Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
|Title:||Therapeutic targeting of BCR-ABL: prognostic markers of response and resistance mechanism in chronic myeloid leukaemia|
|Citation:||Critical Reviews in Oncogenesis, 2012; 17(1):17-30|
|Publisher:||Begell House Inc|
|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|
|Appears in Collections:||Medicine publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.