment of Acute Myeloid Leukemia (AML) and a solution to the high rate of disease relapse experienced by patients. The research found that a protein on the surface of AML cells called CD47 binds to a protein called SIRPα, causing macrophages to develop immune tolerance to AML cells. When SIRPα signalling was absent, macrophages were able to clear human leukemia stem cells (LSC). This finding is significant, as it is believed that relapse of disease is driven by LSCs that survive conventional chemotherapy. The researchers confirmed these results by treating mice that had been engrafted with human AML with a novel protein called SIRPα-Fc that can block CD47 on the leukemia cells. They found that treatment with the protein enhanced phagocytosis of AML cells by macrophages and reduced AML growth in the mice. “This study is an important step forward in our understanding of leukemia stem cells and has opened the door to a new line of therapies that could have a significant clinical impact by preventing relapse of AML,” says Dr. Tom Hudson, President and Scientific Director of Ontario Institute for Cancer Research.
