Document Detail

Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders.
MedLine Citation:
PMID:  12767088     Owner:  NLM     Status:  MEDLINE    
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.
Jorge Cortes; Francis Giles; Susan O'Brien; Deborah Thomas; Maher Albitar; Mary Beth Rios; Moshe Talpaz; Guillermo Garcia-Manero; Stefan Faderl; Laurie Letvak; August Salvado; Hagop Kantarjian
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Cancer     Volume:  97     ISSN:  0008-543X     ISO Abbreviation:  Cancer     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-05-26     Completed Date:  2003-06-20     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0374236     Medline TA:  Cancer     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2760-6     Citation Subset:  AIM; IM    
Copyright Information:
Copyright 2003 American Cancer Society.
Department of Leukemia, The University of Texas, M. D. Anderson Cancer Center, Houston 77030, USA.
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MeSH Terms
Aged, 80 and over
Antineoplastic Agents / therapeutic use*,  toxicity
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy
Leukemia, Myeloid, Acute / drug therapy*
Leukemia, Myelomonocytic, Chronic / drug therapy
Middle Aged
Myelodysplastic Syndromes / drug therapy*
Myeloproliferative Disorders / drug therapy*
Piperazines / therapeutic use*,  toxicity
Polycythemia Vera / drug therapy
Primary Myelofibrosis / drug therapy
Pyrimidines / therapeutic use*,  toxicity
Reg. No./Substance:
0/Antineoplastic Agents; 0/Piperazines; 0/Pyrimidines; 152459-95-5/imatinib

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