613
Views
18
CrossRef citations to date
0
Altmetric
Reviews

The potential for dasatinib in treating chronic lymphocytic leukemia, acute myeloid leukemia, and myeloproliferative neoplasms

Pages 754-763 | Received 29 Oct 2010, Accepted 15 Jan 2011, Published online: 04 Apr 2011

References

  • O'Hare T, Walters DK, Stoffregen E, In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants. Cancer Res 2005;65:4500–4505.
  • Lombardo LJ, Lee FY, Chen P, Discovery of N-(2-chloro-6-methyl-phenyl)- 2-(6-(4-(2-hydroxyethyl)-piperazin-1-yl)- 2-methylpyrimidin-4-ylamino)thiazole-5-carboxamide (BMS-354825), a dual Src/Abl kinase inhibitor with potent antitumor activity in preclinical assays. J Med Chem 2004;47:6658–6661.
  • Chen Z, Lee FY, Bhalla KN, Wu J. Potent inhibition of platelet-derived growth factor-induced responses in vascular smooth muscle cells by BMS-354825 (dasatinib). Mol Pharmacol 2006;69:1527–1533.
  • Schittenhelm MM, Shiraga S, Schroeder A, Dasatinib (BMS-354825), a dual SRC/ABL kinase inhibitor, inhibits the kinase activity of wild-type, juxtamembrane, and activation loop mutant KIT isoforms associated with human malignancies. Cancer Res 2006;66:473–481.
  • Frame MC. Src in cancer: deregulation and consequences for cell behaviour. Biochim Biophys Acta 2002;1602:114–130.
  • Chou MT, Wang J, Fujita DJ. Src kinase becomes preferentially associated with the VEGFR, KDR/Flk-1, following VEGF stimulation of vascular endothelial cells. BMC Biochem 2002;3:32.
  • Williams NK, Lucet IS, Klinken SP, Ingley E, Rossjohn J. Crystal structures of the Lyn protein tyrosine kinase domain in its Apo- and inhibitor-bound state. J Biol Chem 2009;284:284–291.
  • Tokarski JS, Newitt JA, Chang CY, The structure of dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. Cancer Res 2006;66:5790–5797.
  • Shah NP, Tran C, Lee FY, Chen P, Norris D, Sawyers CL. Overriding imatinib resistance with a novel ABL kinase inhibitor. Science 2004;305:399–401.
  • Dasatinib prescribing information [Internet]. Princeton, NJ: Bristol-Myers Squibb Company; 2010. Available from: http://packageinserts.bms.com/pi/pi_sprycel.pdf
  • Shah NP, Kim DW, Kantarjian H, Potent, transient inhibition of BCR-ABL with dasatinib 100 mg daily achieves rapid and durable cytogenetic responses and high transformation-free survival rates in chronic phase chronic myeloid leukemia patients with resistance, suboptimal response or intolerance to imatinib. Haematologica 2010;95:232–240.
  • Kantarjian H, Cortes J, Kim DW, Phase 3 study of dasatinib 140 mg once daily versus 70 mg twice daily in patients with chronic myeloid leukemia in accelerated phase resistant or intolerant to imatinib: 15-month median follow-up. Blood 2009;113:6322–6329.
  • Saglio G, Hochhaus A, Goh YT, Dasatinib in imatinib-resistant or imatinib-intolerant chronic myeloid leukemia in blast phase after 2 years of follow-up in a phase 3 study: efficacy and tolerability of 140 milligrams once daily and 70 milligrams twice daily. Cancer 2010;116:3852–3861.
  • Cortes JE, Jones D, O'Brien S, Results of dasatinib therapy in patients with early chronic-phase chronic myeloid leukemia. J Clin Oncol 2010;28:398–404.
  • Kantarjian H, Shah NP, Hochhaus A, Dasatinib versus imatinib in newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med 2010;362:2260–2270.
  • Hallek M, Cheson BD, Catovsky D, Guidelines for the diagnosis and treatment of chronic lymphocytic leukemia: a report from the International Workshop on Chronic Lymphocytic Leukemia updating the National Cancer Institute-Working Group 1996 guidelines. Blood 2008;111:5446–5456.
  • National Cancer Institute. Surveillance Epidemiology and End Results Cancer Statistics Review 1975-2006. Table 13.6 Chronic Lymphocytic Leukemia2009 [Internet]. Available from: http://seer.cancer.gov/csr/1975_2006/browse_csr.php?section=13&page=sect_13_table.06.html
  • Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ. Cancer statistics, 2009. CA Cancer J Clin 2009;59:225–249.
  • Döhner H, Stilgenbauer S, Benner A, Genomic aberrations and survival in chronic lymphocytic leukemia. N Engl J Med 2000;343:1910–1916.
  • Panasci LC, Xu Z-Y, Aloyz R. Role of nonhomologous end-joining and recombinational DNA repair in resistance to nitrogen mustard and DNA crosslinking agents. DNA repair in cancer therapyIn: Panasci LC, Alaoui-Jamali MA, editors. Totowa, NJ: Humana Press; 2004. pp 9–30.
  • Lin K, Glenn MA, Harris R, c-Abl expression in chronic lymphocytic leukemia cells: clinical and therapeutic implications. Cancer Res 2006;66:7801–7809.
  • Aloyz R, Grzywacz K, Xu ZY, Loignon M, Alaoui-Jamali MA, Panasci L. Imatinib sensitizes CLL lymphocytes to chlorambucil. Leukemia 2004;18:409–414.
  • Hebb JP, Assouline S, Rousseau C, A phase I study of imatinib mesylate in combination with chlorambucil in previously treated chronic lymphocytic leukemia patients. Cancer Chemother Pharmacol [Epub ahead of print].
  • Amrein L, Hernandez TA, Ferrario C, Dasatinib sensitizes primary chronic lymphocytic leukaemia lymphocytes to chlorambucil and fludarabine in vitro. Br J Haematol 2008;143:698–706.
  • Ren CL, Morio T, Fu SM, Geha RS. Signal transduction via CD40 involves activation of lyn kinase and phosphatidylinositol-3-kinase, and phosphorylation of phospholipase Cγ2. J Exp Med 1994;179:673–680.
  • Granziero L, Ghia P, Circosta P, Survivin is expressed on CD40 stimulation and interfaces proliferation and apoptosis in B-cell chronic lymphocytic leukemia. Blood 2001;97:2777–2783.
  • Pedersen IM, Kitada S, Leoni LM, Protection of CLL B cells by a follicular dendritic cell line is dependent on induction of Mcl-1. Blood 2002;100:1795–1801.
  • Chiorazzi N, Rai KR, Ferrarini M. Chronic lymphocytic leukemia. N Engl J Med 2005;352:804–815.
  • Hallaert DYH, Jaspers A, van Noesel CJ, van Oers MH, Kater AP, Eldering E. c-Abl kinase inhibitors overcome CD40-mediated drug resistance in CLL: implications for therapeutic targeting of chemoresistant niches. Blood 2008;112:5141–5149.
  • Mineva ND, Rothstein TL, Meyers JA, Lerner A, Sonenshein GE. CD40 ligand-mediated activation of the de novo RelB NF-KB synthesis pathway in transformed B cells promotes rescue from apoptosis. J Biol Chem 2007;282:17475–17485.
  • Travert M, Ame-Thomas P, Pangault C, CD40 ligand protects from TRAIL-induced apoptosis in follicular lymphomas through NF-KB activation and up-regulation of c-FLIP and Bcl-xL. J Immunol 2008;181:1001–1011.
  • Fiumara P, Younes A. CD40 ligand (CD154) and tumour necrosis factor-related apoptosis inducing ligand (APO-2L) in haematological malignancies. Br J Haematol 2001;113 265–274.
  • Contri A, Brunati AM, Trentin L, Chronic lymphocytic leukemia B cells contain anomalous Lyn tyrosine kinase, a putative contribution to defective apoptosis. J Clin Invest 2005;115:369–378.
  • Ke J, Chelvarajan RL, Sindhava V, Anomalous constitutive Src kinase activity promotes B lymphoma survival and growth. Mol Cancer 2009;8:132.
  • Chakravarty L, Zabel MD, Weis JJ, Weis JH. Depletion of Lyn kinase from the BCR complex and inhibition of B cell activation by excess CD21 ligation. Int Immunol 2002;14:139–146.
  • Dykstra M, Cherukuri A, Sohn HW, Tzeng SJ, Pierce SK. Location is everything: lipid rafts and immune cell signaling. Ann Rev Immunol 2003;21:457–481.
  • Cheng PC, Dykstra ML, Mitchell RN, Pierce SK. A role for lipid rafts in B cell antigen receptor signaling and antigen targeting. J Exp Med 1999;190:1549–1560.
  • Allsup DJ, Kamiguti AS, Lin K, B-cell receptor translocation to lipid rafts and associated signaling differ between prognostically important subgroups of chronic lymphocytic leukemia. Cancer Res 2005;65:7328–7337.
  • Gobessi S, Laurenti L, Longo PG, Inhibition of constitutive and BCR-induced Syk activation downregulates Mcl-1 and induces apoptosis in chronic lymphocytic leukemia B cells. Leukemia 2009;23:686–697.
  • Longo PG, Laurenti L, Gobessi S, Sica S, Leone G, Efremov DG. The Akt/Mcl-1 pathway plays a prominent role in mediating antiapoptotic signals downstream of the B-cell receptor in chronic lymphocytic leukemia B cells. Blood 2008;111:846–855.
  • Veldurthy A, Patz M, Hagist S, The kinase inhibitor dasatinib induces apoptosis in chronic lymphocytic leukemia cells in vitro with preference for a subgroup of patients with unmutated IgVH genes. Blood 2008;112: 1443–1452.
  • Song Z, Lu P, Furman RR, Activities of SYK and PLCgamma2 predict apoptotic response of CLL cells to SRC tyrosine kinase inhibitor dasatinib. Clin Cancer Res 2010;16:587–599.
  • Amrein PC, Attar EC, Takvorian T, Response to dasatinib in patients with relapsed/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) correlates with p-Lyn and p-Syk. Blood 2010;116(Suppl. 1): Abstract 2457.
  • Garg RJ, Wierda W, Fayad L, Estrov Z, Bickel SM, O'Brien S. Phase II study of dasatinib in patients with relapsed CLL abstract. Blood 2008;112(Suppl. 1): Abstract 4197.
  • Pitini V, Arrigo C, Altavilla G. Dasatinib induces a response in chronic lymphocytic leukemia. Blood 2009;113:498.
  • National Cancer Institute. Surveillance Epidemiology and End Results. SEER Stat Fact Sheets: Acute Myeloid Leukemia; 2009 [Internet]. Available from: http://seer.cancer.gov/statfacts/html/amyl.html
  • Tallman MS, Gilliland DG, Rowe JM. Drug therapy for acute myeloid leukemia. Blood 2005;106:1154–1163.
  • Appelbaum FR, Rowe JM, Radich J, Dick JE. Acute myeloid leukemia. Hematology Am Soc Hematol Educ Program2001:62–86.
  • Krause DS, Van Etten RA. Tyrosine kinases as targets for cancer therapy. N Engl J Med 2005;353:172–187.
  • Dos Santos C, Demur C, Bardet V, Prade-Houdellier N, Payrastre B, Récher C. A critical role for Lyn in acute myeloid leukemia. Blood 2008;111:2269–2279.
  • Soupir CP, Vergilio JA, Dal Cin P, Philadelphia chromosome-positive acute myeloid leukemia: a rare aggressive leukemia with clinicopathologic features distinct from chronic myeloid leukemia in myeloid blast crisis. Am J Clin Pathol 2007;127:642–650.
  • Quintás-Cardama A, Cortes J. Molecular biology of bcr-abl1 positive chronic myeloid leukemia. Blood 2009;113:1619–1630.
  • Gilliland DG, Griffin JD. The roles of FLT3 in hematopoiesis and leukemia. Blood 2002;100:1532–1542.
  • Hayakawa F, Towatari M, Kiyoi H, Tandem-duplicated Flt3 constitutively activates STAT5 and MAP kinase and introduces autonomous cell growth in IL-3-dependent cell lines. Oncogene 2000;19:624–631.
  • Okamoto M, Hayakawa F, Miyata Y, Lyn is an important component of the signal transduction pathway specific to FLT3/ITD and can be a therapeutic target in the treatment of AML with FML/ITD. Leukemia 2007;21:403–410.
  • Okamoto M, Hayakawa F, Miyata Y, Lyn is an important component of the signal transduction pathway specific to FLT3/ITD and can be a therapeutic target in the treatment of AML with FLT3/ITD. Leukemia 2007;21:403–410.
  • Choudhary C, Brandts C, Schwable J, Activation mechanisms of STAT5 by oncogenic Flt3-ITD. Blood 2007;110:370–374.
  • Zhou J, Bi C, Janakakumara JV, Enhanced activation of STAT pathways and overexpression of survivin confer resistance to FLT3 inhibitors and could be therapeutic targets in AML. Blood 2009;113:4052–4062.
  • Pardanani A, Tefferi A. Imatinib targets other than bcr/abl and their clinical relevance in myeloid disorders. Blood 2004;104:1931–1939.
  • Lin P, Chen L, Luthra R, Konoplev SN, Wang X, Medeiros LJ. Acute myeloid leukemia harboring t(8;21)(q22;q22): a heterogeneous disease with poor outcome in a subset of patients unrelated to secondary cytogenetic aberrations. Mod Pathol 2008;21:1029–1036.
  • Heinrich MC, Blanke CD, Druker BJ, Corless CL. Inhibition of KIT tyrosine kinase activity: a novel molecular approach to the treatment of KIT-positive malignancies. J Clin Oncol 2002;20:1692–1703.
  • Edling CE, Hallberg B. c-Kit–a hematopoietic cell essential receptor tyrosine kinase. Int J Biochem Cell Biol 2007;39:1995–1998.
  • Cammenga J, Horn S, Bergholz U, Extracellular KIT receptor mutants, commonly found in core binding factor AML, are constitutively active and respond to imatinib mesylate. Blood 2005;106:3958–3961.
  • Pappa V, Kontsioti F, Liakata E, Dasatinib is an effective inhibitor of proliferation and inducer of apoptosis in the KASUMI cell line bearing the t(8;21)(q22;q22) and the N822K KIT mutation abstract. Blood 2008;112(Suppl. 1): Abstract 5054.
  • O'Laughlin-Bunner B, Radosevic N, Taylor ML, Lyn is required for normal stem cell factor-induced proliferation and chemotaxis of primary hematopoietic cells. Blood 2001;98:343–350.
  • Linnekin D, DeBerry CS, Mou S. Lyn associates with the juxtamembrane region of c-Kit and is activated by stem cell factor in hematopoietic cell lines and normal progenitor cells. J Biol Chem 1997;272:27450–27455.
  • Liang X, Wisniewski D, Strife A, Shivakrupa, Clarkson B, Resh MD. Phosphatidylinositol 3-kinase and Src family kinases are required for phosphorylation and membrane recruitment of Dok-1 in c-Kit signaling. J Biol Chem 2002;277:13732–13738.
  • Shrivastava P, Katagiri T, Ogimoto M, Mizuno K, Yakura H. Dynamic regulation of Src-family kinases by CD45 in B cells. Blood 2004;103:1425–1432.
  • Xu Y, Harder KW, Huntington ND, Hibbs ML, Tarlinton DM. Lyn tyrosine kinase: accentuating the positive and the negative. Immunity 2005;22:9–18.
  • Christopher LJ, Cui D, Wu C, Metabolism and disposition of dasatinib after oral administration to humans. Drug Metab Dispos 2008;36:1357–1364.
  • Keung YK, Beaty M, Powell BL, Molnar I, Buss D, Pettenati M. Philadelphia chromosome positive myelodysplastic syndrome and acute myeloid leukemia: retrospective study and review of literature. Leuk Res 2004;28:579–586.
  • Paietta E, Racevskis J, Bennett JM, Biologic heterogeneity in Philadelphia chromosome-positive acute leukemia with myeloid morphology: the Eastern Cooperative Oncology Group experience. Leukemia 1998;12:1881–1885.
  • Kondo T, Tasaka T, Sano F, Philadelphia chromosome-positive acute myeloid leukemia (Ph+ ALL) treated with imatinib mesylate (IM): a report with IM plasma concentration and bcr-abl transcripts. Leuk Res 2009;33: e137–e138.
  • Jentsch-Ullrich K, Pelz AF, Braun H, Complete molecular remission in a patient with Philadelphia- chromosome positive acute myeloid leukemia after conventional therapy and imatinib. Haematologica 2004;89:ECR15.
  • Schalk E, Neum S, Kranz S, Scheinpflug K, Mohren M. Long-term remission in a patient with BCR/ABL-positive acute myeloid leukaemia on maintenance therapy with imatinib. Leuk Res 2009;33:e6–e7.
  • Viniou NA, Vassilakopoulos TP, Giakoumi X, Mantzouranis M, Pangalis GA. Ida-FLAG plus imatinib mesylate-induced molecular remission in a patient with chemoresistant Ph1+ acute myeloid leukemia. Eur J Haematol 2004;72:58–60.
  • Ustun C, Corless CL, Savage N, Chemotherapy and dasatinib induce long-term hematologic and molecular remission in systemic mastocytosis with acute myeloid leukemia with KIT D816V. Leuk Res 2009;33: 735–741.
  • Verstovsek S, Tefferi A, Cortes J, Phase II study of dasatinib in Philadelphia chromosome-negative acute and chronic myeloid diseases, including systemic mastocytosis. Clin Cancer Res 2008;14:3906–3915.
  • Ritchie DS, McBean M, Westerman DA, Kovalenko S, Seymour JF, Dobrovic A. Complete molecular response of e6a2 BCR-ABL-positive acute myeloid leukemia to imatinib then dasatinib. Blood 2008;111:2896–2898.
  • Ravandi F, O'Brien S, Thomas D, First report of phase 2 study of dasatinib with hyper-CVAD for the frontline treatment of patients with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia. Blood 2010;116:2070–2077.
  • Rousselot P, Cayuela J-M, Recher C, Dasatinib (Sprycel®) and chemotherapy for first-line treatment of elderly patients with de novo Philadelphia positive ALL: results of the first 22 patients included in the EWALL-Ph-01 trial (on behalf of the European Working Group on adult ALL (EWALL). Blood 2008;112(Suppl. 1): Abstract 2920.
  • Deininger M, O'Brien SG, Guilhot F. International Randomized Study of Interferon vs STI571 (IRIS) 8-year follow up: sustained survival and low risk for progression or events in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP) treated with imatinib. Blood 2009;114(Suppl. 1): Abstract 1126.
  • Swerdlow S, Campo E, Harris NL, World Health Organization classification of tumours of haematopoietic and lymphoid tissues. 4th edGeneva: WHO; 2008.
  • Cools J, DeAngelo DJ, Gotlib J, A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. N Engl J Med 2003;348:1201–1214.
  • Jovanovic JV, Score J, Waghorn K, Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia. Blood 2007;109:4635–4640.
  • Wang LN, Pan Q, Fu JF, FIP1L1-PDGFRalpha alone or with other genetic abnormalities reveals disease progression in chronic eosinophilic leukemia but good response to imatinib. Chin Med J (Engl) 2008;121:867–873.
  • Jain N, Cortes J, Quintás-Cardama A, Imatinib has limited therapeutic activity for hypereosinophilic syndrome patients with unknown or negative PDGFRalpha mutation status. Leuk Res 2009;33:837–839.
  • Baumgartner C, Gleixner KV, Peter B, Dasatinib inhibits the growth and survival of neoplastic human eosinophils (EOL-1) through targeting of FIP1L1-PDGFRalpha. Exp Hematol 2008;36:1244–1253.
  • Dahabreh IJ, Giannouli S, Zoi C, Dasatinib for the treatment of treatment-refractory hypereosinophilic syndrome and chronic eosinophilic leukemia. Haematologica 2009;94(Suppl. 2): Abstract 0658.
  • Fritsche-Polanz R, Jordan JH, Feix A, Mutation analysis of C-KIT in patients with myelodysplastic syndromes without mastocytosis and cases of systemic mastocytosis. Br J Haematol 2001;113:357–364.
  • Valent P, Spanblöchl E, Sperr WR, Induction of differentiation of human mast cells from bone marrow and peripheral blood mononuclear cells by recombinant human stem cell factor/kit-ligand in long-term culture. Blood 1992;80:2237–2245.
  • Wang B, Tsukada J, Higashi T, Growth suppression of human mast cells expressing constitutively active c-kit receptors by JNK inhibitor SP600125. Genes Cells 2006;11:983–992.
  • Frost MJ, Ferrao PT, Hughes TP, Ashman LK. Juxtamembrane mutant V560GKit is more sensitive to imatinib (STI571) compared with wild-type c-Kit whereas the kinase domain mutant D816VKit is resistant. Mol Cancer Ther 2002;1:1115–1124.
  • Ma Y, Zeng S, Metcalfe DD, The c-KIT mutation causing human mastocytosis is resistant to STI571 and other KIT kinase inhibitors; kinases with enzymatic site mutations show different inhibitor sensitivity profiles than wild-type kinases and those with regulatory-type mutations. Blood 2002;99:1741–1744.
  • Pardanani A, Elliott M, Reeder T, Imatinib for systemic mast-cell disease. Lancet 2003;362:535–536.
  • Shah NP, Lee FY, Luo R, Jiang Y, Donker M, Akin C. Dasatinib (BMS-354825) inhibits KITD816V, an imatinib-resistant activating mutation that triggers neoplastic growth in most patients with systemic mastocytosis. Blood 2006;108:286–291.
  • Chin H, Arai A, Wakao H, Kamiyama R, Miyasaka N, Miura O. Lyn physically associates with the erythropoietin receptor and may play a role in activation of the Stat5 pathway. Blood 1998;91:3734–3745.
  • Wappl M, Jaeger E, Streubel B, Dasatinib inhibits progenitor cell proliferation from polycythaemia vera. Eur J Clin Invest 2008;38:578–584.
  • Pearson TC, Messinezy M, Westwood N, A polycythemia vera update: diagnosis, pathobiology, and treatment. Hematology Am Soc Hematol Educ Program 2000:51–68.
  • Arcaro A, Aubert M, Espinosa del Hierro ME, Critical role of lipid raft-associated Src kinases in activation of PI3K-Akt signalling. Cell Signal 2007;19:1081–1092.
  • Ptasznik A, Prossnitz ER, Yoshikawa D, Smrcka A, Traynor-Kaplan AE, Bokoch GM. A tyrosine kinase signaling pathway accounts for the majority of phosphatidylinositol 3,4,5-triphosphate formation in chemoattractant-stimulated human neutrophils. J Biol Chem 1996;271:25204–25207.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.