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<lom:langstring xml:lang="x-none">10.1038/s41375-025-02593-8</lom:langstring>

  
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<lom:title>
  
<lom:langstring xml:lang="en">DEK::NUP214 acts as an XPO1-dependent transcriptional activator of essential leukemia genes</lom:langstring>

  
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<lom:langstring xml:lang="en">The t(6;9)(p22.3;q34.1) translocation/DEK::NUP214 fusion protein defines a distinct subgroup of younger AML patients classified as a separate disease entity by the World Health Organization. DEK is a nuclear factor with multifunctional roles, including gene regulation, while its fusion partner, NUP214, plays a pivotal role in nuclear export by interacting with transport receptors such as XPO1. However, the precise mechanism by which DEK::NUP214 drives leukemia remains unclear. A comprehensive multi-omics comparison of 57 AML primary samples (including whole genome sequencing, targeted sequencing, transcriptomics, and drug screening with &gt;500 compounds) revealed that t(6;9) cases display a selective response to XPO1 inhibitors (Selinexor &amp; Eltanexor) and a distinct transcriptomic signature characterized by the overexpression of FOXC1 and HOX genes that are key leukemia mediators. CUT&amp;RUN experiments demonstrated the direct binding of DEK::NUP214 to the promoters of FOXC1 and HOXA/B clusters. Strikingly, the expression of these genes and the binding of DEK::NUP214 to their regulatory regions were selectively reduced upon XPO1 inhibition in t(6;9) cells. Altogether, these results identified a novel function of DEK::NUP214 as an XPO1-dependent transcriptional activator of key leukemia drivers and provide a rationale to explore the use of XPO1 inhibitors in this patient population.</lom:langstring>

  
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<lom:language>eng</lom:language>

  
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<lom:langstring xml:lang="en">Acute Myeloid Leukaemia</lom:langstring>

  
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<lom:datetime>2025-11-25T14:40:24.808Z</lom:datetime>

  
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