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1. Full Text AP24534, a Pan-BCR-ABL Inhibitor for Chronic Myeloid Leukemia, Potently Inhibits the T315I Mutant and Overcomes Mutation-Based Resistance
by O'Hare, Thomas and Shakespeare, William C and Zhu, Xiaotian and Eide, Christopher A and Rivera, Victor M and Wang, Yihan and Wang, Frank and Adrian, Lauren T and Zhou, Tianjun and Zhou, Dong and Huang, Wei-Sheng and Xu, Qihong and Metcalf, Chester A and Tyner, Jeffrey W and Loriaux, Marc M and Corbin, Amie S and Wardwell, Scott and Ning, Yaoyu and Keats, Jeffrey A and Sundaramoorthi, Raji and Thomas, Mathew and Snodgrass, Joseph and Commodore, Lois and Sawyer, Tomi K and Dalgarno, David C and Deininger, Michael W.N and Druker, Brian J and Clackson, Tim
Cancer Cell, ISSN 1535-6108, 2009, Volume 16, Issue 5, pp. 401 - 412
Inhibition of BCR-ABL by imatinib induces durable responses in many patients with chronic myeloid leukemia (CML), but resistance attributable to kinase domain... 
CHEMBIO | HUMDISEASE | CHRONIC MYELOGENOUS LEUKEMIA | DASATINIB BMS-354825 | MESYLATE | CML | ONCOLOGY | KINASE DOMAIN MUTATIONS | AMN107 | IMATINIB RESISTANCE | NILOTINIB | Proto-Oncogene Proteins c-abl - antagonists & inhibitors | Humans | Imidazoles - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Crystallography, X-Ray | Pyridazines - pharmacology | Protein Kinase Inhibitors - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Antineoplastic Agents - pharmacology | Fusion Proteins, bcr-abl - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Proto-Oncogene Proteins c-abl - genetics | Cell Growth Processes - drug effects | Proto-Oncogene Proteins c-abl - chemistry | Models, Molecular | Imidazoles - pharmacology | Antineoplastic Agents - chemistry | Mice, SCID | Pyridazines - chemistry | Fusion Proteins, bcr-abl - genetics | Animals | Signal Transduction - drug effects | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Proto-Oncogene Proteins c-abl - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Fusion Proteins, bcr-abl - metabolism | Chronic myeloid leukemia | BCR protein | Imatinib | Mutagenesis | Abl protein | Mutation | Fusion protein | Tumors | Index Medicus | imatinib resistance | dasatinib | nilotinib | compound mutation
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2. Full Text Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival
by Hamilton, Ashley and Helgason, G. Vignir and Schemionek, Mirle and Zhang, Bin and Myssina, Svetlana and Allan, Elaine K and Nicolini, Franck E and Müller-Tidow, Carsten and Bhatia, Ravi and Brunton, Valerie G and Koschmieder, Steffen and Holyoake, Tessa L
Blood, ISSN 0006-4971, 02/2012, Volume 119, Issue 6, pp. 1501 - 1510
Recent evidence suggests chronic myeloid leukemia (CML) stem cells are insensitive to kinase inhibitors and responsible for minimal residual disease in treated... 
CHRONIC MYELOGENOUS LEUKEMIA | SELECTIVE INHIBITOR | POSITIVE CELLS | COLONY-STIMULATING FACTOR | TYROSINE KINASE | PHILADELPHIA-CHROMOSOME | ACUTE LYMPHOBLASTIC-LEUKEMIA | RESIDUAL DISEASE | HEMATOLOGY | HEMATOPOIETIC PROGENITORS | IMATINIB MESYLATE | Antigens, CD34 - metabolism | Apoptosis - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Dose-Response Relationship, Drug | STAT5 Transcription Factor - metabolism | Flow Cytometry | Neoplastic Stem Cells - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | HEK293 Cells | Neoplastic Stem Cells - pathology | Cell Survival - drug effects | Dasatinib | Mice, Transgenic | Nuclear Proteins - metabolism | Gene Expression Regulation, Leukemic | Pyrimidines - pharmacology | Gene Knockout Techniques | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Fusion Proteins, bcr-abl - genetics | Animals | Fusion Proteins, bcr-abl - antagonists & inhibitors | K562 Cells | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Adaptor Proteins, Signal Transducing - metabolism | Fusion Proteins, bcr-abl - metabolism | Index Medicus | Abridged Index Medicus | Myeloid Neoplasia
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3. Full Text BCR-ABL uncouples canonical JAK2-STAT5 signaling in chronic myeloid leukemia
by Hantschel, Oliver and Warsch, Wolfgang and Eckelhart, Eva and Kaupe, Ines and Grebien, Florian and Wagner, Kay-Uwe and Superti-Furga, Giulio and Sexl, Veronika
Nature Chemical Biology, ISSN 1552-4450, 03/2012, Volume 8, Issue 3, pp. 285 - 293
Constitutive activation of STAT5 is critical for the maintenance of chronic myeloid leukemia (CML) characterized by the BCR-ABL oncoprotein. Tyrosine kinase... 
CHRONIC MYELOGENOUS LEUKEMIA | POLYCYTHEMIA-VERA | JAK2 INHIBITOR | TYROSINE PHOSPHORYLATION | PHILADELPHIA-CHROMOSOME | BIOCHEMISTRY & MOLECULAR BIOLOGY | MYELOPROLIFERATIVE NEOPLASMS | FOLLOW-UP | PATIENTS RECEIVING IMATINIB | KINASE INHIBITOR | DNA-BINDING ACTIVITY | Humans | Mice, Inbred C57BL | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Janus Kinase 2 - deficiency | Mice, Knockout | STAT5 Transcription Factor - metabolism | Animals | Signal Transduction - drug effects | U937 Cells | Janus Kinase 2 - metabolism | STAT5 Transcription Factor - antagonists & inhibitors | Fusion Proteins, bcr-abl - antagonists & inhibitors | HEK293 Cells | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Antineoplastic Agents - pharmacology | Mice | Benzamides | Fusion Proteins, bcr-abl - metabolism | Janus Kinase 2 - antagonists & inhibitors | Proteins | Enzymes | Cellular biology | Leukemia | Oncology | Pharmacology | Apoptosis | BCR protein | Animal models | Transformation | Janus kinase 2 | Abl protein | Stat5 protein | Chronic myeloid leukemia | Fusion protein | Protein-tyrosine kinase | Index Medicus
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4. Full Text Targeting the SH2-Kinase Interface in Bcr-Abl Inhibits Leukemogenesis
by Grebien, Florian and Hantschel, Oliver and Wojcik, John and Kaupe, Ines and Kovacic, Boris and Wyrzucki, Arkadiusz M and Gish, Gerald D and Cerny-Reiterer, Sabine and Koide, Shohei and Koide, Akiko and Beug, Hartmut and Pawson, Tony and Valent, Peter and Superti-Furga, Giulio and Argonne National Lab. (ANL), Argonne, IL (United States). Advanced Photon Source (APS)
Cell, ISSN 0092-8674, 10/2011, Volume 147, Issue 2, pp. 306 - 319
Chronic myelogenous leukemia (CML) is caused by the constitutively active tyrosine kinase Bcr-Abl and treated with the tyrosine kinase inhibitor (TKI)... 
CHRONIC MYELOGENOUS LEUKEMIA | TRANSFORMATION | ACTIVATION | PROTEIN-TYROSINE KINASES | C-ABL | BCR/ABL | BIOCHEMISTRY & MOLECULAR BIOLOGY | BINDING-SITE | INDUCTION | CHRONIC MYELOID-LEUKEMIA | SH2 DOMAINS | CELL BIOLOGY | Fusion Proteins, bcr-abl - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Amino Acid Sequence | Signal Transduction | Protein-Tyrosine Kinases - metabolism | Humans | Cells, Cultured | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Models, Molecular | Molecular Sequence Data | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Isoleucine - metabolism | src Homology Domains | Animals | Base Sequence | Fusion Proteins, bcr-abl - antagonists & inhibitors | Protein-Tyrosine Kinases - chemistry | Mice | Protein Kinase Inhibitors - pharmacology | Benzamides | Fusion Proteins, bcr-abl - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Fibronectins | Tyrosine | Enzymes | Universities and colleges | Molecular genetics | Leukemia | Index Medicus | APOPTOSIS | MUTANTS | BASIC BIOLOGICAL SCIENCES | TYROSINE | IN VITRO | LEUKEMOGENESIS | SENSITIVITY | PHOSPHOTRANSFERASES | TARGETS | MICE | LEUKEMIA | 60 APPLIED LIFE SCIENCES
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5. Full Text Human chronic myeloid leukemia stem cells are insensitive to imatinib despite inhibition of BCR-ABL activity
by Corbin, Amie S and Agarwal, Anupriya and Loriaux, Marc and Cortes, Jorge and Deininger, Michael W and Druker, Brian J
Journal of Clinical Investigation, ISSN 0021-9738, 01/2011, Volume 121, Issue 1, pp. 396 - 409
Imatinib therapy, which targets the oncogene product BCR-ABL, has transformed chronic myeloid leukemia (CML) from a life-threatening disease into a chronic... 
CHRONIC MYELOGENOUS LEUKEMIA | PROGENITOR CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | CD34(+) CELLS | MESYLATE DISCONTINUATION | KINASE INHIBITION | HUMAN HEMATOPOIETIC STEM | COMPLETE CYTOGENETIC REMISSION | TYROSINE KINASE | EARLY CHRONIC-PHASE | P-GLYCOPROTEIN | Cell Survival - drug effects | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Drug Resistance, Neoplasm | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Neoplastic Stem Cells - metabolism | Models, Biological | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Fusion Proteins, bcr-abl - antagonists & inhibitors | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Neoplastic Stem Cells - pathology | Antineoplastic Agents - pharmacology | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Benzamides | In Vitro Techniques | Cytokines - pharmacology | Stem cells | Physiological aspects | Genetic aspects | Research | Chronic myeloid leukemia | Drug therapy | Oncogenes | Index Medicus | Abridged Index Medicus
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6. Full Text Impact of Baseline BCR-ABL Mutations on Response to Nilotinib in Patients With Chronic Myeloid Leukemia in Chronic Phase
by Timothy Hughes and Giuseppe Saglio and Susan Branford and Simona Soverini and Dong-Wook Kim and Martin C. Müller and Giovanni Martinelli and Jorge Cortes and Lan Beppu and Enrico Gottardi and Dongho Kim and Philipp Erben and Yaping Shou and Ariful Haque and Neil Gallagher and Jerald Radich and Andreas Hochhaus
Journal of Clinical Oncology, ISSN 0732-183X, 09/2009, Volume 27, Issue 25, pp. 4204 - 4210
Purpose Nilotinib is a second-generation tyrosine kinase inhibitor indicated for the treatment of patients with chronic myeloid leukemia (CML) in chronic phase... 
CHRONIC MYELOGENOUS LEUKEMIA | SELECTIVE INHIBITOR | AMN107 NILOTINIB | ONCOLOGY | KINASE DOMAIN MUTATIONS | FORMERLY AMN107 | BLAST CRISIS | HARMONIZING CURRENT METHODOLOGY | FOLLOW-UP | IMATINIB RESISTANCE | GIMEMA WORKING PARTY | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | United States | Europe | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Treatment Outcome | Antineoplastic Agents - therapeutic use | Piperazines - therapeutic use | Gene Expression Regulation, Leukemic | Imatinib Mesylate | Gene Expression Regulation, Enzymologic | Drug Resistance, Neoplasm - genetics | Fusion Proteins, bcr-abl - genetics | Time Factors | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Benzamides | Mutation | Australia | Korea | Index Medicus | ORIGINAL REPORTS | Hema9
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7. Full Text A long noncoding RNA critically regulates Bcr-Abl-mediated cellular transformation by acting as a competitive endogenous RNA
by Guo, G and Kang, Q and Zhu, X and Chen, Q and Wang, X and Chen, Y and Ouyang, J and Zhang, L and Tan, H and Chen, R and Huang, S and Chen, J.-L
Oncogene, ISSN 0950-9232, 04/2015, Volume 34, Issue 14, pp. 1768 - 1779
Aberrant expression of long noncoding RNAs (lncRNAs) is associated with various human cancers. However, the role of lncRNAs in Bcr-Abl-mediated chronic myeloid... 
STEM-CELLS | NORMAL HEMATOPOIESIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | C-MYC | PTEN | CANCER | CHRONIC MYELOID-LEUKEMIA | MOLECULAR PATHWAYS | CELL BIOLOGY | MESSENGER-RNAS | ONCOLOGY | GENETICS & HEREDITY | GENE-EXPRESSION | TUMOR-SUPPRESSOR | Neoplasm Transplantation | Oligonucleotide Array Sequence Analysis | Apoptosis - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Transplantation, Heterologous | Fusion Proteins, bcr-abl - biosynthesis | PTEN Phosphohydrolase - antagonists & inhibitors | DNA Methylation | MCF-7 Cells | Cell Transformation, Neoplastic - genetics | RNA, Long Noncoding - biosynthesis | HEK293 Cells | Benzamides - pharmacology | PTEN Phosphohydrolase - genetics | Jurkat Cells | RNA, Messenger - genetics | Gene Expression Regulation, Leukemic - drug effects | Mice, Transgenic | RNA, Long Noncoding - genetics | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Hep G2 Cells | Fusion Proteins, bcr-abl - genetics | Animals | Mice, Nude | Fusion Proteins, bcr-abl - antagonists & inhibitors | K562 Cells | Cell Line, Tumor | Mice | MicroRNAs - genetics | Protein Kinase Inhibitors - pharmacology | Proto-Oncogene Proteins c-myc - genetics | Cellular biology | Ribonucleic acid--RNA | Gene expression | Index Medicus
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8. Full Text Charting the Molecular Network of the Drug Target Bcr-Abl
by Marc Brehme and Oliver Hantschel and Jacques Colinge and Ines Kaupe and Melanie Planyavsky and Thomas Köcher and Karl Mechtler and Keiryn L. Bennett and Giulio Superti-Furga and John Kuriyan
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2009, Volume 106, Issue 18, pp. 7414 - 7419
The tyrosine kinase Bcr-Abl causes chronic myeloid leukemia and is the cognate target of tyrosine kinase inhibitors like imatinib. We have charted the... 
Proteins | Phosphatases | K562 cells | Drug interactions | Molecular interactions | Proteomics | Cell lines | Antibodies | Lead | Chronic myeloid leukemia | Protein interaction network tyrosine kinase inhibitor | Imatinib | CHRONIC MYELOGENOUS LEUKEMIA | TRANSFORMATION | PROTEIN | C-ABL | INHIBITORS IMATINIB | TYROSINE KINASE | MULTIDISCIPLINARY SCIENCES | imatinib | MECHANISMS | MASS-SPECTROMETRY | CHRONIC MYELOID-LEUKEMIA | protein interaction network | chronic myeloid leukemia | tyrosine kinase inhibitor | PROTEOMICS | Cell Line | Humans | Fusion Proteins, bcr-abl - antagonists & inhibitors | Multienzyme Complexes - metabolism | Protein Kinase Inhibitors - pharmacology | Multienzyme Complexes - antagonists & inhibitors | Fusion Proteins, bcr-abl - metabolism | Protein Interaction Mapping | Development and progression | Drug targeting | Research | Drug therapy | Observations | Protein-protein interactions | Kinases | Leukemia | Index Medicus | Biological Sciences
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9. Full Text Combined targeting of BCL-2 and BCR-ABL tyrosine kinase eradicates chronic myeloid leukemia stem cells
by Carter, Bing Z and Mak, Po Yee and Mu, Hong and Zhou, Hongsheng and Mak, Duncan H and Schober, Wendy and Leverson, Joel D and Zhang, Bin and Bhatia, Ravi and Huang, Xuelin and Cortes, Jorge and Kantarjian, Hagop and Konopleva, Marina and Andreeff, Michael
Science Translational Medicine, ISSN 1946-6234, 09/2016, Volume 8, Issue 355, pp. 355ra117 - 355ra117
BCR-ABL tyrosine kinase inhibitors (TKIs) are effective against chronic myeloid leukemia (CML), but they rarely eliminate CML stem cells. Disease relapse is... 
CHRONIC MYELOGENOUS LEUKEMIA | PROGENITOR CELLS | CHRONIC PHASE | MEDICINE, RESEARCH & EXPERIMENTAL | AML CELLS | APOPTOSIS | BLAST-CRISIS CML | INHIBITOR ABT-199 | IMATINIB | QUIESCENT | DRUG-RESISTANCE | CELL BIOLOGY | Antigens, CD34 - metabolism | Blast Crisis - drug therapy | Blast Crisis - pathology | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Mice, Transgenic | Proto-Oncogene Proteins c-bcl-2 - metabolism | Animals | Protein Kinase Inhibitors - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Neoplastic Stem Cells - pathology | Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Cell Cycle - drug effects | Fusion Proteins, bcr-abl - metabolism | Index Medicus
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10. Full Text Bcr-Abl kinase domain mutations, drug resistance, and the road to a cure for chronic myeloid leukemia
by O'Hare, Thomas and Eide, Christopher A and Deininger, Michael W. N
Blood, ISSN 0006-4971, 10/2007, Volume 110, Issue 7, pp. 2242 - 2249
Mutations in the kinase domain (KD) of BCR-ABL are the most prevalent mechanism of acquired imatinib resistance in patients with chronic myeloid leukemia... 
CHRONIC MYELOGENOUS LEUKEMIA | CYTOGENETIC RESPONSES | DASATINIB BMS-354825 | IMATINIB-RESISTANT | NILOTINIB AMN107 | CHRONIC-PHASE | TYROSINE KINASE | BLAST CRISIS | CLINICAL RESISTANCE | HEMATOLOGY | GIMEMA WORKING PARTY | Recurrence | Cell Proliferation | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Piperazines - chemistry | Pyrimidines - chemistry | Point Mutation - genetics | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Protein Structure, Tertiary | Risk Factors | Models, Molecular | Piperazines - therapeutic use | Mutation - genetics | Imatinib Mesylate | Drug Resistance, Neoplasm - genetics | Fusion Proteins, bcr-abl - genetics | Animals | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Benzamides | Fusion Proteins, bcr-abl - metabolism | Drug Resistance, Neoplasm - drug effects | Index Medicus | Abridged Index Medicus
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11. Full Text Characterization of AMN107, a selective inhibitor of native and mutant Bcr-Abl
by Weisberg, Ellen and Manley, Paul W and Breitenstein, Werner and Brüggen, Josef and Cowan-Jacob, Sandra W and Ray, Arghya and Huntly, Brian and Fabbro, Doriano and Fendrich, Gabriele and Hall-Meyers, Elizabeth and Kung, Andrew L and Mestan, Jürgen and Daley, George Q and Callahan, Linda and Catley, Laurie and Cavazza, Cara and Mohammed, Azam and Neuberg, Donna and Wright, Renee D and Gilliland, D. Gary and Griffin, James D
Cancer Cell, ISSN 1535-6108, 2005, Volume 7, Issue 2, pp. 129 - 141
The Bcr-Abl tyrosine kinase oncogene causes chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL).... 
CHRONIC MYELOGENOUS LEUKEMIA | IN-VITRO | POSITIVE CELLS | ONCOLOGY | IMATINIB STI571 RESISTANCE | ACUTE LYMPHOBLASTIC-LEUKEMIA | TYROSINE KINASE INHIBITOR | HEMATOPOIETIC-CELL LINES | CHRONIC MYELOID-LEUKEMIA | CHRONIC MYELOMONOCYTIC LEUKEMIA | FARNESYL TRANSFERASE INHIBITOR | CELL BIOLOGY | Phosphorylation | Models, Chemical | Mycoplasma - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Crystallography, X-Ray | Drug Resistance, Neoplasm | Pyrimidines - chemistry | Dose-Response Relationship, Drug | Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy | Retroviridae - genetics | Time Factors | Inhibitory Concentration 50 | Antineoplastic Agents - pharmacology | Cell Line | Bone Marrow Cells - cytology | Cell Survival | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Fusion Proteins, bcr-abl - genetics | Animals | Models, Biological | Hematopoietic Stem Cells - cytology | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Mice | Benzamides | Mutation | Index Medicus
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12. Full Text Transient Potent BCR-ABL Inhibition Is Sufficient to Commit Chronic Myeloid Leukemia Cells Irreversibly to Apoptosis
by Shah, Neil P and Kasap, Corynn and Weier, Christopher and Balbas, Minna and Nicoll, John M and Bleickardt, Eric and Nicaise, Claude and Sawyers, Charles L
Cancer Cell, ISSN 1535-6108, 2008, Volume 14, Issue 6, pp. 485 - 493
The BCR-ABL inhibitor dasatinib achieves clinical remissions in chronic myeloid leukemia (CML) patients using a dosing schedule that achieves potent but... 
CELLCYCLE | LUNG-CANCER | IMATINIB-RESISTANT | INTOLERANT | POSITIVE CELLS | PHARMACOKINETICS | ONCOLOGY | TYROSINE KINASE | GROWTH | DASATINIB | ERLOTINIB | ADDICTION | Dasatinib | Cell Survival | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Receptor, Epidermal Growth Factor - metabolism | Fusion Proteins, bcr-abl - physiology | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Fusion Proteins, bcr-abl - antagonists & inhibitors | K562 Cells | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Benzamides | Kinetics | Apoptosis | Medical colleges | Chronic myeloid leukemia | Lung cancer | Index Medicus
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