MEF2D fusions, a recurrent feature in B-cell precursor acute lymphoblastic leukemia (BCP-ALL), are associated with poor prognosis. Zhang and colleagues dissect the molecular mechanisms underlying the pathogenic function of the… Click to show full abstract
MEF2D fusions, a recurrent feature in B-cell precursor acute lymphoblastic leukemia (BCP-ALL), are associated with poor prognosis. Zhang and colleagues dissect the molecular mechanisms underlying the pathogenic function of the MEF2D-HNRNPUL1 fusion, revealing that it impairs B-cell development. The authors also show that the HDAC inhibitor panobinostat in combination with chemotherapy improves overall survival in a murine model, suggesting a potential targeted intervention for BCP-ALL bearing MEF2D fusions.
               
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