Introduction
Acute myeloid leukemia (AML) with t(6;9)(p23;q34) resulting in the DEK::NUP214 fusion gene represents a rare (0.5-2% of AML) but particularly aggressive subtype classified as adverse-risk in current ELN guidelines. This chromosomal rearrangement frequently co-occurs with FLT3-ITD mutations (present in approximately 78% of cases), creating a dual molecular insult that drives leukemogenesis through disrupted nucleocytoplasmic transport and enhanced FLT3 signaling. Historically, patients with t(6;9) AML have shown poor responses to conventional chemotherapy, with reported 5-year overall survival rates below 20% with chemotherapy alone. Allogeneic hematopoietic stem cell transplantation (allo-HSCT) has emerged as the cornerstone of curative therapy, though comprehensive outcome data specific to this genetic subtype remain limited due to its rarity.
