AsianScientist (Apr. 4, 2016) – Researchers in Singapore have uncovered a molecular pathway that could serve as a potential drug target for the treatment of acute myeloid leukemia (AML). The findings of the study were published in Nature Communications.
Researchers from the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore has uncovered a new clue that may help in the fight against AML, the most common form of cancer of the blood and bone marrow. The findings could lead to the development of more effective disease treatments.
AML usually originates from the bone marrow, where blood cells are produced. It is characterized by an overproduction of impaired white blood cells. The differentiation of immature white blood cell precursors into functional white blood cells is an essential process which mediates the body’s immunity.
The research team found that an enzyme, GCN5, is able to inactivate a protein called C/EBPα in myeloid precursor cells. As a result, healthy white blood cell formation is disrupted. What is more, they discovered that the inactivation of the C/EBPα protein is carried out by acetylation, a process by which GCN5 adds an acetyl group onto C/EBPα. This then leads to a reduced ability of C/EBPα to bind to DNA.
“As AML is a fast-growing cancer, timely treatment soon after diagnosis could increase patients’ chances of survival. The current main treatment strategy for AML is cytotoxic [meaning toxic to cells] chemotherapy,” said Professor Daniel Tenen, corresponding author and director of CSI Singapore.
“Our research results form the basis of an alternative therapeutic strategy that could potentially reduce remission risks and improve cure rates. Moving forward, the team is looking into designing effective GCN5 inhibitors for therapeutic purposes by studying GCN5 in AML further in depth.”
The article can be found at: Bararia et al. (2016) Acetylation of C/EBPα Inhibits its Granulopoietic Function.
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Source: National University of Singapore; Photo: Shutterstock.
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