The molecular pathogenesis of the NUP98-HOXA9 fusion protein in acute myeloid leukemia

This is the authors' abstract. We don't add key points for this paper.

Recurrent chromosomal translocations are common initiation events and have provided important insights into the pathogenesis of AML, paving the way for the introduction of novel targeted therapies. However, clinical outcomes, in particular for patients with adverse cytogenetic features remain suboptimal. The chromosomal translocation t (7;11)(p15, p15), encoding the fusion protein NUP98-HOXA9 (NHA9), is a rare poor risk cytogenetic event in AML associated with a particularly poor prognosis. NHA9 brings the FG repeat-rich portion of the nucleoporin NUP98 upstream of the homeodomain and PBX heterodimerization domains of HOXA9, and acts as oncogenic transcription factor. 1 The pathogenic events underlying NHA9 remain poorly understood and herein, we aim to characterize the downstream mediators of this oncoprotein by determining the effects of the fusion using human cellular models.