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Chen X, Shi X, Wang X, et al. Novel use of old drug: Anti-rheumatic agent auranofin overcomes imatinib-resistance of chronic myeloid leukemia cells. Cancer Cell Microenviron. 2014;1(6)doi: 10.14800/ccm.415.
Chen, X., Shi, X., Wang, X., & Liu, J. (2014). Novel use of old drug: Anti-rheumatic agent auranofin overcomes imatinib-resistance of chronic myeloid leukemia cells. Cancer cell & microenvironment, 1(6), . https://doi.org/10.14800/ccm.415
Chen, Xin, et al. "Novel use of old drug: Anti-rheumatic agent auranofin overcomes imatinib-resistance of chronic myeloid leukemia cells." Cancer cell & microenvironment vol. 1,6 (2014). doi: https://doi.org/10.14800/ccm.415
Chen X, Shi X, Wang X, Liu J. Novel use of old drug: Anti-rheumatic agent auranofin overcomes imatinib-resistance of chronic myeloid leukemia cells. Cancer Cell Microenviron. 2014 Nov 01;1(6). doi: 10.14800/ccm.415. PMID: 25995993; PMCID: PMC4434598.
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Cancer Cell Microenviron. 2014 Nov 01;1(6). doi: 10.14800/ccm.415.

Novel use of old drug: Anti-rheumatic agent auranofin overcomes imatinib-resistance of chronic myeloid leukemia cells.

Cancer cell & microenvironment

Xin Chen, Xianping Shi, Xuejun Wang, Jinbao Liu

Affiliations

  1. State Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Department of Pathophysiology, Guangzhou Medical University, Guangdong 510182, China.
  2. State Key Lab of Respiratory Disease, Protein Modification and Degradation Lab, Department of Pathophysiology, Guangzhou Medical University, Guangdong 510182, China ; Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion, South Dakota 57069, USA.

PMID: 25995993 PMCID: PMC4434598 DOI: 10.14800/ccm.415

Abstract

Patients with chronic myeloid leukemia (CML) are commonly treated with a specific inhibitor of BCR-ABL tyrosine kinase, imatinib mesylate (IM). Unfortunately, CML patients develop IM-resistance, which has emerged as a significant clinical problem. Somatic mutations, especially T315I mutation, in BCR-ABL kinase domain represent the most common mechanism underlying drug resistance to tyrosine kinase inhibitors (TKI), including imatinib. Thus, it is urgent to develop novel therapeutic strategies to overcome TKI-resistance. The anti-rheumatic gold (I) compound Auranofin (AF), was recently approved by US Food and Drug Administration for Phase II clinical trials to treat leukemia. In a recent study, we discovered that AF can selectively inhibit 19S proteasome-associated deubiquitinases (UCHL5 and USP14), which mediates its anticancer effects. More recently studies we have shown that AF inhibits the growth of both Bcr-Abl wild-type cells and IM-resistant Bcr-Abl-T315I mutation cells

Keywords: Bcr-Abl; CML; auranofin; imatinib resistance; proteasomal deubiquitinases; reactive oxygen species

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