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 in | Journal of clinical pathology Vol. 63; no. 8; pp. 737 - 740 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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BMJ Publishing Group
01.08.2010
BMJ Publishing Group LTD |
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| Abstract | 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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| AbstractList | 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 (mu-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. 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. 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. 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-bcrBCR-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. 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 (k-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. |
| Author | Meddeb, Balkis Sennana, Halima Beaufils, Nathalie Bennour, Ayda Gabert, Jean Saad, Ali |
| Author_xml | – sequence: 1 givenname: Ayda surname: Bennour fullname: Bennour, Ayda email: aydabennour@yahoo.fr organization: Department of Cytogenetics Molecular Genetics and Reproductive Biology, Farhat Hached University Teaching Hospital, Sousse, Tunisia – sequence: 2 givenname: Nathalie surname: Beaufils fullname: Beaufils, Nathalie email: aydabennour@yahoo.fr organization: Laboratory of Biochemistry and Molecular Biology, Nord Hospital, Marseille, France – sequence: 3 givenname: Halima surname: Sennana fullname: Sennana, Halima email: aydabennour@yahoo.fr organization: Department of Cytogenetics Molecular Genetics and Reproductive Biology, Farhat Hached University Teaching Hospital, Sousse, Tunisia – sequence: 4 givenname: Balkis surname: Meddeb fullname: Meddeb, Balkis email: aydabennour@yahoo.fr organization: Department of Clinical Hematology Aziza Othmana Hospital, Tunis, Tunisia – sequence: 5 givenname: Ali surname: Saad fullname: Saad, Ali email: aydabennour@yahoo.fr organization: Department of Cytogenetics Molecular Genetics and Reproductive Biology, Farhat Hached University Teaching Hospital, Sousse, Tunisia – sequence: 6 givenname: Jean surname: Gabert fullname: Gabert, Jean email: aydabennour@yahoo.fr organization: Laboratory of Biochemistry and Molecular Biology, Nord Hospital, Marseille, France |
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| Cites_doi | 10.1182/blood.V76.9.1819.1819 10.1038/sj/leu/2401592 10.1016/j.leukres.2007.03.001 10.1038/sj.leu.2403454 10.1038/sj.leu.2404236 10.1002/ajh.21366 10.1080/10428190902930496 10.1182/blood-2005-03-1036 10.1136/jcp.2005.029595 10.1002/hon.822 10.1182/blood-2009-08-215939 |
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| Keywords | Human Resistance Myeloproliferative syndrome Anatomic pathology Imatinib Chronic myelogenous leukemia Genetics Malignant hemopathy Mutation Cancer |
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| References | Saglio, Guerrasio, Rosso 1990; 76 Popovici, Charbonnier, Gisserot 2008; 32 Verma, Fava, Kantarjian 2009; 84 Lee, Kim, Kim 2004; 18 Nicolini, Corm, Lê 2006; 20 Andrikovics, Nahajevszky, Szilvási 2007; 25 Mondal, Majumdar, Dasgupta 2006; 59 Branford, Melo, Hughes 2009; 114 Willis, Lange, Demehri 2005; 106 Van Dongen, Macintyre, Gabert 1999; 13 Mascarenhas, Cunha, Miranda 2009; 50 Saglio (2024053014360391000_63.8.737.1) 1990; 76 2024053014360391000_63.8.737.8 2024053014360391000_63.8.737.9 2024053014360391000_63.8.737.11 2024053014360391000_63.8.737.4 2024053014360391000_63.8.737.5 2024053014360391000_63.8.737.6 2024053014360391000_63.8.737.10 2024053014360391000_63.8.737.7 2024053014360391000_63.8.737.2 2024053014360391000_63.8.737.3 |
| References_xml | – volume: 114 start-page: 5426 year: 2009 article-title: Selecting optimal second-line tyrosine kinase inhibitor therapy for chronic myeloid leukemia patients after imatinib failure: does the BCR–ABL mutation status really matter? publication-title: Blood contributor: fullname: Hughes – volume: 25 start-page: 143 year: 2007 article-title: First and second line imatinib treatment in chronic myelogenous leukemia patients expressing rare e1a2 or e19a2 BCR–ABL transcripts publication-title: Hematol Oncol contributor: fullname: Szilvási – volume: 13 start-page: 1901 year: 1999 article-title: Standardized RT-PCR analysis of fusion gene transcripts from chromosome aberrations in acute leukaemia for detection of minimal residual disease. Report of the BIOMOED-1 Concerted Action: investigation of minimal residual disease in acute leukaemia publication-title: Leukemia contributor: fullname: Gabert – volume: 76 start-page: 1819 year: 1990 article-title: New type of Bcr/Abl junction in Philadelphia chromosome-positive chronic myelogenous leukemia publication-title: Blood contributor: fullname: Rosso – volume: 106 start-page: 2128 year: 2005 article-title: High-sensitivity detection of BCR–ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy publication-title: Blood contributor: fullname: Demehri – volume: 59 start-page: 1102 year: 2006 article-title: e19a2 BCR–ABL fusion transcript in typical chronic myeloid leukaemia: a report of two cases publication-title: J Clin Pathol contributor: fullname: Dasgupta – volume: 50 start-page: 1148 year: 2009 article-title: New mutations detected by denaturing high performance liquid chromatography during screening of exon 6 bcr–abl mutations in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors publication-title: Leuk Lymphoma contributor: fullname: Miranda – volume: 18 start-page: 1539 year: 2004 article-title: Imatinib induces a cytogenetic response in blast crisis or interferon failure chronic myeloid leukemia patients with e19a2 BCR–ABL transcripts publication-title: Leukemia contributor: fullname: Kim – volume: 20 start-page: 1061 year: 2006 article-title: Mutation status and clinical outcome of 89 imatinib mesylate-resistant chronic myelogenous leukemia patients: a retrospectve analysis from the French intergroup of CML (Fi(p)-LMC GROUP) publication-title: Leukemia contributor: fullname: Lê – volume: 32 start-page: 361 year: 2008 article-title: Y253H mutation appearing in a μ-BCR–ABL (e19a2) CML publication-title: Leuk Res contributor: fullname: Gisserot – volume: 84 start-page: 256 year: 2009 article-title: Complexity of BCR–ABL kinase domain mutations during the course of therapy with tyrosine kinase inhibitors in chronic myeloid leukemia publication-title: Am J Hematol contributor: fullname: Kantarjian – volume: 76 start-page: 1819 year: 1990 ident: 2024053014360391000_63.8.737.1 article-title: New type of Bcr/Abl junction in Philadelphia chromosome-positive chronic myelogenous leukemia publication-title: Blood doi: 10.1182/blood.V76.9.1819.1819 contributor: fullname: Saglio – ident: 2024053014360391000_63.8.737.2 doi: 10.1038/sj/leu/2401592 – ident: 2024053014360391000_63.8.737.6 doi: 10.1016/j.leukres.2007.03.001 – ident: 2024053014360391000_63.8.737.9 doi: 10.1038/sj.leu.2403454 – ident: 2024053014360391000_63.8.737.4 doi: 10.1038/sj.leu.2404236 – ident: 2024053014360391000_63.8.737.5 doi: 10.1002/ajh.21366 – ident: 2024053014360391000_63.8.737.3 doi: 10.1080/10428190902930496 – ident: 2024053014360391000_63.8.737.8 doi: 10.1182/blood-2005-03-1036 – ident: 2024053014360391000_63.8.737.10 doi: 10.1136/jcp.2005.029595 – ident: 2024053014360391000_63.8.737.11 doi: 10.1002/hon.822 – ident: 2024053014360391000_63.8.737.7 doi: 10.1182/blood-2009-08-215939 |
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| SubjectTerms | 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 |
| Title | E355G mutation appearing in a patient with e19a2 chronic myeloid leukaemia resistant to imatinib |
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