Report of 34 patients with clonal chromosomal abnormalities in Philadelphia-negative cells during imatinib treatment of Philadelphia-positive chronic myeloid leukemia
Autor: | Odile Maarek, G L Roux, C Leonard, M J Mozziconacci, Franck E. Nicolini, Y Yacouben, M Imbert, C. Charrin, Virginie Eclache, M Vigier, C Gervais, Christine Terré, F Nguyen Khac, J P Vernant, J Roussi, Vincent Leymarie, Franck Viguié, Norbert Vey, Guillaume Laurent, G. Flandrin, Hossein Mossafa, J. N. Bastie, Michel Lessard, Marina Lafage-Pochitaloff, J van den Akker, B Salles, Christian Recher, Pascaline Talmant, Nicole Dastugue, Sylvie Castaigne, Stéphane Giraudier, Philippe Rousselot, Francine Mugneret, N Auger, Frédéric Maloisel |
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Rok vydání: | 2004 |
Předmět: |
Oncology
Adult Male Cancer Research medicine.medical_specialty Myeloid Trisomy 8 Leukemia Myeloid Chronic Atypical BCR-ABL Negative Piperazines hemic and lymphatic diseases Internal medicine Leukemia Myelogenous Chronic BCR-ABL Positive medicine Humans neoplasms Aged Retrospective Studies Chromosome Aberrations Hematology business.industry Incidence Myeloid leukemia Imatinib Middle Aged medicine.disease Aneuploidy Prognosis Clone Cells Leukemia Imatinib mesylate medicine.anatomical_structure Pyrimidines Immunology Benzamides Imatinib Mesylate Female business Tyrosine kinase Chromosomes Human Pair 7 medicine.drug Chromosomes Human Pair 8 |
Zdroj: | Leukemia. 18(8) |
ISSN: | 0887-6924 |
Popis: | Imatinib mesylate (Gleevec), an inhibitor of the BCR-ABL tyrosine kinase, was introduced recently into the therapy of chronic myeloid leukemia (CML). Several cases of emergence of clonal chromosomal abnormalities after therapy with imatinib have been reported, but their incidence, etiology and prognosis remain to be clarified. We report here a large series of 34 CML patients treated with imatinib who developed Philadelphia (Ph)-negative clones. Among 1001 patients with Ph-positive CML treated with imatinib, 34 (3.4%) developed clonal chromosomal abnormalities in Ph-negative cells. Three patients were treated with imatinib up-front. The most common cytogenetic abnormalities were trisomy 8 and monosomy 7 in twelve and seven patients, respectively. In 15 patients, fluorescent in situ hybridization with specific probes was performed in materials archived before the initiation of imatinib. The Ph-negative clone was related to previous therapy in three patients, and represented a minor pre-existing clone that expanded after the eradication of Ph-positive cells with imatinib in two others. However, in 11 patients, the new clonal chromosomal abnormalities were not detected and imatinib may have had a direct effect. No myelodysplasia was found in our cohort. With a median follow-up of 24 months, one patient showed CML acceleration and two relapsed. |
Databáze: | OpenAIRE |
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