In acute myeloid leukaemia or AML, normal bone marrow is replaced with leukaemic cells, leading to a rise of abnormal white blood cells and a drop in healthy blood cells. The rare disease progresses rapidly and can quickly lead to death. Now, a team of British scientists h
The team of researchers from the University of Edinburgh have identified a new possible therapeutic target in or AML. Two molecules that act in synergy to put a brake on the development of leukaemic stem cells in the aggressive blood cancer. 
The haematologist Kamil Kranc and his colleagues have identified genes that act as brakes to stop the development of AML.
Two molecules, hypoxia-inducible factor-1α (HIF-1α) and HIF-2α, work together to stop the formation of leukaemic stem cells in this type of blood cancer.
The work shows that if either HIF-2α or both HIF-1α and HIF-2α are blocked, leukaemia develops much faster. Previously, it had been thought that blocking HIF-1α or HIF-2α would stop leukaemia progression.
“Our discovery that HIF-1α and HIF-2α molecules act together to stop leukaemia development is a major milestone in our efforts to combat leukaemia,” commented Kranc. “We now intend to harness this knowledge to develop curative therapies that eliminate leukaemic stem cells, which are the underlying cause of AML.”
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