Researchers around IBC2 Vice Director Stefan Müller have uncovered a mechanism driving the accelerated growth of leukemia cells with a prevalent genetic mutation. The study focused on acute myeloid leukemia (AML), a life-threatening blood cancer prevalent in adults, with a specific mutation in the NPM1 gene. The investigation revealed that leukemia cells carrying this mutation activate specific genes vital for cellular recycling. Published in Cell Reports, the findings present promising therapeutic possibilities, offering fresh insights into combating AML.

The mutated NPM1 variant, known as NPM1c, plays a pivotal role in leukemia development. The interdisciplinary team at Goethe University identified a novel pathway through which NPM1c influences cellular processes, specifically autophagy. This metabolic pathway facilitates self-recycling, aiding in the removal of defective molecules and providing essential building blocks for cancer cells. By elucidating how NPM1c binds to members of the autophagy modifier family GABARAP, the researchers pave the way for potential drug development to target this interaction, offering a novel approach to impede leukemia cell growth.