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Seminars in Hematology
Volume 46
, Pages S27-S33
, April 2009
New Directions in the Treatment of Imatinib Failure and/or Resistance
References
- . NCCN: Clinical practice guidelines in oncology (Chronic myelogenous leukemia). 2009;© 2006 National Comprehensive Cancer Network, Inc. Version 2. Jenkintown, PA
- Evolving concepts in the management of chronic myeloid leukemia: Recommendations from an expert panel on behalf of the European LeukemiaNet. Blood. 2006;108:1809–1820
- . Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance. Leukemia. 2004;18:1321–1331
- Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy. Leukemia. 2002;16:2190–2196
- . Anticipating clinical resistance to target-directed agents: The BCR-ABL paradigm. Mol Diagn Ther. 2006;10:67–76
- Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science. 2001;293:876–880
- . New insights into the pathophysiology of chronic myeloid leukemia and imatinib resistance. Ann Intern Med. 2006;145:913–923
- The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib. Leukemia. 2006;20:658–663
- . Active transport of imatinib into and out of cells: implications for drug resistance. Blood. 2004;104:3739–3745
- Most CML patients who have a suboptimal response to imatinib have low OCT-1 activity: higher doses of imatinib may overcome the negative impact of low OCT-1 activity. Blood. 2007;110:4064–4072
- . Targeting the silent minority: emerging immunotherapeutic strategies for eradication of malignant stem cells in chronic myeloid leukaemia. Cancer Immunol Immunother. 2005;54:297–306
- . Leukaemia stem cells and the evolution of cancer-stem-cell research. Nat Rev Cancer. 2005;5:311–321
- Dose escalation of imatinib mesylate can overcome resistance to standard-dose therapy in patients with chronic myelogenous leukemia. Blood. 2003;101:473–475
- Imatinib dose escalation is effective in patients with chronic myeloid leukemia in chronic phase (CP-CML). Blood. 2007;110:317a
- Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. Cancer Cell. 2005;7:129–141
- AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia. Clin Cancer Res. 2005;11:4941–4947
- 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
- . Overriding imatinib resistance with a novel ABL kinase inhibitor. Science. 2004;305:399–401
- 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
- Solution conformations and dynamics of ABL kinase-inhibitor complexes determined by NMR substantiate the different binding modes of imatinib/nilotinib and dasatinib. J Biol Chem. 2008;283:18292–18302
- . AMN107: tightening the grip of imatinib. Cancer Cell. 2005;7:117–119
- Nilotinib in patients with imatinib-resistant or –intolerant chronic myelogenous leukemia in chronic phase (CP-CML): updated phase II results [abstract 7010]. J Clin Oncol. 2008;20(Suppl):26 May
- Nilotinib in chronic myelogenous leukaemia in chronic phase (CP-CML) patients with imatinib resistance or –intolerance: updated phase 2 results. Hematologica. 2008;93(Suppl 1):350
- Nilotinib in accelerated phase chronic myelogenous leukemia (AP-CML) patients with imatinib-resistance or –intolerance: update of a phase 2 study. J Clin Oncol. 2008;26:384s
- Nilotinib in imatinib-resistant or -intolerant patients with chronic myelogenous leukaemia in accelerated phase (AP-CML): update of a phase 2 study. Hematologica. 2008;93:47
- Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. N Engl J Med. 2006;354:2542–2551
- Dasatinib in imatinib-resistant Philadelphia chromosome-positive leukemias. N Engl J Med. 2006;354:2531–2541
- Dasatinib induces complete hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in blast crisis. Blood. 2007;109:3207–3213
- Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase. Blood. 2007;109:4143–4150
- Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. Blood. 2007;109:2303–2309
- Dasatinib induces durable cytogenetic responses in patients with chronic myelogenous leukemia in chronic phase with resistance or intolerance to imatinib. Leukemia. 2008;22:1200–1206
- Dasatinib long-term efficacy in patients with chronic myeloid leukemia in chronic phase (CP-CML) with resistance or intolerance to imatinib: a two-year update of the START-C study. Haematologica. 2008;93:372
- Dasatinib 2-year efficacy in patients with chronic-phase chronic myelogenous leukemia (CP-CML) with resistance or intolerance to imatinib (START-C). J Clin Oncol. 2008;26:374s
- Dasatinib efficacy in patients with imatinib-resistant/-intolerant chronic myeloid leukemia in blast phase: 24-month data from the START program. Haematologica. 2008;93:349
- Pleural effusions in patients with chronic myeloid leukaemia treated with dasatinib may have an immune-mediated pathogenesis. Br J Haematol. 2008;141:745–747
- Dasatinib compared with high-dose imatinib in patients with chronic myelogenous leukemia in chronic phase (CP-CML) after failure of standard-dose imatinib—a two-year update of the START-R study. Haematologica. 2008;93:48
- . Dasatinib or high-dose imatinib for patients with chronic myelogenous leukemia chronic-phase (CP-CML) resistant to standard- dose imatinib: 2-year follow-up data from START-R. J Clin Oncol. 2008;26:375s
- 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
- Dasatinib or high-dose imatinib for patients with chronic-phase chronic myeloid leukemia resistant to standard-dose imatinib: 2-year follow-up data from START-R (CA180-017). Blood. 2007;110:226a
- Nilotinib in chronic myelogenous leukemia patients who failed prior imatinib and dasatinib therapy: updated results of an open-label phase 2 study. J Clin Oncol. 2008;26:385s
- . A phase II study of nilotinib administered to patients with imatinib resistant or intolerant chronic myelogenous leukemia (CML) in chronic phase (CP), accelerated phase (AP) or blast crisis (BC) who also failed dasatinib. J Clin Oncol. 2007;25:366s
- Dasatinib (BMS-354825) is active in Philadelphia chromosome-positive chronic myelogenous leukemia after imatinib and nilotinib (AMN107) therapy failure. Blood. 2007;109:497–499
- In vitro and in vivo activity of SKI-606, a novel Src-Abl inhibitor, against imatinib-resistant Bcr-Abl+ neoplastic cells. Cancer Res. 2006;66:11314–11322
- SKI-606, a 4-anilino-3-quinolinecarbonitrile dual inhibitor of Src and Abl kinases, is a potent antiproliferative agent against chronic myelogenous leukemia cells in culture and causes regression of K562 xenografts in nude mice. Cancer Res. 2003;63:375–381
- Efficacy and safety of bosutinib (SKI-606) among patients with chronic phase Ph+ chronic myelogenous leukemia (CML). Blood. 2007;110:225a
- NS-187, a potent and selective dual Bcr-Abl/Lyn tyrosine kinase inhibitor, is a novel agent for imatinib-resistant leukemia. Blood. 2005;106:3948–3954
- Comparison of imatinib, dasatinib, nilotinib and INNO-406 in imatinib-resistant cell lines. Leuk Res. 2008;32:980–983
- A phase I study of INNO-406 in patients with advanced Philadelphia (Ph+) chromosome-positive leukemias who are resistant or intolerant to imatinib and second generation tyrosine kinase inhibitors. Blood. 2007;110:144a
- Inhibition of wild-type and mutant Bcr-Abl by AP23464, a potent ATP-based oncogenic protein kinase inhibitor: implications for CML. Blood. 2004;104:2532–2539
- Activity of dual SRC-ABL inhibitors highlights the role of BCR/ABL kinase dynamics in drug resistance. Proc Natl Acad Sci U S A. 2006;103:9244–9249
- 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
- Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases. Proc Natl Acad Sci U S A. 2005;102:11011–11016
- . MK-0457, a novel kinase inhibitor, is active in patients with chronic myeloid leukemia or acute lymphocytic leukemia with the T315I BCR-ABL mutation. Blood. 2007;109:500–502
- Simultaneous targeting of aurora kinases and Bcr-Abl kinase by the small molecule inhibitor PHA-739358 is effective against imatinib-resistant BCR-ABL mutations including T315I. Blood. 2008;111:4355–4364
- ABT-737 is a useful component of combinatory chemotherapies for chronic myeloid leukaemias with diverse drug-resistance mechanisms. Br J Haematol. 2008;140:181–190
- . New targeted approaches in chronic myeloid leukemia. J Clin Oncol. 2005;23:6316–6324
- Tasigna (nilotinib) [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2007;
- Sprycel (dasatinib) [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; 2007;
Editorial support was provided by Jeni Fagan (Health Interactions) on behalf of Novartis Oncology.
STATEMENT OF CONFLICT OF INTEREST: Dr Giles received research support from Novartis Pharmaceuticals Corp.
PII: S0037-1963(09)00022-5
doi: 10.1053/j.seminhematol.2009.01.011
© 2009 Elsevier Inc. All rights reserved.
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Seminars in Hematology
Volume 46
, Pages S27-S33
, April 2009
