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Blood, 15 August 2006, Vol. 108, No. 4, pp. 1370-1373. Prepublished online as a Blood First Edition Paper on April 20, 2006; DOI 10.1182/blood-2006-02-003145. This Article Full Text (PDF) All Versions of this Article: blood-2006-02-003145v1 108/4/1370    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Jordanides, N. E Articles by Mountford, J. C Search for Related Content PubMed PubMed Citation Articles by Jordanides, N. E Articles by Mountford, J. C Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 16, 2006 Accepted April 6, 2006 Functional ABCG2 is over-expressed on primary CML CD34+ cells and is inhibited by imatinib mesylate Niove E Jordanides, Heather G Jorgensen, Tessa L Holyoake, and Joanne C Mountford* From Experimental Haematology & Haemopoietic Stem Cells, University of Glasgow * Corresponding author; email: jcm7n{at}clinmed.gla.ac.uk. Imatinib mesylate (IM) therapy for chronic myeloid leukemia (CML) has transformed the treatment of this disease. However, the vast majority of patients, despite major responses, still harbor Philadelphia chromosome positive (Ph+) cells. We have described a population of primitive Ph+ cells that are insensitive to IM and may be a source of IM resistance. Cell line studies have suggested that the drug transporter ABCG2 may be a mediator of IM resistance, however there is considerable debate about whether IM is an ABCG2 substrate or inhibitor. We demonstrate here that primitive CML CD34+ cells aberrantly over-express functional ABCG2 but that co-treatment with IM and an ABCG2 inhibitor does not potentiate the effect of IM. We definitively show that IM is an inhibitor of, but not a substrate for ABCG2 and that therefore, ABCG2 does not modulate intracellular concentrations of IM in this clinically relevant cell population. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Imatinib and ABCG2: who controls whom? Junia V. Melo Blood 2006 108: 1116-1117. [Full Text] [PDF] This article has been cited by other articles: B. Chapuy, M. Panse, U. Radunski, R. Koch, D. Wenzel, N. Inagaki, D. Haase, L. Truemper, and G. G. Wulf ABC transporter A3 facilitates lysosomal sequestration of imatinib and modulates susceptibility of chronic myeloid leukemia cell lines to this drug Haematologica, November 1, 2009; 94(11): 1528 - 1536. [Abstract] [Full Text] [PDF] D. H. Kim, L. Sriharsha, W. Xu, S. Kamel-Reid, X. Liu, K. Siminovitch, H. A. Messner, and J. H. Lipton Clinical Relevance of a Pharmacogenetic Approach Using Multiple Candidate Genes to Predict Response and Resistance to Imatinib Therapy in Chronic Myeloid Leukemia Clin. Cancer Res., July 15, 2009; 15(14): 4750 - 4758. [Abstract] [Full Text] [PDF] D. H. Kim, W. Xu, C. Ma, X. Liu, K. Siminovitch, H. A. Messner, and J. H. Lipton Genetic variants in the candidate genes of the apoptosis pathway and susceptibility to chronic myeloid leukemia Blood, March 12, 2009; 113(11): 2517 - 2525. [Abstract] [Full Text] [PDF] D. K. Hiwase, V. Saunders, D. Hewett, A. Frede, S. Zrim, P. Dang, L. Eadie, L. B. To, J. Melo, S. Kumar, et al. 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Manley, and T. P. Hughes Imatinib increases the intracellular concentration of nilotinib, which may explain the observed synergy between these drugs Blood, April 15, 2007; 109(8): 3609 - 3610. [Full Text] [PDF] Y. Wang, D. Cai, C. Brendel, C. Barett, P. Erben, P. W. Manley, A. Hochhaus, A. Neubauer, and A. Burchert Adaptive secretion of granulocyte-macrophage colony-stimulating factor (GM-CSF) mediates imatinib and nilotinib resistance in BCR/ABL+ progenitors via JAK-2/STAT-5 pathway activation Blood, March 1, 2007; 109(5): 2147 - 2155. [Abstract] [Full Text] [PDF]

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