We are delighted that Drs. Jourdan and Dastugue of the Bordeau, Grenoble, Marseille, Toulouse (BGMT) intergroup confirmed most of our findings in de novo acute myeloid leukemia (AML) with t(6;11)(q27;q23). In light of our experience, it would be interesting to know whether any of the patients in the BGMT series underwent transplantation, including the patient who survived for 47 months.

We are now able to provide additional follow-up information on the two long-term survivors from our article.1 At last follow-up, Patient 1 remained alive and in remission at 73 months after diagnosis. However, Patient 2, who was the only Cancer and Leukemia Group B (CALGB) patient to undergo allogeneic transplantation in first complete remission (CR1), developed a recurrence nearly 6 years after undergoing transplantation. Cytogenetic analysis at the time of recurrence revealed t(6;11)(q27;q23) and del(13)(q12q21) in all 15 metaphase cells studied. The patient achieved a second CR after reinduction chemotherapy followed by infusion of additional donor cells and remained in remission at last follow-up 5 months later, 76 months after initial diagnosis. In addition, we recently identified another patient with de novo AML and t(6;11) from CALGB 9621. The patient was an African-American man age 23 years who presented with AML (French–American–British subtype M1), white blood cell count 1 × 109/L, hemoglobin 10 g/dL, platelets 138 × 109/L, and no organ involvement. The karyotype at diagnosis was 46,XY,del(5)(q13q33), t(6;11)(q27;q23)[20]. He achieved a CR with induction therapy and underwent an autologous transplantation in CR1, but he developed a recurrence at 14 months and died at 24 months after diagnosis. These data are consistent with those reported previously on the CALGB and literature patients and further support the notion that t(6;11) occurs with greater frequency among African Americans.1

Clearly, additional basic research and new therapies are necessary for this rare but high-risk subset of patients. Elucidation of the role of the AF6 gene, the fusion partner of the MLL gene in t(6;11)(q27;q23), may help to identify new targets for therapy. For example, AF6 may have an important role in Ras-dependent activation of the Ras-Raf protein kinase cascade.2 If the interaction of AF6 and Ras is perturbed in t(6;11) AML, then targeting Ras activity through new agents, such as farnesyl transferase inhibitors, may be an attractive investigational therapy in this rare form of leukemia.


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William Blum M.D.*, Krzysztof Mrózek M.D., Ph.D.*, Amy S. Ruppert M.A.S.* †, Clara D. Bloomfield M.D*, * For Cancer and Leukemia Group B, Division of Hematology and Oncology, Department of Internal Medicine, Comprehensive Cancer Center, The Ohio State University, Columbus, Ohio, † Cancer and Leukemia Group B Statistical Center, Durham, North Carolina.