Dasatinib treatment of chronic-phase chronic myeloid leukemia: analysis of responses according to preexisting BCR-ABL mutations.
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Martin C. Müller | J. Radich | L. Ploughman | B. Druker | J. Cortes | P. Erben | A. Hochhaus | Dong-Wook Kim | T. Hughes | S. Branford | R. Pasquini | J. Mukhopadhyay | T. Hughes
[1] H. Kantarjian,et al. Long-term outcome of patients with chronic myeloid leukemia treated with second-generation tyrosine kinase inhibitors after imatinib failure is predicted by the in vitro sensitivity of BCR-ABL kinase domain mutations. , 2009, Blood.
[2] Martin C. Müller,et al. Impact of baseline BCR-ABL mutations on response to nilotinib in patients with chronic myeloid leukemia in chronic phase. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[3] Rocco Piazza,et al. Activity of bosutinib, dasatinib, and nilotinib against 18 imatinib-resistant BCR/ABL mutants. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[4] M. Pirmohamed,et al. Effective dasatinib uptake may occur without human organic cation transporter 1 (hOCT1): implications for the treatment of imatinib-resistant chronic myeloid leukemia. , 2008, Blood.
[5] D. Marin,et al. Finding of kinase domain mutations in patients with chronic phase chronic myeloid leukemia responding to imatinib may identify those at high risk of disease progression. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[6] J. Bajpai. Dasatinib or High-dose Imatinib for Chronic-phase Chronic Myeloid Leukemia After Failure of First-line Imatinib: a Randomized Phase 2 Trial , 2008 .
[7] Martin C. Müller,et al. ABL single nucleotide polymorphisms may masquerade as BCR-ABL mutations associated with resistance to tyrosine kinase inhibitors in patients with chronic myeloid leukemia , 2008, Haematologica.
[8] N. Donato,et al. Association between imatinib-resistant BCR-ABL mutation-negative leukemia and persistent activation of LYN kinase. , 2008, Journal of the National Cancer Institute.
[9] Andreas Hochhaus,et al. Intermittent target inhibition with dasatinib 100 mg once daily preserves efficacy and improves tolerability in imatinib-resistant and -intolerant chronic-phase chronic myeloid leukemia. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[10] D. Marin,et al. In vivo kinetics of kinase domain mutations in CML patients treated with dasatinib after failing imatinib. , 2008, Blood.
[11] Martin C. Müller,et al. Dynamics of BCR-ABL mutated clones prior to hematologic or cytogenetic resistance to imatinib , 2008, Haematologica.
[12] H. Kantarjian,et al. Characteristics and outcomes of patients with chronic myeloid leukemia and T315I mutation following failure of imatinib mesylate therapy. , 2007, Blood.
[13] T. Brümmendorf,et al. Efficacy and safety of dasatinib in imatinib-resistant or -intolerant patients with chronic myeloid leukemia in blast phase , 2008, Leukemia.
[14] H. Kantarjian,et al. Dynamics of BCR-ABL kinase domain mutations in chronic myeloid leukemia after sequential treatment with multiple tyrosine kinase inhibitors. , 2007, Blood.
[15] P. Manley,et al. 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. , 2007, Blood.
[16] G. Rosti,et al. Efficacy of Dasatinib in Patients with Accelerated-Phase Chronic Myelogenous Leukemia with Resistance or Intolerance to Imatinib: 2-Year Follow-Up Data from START-A (CA180-005). , 2007 .
[17] J. Apperley. Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia. , 2007, The Lancet. Oncology.
[18] C. Sawyers,et al. Sequential ABL kinase inhibitor therapy selects for compound drug-resistant BCR-ABL mutations with altered oncogenic potency. , 2007, The Journal of clinical investigation.
[19] B. Druker,et al. Applying the discovery of the Philadelphia chromosome. , 2007, The Journal of clinical investigation.
[20] R. Larson,et al. Dasatinib induces significant hematologic and cytogenetic responses in patients with imatinib-resistant or -intolerant chronic myeloid leukemia in accelerated phase. , 2007, Blood.
[21] M. Baccarani,et al. Dasatinib induces notable hematologic and cytogenetic responses in chronic-phase chronic myeloid leukemia after failure of imatinib therapy. , 2007, Blood.
[22] M. Deininger,et al. Bcr-Abl kinase domain mutations and the unsettled problem of Bcr-AblT315I: looking into the future of controlling drug resistance in chronic myeloid leukemia. , 2007, Clinical lymphoma & myeloma.
[23] M. Baccarani,et al. Resistance to dasatinib in Philadelphia-positive leukemia patients and the presence or the selection of mutations at residues 315 and 317 in the BCR-ABL kinase domain. , 2007, Haematologica.
[24] C. Preudhomme,et al. The prognosis impact of BCR-ABL P-loop mutations: worse or not worse? , 2007, Leukemia.
[25] S. Branford. Chronic myeloid leukemia: molecular monitoring in clinical practice. , 2007, Hematology. American Society of Hematology. Education Program.
[26] M. Baccarani,et al. 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 , 2006, Clinical Cancer Research.
[27] Francisco Cervantes,et al. Five-year follow-up of patients receiving imatinib for chronic myeloid leukemia. , 2006, The New England journal of medicine.
[28] H. Kantarjian,et al. Frequency and clinical significance of BCR-ABL mutations in patients with chronic myeloid leukemia treated with imatinib mesylate , 2006, Leukemia.
[29] Simona Soverini,et al. 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. , 2006, Blood.
[30] M. Wittekind,et al. The structure of Dasatinib (BMS-354825) bound to activated ABL kinase domain elucidates its inhibitory activity against imatinib-resistant ABL mutants. , 2006, Cancer research.
[31] J. Mestan,et al. In vitro activity of Bcr-Abl inhibitors AMN107 and BMS-354825 against clinically relevant imatinib-resistant Abl kinase domain mutants. , 2005, Cancer research.
[32] Martin C. Müller,et al. Response and resistance in 300 patients with BCR‐ABL–positive leukemias treated with imatinib in a single center , 2005, Cancer.
[33] B. Druker,et al. Oncogenes and Tumor Suppressors (795 articles) , 2004 .
[34] Jorge Cortes,et al. Natural history and staging of chronic myelogenous leukemia. , 2004, Hematology/oncology clinics of North America.
[35] Susan Branford,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. , 2003, Blood.
[36] N. Donato,et al. BCR-ABL independence and LYN kinase overexpression in chronic myelogenous leukemia cells selected for resistance to STI571. , 2003, Blood.
[37] B. Druker,et al. Molecular and chromosomal mechanisms of resistance to imatinib (STI571) therapy , 2002, Leukemia.