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dc.contributor.authorSerpa, Mariana [UNIFESP]
dc.contributor.authorSanabani, Sabri S. [UNIFESP]
dc.contributor.authorDorlhiac-Llacer, Pedro Enrique
dc.contributor.authorNardinelli, Luciana
dc.contributor.authorFerreira, Patricia de Barros
dc.contributor.authorBorges Martins, Thays Fernanda
dc.contributor.authorSeguro, Fernanda [UNIFESP]
dc.contributor.authorBendit, Israel
dc.date.accessioned2016-01-24T14:17:46Z
dc.date.available2016-01-24T14:17:46Z
dc.date.issued2012-01-01
dc.identifierhttp://dx.doi.org/10.1159/000333092
dc.identifier.citationActa Haematologica. Basel: Karger, v. 127, n. 1, p. 56-59, 2012.
dc.identifier.issn0001-5792
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/34495
dc.description.abstractDespite 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. Copyright (C) 2011 S. Karger AG, Baselen
dc.description.sponsorshipFundacao Maria Cecilia Souto Vidigal
dc.format.extent56-59
dc.language.isoeng
dc.publisherKarger
dc.relation.ispartofActa Haematologica
dc.rightsAcesso restrito
dc.subjectBCR-ABL kinaseen
dc.subjectChronic myelogenous leukemiaen
dc.subjectF359I point mutationen
dc.subjectKinase inhibitorsen
dc.subjectSuboptimal responseen
dc.titleDasatinib Overrides Imatinib Resistance Mediated by the F359I Residue Mutation in Two Patients with Chronic Myeloid Leukemiaen
dc.typeArtigo
dc.rights.licensehttp://www.karger.com/Services/RightsPermissions
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv São Paulo, Dept Hematol, Sch Med, Fac Med, BR-05403000 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Clin Immunol & Allergy Div, BR-05403000 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Dept Infect Dis, BR-05403000 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Canc Inst São Paulo, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Translat Med, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Canc Inst São Paulo, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Translat Med, São Paulo, Brazil
dc.identifier.doi10.1159/000333092
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000297372400013


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