Deregulated gene expression profiles and regulatory networks in RUNX1/RUNX1T1-positive AML patients
- 1. Department of Hematology, Venizeleio General Hospital of Heraklion, Crete, Greece
- 2. Department of Biochemistry and Molecular Biology, Institute for Personalized Medicine, The Pennsylvania State University College of Medicine, Hershey, PA 17033, USA
- 3. Department of Life Sciences, School of Sciences, European University Cyprus, 1516, Nicosia, Cyprus; Cancer Genetics, Genomics and Systems Biology laboratory, Basic and Translational Cancer Research Center (BTCRC), Nicosia 1516, Cyprus
Contributors
Contact person:
- 1. Department of Life Sciences, School of Sciences, European University Cyprus, 1516, Nicosia, Cyprus; Cancer Genetics, Genomics and Systems Biology laboratory, Basic and Translational Cancer Research Center (BTCRC), Nicosia 1516, Cyprus
Description
AML is a heterogeneous and complex disease. RUNX1/RUNX1T1 is a fusion oncogene resulting from the chromosomal translocation t(8;21) and plays a crucial role in AML. However, its impact on the transcriptomic profile of different groups of age among AML patients is not completely understood. We aimed to investigate the deregulated gene expression profiles in RUNX1/RUNX1T1-positive AML patients, and compare their functions and regulatory networks between adult and pediatric patients. Our data corroborate that the RUNX1/RUNX1T1 fusion reprograms a large transcriptional network to establish and maintain leukemia via intricate PPI interactions and kinase-driven phosphorylation events.
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