Heterodimerization of AML1/ETO with CBFβ is required for leukemogenesis but not for myeloproliferation
Just published as an original article in Leukemia are now the results from a cooperative study involving several of the groups of the SFB 1074 project at Ulm University, which we are also a member of.
Its focus was one of the core-binding factor (CBF) variants of acute myeloid leukemia (AML), which is defined by a translocation between chromosomes 8 and 21 and generates the AML1/ETO fusion protein. Using mouse models and a lot of wet-lab work and experiments, our cooperation partners sought to study how this fusion protein mediates leukemic transformation. We supported their work by validating with Illumina RNA sequencing data that the leukemia-initiating murine isoform of AML1/ETO, which they characterized in this work, is i) also expressed in human CBF-AML and ii) not expressed in another AML subtype.