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Therapeutic targeting of BCR-ABL: prognostic markers of response and resistance mechanism in chronic myeloid leukaemia

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dc.contributor.authorYeung, D.
dc.contributor.authorHughes, T.
dc.date.issued2012
dc.description.abstractChronic myeloid leukemia (CML) is caused by the formation of the BCR-ABL fusion protein as a result of the t(9;22) chromosomal translocation. The elucidation of its molecular pathogenesis led to the identification of a therapeutic target and the subsequent synthesis and introduction of a small-molecule inhibitor for this target, imatinib. Because CML is the first disease successfully treated by targeted kinase inhibition, it served as a paradigm for discovery of disease mechanism and drug development in other diseases in which constitutive kinase expression plays a central role in pathogenesis. Despite the spectacular success of imatinib, not all CML patients derive great benefit from it. This review will cover some of the currently known prognostic markers of disease response and potential resistance mechanisms.
dc.description.statementofresponsibilityD.T. Yeung, T.P. Hughes
dc.identifier.citationCritical Reviews in Oncogenesis, 2012; 17(1):17-30
dc.identifier.doi10.1615/CritRevOncog.v17.i1.30
dc.identifier.issn0893-9675
dc.identifier.issn2162-6448
dc.identifier.orcidYeung, D. [0000-0002-7558-9927]
dc.identifier.orcidHughes, T. [0000-0002-0910-3730] [0000-0002-7990-4509]
dc.identifier.urihttp://hdl.handle.net/2440/72664
dc.language.isoen
dc.publisherBegell House Inc
dc.rightsCopyright status unknown
dc.source.urihttps://doi.org/10.1615/critrevoncog.v17.i1.30
dc.subjectAnimals
dc.subjectHumans
dc.subjectFusion Proteins, bcr-abl
dc.subjectAntineoplastic Agents
dc.subjectProtein Kinase Inhibitors
dc.subjectPrognosis
dc.subjectSignal Transduction
dc.subjectDrug Resistance, Neoplasm
dc.subjectLeukemia, Myelogenous, Chronic, BCR-ABL Positive
dc.subjectBiomarkers, Pharmacological
dc.subjectMolecular Targeted Therapy
dc.subjectBiomarkers, Tumor
dc.titleTherapeutic targeting of BCR-ABL: prognostic markers of response and resistance mechanism in chronic myeloid leukaemia
dc.typeJournal article
pubs.publication-statusPublished

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