« Previous
Next »
Seminars in Hematology
Volume 46
, Pages S22-S26
, April 2009
Understanding the Role of Mutations in Therapeutic Decision Making for Chronic Myeloid Leukemia
References
- . Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining. Nature. 1973;243:290–293
- Translocation of c-ab1 oncogene correlates with the presence of a Philadelphia chromosome in chronic myelocytic leukaemia. Nature. 1983;306:277–280
- . Mechanisms and implications of imatinib resistance mutations in BCR-ABL. Curr Opin Hematol. 2004;11:35–43
- Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate. Leukemia. 2006;20:1767–1773
- Presence or the emergence of a F317L BCR-ABL mutation may be associated with resistance to dasatinib in Philadelphia chromosome-positive leukemia. J Clin Oncol. 2006;24:e51–e52
- . Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia. Lancet Oncol. 2007;8:1018–1029
- . Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. Blood. 2003;101:4611–4614
- 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;102:276–283
- . Monitoring the response and course of chronic myeloid leukemia in the modern era of BCR-ABL tyrosine kinase inhibitors: practical advice on the use and interpretation of monitoring methods. Blood. 2008;111:1774–1780
- Monitoring CML patients responding to treatment with tyrosine kinase inhibitors: review and recommendations for harmonizing current methodology for detecting BCR-ABL transcripts and kinase domain mutations and for expressing results. Blood. 2006;108:28–37
- 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
- Contribution of ABL kinase domain mutations to imatinib resistance in different subsets of Philadelphia-positive patients: by the GIMEMA Working Party on Chronic Myeloid Leukemia. Clin Cancer Res. 2006;12:7374–7379
- 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;2:117–125
- . Mechanisms of autoinhibition and STI-571/imatinib resistance revealed by mutagenesis of BCR-ABL. Cell. 2003;112:831–843
- Dynamics of BCR-ABL kinase domain mutations in chronic myeloid leukemia after sequential treatment with multiple tyrosine kinase inhibitors. Blood. 2007;110:4005–4011
- Characteristics and outcome of chronic myeloid leukemia patients with F317L BCR-ABL kinase domain mutation after therapy with tyrosine kinase inhibitors. Blood. 2008;112:4839–4842
- Clinical outcome of 27 imatinib mesylate-resistant chronic myelogenous leukemia patients harboring a T315I BCR-ABL mutation. Haematologica. 2007;92:1238–1241
- Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy. Blood. 2008;112:53–55
- Impact of imatinib mesylate dose escalation on resistance and sub-optimal responses to standard-dose therapy in patients (pts) with chronic myeloid leukemia (CML). Blood. 2007;110:313a–314a
- Imatinib mesylate dose escalation is associated with durable responses in patients with chronic myeloid leukemia post cytogenetic failure on standard-dose imatinib therapy. Blood. 2008;Dec 5. [Epub ahead of print]
- 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
- 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
- . Overriding imatinib resistance with a novel ABL kinase inhibitor. Science. 2004;305:399–401
- 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
- Response to nilotinib in chronic myelogenous leukemia patients in chronic phase (CML-CP) according to BCR-ABL mutations at baseline. Haematologica. 2008;93:21
- Response to nilotinib in chronic myelogenous leukemia patients in chronic phase (CML-CP) according to BCR-ABL mutations at baseline. J Clin Oncol. 2008;26:387s
- Dasatinib efficacy by dosing schedule across individual baseline BCR-ABL mutations in chronic phase chronic myelogenous leukemia (CML-CP) after imatinib failure. J Clin Oncol. 2008;26(May 20 suppl):375s
- Dasatinib efficacy after imatinib failure by dosing schedule and baseline BCR-ABL mutation status in patients with chronic myeloid leukemia in chronic phase (CML-CP). Haematologica. 2008;93(Suppl 1):371–372
- Comparison of imatinib, dasatinib, nilotinib and INNO-406 in imatinib-resistant cell lines. Leuk Res. 2008;32:980–983
- . 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;102:3395–3400
- 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
- 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
- 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
- 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
- . Efficacy of subcutaneous homoharringtonine in chronic myeloid leukemia patients resistant to tyrosine kinase inhibitors and harboring a BCR-ABL mutation. Haematologica. 2008;93(s1):56
- Data from a multicenter open label study of subcutaneous omacetaxine mepesuccinate in imatinib-resistant chronic myeloid leukemia patients with T315I mutation. Haematologica. 2008;93(Suppl 1):48–49
- . 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
- Inhibition of drug-resistant mutants of ABL, KIT, and EGF receptor kinases. Proc Natl Acad Sci U S A. 2005;102:11011–11016
- . NCCN: Clinical practice guidelines in oncology (Chronic myelogenous leukemia). 2009;© 2006 National Comprehensive Cancer Network, Inc. Version 2. Jenkintown, PA
- 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;106:2128–2137
- The presence of a BCR-ABL mutant allele in CML does not always explain clinical resistance to imatinib. Leukemia. 2006;20:658–663
- Mutations of the BCR-ABL-kinase domain occur in a minority of patients with stable complete cytogenetic response to imatinib. Leukemia. 2007;21:489–493
Editorial support was provided by Daniel Hutta, PhD, and Michael Mandola, PhD (Health Interactions) on behalf of Novartis Oncology.
STATEMENT OF CONFLICT OF INTEREST: Dr Jabbour is on the Speakers Bureau for Novartis Pharmaceuticals Corp. Dr Soverini has no relationships with the supplement sponsor to disclose.
PII: S0037-1963(09)00020-1
doi: 10.1053/j.seminhematol.2009.01.009
« Previous
Next »
Seminars in Hematology
Volume 46
, Pages S22-S26
, April 2009
