
In t(6;9) AML, DEK::NUP214 acts as a transcriptional activator of FOXC1 and HOX genes. Multi-omics analysis of 57 AML samples showed selective sensitivity to XPO1 inhibitors, notably Selinexor and Eltanexor. DEK::NUP214 binds FOXC1 and HOXA/B promoters, a process reversed by XPO1 inhibition, supporting a mechanistic rationale for targeted therapy in this distinct AML subtype.
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