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dc.date.accessioned2018-06-28T14:38:40Z
dc.date.issued2012
dc.identifierhttp://publications.icr.ac.uk/11549/
dc.identifier.citationAMERICAN JOURNAL OF HEMATOLOGY, 2012, 87 (3), pp. 298 - 304
dc.identifier.issn0361-8609
dc.identifier.urihttps://repository.icr.ac.uk/handle/internal/1966
dc.description.abstractThe introduction of tyrosine kinase inhibitors (TKIs), starting with imatinib and followed by second and third generation TKIs, has significantly changed the clinical management of patients with chronic myeloid leukemia (CML). Despite their unprecedented clinical success, a proportion of patients fail to achieve complete cytogenetic remission by 12 months of treatment (primary resistance) while others experience progressive resistance after an initial response (secondary resistance). BCR-ABL1 kinase domain (KD) mutations have been detected in a proportion of patients at the time of treatment failure, and therefore their identification and monitoring plays an important role in therapeutic decisions particularly when switching TKIs. When monitoring KD mutations in a clinical laboratory, the choice of method should take into account turnaround time, cost, sensitivity, specificity, and ability to accurately quantify the size of the mutant clone. In this article, we describe in a manual style the methods most widely used in our laboratory to monitor KD mutations in patients with CML including direct sequencing, D-HPLC, and pyrosequencing. Advantages, disadvantages, interpretation of results, and their clinical applications are reviewed for each method. Am. J. Hematol., 2012. (c) 2011 Wiley Periodicals, Inc.
dc.format.extent298 - 304
dc.languageeng
dc.language.isoeng
dc.subjectchronic myeloid-leukemia chronic myelogenous leukemia acute lymphoblastic-leukemia bcr-abl mutations philadelphia-positive patients clonal cytogenetic evolution gimema working party chronic-phase imatinib resistance point mutations
dc.titleBCR-ABL1 kinase domain mutations: Methodology and clinical evaluation
dc.typeJournal Article
rioxxterms.licenseref.startdate2012
rioxxterms.typeJournal Article/Review
dc.relation.isPartOfAMERICAN JOURNAL OF HEMATOLOGY
pubs.issue3
pubs.notesISI Document Delivery No.: 894TF Times Cited: 0 Cited Reference Count: 87 Alikian, Mary Gerrard, Gareth Subramanian, Papagudi G. Mudge, Katherine Foskett, Pierre Khorashad, Jamshid Sorouri Lim, Ai Chiin Marin, David Milojkovic, Dragana Reid, Alistair Rezvani, Katy Goldman, John Apperley, Jane Foroni, Letizia Leukaemia and Lymphoma Research (LLR)[08065] Contract grant sponsor: Leukaemia and Lymphoma Research (LLR); Contract grant number: 08065. Wiley-blackwell Malden none The introduction of tyrosine kinase inhibitors (TKIs), starting with imatinib and followed by second and third generation TKIs, has significantly changed the clinical management of patients with chronic myeloid leukemia (CML). Despite their unprecedented clinical success, a proportion of patients fail to achieve complete cytogenetic remission by 12 months of treatment (primary resistance) while others experience progressive resistance after an initial response (secondary resistance). BCR-ABL1 kinase domain (KD) mutations have been detected in a proportion of patients at the time of treatment failure, and therefore their identification and monitoring plays an important role in therapeutic decisions particularly when switching TKIs. When monitoring KD mutations in a clinical laboratory, the choice of method should take into account turnaround time, cost, sensitivity, specificity, and ability to accurately quantify the size of the mutant clone. In this article, we describe in a manual style the methods most widely used in our laboratory to monitor KD mutations in patients with CML including direct sequencing, D-HPLC, and pyrosequencing. Advantages, disadvantages, interpretation of results, and their clinical applications are reviewed for each method. Am. J. Hematol., 2012. (c) 2011 Wiley Periodicals, Inc.
pubs.notesNot known
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Cancer Biomarkers
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Cancer Biomarkers
pubs.organisational-group/ICR
pubs.organisational-group/ICR/Primary Group
pubs.organisational-group/ICR/Primary Group/ICR Divisions
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Cancer Therapeutics/Cancer Biomarkers
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies
pubs.organisational-group/ICR/Primary Group/ICR Divisions/Clinical Studies/Cancer Biomarkers
pubs.volume87en_US
pubs.embargo.termsNot known
icr.researchteamCancer Biomarkersen_US
dc.contributor.icrauthorLim, Ai Chiinen


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