CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate
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in complete cytogenetic remission on imatinib mesylate treatment. Blood 2005;105:2093-8. 72. Sherbenou DW, Wong MJ, Humayun A, McGreevey LS, Harrell P, Yang R, et al. Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinib. Leukemia 2007;21:489-93. 73. Khorashad JS, Anand M, Marin D, Saunders S, Al-Jabary T, Iqbal A, Margerison S, et al. The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib. Leukemia 2006;20:658-63. 74. Soverini S, Martinelli G, Rosti G, Bassi S, Amabile M, Poerio A, et al. ABL mutations in late chronic phase chronic myeloid leukemia patients with up-front cytogenetic resistance to imatinib are associated with a greater likelihood of progression to blast crisis and shorter survival: a study by the GIMEMA Working Party on Chronic Myeloid Leukemia. J Clin Oncol 2005;23:4100-9. 75. Soverini S, Colarossi S, Gnani A, Rosti G, Castagnetti F, Poerio A, et al. Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: by the GIMEMA Working Party on Chronic Myeloid Leukemia. Clin Cancer Res 2006;12:7374-9. 76. Martinelli G, Iacobucci I, Soverini S, Cilloni D, Saglio G, Pane F, Baccarani M. Monitoring minimal residual disease and controlling drug resistance in chronic myeloid leukaemia patients in treatment with imatinib as a guide to clinical management. Hematol Oncol 2006;24:196-204. 77. Peng B, Lloyd P, Schran H. Clinical pharmacokinetics of imatinib. Clin Pharmacokinet 2005;44:879-94. 78. Talpaz M, Silver RT, Druker BJ, Goldman JM, GambacortiPasserini C, Guilhot F, et al. Imatinib induces durable hematologic and cytogenetic responses in patients with accelerated phase chronic myeloid leukemia: results of a phase 2 study. Blood 2002;99:1928-37. 79. Picard S, Titier K, Etienne G, Teilhet E, Ducint D, Bernard MA, et al. Trough imatinib plasma levels are associated with both cytogenetic and molecular responses to standard-dose imatinib in chronic myeloid leukemia. Blood 2007;109:3496-9. 80. White DL, Saunders VA, Dang P, Engler J, Zannettino AC, Cambareri AC, et al. OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib. Blood 2006;108:697704. 81. Mahon FX, Belloc F, Lagarde V, Chollet C, Moreau-Gaudry F, Reiffers J, et al. MDR1 gene overexpression confers resistance to imatinib mesylate in leukemia cell line models. Blood 2003;101:2368-73. 82. Thomas J, Wang L, Clark RE, Pirmohamed M. Active transport of imatinib into and out of cells: implications for drug resistance. Blood 2004;104:3739-45. 83. Burger H, van Tol H, Boersma AW, Brok M, Wiemer EA, Stoter G, Nooter K. Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump. Blood 2004;104:2940-2. 84. Gurney H, Wong M, Balleine RL, Rivory LP, McLachlan AJ, Hoskins JM, et al. Imatinib disposition and ABCB1 (MDR1, P-glycoprotein) genotype. Clin Pharmacol Ther 2007;82:33-40. 85. Sorel N, Chazelas F, Brizard A, Chomel JC. Double-gradient-denaturing-gradient gel electrophoresis for mutation screening of the BCR-ABL tyrosine kinase domain in chronic myeloid leukemia patients. Clin Chem 2005; 51:1263-6. 86. Kreuzer KA, Le Coutre P, Landt O, Na IK, Schwarz M, Schultheis K, et al. Preexistence and evolution of imatinib mesylate-resistant clones in chronic myelogenous leukemia detected by a PNA-based PCR clamping technique. Ann Hematol 2003;82:284-9. 87. Gruber FX, Lamark T, Anonli A, Sovershaev MA, Olsen M, Gedde-Dahl T, et al. Selecting and deselecting imatinibresistant clones: observations made by longitudinal, quantitative monitoring of mutated BCR-ABL. Leukemia 2005; 19:2159-65. 88. Nardi V, Raz T, Cao X, Wu CJ, Stone RM, Cortes J, et al. Quantitative monitoring by polymerase colony assay of known mutations resistant to ABL kinase inhibitors. Oncogene 2007 [Epub ahead of print]. 89. Vivante A, Amariglio N, Koren-Michowitz M, AshurFabian O, Nagler A, Rechavi G, et al. High-throughput, sensitive and quantitative assay for the detection of BCRABL kinase domain mutations. Leukemia 2007;21:131821. Editorials & Perspectives
منابع مشابه
Detection of BCR-ABL Kinase Mutations in CD34+ cells from Chronic Myelogenous Leukemia Patients in Complete Cytogenetic Remission on Imatinib Mesylate Treatment Short title: Kinase mutations in CML patients in CCR on Imatinib
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Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment.
The BCR-ABL kinase inhibitor imatinib mesylate induces complete cytogenetic response (CCR) in a high proportion of chronic myelogenous leukemia (CML) patients. However, patients in CCR usually demonstrate evidence of residual BCR-ABL-positive progenitors. The mechanisms underlying persistence of small numbers of malignant progenitors in imatinib-sensitive patients are unclear. BCR-ABL kinase do...
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The BCR/ABL tyrosine kinase inhibitor imatinib mesylate (Gleevec, STI571; Novartis, Basel, Switzerland) has shown remarkable efficacy in the treatment of chronic myelogenous leukemia (CML), with a high proportion of patients achieving complete cytogenetic responses (CCRs). However, it is not clear whether remissions will be durable and whether imatinib mesylate can eliminate the malignant primi...
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Imatinib mesylate treatment markedly reduces the burden of leukemia cells in chronic myelogenous leukemia (CML) patients. However, patients remain at risk for relapse on discontinuing treatment. We have previously shown that residual BCR-ABL progenitors can be detected in CML patients within the first 2 years of imatinib treatment. However, reduced rates of relapse and continued decline of BCR-...
متن کاملPersistence of leukemia stem cells in chronic myelogenous leukemia patients in prolonged remission with imatinib treatment.
Imatinib mesylate treatment markedly reduces the burden of leukemia cells in chronic myelogenous leukemia (CML) patients. However, patients remain at risk for relapse on discontinuing treatment. We have previously shown that residual BCR-ABL(+) progenitors can be detected in CML patients within the first 2 years of imatinib treatment. However, reduced rates of relapse and continued decline of B...
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Imatinib mesylate, showed encouraging activity in chronic myelogenous leukemia. However, there are few data regarding his efficacy and response monitoring in Sub-Saharan African patients. Our objective was to assess response to imatinib mesylate (Glivec) in Côte d'Ivoire patients with newly diagnosed Chronic Myeloid Leukemia (CML). From May 2005 to September 2009, we treated 42 patients (40 yea...
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تاریخ انتشار 2008