A01
Role of FBXO41 in maintaining the undifferentiated state in acute myeloid leukemia
Project Summary
Acute myeloid leukemia (AML) is the most common form of acute leukemia and mainly affects elderly people. It is a highly heterogeneous disease marked by the sequential acquisition of driver mutations leading to a differentiation block in hematopoiesis of the myeloid lineage coupled with extensive proliferation, which increases the number of immature myeloblasts in the blood and bone marrow. Even though next-generation sequencing facilitated risk stratification strategies, genetic characterizations of this disease largely failed to identify novel targeted treatment approaches, keeping the 5-year survival rate as low as 30%. Therefore, investigating post-translational mechanisms such as ubiquitylation holds great promise to identify new actionable targets in AML.
In this study, we aim to identify new vulnerabilities of the ubiquitin-proteasome system (UPS) in AML to understand the underlying mechanisms of the differentiation block on a post-translational level.
