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• W2143459158 abstract "American Journal of HematologyVolume 84, Issue 10 p. 679-682 Solving Clinical Problems in Blood DiseasesFree Access A 51-year-old male CML patient with progressive hearing loss, confusion, ataxia, and aphasia during imatinib treatment† ‡ Jeroen J.W.M. Janssen, Corresponding Author Jeroen J.W.M. Janssen [email protected] Department of Hematology, VU University Medical Center, HV Amsterdam, The NetherlandsDepartment of Hematology, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The NetherlandsSearch for more papers by this authorHenk W. Berendse, Henk W. Berendse Department of Neurology, VU University Medical Center, HV Amsterdam, The NetherlandsSearch for more papers by this authorGerrit-Jan Schuurhuis, Gerrit-Jan Schuurhuis Department of Hematology, VU University Medical Center, HV Amsterdam, The NetherlandsSearch for more papers by this authorPauline A. Merle, Pauline A. Merle Department of Hematology, VU University Medical Center, HV Amsterdam, The NetherlandsSearch for more papers by this authorGert J. Ossenkoppele, Gert J. Ossenkoppele Department of Hematology, VU University Medical Center, HV Amsterdam, The NetherlandsSearch for more papers by this author Jeroen J.W.M. Janssen, Corresponding Author Jeroen J.W.M. Janssen [email protected] Department of Hematology, VU University Medical Center, HV Amsterdam, The NetherlandsDepartment of Hematology, VU University Medical Center, De Boelelaan 1117, 1081 HV Amsterdam, The NetherlandsSearch for more papers by this authorHenk W. Berendse, Henk W. Berendse Department of Neurology, VU University Medical Center, HV Amsterdam, The NetherlandsSearch for more papers by this authorGerrit-Jan Schuurhuis, Gerrit-Jan Schuurhuis Department of Hematology, VU University Medical Center, HV Amsterdam, The NetherlandsSearch for more papers by this authorPauline A. Merle, Pauline A. Merle Department of Hematology, VU University Medical Center, HV Amsterdam, The NetherlandsSearch for more papers by this authorGert J. Ossenkoppele, Gert J. Ossenkoppele Department of Hematology, VU University Medical Center, HV Amsterdam, The NetherlandsSearch for more papers by this author First published: 30 June 2009 https://doi.org/10.1002/ajh.21489Citations: 4 † Conflict of interest: Nothing to report. ‡ A physician or group of physicians considers presentation and evolution of a real clinical case, reacting to clinical information and data (boldface type). This is followed by a discussion/commentary. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL References 1 Druker BJ,Guilhot F,O'Brien SG, et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med 2006; 355: 2408– 2417. 2 Druker BJ,Sawyers CL,Kantarjian H, et al. Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome. N Engl J Med 2001; 344: 1038– 1042. 3 Leis JF,Stepan DE,Curtin PT, et al. Central nervous system failure in patients with chronic myelogenous leukemia lymphoid blast crisis and Philadelphia chromosome positive acute lymphoblastic leukemia treated with imatinib (STI-571). Leuk Lymphoma 2004; 45: 695– 698. 4 Matsuda M,Morita Y,Shimada T, et al. Extramedullary blast crisis derived from 2 different clones in the central nervous system and neck during complete cytogenetic remission of chronic myelogenous leukemia treated with imatinib mesylate. Int J Hematol 2005; 81: 307– 309. 5 Altintas A,Cil T,Kilinc I, et al. Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: A case report. J Neurooncol 2007; 84: 103– 105. 6 Alimena G,Breccia M,Latagliata R, et al. Sudden blast crisis in patients with Philadelphia chromosome-positive chronic myeloid leukemia who achieved complete cytogenetic remission after imatinib therapy. Cancer 2006; 107: 1008– 1013. 7 Aichberger KJ,Herndlhofer S,Agis H, et al. Liposomal cytarabine for treatment of myeloid central nervous system relapse in chronic myeloid leukaemia occurring during imatinib therapy. Eur J Clin Invest 2007; 37: 808– 813. 8 Rajappa S,Uppin SG,Raghunadharao D, et al. Isolated central nervous system blast crisis in chronic myeloid leukemia. Hematol Oncol 2004; 22: 179– 181. 9 Petzer AL,Gunsilius E,Hayes M, et al. Low concentrations of STI571 in the cerebrospinal fluid: A case report. Br J Haematol 2002; 117: 623– 625. 10 Janssen JJWM,Hochhaus A,van Oostveen JW, et al. Secondary imatinib resistance associated with an aberrant bcr-abl fusion gene. Leukemia 2004; 18: 1020– 1021. 11 Jabbour E,Kantarjian H,O'Brien S, et al. Sudden blastic transformation in patients with chronic myeloid leukemia treated with imatinib mesylate. Blood 2006; 107: 480– 482. 12 Simpson E,O'Brien SG,Reilly JT. Extramedullary blast crises in CML patients in complete hematological remission treated with imatinib mesylate. Clin Lab Haematol 2006; 28: 215– 216. 13 Graham SM,Jorgensen HG,Allan E, et al. Primitive, quiescent, Philadelphia-positive stem cells from patients with chronic myeloid leukemia are insensitive to STI571 in vitro. Blood 2002; 99: 319– 325. 14 Neville K,Parise RA,Thompson P, et al. Plasma and cerebrospinal fluid pharmacokinetics of imatinib after administration to nonhuman primates. Clin Cancer Res 2004; 10: 2525– 2529. 15 Bornhauser M,Jenke A,Freiberg-Richter J, et al. CNS blast crisis of chronic myelogenous leukemia in a patient with a major cytogenetic response in bone marrow associated with low levels of imatinib mesylate and its N-desmethylated metabolite in cerebral spinal fluid. Ann Hematol 2004: 83: 401– 402. 16 le Coutre P,Kreuzer KA,Pursche S, et al. Pharmacokinetics and cellular uptake of imatinib and its main metabolite CGP74588. Cancer Chemother Pharmacol 2004; 53: 313– 323. 17 Wolff NC,Richardson JA,Egorin M, et al. The CNS is a sanctuary for leukemic cells in mice receiving imatinib mesylate for Bcr/Abl-induced leukemia. Blood 2003; 101: 5010– 5013. 18 Takayama N,Sato N,O'Brien SG, et al. Imatinib mesylate has limited activity against the central nervous system involvement of Philadelphia chromosome-positive acute lymphoblastic leukaemia due to poor penetration into cerebrospinal fluid. Br J Haematol 2002; 119: 106– 108. 19 Breedveld P,Pluim D,Cipriani G, et al. The effect of Bcrp1 (Abcg2) on the in vivo pharmacokinetics and brain penetration of imatinib mesylate (Gleevec): Implications for the use of breast cancer resistance protein and P-glycoprotein inhibitors to enable the brain penetration of imatinib in patients. Cancer Res 2005; 65: 2577– 2582. 20 Giannoudis A,Davies A,Lucas CM, et al. Effective dasatinib uptake may occur without human organic Cation Transporter 1 (hOCT1): Implications for the treatment of imatinib resistant chronic myeloid leukaemia. Blood 2008; 112: 3348– 3354. 21 Hiwase DK,Saunders V,Hewett D, et al. Dasatinib cellular uptake and efflux in chronic myeloid leukemia cells: Therapeutic implications. Clin Cancer Res 2008; 14: 3881– 3888. 22 Porkka K,Koskenvesa P,Lundan T, et al. Dasatinib crosses the blood-brain barrier and is an efficient therapy for central nervous system Philadelphia chromosome-positive leukemia. Blood 2008; 112: 1005– 1012. 23 Chen Y,Agarwal S,Shaik NM, et al. P-glycoprotein and breast cancer resistance protein influence brain distribution of dasatinib. J Pharmacol Exp Ther. 10.1124/jpet.109.154781. 24 Lagas JS,van Waterschoot RA,van Tilburg VA, et al. Brain accumulation of dasatinib is restricted by P-glycoprotein (ABCB1) and breast cancer resistance protein (ABCG2) and can be enhanced by elacridar treatment. Clin Cancer Res 2009; 15: 2344– 2351. 25 Yokota A,Kimura S,Masuda S, et al. INNO-406, a novel BCR-ABL/Lyn dual tyrosine kinase inhibitor, suppresses the growth of Ph+ leukemia cells in the central nervous system, and cyclosporine A augments its in vivo activity. Blood 2007; 109: 306– 314. Citing Literature Volume84, Issue10October 2009Pages 679-682 ReferencesRelatedInformation" @default.
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