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Dr. Cortes is a clinical research scholar for The Leukemia and Lymphoma Society, White Plains, New York.
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Original Article
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Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders†
Article first published online: 19 MAY 2003
DOI: 10.1002/cncr.11416
Copyright © 2003 American Cancer Society
Additional Information
How to Cite
Cortes, J., Giles, F., O'Brien, S., Thomas, D., Albitar, M., Rios, M. B., Talpaz, M., Garcia-Manero, G., Faderl, S., Letvak, L., Salvado, A. and Kantarjian, H. (2003), Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders. Cancer, 97: 2760–2766. doi: 10.1002/cncr.11416
- †
Dr. Armand Keating served as guest editor on this article.
Publication History
- Issue published online: 19 MAY 2003
- Article first published online: 19 MAY 2003
- Manuscript Accepted: 27 FEB 2003
- Manuscript Revised: 24 FEB 2003
- Manuscript Received: 13 DEC 2002
- Abstract
- Article
- References
- Cited By
Keywords:
- imatinib mesylate;
- acute myeloid leukemia;
- myelodysplastic syndrome;
- platelet-derived growth factor;
- myelofibrosis;
- polythemia vera
Abstract
BACKGROUND
Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R). c-kit is expressed in most patients with acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) and PDGF has been implicated in the pathogenesis of myeloproliferative disorders (MPD).
METHODS
The authors investigated the efficacy of imatinib in patients with these disorders. Forty-eight patients with AML (n = 10), MDS (n = 8), myelofibrosis (n = 18), atypical chronic myeloid leukemia (CML; n = 7), chronic myelomonocytic leukemia (CMML; n = 3), or polycythemia vera (n = 2) were treated with imatinib 400 mg daily.
RESULTS
None of the patients with AML or MDS responded. Among patients with myelofibrosis, 10 of 14 patients with splenomegaly (71%) had a 30% or greater reduction in spleen size, 1 patient had trilineage hematologic improvement, 2 had erythroid hematologic improvement, and 1 had improvement in platelet count. One patient with atypical CML had erythroid hematologic improvement. Both patients with polycythemia vera needed fewer phlebotomies (from 2–3 per year to none during the 8 months of therapy and from 3–6 per year to 1 during 9 months of therapy). None of the three patients with CMML responded. Treatment was well tolerated. The side effects were similar to those observed in patients with CML.
CONCLUSIONS
Within these small subgroups of disease types, single-agent imatinib did not achieve a significant clinical response among patients with AML, MDS, atypical CML, or CMML without PDGF-R fusion genes. Preliminary data on polycythemia vera are promising and deserve further investigation. Responses among myelofibrosis patients were minor. Therefore, a combination treatment regimen including imatinib may be more effective. Cancer 2003;97:2760–6. © 2003 American Cancer Society.
DOI 10.1002/cncr.0000