Cohen P. Protein kinases: the major drug targets of the twenty-first century? Nat Rev Drug Discov 2002; 1(4): 309–15 ArticlePubMedCAS Google Scholar
Dancey J, Sausville EA. Issues and progress with protein kinase inhibitors for cancer treatment. Nat Rev Drug Discov 2003; 2(4): 296–313 ArticlePubMedCAS Google Scholar
Noble ME, Endicott JA, Johnson LN. Protein kinase inhibitors: insights into drug design from structure. Science 2004; 303(5665): 1800–5 ArticlePubMedCAS Google Scholar
Nowell P, Hungerford D. A minute chromosome in human chronic granulocytic leukemia [abstract]. Science 1960; 132: 1497 Google Scholar
Rowley JD. A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining [letter]. Nature 1973; 243(5405): 290–3 ArticlePubMedCAS Google Scholar
Kelliher MA, McLaughlin J, Witte ON, et al. Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL. Proc Natl Acad sci USA 1990; 87(17): 6649–53 ArticlePubMedCAS Google Scholar
Goldman JM, Melo JV. Chronic myeloid leukemia: advances in biology and new approaches to treatment. N Engl J Med 2003; 349(15): 1451–64 ArticlePubMedCAS Google Scholar
Deininger MW, Goldman JM, Melo JV. The molecular biology of chronic myeloid leukemia. Blood 2000; 96(10): 3343–56 PubMedCAS Google Scholar
Deininger M, Buchdunger E, Druker BJ. The development of imatinib as a therapeutic agent for chronic myeloid leukemia. Blood 2005; 105(7): 2640–53 ArticlePubMedCAS Google Scholar
Daley GQ, Van Etten RA, Baltimore D. Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome. Science 1990; 247(4944): 824–30 ArticlePubMedCAS Google Scholar
Daley GQ, Van Etten RA, Baltimore D. Blast crisis in a murine model of chronic myelogenous leukemia. Proc Natl Acad sci U S A 1991; 88(24): 11335–8 ArticlePubMedCAS Google Scholar
Kantarjian HM, O’Brien S, Cortes JE, et al. Complete cytogenetic and molecular responses to interferon-alpha-based therapy for chronic myelogenous leukemia are associated with excellent long-term prognosis. Cancer 2003; 97(4): 1033–41 ArticlePubMedCAS Google Scholar
Hehlmann R, Berger U, Hochhaus A. Chronic myeloid leukemia: a model for oncology. Ann Hematol 2005 Aug; 84(8): 487–97 ArticlePubMed Google Scholar
Druker BJ, Tamura S, Buchdunger E, et al. Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr-Abl positive cells. Nat Med 1996; 2(5): 561–6 ArticlePubMedCAS Google Scholar
Druker BJ, Talpaz M, Resta DJ, 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(14): 1031–7 ArticlePubMedCAS Google Scholar
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(14): 1038–42 ArticlePubMedCAS Google Scholar
Kantarjian H, Sawyers C, Hochhaus A, et al. Hematologic and cytogenetic responses to imatinib mesylate in chronic myelogenous leukemia. N Engl J Med 2002; 346(9): 645–52 ArticlePubMedCAS Google Scholar
Talpaz M, Silver RT, Druker BJ, 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(6): 1928–37 ArticlePubMedCAS Google Scholar
Sawyers CL, Hochhaus A, Feldman E, 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(10): 3530–9 ArticlePubMedCAS Google Scholar
Mahon FX, Deininger MW, Schultheis B, et al. Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance. Blood 2000; 96(3): 1070–9 PubMedCAS Google Scholar
le Coutre P, Tassi E, Varella-Garcia M, et al. Induction of resistance to the Abelson inhibitor STI571 in human leukemic cells through gene amplification. Blood 2000; 95(5): 1758–66 PubMed Google Scholar
Weisberg E, Griffin JD. Mechanism of resistance to the ABL tyrosine kinase inhibitor STI571 in BCR/ABL-transformed hematopoietic cell lines. Blood 2000; 95(11): 3498–505 PubMedCAS Google Scholar
Gorre ME, Mohammed M, Ellwood K, et al. Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science 2001; 293(5531): 876–80 ArticlePubMedCAS Google Scholar
Shah NP, Nicoll JM, Nagar B, et al. Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. Cancer Cell 2002; 2(2): 117–25 ArticlePubMedCAS Google Scholar
Shah NP, Sawyers CL. Mechanisms of resistance to STI571 in Philadelphia chromosome-associated leukemias. Oncogene 2003; 22(47): 7389–95 ArticlePubMedCAS Google Scholar
Gorre ME, Sawyers CL. Molecular mechanisms of resistance to STI571 in chronic myeloid leukemia. Curr Opin Hematol 2002; 9(4): 303–7 ArticlePubMed Google Scholar
Donate NJ, Wu JY, Stapley J, et al. BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. Blood 2003; 101(2): 690–8 Article Google Scholar
Dai Y, Rahmani M, Corey SJ, et al. 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(33): 34227–39 ArticlePubMedCAS Google Scholar
Donate NJ, Wu JY, Stapley J, et al. Imatinib mesylate resistance through BCR-ABL independence in chronic myelogenous leukemia. Cancer Res 2004; 64(2): 672–7 Article Google Scholar
Hochhaus A, La Rosee P. Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance. Leukemia 2004; 18(8): 1321–31 ArticlePubMedCAS Google Scholar
Nardi V, Azam M, Daley GQ. Mechanisms and implications of imatinib resistance mutations in BCR-ABL. Curr Opin Hematol 2004; 11(1): 35–43 ArticlePubMedCAS Google Scholar
Van Etten RA. Cycling, stressed-out and nervous: cellular functions of c-Abl. Trends Cell Biol 1999; 9(5): 179–86 ArticlePubMed Google Scholar
Hantschel O, Superti-Furga G. Regulation of the c-Abl and Bcr-Abl tyrosine kinases. Nat Rev Mol Cell Biol 2004; 5(1): 33–44 ArticlePubMedCAS Google Scholar
Azam M, Latek RR, Daley GQ. Mechanisms of autoinhibition and STI-571/ imatinib resistance revealed by mutagenesis of BCR-ABL. Cell 2003; 112(6): 831–43 ArticlePubMedCAS Google Scholar
Nagar B, Hantschel O, Young MA, et al. Structural basis for the autoinhibition of c-Abl tyrosine kinase. Cell 2003; 112(6): 859–71 ArticlePubMedCAS Google Scholar
Hantschel O, Nagar B, Guettler S, et al. A myristoyl/phosphotyrosine switch regulates c-Abl. Cell 2003; 112(6): 845–57 ArticlePubMedCAS Google Scholar
Schindler T, Bornmann W, Pellicena P, et al. Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. Science 2000; 289(5486): 1938–42 ArticlePubMedCAS Google Scholar
Nagar B, Bornmann WG, Pellicena P, 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(15): 4236–43 PubMedCAS Google Scholar
Hochhaus A, Kreil S, Corbin A, et al. Roots of clinical resistance to STI-571 cancer therapy. Science 2001; 293(5538): 2163 ArticlePubMedCAS Google Scholar
Roche-Lestienne C, Soenen-Cornu V, Grardel-Duflos N, et al. Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment. Blood 2002; 100(3): 1014–8 ArticlePubMedCAS Google Scholar
Roche-Lestienne C, Preudhomme C. Mutations in the ABL kinase domain pre-exist the onset of imatinib treatment. Semin Hematol 2003; 40(2 Suppl. 2): 80–2 ArticlePubMedCAS Google Scholar
Roumiantsev S, Shah NP, Gorre ME, et al. Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop. Proc Natl Acad sci U S A 2002; 99(16): 10700–5 ArticlePubMedCAS Google Scholar
Branford S, Rudzki Z, Walsh S, et al. High frequency of point mutations clustered within the adenosine triphosphate-binding region of BCR/ABL in patients with chronic myeloid leukemia or Ph-positive acute lymphoblastic leukemia who develop imatinib (STI571) resistance. Blood 2002; 99(9): 3472–5 ArticlePubMedCAS Google Scholar
Branford S, Rudzki Z, Walsh S, et al. Detection of BCR-ABL mutations in patients with CML treated with imatinib is virtually always accompanied by clinical resistance, and mutations in the ATP phosphate-binding loop (P-loop) are associated with a poor prognosis. Blood 2003; 102(1): 276–83 ArticlePubMedCAS Google Scholar
Chu S, Xu H, Shah NP, 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(5): 2093–8 ArticlePubMedCAS Google Scholar
Corbin AS, La Rosee P, Stoffregen EP, et al. Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. Blood 2003; 101(11): 4611–4 ArticlePubMedCAS Google Scholar
Piazza RG, Magistroni V, Gasser M, et al. Evidence for D276G and L364I Bcr-Abl mutations in Ph+ leukaemic cells obtained from patients resistant to Imatinib. Leukemia 2005; 19(1): 132–4 PubMedCAS Google Scholar
Soverini S, Martinelli G, Rosti G, 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(18): 4100–9 ArticlePubMedCAS Google Scholar
Branford S, Rudzki Z, Parkinson I, et al. Real-time quantitative PCR analysis can be used as a primary screen to identify patients with CML treated with imatinib who have BCR-ABL kinase domain mutations. Blood 2004; 104(9): 2926–32 ArticlePubMedCAS Google Scholar
Barthe C, Cony-Makhoul P, Melo JV, et al. Roots of clinical resistance to STI-571 cancer therapy. Science 2001; 293(5538): 2163 ArticlePubMedCAS Google Scholar
von Bubnoff N, Schneller F, Peschel C, et al. BCR-ABL gene mutations in relation to clinical resistance of Philadelphia-chromosome-positive leukaemia to STI571: a prospective study. Lancet 2002; 359(9305): 487–91 Article Google Scholar
Daub H, Specht K, Ullrich A. Strategies to overcome resistance to targeted protein kinase inhibitors. Nat Rev Drug Discov 2004; 3(12): 1001–10 ArticlePubMedCAS Google Scholar
Al-Ali HK, Heinrich MC, Lange T, et al. High incidence of BCR-ABL kinase domain mutations and absence of mutations of the PDGFR and KIT activation loops in CML patients with secondary resistance to imatinib. Hematol J 2004; 5(1): 55–60 ArticlePubMedCAS Google Scholar
Willis SG, Lange T, Demehri S, et al. High-sensitivity detection of BCR-ABL kinase domain mutations in imatinib-naive patients: correlation with clonal cytogenetic evolution but not response to therapy. Blood 2005; 106(6): 2128–37 ArticlePubMedCAS Google Scholar
Azam M, Raz T, Nardi V, et al. A screen to identify drug resistant variants to target-directed anti-cancer agents. Biol Proced Online 2003; 5: 204–10 ArticlePubMedCAS Google Scholar
Martinelli G, Soverini S, Rosti G, et al. New tyrosine kinase inhibitors in chronic myeloid leukemia. Haematologica 2005; 90(4): 534–41 PubMedCAS Google Scholar
Paez JG, Janne PA, Lee JC, et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science 2004; 304(5676): 1497–500 ArticlePubMedCAS Google Scholar
Sordella R, Bell DW, Haber DA, et al. Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways. Science 2004; 305(5687): 1163–7 ArticlePubMedCAS Google Scholar
Lynch TJ, Bell DW, Sordella R, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med 2004; 350(21): 2129–39 ArticlePubMedCAS Google Scholar
Liu Y, Shah K, Yang F, et al. A molecular gate which controls unnatural ATP analogue recognition by the tyrosine kinase v-Src. Bioorg Med Chem 1998; 6(8): 1219–26 ArticlePubMedCAS Google Scholar
Bishop AC. A hot spot for protein kinase inhibitor sensitivity. Chem Biol 2004; 11(5): 587–9 ArticlePubMedCAS Google Scholar
Nolen B, Taylor S, Ghosh G. Regulation of protein kinases; controlling activity through activation segment conformation. Mol Cell 2004; 15(5): 661–75 ArticlePubMedCAS Google Scholar
Tamborini E, Bonadiman L, Greco A, et al. A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient. Gastroenterology 2004; 127(1): 294–9 ArticlePubMedCAS Google Scholar
Cools J, DeAngelo DJ, Gotlib J, et al. 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(13): 1201–14 ArticlePubMedCAS Google Scholar
Kwak EL, Sordella R, Bell DW, et al. Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib. Proc Natl Acad sci U S A 2005; 102(21): 7665–70 ArticlePubMedCAS Google Scholar
Kobayashi S, Boggon TJ, Dayaram T, et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N Engl J Med 2005; 352(8): 786–92 ArticlePubMedCAS Google Scholar
Wakai T, Kanda T, Hirota S, et al. Late resistance to imatinib therapy in a metastatic gastrointestinal stromal tumour is associated with a second KIT mutation. Br J Cancer 2004; 90(11): 2059–61 PubMedCAS Google Scholar
Ma Y, Zeng S, Metcalfe DD, et al. 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(5): 1741–4 ArticlePubMedCAS Google Scholar
Dorsey JF, Jove R, Kraker AJ, et al. The pyrido[2,3-d]pyrimidine derivative PD180970 inhibits p210Bcr-Abl tyrosine kinase and induces apoptosis of K562 leukemic cells. Cancer Res 2000; 60(12): 3127–31 PubMedCAS Google Scholar
Wisniewski D, Lambek CL, Liu C, et al. Characterization of potent inhibitors of the Bcr-Abl and the c-kit receptor tyrosine kinases. Cancer Res 2002; 62(15): 4244–55 PubMedCAS Google Scholar
von Bubnoff N, Veach DR, Miller WT, et al. Inhibition of wild-type and mutant Bcr-Abl by pyrido-pyrimidine-type small molecule kinase inhibitors. Cancer Res 2003; 63(19): 6395–404 Google Scholar
Shah NP, Tran C, Lee FY, et al. Overriding imatinib resistance with a novel ABL kinase inhibitor. Science 2004; 305(5682): 399–401 ArticlePubMedCAS Google Scholar
Weisberg E, Manley PW, Breitenstein W, et al. Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell 2005; 7(2): 129–41 ArticlePubMedCAS Google Scholar
Burgess MR, Skaggs BJ, Shah NP, et al. Comparative analysis of two clinically active BCR-ABL kinase inhibitors reveals the role of conformation-specific binding in resistance. Proc Natl Acad sci U S A 2005; 102(9): 3395–400 ArticlePubMedCAS Google Scholar