From left to right: Prof. Dr. Thomas Klingebiel, Prof. Dr. Hubert Serve, Karin Einhold-Kranz, Prof. Dr. Jan-Henning Klusmann, Prof. Dr. Enrico Schleiff. The image was taken from https://www.kinderkrebs-frankfurt.de/eine-million-euro-forschungsgelder-fuer-krebskranke-kinder/.

RUNX1 isoform disequilibrium promotes the development of ML-DS

Recently, our long running project on the transcription factor RUNX1 was published in BLOOD. We are happy to share a publication that shows the importance of the equilibrium between different RUNX1 isoforms in Down syndrome associated AML. More specifically, we provide proof on how the overexpression of RUNX1A, due to aneuploidy of Chromosome 21 in ML-DS, promotes cell proliferation and malignancy. The effects of RUNX1A overexpression have been linked to a synergistic effect with GATA1s expression and an downstream interaction with MYC:MAX dimerization, therefore promoting oncogenesis.

We like to thank all the contributors of this collaborative work adding to our understanding of ML-DS.

Sofia Gialesaki, et al., RUNX1 isoform disequilibrium promotes the development of trisomy 21 associated myeloid leukemia. Blood 2022; blood.2022017619. doi: https://doi.org/10.1182/blood.2022017619

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