The level of BCR-ABL1 kinase activity before treatment does not identify chronic myeloid leukemia patients who fail to achieve a complete cytogenetic response on imatinib

Haematologica

Volumn 94, Issue 6, 2009, Pages 861-864

  Khorashad, Jamshid Sorouri ^a   Wagner, Simon ^a   Greener, Liat ^a   Marin, David ^a   Reid, Alistair ^a   Milojkovic, Dragana ^a   Patel, Hetal ^a   Willimott, Shaun ^a   Rezvani, Katy ^a   Gerrard, Gareth ^a   Loaiza, Sandra ^a   Davis, John ^a   Goldman, John ^a   Melo, Junia ^a   Apperley, Jane ^a   Foroni, Letizia ^a  

^a HAMMERSMITH HOSPITAL   (United Kingdom)

Author keywords

CD34; CML; Imatinib; p Crkl

Indexed keywords

BCR ABL PROTEIN; IMATINIB; PROTEIN BCR ABL 1; UNCLASSIFIED DRUG;

ARTICLE; AUTOPHOSPHORYLATION; CHROMOSOME ANALYSIS; CHRONIC MYELOID LEUKEMIA; CONTROLLED STUDY; DRUG DOSE INCREASE; DRUG INHIBITION; FLOW CYTOMETRY; GENETIC VARIABILITY; HUMAN; HUMAN CELL; IN VITRO STUDY; MAJOR CLINICAL STUDY;

ADAPTOR PROTEINS, SIGNAL TRANSDUCING; ANTIGENS, CD4; ANTINEOPLASTIC AGENTS; CELLS, CULTURED; DOSE-RESPONSE RELATIONSHIP, DRUG; DRUG RESISTANCE; FLOW CYTOMETRY; FUSION PROTEINS, BCR-ABL; HL-60 CELLS; HUMANS; IN SITU HYBRIDIZATION, FLUORESCENCE; K562 CELLS; LEUKEMIA, MYELOGENOUS, CHRONIC, BCR-ABL POSITIVE; LEUKOCYTES, MONONUCLEAR; NEUTROPHILS; NUCLEAR PROTEINS; PHOSPHORYLATION; PIPERAZINES; PROTEIN-TYROSINE KINASES; PYRIMIDINES; TREATMENT OUTCOME;

EID: 66749138981     PISSN: 03906078     EISSN: 15928721     Source Type: Journal    
DOI: 10.3324/haematol.2008.003715     Document Type: Article

References (22)

1. Gambacorti-Passerini C, le Coutre P, Mologni L, Fanelli M, Bertazzoli C, Marchesi E, et al. Inhibition of the ABL kinase activity blocks the proliferation of BCR/ABL+ leukemic cells and induces apoptosis. Blood Cells Mol Dis 1997;23:380-394
2. Goldman JM. How I treat chronic myeloid leukemia in the imatinib era. Blood 2007;110:2828-2837 (Pubitemid 350006935)
3. de Lavallade H, Apperley JF, Khorashad JS, Milojkovic D, Reid AG, Bua M, et al. Imatinib for Newly Diagnosed Patients With Chronic Myeloid Leukemia: Incidence of Sustained Responses in an Intention-to-Treat Analysis. J Clin Oncol 2008;26:3358-3363
4. Apperley JF. Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia. Lancet Oncol 2007;8:1018-1029 (Pubitemid 47629897)
5. Schultheis B, Szydlo R, Mahon FX, Apperley JF, Melo JV. Analysis of total phosphotyrosine levels in CD34+ cells from CML patients to predict the response to imatinib mesylate treatment. Blood 2005;105:4893-4894 (Pubitemid 40807320)
6. Yong AS, Szydlo RM, Goldman JM, Apperley JF, Melo JV. Molecular profiling of CD34+ cells identifies low expression of CD7, along with high expression of proteinase 3 or elastase, as predictors of longer survival in patients with CML. Blood 2006;107:205-212 (Pubitemid 43053545)
7. Hamilton A, Elrick L, Myssina S, Copland M, Jørgensen H, Melo JV, Holyoake T. BCR-ABL activity and its response to drugs can be determined in CD34+ CML stem cells by CrkL phosphorylation status using flow cytometry. Leukemia 2006;20:1035-1039 (Pubitemid 43797294)
8. Druker BJ, Talpaz M, Resta DJ, Peng B, Buchdunger E, Ford JM, et al. Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 2001;344:1031-1037 (Pubitemid 32267972)
9. Goldman JM, Melo JV. Targeting the BCR-ABL tyrosine kinase in chronic myeloid leukemia. N Engl J Med 2001;344:1084-1086 (Pubitemid 32267980)
10. Patel H, Marley SB, Gordon MY. Detection in primary chronic myeloid leukaemia cells of p210BCR-ABL1 in complexes with adaptor proteins CBL, CRKL, and GRB2. Genes Chromosomes Cancer 2006;45:1121-1129 (Pubitemid 44763440)
11. Maxwell SA, Kurzrock R, Parsons SJ, Talpaz M, Gallick GE, Kloetzer WS, et al. Analysis of P210bcr-abl tyrosine protein kinase activity in various subtypes of Philadelphia chromosome-positive cells from chronic myelogenous leukemia patients. Cancer Res 1987;47:1731-1739 (Pubitemid 17044512)
12. Nichols GL, Raines MA, Vera JC, Lacomis L, Tempst P, Golde DW. Identification of CRKL as the constitutively phosphorylated 39-kD tyrosine phosphoprotein in chronic myelogenous leukemia cells. Blood 1994;84:2912-2918 (Pubitemid 24328078)
13. ten Hoeve J, Arlinghaus RB, Guo JQ, Heisterkamp N, Groffen J. Tyrosine phosphorylation of CRKL in Philadelphia+ leukemia. Blood 1994;84:1731-1736
14. Patel H, Marley SB, Greener L, Gordon MY. Subcellular distribution of p210 (BCR-ABL) in CML cell lines and primary CD34+ CML cells. Leukemia 2008;22:559-571
15. de Jong R, ten Hoeve J, Heisterkamp N, Groffen J. Tyrosine 207 in CRKL is the BCR/ABL phosphorylation site. Oncogene 1997;14:507-513
16. Nichols GL, Raines MA, Vera JC, Lacomis L, Tempst P, Golde DW. Identification of CRKL as the constitutively phosphorylated 39-kD tyrosine phosphoprotein in chronic myelogenous leukemia cells. Blood 1994;84:2912-2918 (Pubitemid 24328078)
17. White D, Saunders V, Grigg A, Arthur C, Filshie R, Leahy MF, et al. Measurement of in vivo BCR-ABL kinase inhibition to monitor imatinib-induced target blockade and predict response in chronic myeloid leukemia. J Clin Oncol 2007;25:4445-4451 (Pubitemid 350013851)
18. White D, Saunders V, Lyons AB, Branford S, Grigg A, To LB, et al. In vitro sensitivity to imatinib-induced inhibition of ABL kinase activity is predictive of molecular response in patients with de novo CML. Blood 2005;106:2520-2526
19. Khorashad JS, Anand M, Marin D, Saunders S, Al-Jabary T, Iqbal A, et al. The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib. Leukemia 2006;20:658-663
20. Donato NJ, Wu JY, Stapley J, Lin H, Arlinghaus R, Aggarwal BB, et al. Imatinib mesylate resistance through BCR-ABL independence in chronic myelogenous leukemia. Cancer Res 2004;64:672-677 (Pubitemid 38120909)
21. Wang Y, Cai D, Brendel C, Barett C, Erben P, Manley PW, et al. 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 2007;109:2147-2155 (Pubitemid 46348217)
22. Jilani I, Kantarjian H, Gorre M, Cortes J, Ottmann O, Bhalla K, et al. Phosphorylation levels of BCR-ABL, CrkL, AKT and STAT5 in imatinib-resistant chronic myeloid leukemia cells implicate alternative pathway usage as a survival strategy. Leuk Res 2008;32:643-649