E355G mutation appearing in a patient with e19a2 chronic myeloid leukaemia resistant to imatinib

The development of imatinib is a milestone in the treatment of chronic myeloid leukaemia (CML), and its therapeutic effect has been extensively investigated in patients with CML who carry M-bcr and m-bcr BCR–ABL fusion transcripts. However, knowledge about its therapeutic effect on patients with CML...

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Published inJournal of clinical pathology Vol. 63; no. 8; pp. 737 - 740
Main Authors Bennour, Ayda, Beaufils, Nathalie, Sennana, Halima, Meddeb, Balkis, Saad, Ali, Gabert, Jean
Format Journal Article
LanguageEnglish
Published London BMJ Publishing Group 01.08.2010
BMJ Publishing Group LTD
Subjects
Adult
Antineoplastic Agents - therapeutic use
Benzamides
Biological and medical sciences
DNA Mutational Analysis - methods
DNA, Neoplasm - genetics
Drug Resistance, Neoplasm - genetics
Female
Fusion Proteins, bcr-abl - genetics
Hematologic and hematopoietic diseases
Humans
Imatinib Mesylate
Investigative techniques, diagnostic techniques (general aspects)
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Medical sciences
Mutation
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Piperazines - therapeutic use
Pyrimidines - therapeutic use
Reverse Transcriptase Polymerase Chain Reaction - methods
Human
Resistance
Myeloproliferative syndrome
Anatomic pathology
Imatinib
Chronic myelogenous leukemia
Genetics
Malignant hemopathy
Mutation
Cancer
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Summary:The development of imatinib is a milestone in the treatment of chronic myeloid leukaemia (CML), and its therapeutic effect has been extensively investigated in patients with CML who carry M-bcr and m-bcr BCR–ABL fusion transcripts. However, knowledge about its therapeutic effect on patients with CML who have the rare BCR–ABL fusion transcript e19a2 (μ-bcr) remains sparse. This report describes a patient with Philadelphia-positive chronic myeloid leukaemia with e19a2 rearrangement, in whom E355G mutation had been acquired. The patient was resistant to imatinib treatment based on conventional cytogenetic and fluorescence in situ hybridisation analysis.
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ISSN:0021-9746
1472-4146
DOI:10.1136/jcp.2010.078311