1,588
Views
72
CrossRef citations to date
0
Altmetric
Review

Src-family kinases in the development and therapy of Philadelphia chromosome-positive chronic myeloid leukemia and acute lymphoblastic leukemia

Pages 19-26 | Received 25 Sep 2007, Accepted 27 Sep 2007, Published online: 01 Jul 2009

References

  • Rowley J D. Letter: a new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature 1973; 243: 290–293
  • Heisterkamp N, Jenster G, Ten H J, Zovich D, Pattengale P K, Groffen J. Acute leukaemia in bcr/abl transgenic mice. Nature 1990; 344: 251–253
  • Daley G Q, Van Etten R A, Baltimore D. Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. Science 1990; 247: 824–830
  • Pear W S, Miller J P, Xu L, Pui J C, Soffer B, Quackenbush R C, et al. Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow. Blood 1998; 92: 3780–3792
  • Kurzrock R, Gutterman J U, Talpaz M. The molecular genetics of Philadelphia chromosome-positive leukemias. N Engl J Med 1988; 319: 990–998
  • Kantarjian H M, Giles F, Quintas-Cardama A, Cortes J. Important therapeutic targets in chronic myelogenous leukemia. Clin Cancer Res 2007; 13: 1089–1097
  • Hochhaus A, Hughes T. Clinical resistance to imatinib: mechanisms and implications. Hematol Oncol Clin North Am 2004; 18: 641–656
  • Gambacorti C, Talpaz M, Sawyers C L, Druker B J, Hochhaus A, Schiffer C, et al. Five year follow-up results of a phase II trial in patients with late chronic phase (L-CP) chronic myeloid leukemia (CML) treated with imatinib who are refractory/intolerant of interferon-α. Blood 2005; 106: 1089
  • Druker B J, Guilhot F, O'Brien S, Larson N, on behalf of the IRIS (International Randomized IF). Long-term benefits of imatinib (IM) for patients newly diagnosed with chronic myelogenous leukemia in chronic phase (CML-CP): the 5-year update from the IRIS study. J Clin Oncol 2006; 24(Suppl 18S)6506
  • O'Brien S G, Guilhot F, Larson R A, Gathmann I, Baccarani M, Cervantes F, et al. Imatinib compared with interferon and low-dose cytarabine for newly diagnosed chronic-phase chronic myeloid leukemia. N Engl J Med 2003; 348: 994–1004
  • Druker B J, Guilhot F, O'Brien S G, Gathmann I, Kantarjian H, Gattermann N, et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. N Engl J Med 2006; 355: 2408–2417
  • Sawyers C L, Hochhaus A, Feldman E, Goldman J M, Miller C B, Ottmann O G, et al. Imatinib induces hematologic and cytogenetic responses in patients with chronic myelogenous leukemia in myeloid blast crisis: results of a phase II study. Blood 2002; 99: 3530–3539
  • Talpaz M, Silver R T, Druker B J, Goldman J M, Gambacorti-Passerini 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: 1928–1937
  • Talpaz M, Goldman J, Sawyers C, Hochhaus A, Silver R T, Smith B D, et al. High dose imatinib (STI571, Gleevec) provides durable long-term outcomes for patients (Pts) with chronic myeloid leukemia (CML) in accelerated phase (AP) or myeloid blast crisis (BC): follow-up of the phase II studies. Blood 2003; 102: 3369
  • Graham S M, Jorgensen H G, Allan E, Pearson C, Alcorn M J, Richmond L, 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
  • Marley S B, Deininger M W, Davidson R J, Goldman J M, Gordon M Y. The tyrosine kinase inhibitor STI571, like interferon-α, preferentially reduces the capacity for amplification of granulocyte-macrophage progenitors from patients with chronic myeloid leukemia. Exp Hematol 2000; 28: 551–557
  • Warmuth M, Bergmann M, Priess A, Hauslmann K, Emmerich B, Hallek M. The Src family kinase Hck interacts with Bcr-Abl by a kinase-independent mechanism and phosphorylates the Grb2-binding site of Bcr. J Biol Chem 1997; 272: 33260–33270
  • Danhauser-Riedl S, Warmuth M, Druker B J, Emmerich B, Hallek M. Activation of Src kinases p53/56lyn and p59hck by p210bcr/abl in myeloid cells. Cancer Res 1996; 56: 3589–3596
  • Roginskaya V, Zuo S, Caudell E, Nambudiri G, Kraker A J, Corey S J. Therapeutic targeting of Src-kinase Lyn in myeloid leukemic cell growth. Leukemia 1999; 13: 855–861
  • Lionberger J M, Wilson M B, Smithgall T E. Transformation of myeloid leukemia cells to cytokine independence by Bcr-Abl is suppressed by kinase-defective Hck. J Biol Chem 2000; 275: 18581–18585
  • Donato N J, Wu J Y, Stapley J, Gallick G, Lin H, Arlinghaus R, et al. BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. Blood 2003; 101: 690–698
  • Dai Y, Rahmani M, Corey S J, Dent P, Grant S. A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2. J Biol Chem 2004; 279: 34227–34239
  • Hu Y, Swerdlow S, Duffy T M, Weinmann R, Lee F Y, Li S. Targeting multiple kinase pathways in leukemic progenitors and stem cells is essential for improved treatment of Ph+ leukemia in mice. Proc Natl Acad Sci USA 2006; 103: 16870–16875
  • Ptasznik A, Nakata Y, Kalota A, Emerson S G, Gewirtz A M. Short interfering RNA (siRNA) targeting the Lyn kinase induces apoptosis in primary, and drug-resistant, BCR-ABL1(+) leukemia cells. Nat Med 2004; 10: 1187–1189
  • Hu Y, Liu Y, Pelletier S, Buchdunger E, Warmuth M, Fabbro D, et al. Requirement of Src kinases Lyn, Hck and Fgr for BCR-ABL1-induced B-lymphoblastic leukemia but not chronic myeloid leukemia. Nat Genet 2004; 36: 453–461
  • Donato N J, Wu J Y, Stapley J, Lin H, Arlinghaus R, Aggarwal B B, et al. Imatinib mesylate resistance through BCR-ABL independence in chronic myelogenous leukemia. Cancer Res 2004; 64: 672–677
  • Donato N J, Wu J, Kong L Y, Meng F, Lee F, Talpaz M. Constitutive activation of SRC-family kinases in chronic myelogenous leukemia patients resistant to imatinib mesylate in the absence of BCR-ABL mutations: a rationale for use of SRC/ABL dual kinase inhibitor-based therapy. Blood 2005; 106: 1087
  • Faderl S, Kantarjian H M, Thomas D A, Cortes J, Giles F, Pierce S, et al. Outcome of Philadelphia chromosome-positive adult acute lymphoblastic leukemia. Leuk Lymphoma 2000; 36: 263–273
  • Lugo T G, Pendergast A M, Muller A J, Witte O N. Tyrosine kinase activity and transformation potency of bcr-abl oncogene products. Science 1990; 247: 1079–1082
  • Van Etten R A. Mechanisms of transformation by the BCR-ABL oncogene: new perspectives in the post-imatinib era. Leuk Res 2004; 28(Suppl 1)S21–S28
  • Puil L, Liu J, Gish G, Mbamalu G, Bowtell D, Pelicci P G, et al. Bcr-Abl oncoproteins bind directly to activators of the Ras signalling pathway. EMBO J 1994; 13: 764–773
  • Jiang X, Lopez A, Holyoake T, Eaves A, Eaves C. Autocrine production and action of IL-3 and granulocyte colony-stimulating factor in chronic myeloid leukemia. Proc Natl Acad Sci USA 1999; 96: 12804–12809
  • Gordon M Y, Dowding C R, Riley G P, Goldman J M, Greaves M F. Altered adhesive interactions with marrow stroma of haematopoietic progenitor cells in chronic myeloid leukaemia. Nature 1987; 328: 342–344
  • Bedi A, Zehnbauer B A, Barber J P, Sharkis S J, Jones R J. Inhibition of apoptosis by BCR-ABL in chronic myeloid leukemia. Blood 1994; 83: 2038–2044
  • Deutsch E, Dugray A, AbdulKarim B, Marangoni E, Maggiorella L, Vaganay S, et al. BCR-ABL down-regulates the DNA repair protein DNA-PKcs. Blood 2001; 97: 2084–2090
  • Slupianek A, Schmutte C, Tombline G, Nieborowska-Skorska M, Hoser G, Nowicki M O, et al. BCR/ABL regulates mammalian RecA homologs, resulting in drug resistance. Mol Cell 2001; 8: 795–806
  • Abram C L, Courtneidge S A. Src family tyrosine kinases and growth factor signaling. Exp Cell Res 2000; 254: 1–13
  • Boggon T J, Eck M J. Structure and regulation of Src family kinases. Oncogene 2004; 23: 7918–7927
  • Li S. Src kinases as targets for B cell acute lymphoblastic leukaemia therapy. Expert Opin Ther Targets 2005; 9: 329–341
  • Warmuth M, Damoiseaux R, Liu Y, Fabbro D, Gray N. SRC family kinases: potential targets for the treatment of human cancer and leukemia. Curr Pharm Des 2003; 9: 2043–2059
  • Lowell C A, Soriano P. Knockouts of Src-family kinases: stiff bones, wimpy T cells, and bad memories. Genes Dev 1996; 10: 1845–1857
  • Overell R W, Watson J D, Gallis B, Weisser K E, Cosman D, Widmer M B. Nature and specificity of lymphokine independence induced by a selectable retroviral vector expressing v-src. Mol Cell Biol 1987; 7: 3394–3401
  • Watson J D, Eszes M, Overell R, Conlon P, Widmer M, Gillis S. Effect of infection with murine recombinant retroviruses containing the v-src oncogene on interleukin 2- and interleukin 3-dependent growth states. J Immunol 1987; 139: 123–129
  • Anderson S M, Carroll P M, Lee F D. Abrogation of IL-3 dependent growth requires a functional v-src gene product: evidence for an autocrine growth cycle. Oncogene 1990; 5: 317–325
  • Engelman A, Rosenberg N. bcr/abl and src but not myc and ras replace v-abl in lymphoid transformation. Mol Cell Biol 1990; 10: 4365–4369
  • Keller G, Wagner E F. Expression of v-src induces a myeloproliferative disease in bone-marrow-reconstituted mice. Genes Dev 1989; 3: 827–837
  • Meyn M A, III, Wilson M B, Abdi F A, Fahey N, Schiavone A P, Wu J, et al. Src family kinases phosphorylate the Bcr-Abl SH3-SH2 region and modulate Bcr-Abl transforming activity. J Biol Chem 2006; 281: 30907–30916
  • Wilson M B, Schreiner S J, Choi H J, Kamens J, Smithgall T E. Selective pyrrolo-pyrimidine inhibitors reveal a necessary role for Src family kinases in Bcr-Abl signal transduction and oncogenesis. Oncogene 2002; 21: 8075–8088
  • Tanis K Q, Veach D, Duewel H S, Bornmann W G, Koleske A J. Two distinct phosphorylation pathways have additive effects on Abl family kinase activation. Mol Cell Biol 2003; 23: 3884–3896
  • Klejman A, Schreiner S J, Nieborowska-Skorska M, Slupianek A, Wilson M, Smithgall T E, et al. The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells. EMBO J 2002; 21: 5766–5774
  • Ptasznik A, Urbanowska E, Chinta S, Costa M A, Katz B A, Stanislaus M A, et al. Crosstalk between BCR/ABL oncoprotein and CXCR4 signaling through a Src family kinase in human leukemia cells. J Exp Med 2002; 196: 667–678
  • Ilaria R L, Jr, Hawley R G, Van Etten R A. Dominant negative mutants implicate STAT5 in myeloid cell proliferation and neutrophil differentiation. Blood 1999; 93: 4154–4166
  • Nosaka T, Kawashima T, Misawa K, Ikuta K, Mui A L, Kitamura T. STAT5 as a molecular regulator of proliferation, differentiation and apoptosis in hematopoietic cells. EMBO J 1999; 18: 4754–4765
  • Kieslinger M, Woldman I, Moriggl R, Hofmann J, Marine J C, Ihle J N, et al. Antiapoptotic activity of Stat5 required during terminal stages of myeloid differentiation. Genes Dev 2000; 14: 232–244
  • Warmuth M, Simon N, Mitina O, Mathes R, Fabbro D, Manley P W, et al. Dual-specific Src and Abl kinase inhibitors, PP1 and CGP76030, inhibit growth and survival of cells expressing imatinib mesylate-resistant Bcr-Abl kinases. Blood 2003; 101: 664–672
  • Skorski T, Bellacosa A, Nieborowska-Skorska M, Majewski M, Martinez R, Choi J K, et al. Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway. EMBO J 1997; 16: 6151–6161
  • Druker B J, Sawyers C L, Kantarjian H, Resta D J, Reese S F, Ford J M, 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
  • Ottmann O G, Druker B J, Sawyers C L, Goldman J M, Reiffers J, Silver R T, et al. A phase 2 study of imatinib in patients with relapsed or refractory Philadelphia chromosome-positive acute lymphoid leukemias. Blood 2002; 100: 1965–1971
  • Hochhaus A, La Rosee P. Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance. Leukemia 2004; 18: 1321–1331
  • Nagar B, Bornmann W G, Pellicena P, Schindler T, Veach D R, Miller W T, et al. Crystal structures of the kinase domain of c-Abl in complex with the small molecule inhibitors PD173955 and imatinib (STI-571). Cancer Res 2002; 62: 4236–4243
  • Schindler T, Bornmann W, Pellicena P, Miller W T, Clarkson B, Kuriyan J. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Science 2000; 289: 1938–1942
  • Azam M, Latek R R, Daley G Q. Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL. Cell 2003; 112: 831–843
  • Chu S, Xu H, Shah N P, Snyder D S, Forman S J, Sawyers C L, et al. Detection of BCR-ABL kinase mutations in CD34+ cells from chronic myelogenous leukemia patients in complete cytogenetic remission on imatinib mesylate treatment. Blood 2005; 105: 2093–2098
  • Tipping A J, Baluch S, Barnes D J, Veach D R, Clarkson B M, Bornmann W G, et al. Efficacy of dual-specific Bcr-Abl and Src-family kinase inhibitors in cells sensitive and resistant to imatinib mesylate. Leukemia 2004; 18: 1352–1356
  • Azam M, Daley G Q. Anticipating clinical resistance to target-directed agents: the BCR-ABL paradigm. Mol Diagn Ther 2006; 10: 67–76
  • Kantarjian H M, Talpaz M, Giles F, O'Brien S, Cortes J. New insights into the pathophysiology of chronic myeloid leukemia and imatinib resistance. Ann Intern Med 2006; 145: 913–923
  • O'hare T, Walters D K, Stoffregen E P, Jia T, Manley P W, Mestan J, et al. 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
  • Shah N P, Tran C, Lee F Y, Chen P, Norris D, Sawyers C L. Overriding imatinib resistance with a novel ABL kinase inhibitor. Science 2004; 305: 399–401
  • Tokarski J S, Newitt J A, Chang C Y, Cheng J D, Wittekind M, Kiefer S E, et al. 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
  • Lee F Y, Lombardo L, Camuso A, Castaneda S, Fager K, Flefleh C, et al. BMS-354825 potently inhibits multiple selected oncogenic tyrosine kinases and possesses broad-spectrum antitumor activities in vitro and in vivo. Proc Am Assoc Cancer Res 2005; 46: 159, (abstr. 675)
  • Lombardo L J, Lee F Y, Chen P, Norris D, Barrish J C, Behnia K, et al. 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
  • Nam S, Kim D, Cheng J Q, Zhang S, Lee J H, Buettner R, et al. Action of the Src family kinase inhibitor, dasatinib (BMS-354825), on human prostate cancer cells. Cancer Res 2005; 65: 9185–9189
  • Schittenhelm M M, Shiraga S, Schroeder A, Corbin A S, Griffith D, Lee F Y, et al. 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
  • Talpaz M, Shah N P, Kantarjian H, Donato N, Nicoll J, Paquette R, et al. Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med 2006; 354: 2531–2541
  • Baccarani M, Kantarjian H M, Apperley J F, Lipton J H, Druker B, Countouriotis A, et al. Efficacy of dasatinib (SPRYCEL) in patients (pts) with chronic phase chronic myelogenous leukemia (CP-CML) resistant to or intolerant of imatinib: updated results of the CA180013 START-C phase II study. Blood 2006; 108(Suppl.)164
  • Cortes J, Kim D W, Guilhot F, Rosti G, Silver R T, Gollerkeri A, et al. Dasatinib (SPRYCEL) in patients (pts) with chronic myelogenous leukemia in accelerated phase (AP-CML) that is imatinib-resistant (im-r) or -intolerant (im-i): updated results of the CA180-005 START-A phase II study. Blood 2006; 108(Suppl.)2160
  • Martinelli G, Hochhaus A, Coutre S, Apperley J F, Shah N, Gollerkeri A, et al. Dasatinib (SPRYCEL) efficacy and safety in patients (pts) with chronic myelogenous leukemia in lymphoid (CML-LB) or myeloid blast (CML-MB) phase who are imatinib-resistant (im-r) or -intolerant (im-i). Blood 2006; 108(Suppl.)745
  • Dombret H, Ottman O G, Rosti G, Simonsson B, Larson R A, Gollerkeri A, et al. Dasatinib (SPRYCEL) in patients (pts) with Philadelphia chromosome-positive acute lymphoblastic leukemia who are imatinib-resistant (im-r) or -intolerant (im-i): updated results from the CA180-015 START-L study. Blood 2006; 108(Suppl.)286
  • Kantarjian H, Pasquini R, Hamerschlak N, Rousselot P, Holowiecki J, Jootar S, et al. Dasatinib or high-dose imatinib for chronic-phase chronic myeloid leukemia after failure of first-line imatinib: a randomized phase 2 trial. Blood 2007; 109: 5143–5150
  • Hochhaus A, Branford S, Radich J, Mueller M C, Shah N, Erben P, et al. Efficacy of dasatinib in chronic phase chronic myelogenous leukemia patients after imatinib failure according to baseline BCR-ABL mutations. J Clin Oncol 2007; 25(Suppl 18S)7023
  • Quintas-Cardama A, Kantarjian H, Jones D, Nicaise C, O'Brien S, Giles F, et al. Dasatinib (BMS-354825) is active in Philadelphia chromosome-positive chronic myelogenous leukemia after imatinib and nilotinib (AMN107) therapy failure. Blood 2007; 109: 497–499
  • Larson R, Ottmann O, Kantarjian H, le Coutre P, Baccarani M, Weitzman A, et al. A phase II study of nilotinib administered to imatinib resistant or intolerant patients with chronic myelogenous leukemia (CML) in blast crisis (BC) or relapsed/refractory Ph+ acute lymphoblastic leukemia (ALL). J Clin Oncol 2007; 25(Suppl 18S)7040
  • Druker B J. Circumventing resistance to kinase-inhibitor therapy. N Engl J Med 2006; 354: 2594–2596
  • Kantarjian H M, Talpaz M, O'Brien S, Smith T L, Giles F J, Faderl S, et al. Imatinib mesylate for Philadelphia chromosome-positive, chronic-phase myeloid leukemia after failure of interferon-α: follow-up results. Clin Cancer Res 2002; 8: 2177–2187
  • Kantarjian H M, Shan J, Smith T, Talpaz M, Kozuch P, Rios M B, et al. Response to therapy is independently associated with survival prolongation in chronic myelogenous leukemia in the blastic phase. Cancer 2001; 92: 2501–2507
  • Marin D, Marktel S, Bua M, Szydlo R M, Franceschino A, Nathan I, et al. Prognostic factors for patients with chronic myeloid leukaemia in chronic phase treated with imatinib mesylate after failure of interferon α. Leukemia 2003; 17: 1448–1453
  • Kantarjian H, O'Brien S, Cortes J, Giles F, Shan J, Rios M B, et al. Survival advantage with imatinib mesylate therapy in chronic-phase chronic myelogenous leukemia (CML-CP) after IFN-α failure and in late CML-CP, comparison with historical controls. Clin Cancer Res 2004; 10: 68–75
  • Kantarjian H, Schiffer C, Sawyers C L, Hochhaus A, Guilhot F, Niederwieser D W, et al. Imatinib (Gleevec) maintains favorable long-term outcomes in chronic-phase chronic myeloid leukemia (CML) for patients failing interferon-α (IFN) follow-up of a phase II study. Blood 2003; 102: 3368
  • Branford S, Rudzki Z, Harper A, Grigg A, Taylor K, Durrant S, et al. Imatinib produces significantly superior molecular responses compared to interferon α plus cytarabine in patients with newly diagnosed chronic myeloid leukemia in chronic phase. Leukemia 2003; 17: 2401–2409
  • Quintas-Cardama A, Kantarjian H, O'Brien S, Jones D, Borthakur G, Nicaise C, et al. Dasatinib is safe and effective in patients with previously untreated chronic myelogenous leukemia (CML) in chronic phase (CML-CP). Haematologica 2007; 92(Suppl 1)0360