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Experts from the University of Nottingham have discovered how a common genetic mutation disrupts the positioning of a key protein during cell division, revealing a new mechanism behind acute myeloid leukemia and a potential avenue for future treatment.

Acute myeloid leukemia (AML) is an aggressive blood cancer that disrupts the production of healthy blood cells. Around one-third of patients carry a mutation in a gene called NPM1, which causes its protein to accumulate in the wrong part of the cell and plays a key role in driving the disease.

Until now, research has largely focused on how the mutated protein moves between the cell's nucleus and the surrounding cytoplasm. But a new study, led by Dr. Daniel Booth and Dr. Claire Seedhouse at the University of Nottingham's School of Medicine, reveals that what happens during cell division itself is also critical.

Published in Nature Communications, the findings uncover a previously unknown mechanism that helps explain how the mutation disrupts the normal organization of proteins inside leukemia cells.

"For many years, researchers have focused on how this mutated protein is transported around the cell. What we've discovered is that something important happens during cell division itself. The surface of chromosomes acts like a temporary docking station, helping proteins find their way back to the right place after a cell divides. In leukemia cells, this process doesn't work properly," said Booth.

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