Despite intensive induction therapies, disease relapse remains the major clinical challenge in the treatment of acute myeloid leukemia (AML). This is largely driven by persister cells and resistant subclones that endure the selective pressure of chemotherapy through phenotypic plasticity.

The research project investigates the molecular survival strategies of these cells at the intersection of gene expression and cellular metabolism. While transcript levels often remain stable under cytostatic stress, persister cells selectively modulate their translational efficiency: survival and stress programs are preferentially translated into proteins at the ribosomes.

By integrating translatomic and metabolomic profiling, the scientists identify vulnerabilities within this adaptive network. The goal is to uncover tumor-specific dependencies and develop targeted therapeutic strategies that selectively eradicate persister cells and prevent leukemia relapse.