1. Reduced toxicity (FluBu3) versus myeloablative (BuCy) conditioning in acute myeloid leukemia patients who received first allogeneic hematopoietic stem cell transplantation in measurable residual disease-negative CR1.
- Author
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Park S, Bang SY, Kwag D, Lee JH, Kim TY, Lee J, Min GJ, Park SS, Yahng SA, Jeon YW, Shin SH, Yoon JH, Lee SE, Cho BS, Eom KS, Kim YJ, Lee S, Min CK, Cho SG, Lee JW, and Kim HJ
- Subjects
- Humans, Middle Aged, Male, Female, Adult, Neoplasm, Residual, Transplantation, Homologous methods, Aged, Adolescent, Young Adult, Myeloablative Agonists therapeutic use, Allografts, Transplantation Conditioning methods, Leukemia, Myeloid, Acute therapy, Leukemia, Myeloid, Acute mortality, Hematopoietic Stem Cell Transplantation methods
- Abstract
In the present study, reduced toxicity (FluBu3) and myeloablative (BuCy) conditioning were compared in patients with AML who received first allogeneic HSCT in MRD-negative CR1. The study included 124 adult patients who underwent HSCT from an HLA-matched (8/8) sibling, unrelated, or 1-locus mismatched (7/8) unrelated donor (MMUD). The median age was 45 years and intermediate cytogenetics comprised majority (71.8%). The 2-year OS, RFS, CIR and NRM for BuCy (n = 78, 62.9%) and FluBu3 (n = 46, 37.1%) groups were 78.3% and 84.5% (p = 0.358), 78.0% and 76.3% (p = 0.806), 7.7% and 21.5% (p = 0.074) and 14.3% and 2.2% (p = 0.032), respectively. At the time of data cut-off, relapse and NRM were the main causes of HSCT failure in each of the FluBu3 and BuCy arms. Among patients, 75% of relapsed FluBu3 patients had high-risk features of either poor cytogenetics or FLT3-ITD mutation compared with 16.7% of BuCy patients. The majority of NRM in the BuCy group was due to GVHD (73%), half of whom received MMUD transplantation. To conclude, the FluBu3 reduced toxicity conditioning showed comparable post-transplant OS and RFS to BuCy and was associated with significantly reduced NRM that was offset by a trend towards higher risk of relapse even in MRD-negative CR1 population., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)
- Published
- 2024
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