Inversion 16 AML or translocation 16 AML with the co-binding factor CBFB-MYH11 fusion gene is considered to be favorable risk AML. However, most of these patients had the co-mutation either in the receptor tyrosine kinase, or KIT, or FLT3, or NRAS, KRAS, and others. And there is a recent publication from a French group in Blood, 2026, that patients with the inversion 16, but if they have the KIT mutation, or the FLT3 mutation, and especially with MRD positive, are doing worse...
Inversion 16 AML or translocation 16 AML with the co-binding factor CBFB-MYH11 fusion gene is considered to be favorable risk AML. However, most of these patients had the co-mutation either in the receptor tyrosine kinase, or KIT, or FLT3, or NRAS, KRAS, and others. And there is a recent publication from a French group in Blood, 2026, that patients with the inversion 16, but if they have the KIT mutation, or the FLT3 mutation, and especially with MRD positive, are doing worse. So we want to look at this in the context of allogeneic transplantation, and we have 725 patients, 554 with no FLT3, and 171 with FLT3. All are inversion or translocation 16. And there were some caveats that FLT3 received more myeloablative conditioning. They were more transplanted at CR1, and they have less MRD negativity. Because usually we transplant these patients in CR2, and of course, if they have a physician, if they have FLT3 or MRD positive, or they receive more myeloablative conditioning and were transplanted in CR1. So overall, the overall survival was 76%, leukemia-free survival was 68%, relapse 18%, and non-relapse mortality 14%. And when we look at the patients with or without FLT3, there was no difference. So for instance, the two-year overall survival was 74 compared to 78. Leukemia-free survival was both 69%. Relapse in both was less than 20%. And non-relapse mortality was about 12 or 13%. With 30% acute GVHD, about 10% severe acute GVHD, 40% chronic GVHD, and 10% extensive. We also look at CR1, CR2, and the results were similar. So we conclude that there was no interaction between MRD and FLT3. So we conclude that, yes, transplantation in the co-binding factor is with good results. And patients with or without the co-mutation in FLT3 do exactly the same. So maybe the transplantation can overcome the bad prognosis of FLT3. And for future direction, we think that we still need to go in the patient with co-binding factor to see if there is some group of high-risk patients that can benefit from transplant. And of course, now that we can give these patients FLT3 inhibitor or gemtuzumab pre-transplant, maybe the result will be even better.
This transcript is AI-generated. While we strive for accuracy, please verify this copy with the video.