| Literature DB >> 31102734 |
Daniel Nisakar Meenakshi Sundaram1, Xiaoyan Jiang2, Joseph M Brandwein3, Juliana Valencia-Serna4, K C Remant4, Hasan Uludağ5.
Abstract
Chronic myeloid leukemia cells are armed with several resistance mechanisms that can make current drugs ineffective. A better understanding of resistance mechanisms is yielding new approaches to management of the disease. Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm the hallmark of which, the breakpoint cluster region-Abelson (BCR-ABL) oncogene, has been the target of tyrosine kinase inhibitors (TKIs), which have significantly improved the survival of patients with CML. However, because of an increase in TKI resistance, it is becoming imperative to identify resistance mechanisms so that drug therapies can be better prescribed and new agents developed. In this review, we discuss the various BCR-ABL-dependent and -independent mechanisms of resistance observed in CML, and the range of therapeutic solutions available to overcome such resistance and to ultimately improve the survival of patients with CML.Entities:
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Year: 2019 PMID： 31102734 DOI： 10.1016/j.drudis.2019.05.007
Source DB: PubMed Journal: Drug Discov Today ISSN： 1359-6446 Impact factor: 7.851