Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells define commitment to apoptosis

Division of Hematology and Hematologic Malignancies, University of Utah, Huntsman Cancer Institute, Salt Lake City, UT Division of Hematology and Medical Oncology, Oregon Heath & Science University, Portland, OR Knight Cancer Institute, Portland, OR Howard Hughes Medical Institute, Portland, OR Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR Bioanalytical Shared Resource/Pharmacokinetics Core, Oregon Health & Science University, Portland, OR Life Technologies, Madison, WI BD Biosciences, San Diego, CA Department of Cell and Developmental Biology, Oregon Health & Science University, Portland, OR * These authors contributed equally to this work.

[1]  I. Flinn,et al.  Ponatinib in refractory Philadelphia chromosome-positive leukemias. , 2012, The New England journal of medicine.

[2]  M. Deininger,et al.  Pushing the limits of targeted therapy in chronic myeloid leukaemia , 2012, Nature Reviews Cancer.

[3]  B. Druker,et al.  Cryptic Intracellular Retention of ABL Tyrosine Kinase Inhibitors within CML Cells Mediates Apoptosis Commitment Following Acute Drug Exposure , 2011 .

[4]  T. Clackson,et al.  ATP Dependent Efflux Transporters ABCB1 and ABCG2 Are Unlikely to Impact the Efficacy, or Mediate Resistance to the Tyrosine Kinase Inhibitor, Ponatinib , 2011 .

[5]  Xi-shan Wang,et al.  Novel irreversible EGFR tyrosine kinase inhibitor 324674 sensitizes human colon carcinoma HT29 and SW480 cells to apoptosis by blocking the EGFR pathway. , 2011, Biochemical and biophysical research communications.

[6]  B. Druker,et al.  The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profile. , 2011, Cancer research.

[7]  L. Stewart,et al.  Conformational control inhibition of the BCR-ABL1 tyrosine kinase, including the gatekeeper T315I mutant, by the switch-control inhibitor DCC-2036. , 2011, Cancer cell.

[8]  S. Bates,et al.  Comparison of ATP-Binding Cassette Transporter Interactions with the Tyrosine Kinase Inhibitors Imatinib, Nilotinib, and Dasatinib , 2010, Drug Metabolism and Disposition.

[9]  J. Melo,et al.  Nilotinib-mediated inhibition of ABCB1 increases intracellular concentration of dasatinib in CML cells: implications for combination TKI therapy , 2010, Leukemia.

[10]  T. Clackson,et al.  AP24534, a pan-BCR-ABL inhibitor for chronic myeloid leukemia, potently inhibits the T315I mutant and overcomes mutation-based resistance. , 2009, Cancer cell.

[11]  M. Pirmohamed,et al.  Nilotinib concentration in cell lines and primary CD34+ chronic myeloid leukemia cells is not mediated by active uptake or efflux by major drug transporters , 2009, Leukemia.

[12]  R. Koch,et al.  ABC transporter A3 facilitates lysosomal sequestration of imatinib and modulates susceptibility of chronic myeloid leukemia cell lines to this drug , 2009, Haematologica.

[13]  G. Szakács,et al.  Interaction of nilotinib, dasatinib and bosutinib with ABCB1 and ABCG2: implications for altered anti‐cancer effects and pharmacological properties , 2009, British journal of pharmacology.

[14]  K. Zaman,et al.  Therapeutic Drug Monitoring of the new targeted anticancer agents imatinib, nilotinib, dasatinib, sunitinib, sorafenib and lapatinib by LC tandem mass spectrometry. , 2009, Journal of chromatography. B, Analytical technologies in the biomedical and life sciences.

[15]  U. Singh,et al.  Development and Applications of a Broad-Coverage, TR-FRET-Based Kinase Binding Assay Platform , 2009, Journal of biomolecular screening.

[16]  J. Melo,et al.  Short-term intense Bcr–Abl kinase inhibition with nilotinib is adequate to trigger cell death in BCR-ABL+ cells , 2009, Leukemia.

[17]  B. Druker,et al.  Acute dasatinib exposure commits Bcr-Abl-dependent cells to apoptosis. , 2007, Blood.

[18]  Christopher Weier,et al.  Transient potent BCR-ABL inhibition is sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis. , 2008, Cancer cell.

[19]  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.

[20]  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.

[21]  Wolfgang Jahnke,et al.  Solution Conformations and Dynamics of ABL Kinase-Inhibitor Complexes Determined by NMR Substantiate the Different Binding Modes of Imatinib/Nilotinib and Dasatinib*♦ , 2008, Journal of Biological Chemistry.

[22]  J. Melo,et al.  Dasatinib Cellular Uptake and Efflux in Chronic Myeloid Leukemia Cells: Therapeutic Implications , 2008, Clinical Cancer Research.

[23]  P. Erben,et al.  Phospho-CRKL monitoring for the assessment of BCR-ABL activity in imatinib-resistant chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia patients treated with nilotinib , 2008, Haematologica.

[24]  Tillmann Krahnke,et al.  Imatinib pharmacokinetics and its correlation with response and safety in chronic-phase chronic myeloid leukemia: a subanalysis of the IRIS study. , 2008, Blood.

[25]  R. Pazdur,et al.  Sprycel for Chronic Myeloid Leukemia and Philadelphia Chromosome–Positive Acute Lymphoblastic Leukemia Resistant to or Intolerant of Imatinib Mesylate , 2008, Clinical Cancer Research.

[26]  G. Superti-Furga,et al.  Target spectrum of the BCR-ABL inhibitors imatinib, nilotinib and dasatinib , 2008, Leukemia & lymphoma.

[27]  Zheng Yang,et al.  Dasatinib (BMS-354825) Pharmacokinetics and Pharmacodynamic Biomarkers in Animal Models Predict Optimal Clinical Exposure , 2006, Clinical Cancer Research.

[28]  D. Haber,et al.  A common signaling cascade may underlie "addiction" to the Src, BCR-ABL, and EGF receptor oncogenes. , 2006, Cancer cell.

[29]  R. Copeland,et al.  Drug–target residence time and its implications for lead optimization , 2006, Nature Reviews Drug Discovery.

[30]  M. Fischbach,et al.  “Oncogenic Shock”: Explaining Oncogene Addiction through Differential Signal Attenuation , 2006, Clinical Cancer Research.

[31]  P. Manley,et al.  OCT-1-mediated influx is a key determinant of the intracellular uptake of imatinib but not nilotinib (AMN107): reduced OCT-1 activity is the cause of low in vitro sensitivity to imatinib. , 2006, Blood.

[32]  K. Bhalla,et al.  Nilotinib in imatinib-resistant CML and Philadelphia chromosome-positive ALL. , 2006, The New England journal of medicine.

[33]  E. Scholar,et al.  Role of Tyrosine Kinase Inhibitors in Cancer Therapy , 2005, Journal of Pharmacology and Experimental Therapeutics.

[34]  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.

[35]  Donna Neuberg,et al.  Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl. , 2005, Cancer cell.

[36]  Ping Chen,et al.  Overriding Imatinib Resistance with a Novel ABL Kinase Inhibitor , 2004, Science.

[37]  D. Hedley,et al.  Immunoreactivity of Stat5 phosphorylated on tyrosine as a cell‐based measure of Bcr/Abl kinase activity , 2003, Cytometry. Part A : the journal of the International Society for Analytical Cytology.

[38]  G. Superti-Furga,et al.  Structural Basis for the Autoinhibition of c-Abl Tyrosine Kinase , 2003, Cell.

[39]  A. Pendergast,et al.  Activated c-Abl is degraded by the ubiquitin-dependent proteasome pathway , 2001, Current Biology.

[40]  C. Sawyers,et al.  Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. , 2001, The New England journal of medicine.

[41]  P. Seeburg,et al.  Structural mechanism for STI-571 inhibition of abelson tyrosine kinase. , 2000, Science.

[42]  E. Buchdunger,et al.  In vivo eradication of human BCR/ABL-positive leukemia cells with an ABL kinase inhibitor. , 1999, Journal of the National Cancer Institute.