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Role of the RUNX1-EVI1 fusion gene in leukemogenesis Maki K; Yamagata T; Mitani KCancer Sci 2008[Oct]; 99 (10): 1878-83RUNX1-EVI1 is a chimeric gene generated by t(3;21)(q26;q22) observed in patients with aggressive transformation of myelodysplastic syndrome or chronic myelogenous leukemia. RUNX1-EVI1 has oncogenic potentials through dominant-negative effect over wild-type RUNX1, inhibition of Jun kinase (JNK) pathway, stimulation of cell growth via AP-1, suppression of TGF-beta-mediated growth inhibition and repression of C/EBPalpha. Runx1-EVI1 heterozygous knock-in mice die in uteri due to central nervous system (CNS) hemorrhage and severe defects in definitive hematopoiesis as Runx1-/- mice do, indicating that RUNX1-EVI1 dominantly suppresses functions of wild-type RUNX1 in vivo. Acute myelogenous leukemia is induced in mice transplanted with bone marrow cells expressing RUNX1-EVI1, and a Runx1-EVI1 knock-in chimera mouse developed acute megakaryoblastic leukemia. These results suggest that RUNX1-EVI1 plays indispensable roles in leukemogenesis of t(3;21)-positive leukemia. Major leukemogenic effect of RUNX1-EVI1 is mainly through histone deacetyltransferase recruitment via C-terminal binding protein. Histone deacetyltransferase could be a target in molecular therapy of RUNX1-EVI1-expressing leukemia.|*DNA-Binding Proteins/physiology[MESH]|*Proto-Oncogenes[MESH]|*Transcription Factors[MESH]|Alcohol Oxidoreductases/physiology[MESH]|Animals[MESH]|Chromosomes, Human, Pair 21[MESH]|Chromosomes, Human, Pair 3[MESH]|Core Binding Factor Alpha 2 Subunit/*genetics/metabolism[MESH]|Humans[MESH]|Leukemia/*genetics[MESH]|MDS1 and EVI1 Complex Locus Protein[MESH]|Mice[MESH]|Oncogene Proteins, Fusion/*genetics/metabolism[MESH]|Translocation, Genetic[MESH] |
