IMAGE: In the femur of a control mouse (left), AML cells (white arrowhead) have displaced most of the normal bone marrow cells (black arrowhead). But the situation is reversed upon treatment… view more
Credit: Mitchell et al., 2018
Researchers from the Albert Einstein College of Medicine in New York have discovered that a signaling protein elevated in patients with acute myeloid leukemia (AML) plays a much wider role in the disease than previously thought. The study, which will be published May 17 in the Journal of Experimental Medicine, raises hopes that current efforts to target this signaling protein could be a successful strategy to treat AML and other blood cancers.
AML is driven by leukemic stem cells that differentiate abnormally and proliferate excessively, eventually displacing normal, healthy blood stem cells from the bone marrow. Leukemic stem cells are usually resistant to traditional chemotherapies, and so researchers are trying to develop new, more targeted approaches to eliminate these crucial cells.
One possible target is a protein called interleukin-1 receptor accessory protein (IL1RAP), which is often highly expressed on the surface of leukemic stem cells but largely absent from normal blood stem cells. But whether leukemic stem cells require IL1RAP to
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