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Translocation t(6;9) is a rare cytogenetic abnormality found in fewer than 5% of pediatric and adult cases of acute myelogenous leukemia (AML). The outcomes of t(6;9) AML are generally poor, with low five-year overall survival and increased risk for relapse. Furthermore, FLT3-ITD is one of the most common molecular abnormalities found in AML that is associated with increased risk of treatment failure and mortality. Allogeneic hematopoietic cell transplantation (HCT) with the best available donor is a standard treatment option for these cases once remission is achieved. We report a challenging case of t(6;9) and FLT3-positive AML in a young adult male. After failing multiple standard induction regimens, morphologic remission was eventually achieved with a FLT3 inhibitor (sorafenib) and a hypomethylating agent (azacytidine). However, despite allogeneic HCT and re-initiation of sorafenib in the post-HCT setting, he experienced early relapse with the original [FLT3-ITD and t(6;9)] and new (FLT3-D835 and +8) molecular and cytogenetic markers, respectively. This case highlights the need for improved strategies in the post-HCT setting for high-risk AML.

The Challenge of t(6;9) and FLT3-Positive Acute Myelogenous Leukemia in a Young Adult