Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/72664
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Type: Journal article
Title: Therapeutic targeting of BCR-ABL: prognostic markers of response and resistance mechanism in chronic myeloid leukaemia
Author: Yeung, D.
Hughes, T.
Citation: Critical Reviews in Oncogenesis, 2012; 17(1):17-30
Publisher: Begell House Inc
Issue Date: 2012
ISSN: 0893-9675
2162-6448
Statement of
Responsibility: 
D.T. Yeung, T.P. Hughes
Abstract: Chronic 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.
Keywords: Animals
Humans
Fusion Proteins, bcr-abl
Antineoplastic Agents
Protein Kinase Inhibitors
Prognosis
Signal Transduction
Drug Resistance, Neoplasm
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Biomarkers, Pharmacological
Molecular Targeted Therapy
Biomarkers, Tumor
Rights: Copyright status unknown
DOI: 10.1615/CritRevOncog.v17.i1.30
Published version: http://dx.doi.org/10.1615/critrevoncog.v17.i1.30
Appears in Collections:Aurora harvest
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