Project A3: Notch signaling as a novel target of AML/ETO
AML1-ETO9a (AE9a) is an alternatively spliced isoform of the t(8;21) fusion protein and is clinically associated with poor prognosis. In a retroviral bone marrow transplantation model we con-firmed the high oncogenic potential of AE9a. However, in a conditional mouse model of AE9a expression in hematopoietic cells leukemia induction failed. This discrepancy points towards the requirement of additional events (deregulated expression of genes/protein, signals from the niche, etc.) in AE9a-mediated leukemogen-esis in our mouse model. These factors might represent novel promising targets to inhibit leukemia develop-ment. Retroviral insertion mutagenesis will be applied in the genomic mouse model followed by validation of potential candidates using molecular biological/biochemical approaches as well as via comparative analyses of clinical gene expression data sets.
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