Dissecting the role of lymphoid enhancer factor 1 (LEF1) in acute myeloid leukemia

AML is the most frequent acute leukemia in adults and is still associated with a high mortality despite intensive chemotherapy and approaches such as allogeneic transplantation. Thus, there is still an urgent need for innovative treatment options. One prerequisite is a better understanding of the biology of AML. The aim of this thesis was to understand differences in expression of LEF1 isoforms between normal and AML stem cells and based on this to explore the possibility to target AML cells by interfering with the binding of LEF1 to β-catenin. A second goal was to identify factors which collaborate with LEF1 to induce AML as LEF1 alone is only able to induce AML after long latency and only in a part of transplanted mice in a murine bone marrow transplantation model