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Not all imatinib resistance in CML are BCR-ABL kinase domain mutations.

Journal article
Authors Yuan Wei
Mats Hardling
Bob Olsson
Rahil Hezaveh
Anne Ricksten
Dick Stockelberg
Hans Wadenvik
Published in Annals of hematology
Volume 85
Issue 12
Pages 841-7
ISSN 0939-5555
Publication year 2006
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Institute of Medicine, Department of Internal Medicine
Pages 841-7
Language en
Links dx.doi.org/10.1007/s00277-006-0171-...
Keywords Adult, Aged, Aged, 80 and over, Antineoplastic Agents, therapeutic use, Drug Resistance, Neoplasm, genetics, Female, Fusion Proteins, bcr-abl, genetics, Gene Frequency, Humans, Leukemia, Myeloid, Chronic, diagnosis, drug therapy, genetics, pathology, Male, Middle Aged, Mutation, Neoplasm Staging, Piperazines, therapeutic use, Prognosis, Protein Kinases, genetics, Protein Structure, Tertiary, genetics, Pyrimidines, therapeutic use, Treatment Outcome
Subject categories Hematology

Abstract

Point mutations within the ABL kinase domain of the BCR-ABL gene are associated with clinical resistance to imatinib mesylate in chronic myeloid leukemia (CML). To obtain more information about the association between BCR-ABL mutations and type of imatinib resistance, we studied 30 early chronic phase (CP) CML patients, commencing imatinib therapy, using a conventional sequencing technique. Seven patients treated in late CP and three patients treated in the accelerated phase were included for comparison. Blood samples were collected before and every third month during imatinib therapy. Mutations were not seen in any blood sample collected before start of therapy. During imatinib treatment, 2 of the 30 early CP patients acquired point mutations and both of them had other signs of imatinib resistance. None of the five early CP patients with a complete hematologic response (HR), but no cytogenetic response at 12 months, displayed any missense mutation. Likewise, none of 12 early CP patients with detectable BCR-ABL transcripts but in complete hematologic and cytogenetic remission at 12 months displayed any mutation. We conclude that screening early CP patients for BCR-ABL mutations before start of imatinib therapy is not cost-effective. BCR-ABL kinase domain mutations do not appear to explain cytogenetic or molecular (detectable BCR-ABL transcripts by polymerase chain reaction) disease persistence in patients otherwise in stable disease. However, in patients with signs of expanding disease burden, a search for BCR-ABL mutations is warranted.

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