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Vol. 127, No. 1, 2012
Issue release date: December 2011
Section title: Case Report
Acta Haematol 2012;127:56–59
(DOI:10.1159/000333092)

Dasatinib Overrides Imatinib Resistance Mediated by the F359I Residue Mutation in Two Patients with Chronic Myeloid Leukemia

Serpa M.a, d · Sanabani S.S.b, c, e · Dorlhiac-Llacer P.E.a · Nardinelli L.a · de Barros Ferreira P.a · Borges Martins T.F.a · Seguro F.a, d · Bendit I.a
aDepartment of Hematology, Faculty of Medicine, bClinical Immunology and Allergy Division, and cDepartment of Infectious Disease, University of São Paulo, dCancer Institute of São Paulo, and eDepartment of Translational Medicine, Federal University of São Paulo, São Paulo, Brazil

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Article / Publication Details

First-Page Preview
Abstract of Case Report

Received: 6/9/2011 5:24:43 PM
Accepted: 8/11/2011
Published online: 11/17/2011
Issue release date: December 2011

Number of Print Pages: 4
Number of Figures: 1
Number of Tables: 0

ISSN: 0001-5792 (Print)
eISSN: 1421-9662 (Online)

For additional information: http://www.karger.com/AHA

Abstract

Despite the beneficial effects of imatinib mesylate, some patients may either not respond or respond suboptimally. Here, we report two chronic myelogenous leukemia patients; one had a suboptimal response according to European LeukemiaNet criteria (a major molecular response was not achieved after 18 months of standard-dose imatinib therapy) and the other had failure with a standard dose of imatinib. At the time of the suboptimal response in patient 1 and the failure in patient 2, we were able to detect the F359I mutation in the BCR-ABL tyrosine kinase domain using DNA sequencing in both patients. Therefore, it was decided to change the therapeutic regimen to dasatinib at a dose of 100 mg once daily in both patients. This change resulted in the achievement of complete cytogenetic remission in patient 1 after 4 months and a major molecular response within 2 and 3 months in both patients. Detection of the F359I mutation in our two cases likely explains the suboptimal response to imatinib in case 1 and the failure in case 2. This implies that in such cases dasatinib should be considered to effectively suppress the mutated clones.


  

Author Contacts

Israel Bendit, MD, PhD
Department of Hematology, University of Sao Paulo Medical School
Av Dr Eneas de Carvalho Aguiar 155, 1st Floor, Room 30
São Paulo 05403-000 (Brazil)
Tel. +55 11 3061 5544, ext. 312, E-Mail isbendit@usp.br

  

Article Information

Received: June 9, 2011
Accepted after revision: August 11, 2011
Published online: November 17, 2011
Number of Print Pages : 4
Number of Figures : 1, Number of Tables : 0, Number of References : 19

  

Publication Details

Acta Haematologica

Vol. 127, No. 1, Year 2012 (Cover Date: December 2011)

Journal Editor: Ben-Bassat I. (Qiryat-Ono)
ISSN: 0001-5792 (Print), eISSN: 1421-9662 (Online)

For additional information: http://www.karger.com/AHA


Article / Publication Details

First-Page Preview
Abstract of Case Report

Received: 6/9/2011 5:24:43 PM
Accepted: 8/11/2011
Published online: 11/17/2011
Issue release date: December 2011

Number of Print Pages: 4
Number of Figures: 1
Number of Tables: 0

ISSN: 0001-5792 (Print)
eISSN: 1421-9662 (Online)

For additional information: http://www.karger.com/AHA


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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