Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
|Title:||Mechanisms of resistance to BCR-ABL kinase inhibitors|
Vaz de Melo, J.
|Citation:||Leukemia and Lymphoma, 2011; 52(SUPPL. 1):12-22|
|Publisher:||Taylor & Francis Ltd|
|Joana M. Diamond & Junia V. Melo|
|Abstract:||Since the introduction of imatinib mesylate (IM) for the treatment of chronic myeloid leukemia (CML), impressive clinical responses have been observed in the majority of patients in chronic phase. However, not all patients experience an optimal response to IM or even to the more potent, second-generation tyrosine kinase inhibitors (TKIs). Furthermore, responses are not sustained in a number of patients, and it is yet unclear whether the inhibitors can be safely discontinued in patients who achieve long-term remission. The emergence of resistance to TKIs has become a significant problem that has led to extensive studies on the causal mechanisms. This review describes our current state of knowledge on why and how CML cells can develop resistance to TKIs.|
|Rights:||© 2011 Informa UK, Ltd.|
|Appears in Collections:||Aurora harvest|
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.