Journal
LEUKEMIA RESEARCH
Volume 35, Issue 2, Pages 237-242Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.leukres.2010.07.041
Keywords
Chronic myelogenous leukemia; Imatinib; Resistance; Bcr-Abl; Src; Inhibitor
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Funding
- National Natural Science Foundation of China [30772584]
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We have previously shown the inhibition of the small-molecule inhibitor FB2 on imatinib-sensitive and resistance CML cell lines with the wild-type Bcr-Abl fusion gene. Here we report the potent and selective antiproliferation on FB2 on transfected Ba/F3 p210 cell lines expressing various isoforms of Bcr-Abl (wild-type, Y253F, T315I). FB2 which orients Bcr-Abl and Src kinase activities, is shown to override imatinib-resistance CML involving Y253F mutation in the Abl kinase domain of the fusion protein except T315I in vivo and in vitro. Thus, we present FB2 that displays potency toward Bcr-Abl and Src as the molecular target, and which could potentially be used to override drug resistance in CML. (C) 2010 Elsevier Ltd. All rights reserved.
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