Abstract
In the LAME89/91 protocol, children with acute myeloid leukemia (AML) who achieved complete remission (CR) after induction chemotherapy, were treated either with allogeneic bone marrow transplantation (BMT) if they had an HLA-compatible related donor or with chemotherapy including high-dose cytarabine. The objectives of this study were to describe the overall results of this strategy and to compare the two post-remission arms. Two hundred and thirty-one children were enrolled in the protocol. Induction chemotherapy consisted of a combination of cytarabine and mitoxantrone. A CR was achieved in 204 children (88%). Fifty-one of them had an HLA-identical sibling donor and were eligible for BMT. These 51 patients, as well as two additional children who had a one antigen HLA-mismatched father, received BMT during first CR. Consequently, 53 patients were analysed in the BMT group and 151 in the chemotherapy group. With a mean follow up duration in the study of 38 ± 2 months, overall event-free survival (EFS) was 47 ± 7% at 4 years for the 231 patients entered into the protocol. The 4-year disease-free survival (DFS) was 53 ± 8% for the 204 patients who achieved complete remission after induction therapy. The 4-year probability of relapse was 28 ± 14% in the BMT group and 47 ± 9% in the chemotherapy group (p = 0.02). The risk of therapy-related death was 6.2% for BMT and 8.1% for chemotherapy. DFS was 68 ± 14% in the BMT group and 48 ± 9% in the chemotherapy group (p = 0.02). We conclude that allogeneic BMT from a matched sibling donor is the treatment of choice for reducing the relapse risk and for increasing DFS in children with AML in first CR.
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Research grant support: Supported by “l’Association pour la Recherche contre le Cancer (ARC)”
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Michel, G., Baruchel, A., Tabone, M.D. et al. Induction chemotherapy followed by allogeneic bone marrow transplantation or aggressive consolidation chemotherapy in childhood acute myeloblastic leukemia: A prospective study from the French Society of Pediatric Hematology and Immunology (SHIP). Hematol Cell Ther 38, 169–176 (1996). https://doi.org/10.1007/s00282-996-0169-7
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DOI: https://doi.org/10.1007/s00282-996-0169-7