BCR-ABL V280G Mutation, Potential Role in Imatinib Resistance: First Case Report
Introduction: The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL tyrosine kinase inhibitors in 2001 have revolutionized disease management, leading to a reduction in mortality rates and accordingly an increase...
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| Published in: | Clinical Medicine Insights. Oncology Vol. 11; pp. 1 - 5-007 |
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| Main Authors: | , , , , , |
| Format: | Journal Article |
| Language: | English |
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2017
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| Abstract | Introduction: The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL tyrosine kinase inhibitors in 2001 have revolutionized disease management, leading to a reduction in mortality rates and accordingly an increase in the estimated prevalence of CML. Case report: Based on medical records and clinical follow-up, the authors present the case of a Philadelphia chromosome-positive CML patient who developed resistance to imatinib. Quantitative reverse transcription-polymerase chain reaction testing revealed a V280G BCR-ABL mutation. Discussion and conclusions: This is the first report describing a new BCR-ABL kinase domain mutation－V280G－that might be associated with resistance to imatinib. Approximately 15% to 30% of patients treated with imatinib discontinue treatment due to resistance or intolerance. More than 90 BCR-ABL mutations were detected so far, conferring variable degrees of drug resistance, with consequent clinical, therapeutic, and prognostic impact. |
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| AbstractList | The identification of
as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of
tyrosine kinase inhibitors in 2001 have revolutionized disease management, leading to a reduction in mortality rates and accordingly an increase in the estimated prevalence of CML.
Based on medical records and clinical follow-up, the authors present the case of a Philadelphia chromosome-positive CML patient who developed resistance to imatinib. Quantitative reverse transcription-polymerase chain reaction testing revealed a V280G
mutation.
This is the first report describing a new
kinase domain mutation-V280G-that might be associated with resistance to imatinib. Approximately 15% to 30% of patients treated with imatinib discontinue treatment due to resistance or intolerance. More than 90
mutations were detected so far, conferring variable degrees of drug resistance, with consequent clinical, therapeutic, and prognostic impact. Introduction:The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL tyrosine kinase inhibitors in 2001 have revolutionized disease management, leading to a reduction in mortality rates and accordingly an increase in the estimated prevalence of CML.Case report:Based on medical records and clinical follow-up, the authors present the case of a Philadelphia chromosome–positive CML patient who developed resistance to imatinib. Quantitative reverse transcription-polymerase chain reaction testing revealed a V280G BCR-ABL mutation.Discussion and conclusions:This is the first report describing a new BCR-ABL kinase domain mutation—V280G—that might be associated with resistance to imatinib. Approximately 15% to 30% of patients treated with imatinib discontinue treatment due to resistance or intolerance. More than 90 BCR-ABL mutations were detected so far, conferring variable degrees of drug resistance, with consequent clinical, therapeutic, and prognostic impact. Introduction: The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL tyrosine kinase inhibitors in 2001 have revolutionized disease management, leading to a reduction in mortality rates and accordingly an increase in the estimated prevalence of CML. Case report: Based on medical records and clinical follow-up, the authors present the case of a Philadelphia chromosome-positive CML patient who developed resistance to imatinib. Quantitative reverse transcription-polymerase chain reaction testing revealed a V280G BCR-ABL mutation. Discussion and conclusions: This is the first report describing a new BCR-ABL kinase domain mutation－V280G－that might be associated with resistance to imatinib. Approximately 15% to 30% of patients treated with imatinib discontinue treatment due to resistance or intolerance. More than 90 BCR-ABL mutations were detected so far, conferring variable degrees of drug resistance, with consequent clinical, therapeutic, and prognostic impact. Introduction: The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL tyrosine kinase inhibitors in 2001 have revolutionized disease management, leading to a reduction in mortality rates and accordingly an increase in the estimated prevalence of CML. Case report: Based on medical records and clinical follow-up, the authors present the case of a Philadelphia chromosome–positive CML patient who developed resistance to imatinib. Quantitative reverse transcription-polymerase chain reaction testing revealed a V280G BCR-ABL mutation. Discussion and conclusions: This is the first report describing a new BCR-ABL kinase domain mutation—V280G—that might be associated with resistance to imatinib. Approximately 15% to 30% of patients treated with imatinib discontinue treatment due to resistance or intolerance. More than 90 BCR-ABL mutations were detected so far, conferring variable degrees of drug resistance, with consequent clinical, therapeutic, and prognostic impact. |
| Author | Maria D Alberca Ana P Azevedo Fernando Lima Purificacao Tavares Alice Reichert Celina Afonso |
| AuthorAffiliation | 1 Department of Clinical Pathology, Hospital São Francisco Xavier, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal 4 Department of Oncology, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal 3 Department of Hematology, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal 2 Centre for Toxicogenomics and Human Health, Genetics, Oncology and Human Toxicology, NOVA Medical School/Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisboa, Portugal 5 CGC-Genetics/Centro de Genética Clínica, Lisboa, Portugal |
| AuthorAffiliation_xml | – name: 1 Department of Clinical Pathology, Hospital São Francisco Xavier, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal – name: 5 CGC-Genetics/Centro de Genética Clínica, Lisboa, Portugal – name: 3 Department of Hematology, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal – name: 2 Centre for Toxicogenomics and Human Health, Genetics, Oncology and Human Toxicology, NOVA Medical School/Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisboa, Portugal – name: 4 Department of Oncology, Centro Hospitalar de Lisboa Ocidental, Lisboa, Portugal |
| Author_xml | – sequence: 1 givenname: Ana P surname: Azevedo fullname: Azevedo, Ana P email: anpazevedo@gmail.com – sequence: 2 givenname: Alice surname: Reichert fullname: Reichert, Alice – sequence: 3 givenname: Celina surname: Afonso fullname: Afonso, Celina – sequence: 4 givenname: Maria D surname: Alberca fullname: Alberca, Maria D – sequence: 5 givenname: Purificação surname: Tavares fullname: Tavares, Purificação – sequence: 6 givenname: Fernando surname: Lima fullname: Lima, Fernando |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28469513$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1007_s00044_019_02318_4 crossref_primary_10_1155_2023_6673144 crossref_primary_10_1007_s40278_018_40295_3 crossref_primary_10_1002_cnr2_1111 crossref_primary_10_3390_pharmaceutics14061294 crossref_primary_10_1186_s43042_022_00379_6 |
| Cites_doi | 10.6004/jnccn.2016.0197 10.1093/jnci/90.11.850 10.3109/10428194.2011.591013 10.1158/1078-0432.CCR-06-1516 10.1038/sj.leu.2404236 10.1200/JCO.2015.64.8899 10.1038/leu.2016.5 10.6004/jnccn.2016.0016 10.1016/j.clinbiochem.2016.12.006 10.1182/blood-2010-12-326405 10.1182/blood.V63.4.789.789 10.1371/journal.pone.0141665 10.1016/j.leukres.2013.09.011 10.1182/asheducation-2015.1.257 10.1002/cncr.26391 10.1182/blood-2013-05-501569 10.1002/cncr.24928 10.1182/blood-2010-12-319038 10.1038/nrc2126 10.3109/10428194.2014.893307 10.1016/j.clml.2015.02.035 10.1111/j.1365-2141.2010.08245.x 10.3892/or.2012.2153 10.1158/0008-5472.CAN-10-1438 10.1056/NEJMoa062867 10.1111/cas.12284 10.6004/jnccn.2014.0159 10.12788/jcso.0042 10.1007/s00432-014-1845-6 |
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| Keywords | mutation imatinib CML nilotinib BCR-ABL |
| Language | English |
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bibr11-1179554917702870 publication-title: PLoS ONE doi: 10.1371/journal.pone.0141665 contributor: fullname: Liu LL – ident: bibr27-1179554917702870 doi: 10.1016/j.leukres.2013.09.011 – ident: bibr25-1179554917702870 doi: 10.1182/asheducation-2015.1.257 – ident: bibr29-1179554917702870 doi: 10.1002/cncr.26391 – ident: bibr24-1179554917702870 doi: 10.1182/blood-2013-05-501569 – ident: bibr3-1179554917702870 doi: 10.1002/cncr.24928 – ident: bibr9-1179554917702870 doi: 10.1182/blood-2010-12-319038 – ident: bibr4-1179554917702870 doi: 10.1038/nrc2126 – ident: bibr16-1179554917702870 doi: 10.3109/10428194.2014.893307 – ident: bibr22-1179554917702870 doi: 10.1016/j.clml.2015.02.035 – ident: bibr14-1179554917702870 doi: 10.1111/j.1365-2141.2010.08245.x – ident: bibr10-1179554917702870 doi: 10.3892/or.2012.2153 – ident: bibr30-1179554917702870 doi: 10.1158/0008-5472.CAN-10-1438 – ident: bibr21-1179554917702870 doi: 10.1056/NEJMoa062867 – ident: bibr13-1179554917702870 doi: 10.1111/cas.12284 – ident: bibr23-1179554917702870 doi: 10.6004/jnccn.2014.0159 – ident: bibr2-1179554917702870 doi: 10.12788/jcso.0042 – ident: bibr28-1179554917702870 doi: 10.1007/s00432-014-1845-6 |
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| Snippet | Introduction: The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL... Introduction: The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL... The identification of as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of tyrosine kinase inhibitors in 2001 have... Introduction:The identification of BCR-ABL expression as the defining leukemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL... |
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| SubjectTerms | Authorship Blood tests Bone marrow Case Report Case reports Data analysis Family medical history Kinases Leukemia Mutation Patients Peer review Studies Targeted cancer therapy Ultrasonic imaging |
| Title | BCR-ABL V280G Mutation, Potential Role in Imatinib Resistance: First Case Report |
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