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1. Full Text Molecular pathways: BCR-ABL
by Cilloni, Daniela and Saglio, Giuseppe
Clinical Cancer Research, ISSN 1078-0432, 02/2012, Volume 18, Issue 4, pp. 930 - 937
Aberrant tyrosine kinase activity plays a critical role in many hematologic disorders, including chronic myeloid leukemia characterized by the constitutive... 
CHRONIC MYELOGENOUS LEUKEMIA | HEMATOPOIETIC-CELLS | STEM-CELLS | SIGNALING PATHWAYS | CHRONIC-PHASE | ONCOLOGY | BONE-MARROW | CHROMOSOME-POSITIVE CELLS | ANTITUMOR-ACTIVITY | CHRONIC MYELOID-LEUKEMIA | DNA-BINDING ACTIVITY | Humans | Translational Medical Research | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Antineoplastic Agents - therapeutic use | Animals | Signal Transduction - drug effects | Protein Kinase Inhibitors - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Antineoplastic Agents - pharmacology | Mice | Protein Kinase Inhibitors - pharmacology | Fusion Proteins, bcr-abl - metabolism
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2. Full Text Modular PROTAC Design for the Degradation of Oncogenic BCR‐ABL
by Lai, Ashton C and Toure, Momar and Hellerschmied, Doris and Salami, Jemilat and Jaime‐Figueroa, Saul and Ko, Eunhwa and Hines, John and Crews, Craig M
Angewandte Chemie International Edition, ISSN 1433-7851, 01/2016, Volume 55, Issue 2, pp. 807 - 810
Proteolysis Targeting Chimera (PROTAC) technology is a rapidly emerging alternative therapeutic strategy with the potential to address many of the challenges... 
inhibitors | cancer | drug design | E3 ubiquitin ligases | protein degradation | COMPLEX | DOMAIN | C-ABL | SMALL-MOLECULE INHIBITORS | TYROSINE KINASE | CHEMISTRY, MULTIDISCIPLINARY | Cell Line, Tumor | Cell Line | Proteolysis | Humans | Fusion Proteins, bcr-abl - metabolism | Ubiquitin | Developmental biology | Ligases | Binding | BCR protein | Modular design | Abl protein | Drug development | Recruitment | Proteins | Degradation | Ubiquitination | Inhibitors | Technology | Strategy | Fusion protein | Ubiquitin-protein ligase | Drug Design
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3. 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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4. 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 | Myeloid Neoplasia
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5. Full Text Expansion of Bcr-Abl-Positive Leukemic Stem Cells Is Dependent on Hedgehog Pathway Activation
by Dierks, Christine and Beigi, Ronak and Guo, Gui-Rong and Zirlik, Katja and Stegert, Mario R and Manley, Paul and Trussell, Christopher and Schmitt-Graeff, Annette and Landwerlin, Klemens and Veelken, Hendrik and Warmuth, Markus
Cancer Cell, ISSN 1535-6108, 2008, Volume 14, Issue 3, pp. 238 - 249
Resistance of Bcr-Abl-positive leukemic stem cells (LSCs) to imatinib treatment in patients with chronic myeloid leukemia (CML) can cause relapse of disease... 
STEMCELL | CELLCYCLE | CHRONIC MYELOGENOUS LEUKEMIA | HEMATOPOIETIC-CELLS | MOLECULAR REMISSION | ONCOLOGY | SONIC HEDGEHOG | SIGNALING PATHWAY | PHILADELPHIA-CHROMOSOME | NEURAL-TUBE | IMATINIB MESYLATE DISCONTINUATION | MICE | CHRONIC MYELOID-LEUKEMIA | CELL BIOLOGY | Cell Proliferation | Fetal Stem Cells - cytology | Gene Expression - drug effects | Receptors, G-Protein-Coupled - metabolism | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Fetal Stem Cells - metabolism | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Hedgehog Proteins - physiology | Hematopoiesis - drug effects | Neoplastic Stem Cells - metabolism | Kruppel-Like Transcription Factors - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Smoothened Receptor | Bone Marrow Transplantation | Veratrum Alkaloids - pharmacology | Neoplastic Stem Cells - pathology | Bone Marrow Cells - drug effects | Hematopoiesis - physiology | Patched Receptors | Drug Therapy, Combination | Veratrum Alkaloids - therapeutic use | Mice, Inbred C57BL | Bone Marrow Cells - pathology | Receptors, Cell Surface - metabolism | Mice, Transgenic | Pyrimidines - pharmacology | Mice, Knockout | Fusion Proteins, bcr-abl - genetics | Animals | Signal Transduction - drug effects | Pyrimidines - therapeutic use | Survival Analysis | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Signal Transduction - physiology | Fetal Stem Cells - transplantation | Mice | Receptors, G-Protein-Coupled - genetics | Zinc Finger Protein GLI1 | Kruppel-Like Transcription Factors - genetics | Bone Marrow Cells - metabolism | Fusion Proteins, bcr-abl - metabolism | Receptors, Cell Surface - genetics | Genetic research | Flexible response (Strategy) | Drug resistance | Deterrence (Strategy) | Leukemia | Stem cells
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6. 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
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7. 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 | APOPTOSIS | MUTANTS | BASIC BIOLOGICAL SCIENCES | TYROSINE | IN VITRO | LEUKEMOGENESIS | SENSITIVITY | PHOSPHOTRANSFERASES | TARGETS | MICE | LEUKEMIA | 60 APPLIED LIFE SCIENCES
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8. Full Text Ablation of PI3K blocks BCR-ABL leukemogenesis in mice, and a dual PI3K/mTOR inhibitor prevents expansion of human BCR-ABL+ leukemia cells
by Kharas, Michael G and Janes, Matthew R and Scarfone, Vanessa M and Lilly, Michael B and Knight, Zachary A and Shokat, Kevan M and Fruman, David A
Journal of Clinical Investigation, ISSN 0021-9738, 09/2008, Volume 118, Issue 9, pp. 3038 - 3050
Some cases of pre-B cell acute lymphoblastic leukemia (pre-B-ALL) are caused by the Philadelphia (Ph) chromosome-encoded BCR-ABL oncogene, and these tend to... 
MAMMALIAN TARGET | RAPAMYCIN | TRANSFORMATION | MEDICINE, RESEARCH & EXPERIMENTAL | BCR/ABL | PHOSPHORYLATION | GROWTH | AKT | REGULATED KINASE KINASE | PHOSPHOINOSITIDE 3-KINASE | SUBUNIT | Protein Kinases - metabolism | Cell Proliferation | Antigens, CD34 - biosynthesis | Humans | Phosphatidylinositol 3-Kinases - metabolism | Gene Expression Regulation, Leukemic | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Animals | Antigens, CD19 - biosynthesis | Cell Transformation, Neoplastic | Models, Biological | Burkitt Lymphoma - genetics | Cell Line, Tumor | Antineoplastic Agents - pharmacology | Mice | TOR Serine-Threonine Kinases | Fusion Proteins, bcr-abl - metabolism | Cell proliferation | Control | Translocation (Genetics) | Physiological aspects | Genetic aspects | Research | Chronic myeloid leukemia | Risk factors
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9. Full Text Targeting Bcr-Abl by combining allosteric with ATP-binding-site inhibitors
by Ding, Qiang and Jahnke, Wolfgang and Adrián, Francisco J and Guo, Gui-Rong and Warmuth, Markus and Deng, Xianming and Grzesiek, Stephan and Bursulaya, Badry and Gray, Nathanael S and Okram, Barun and Tuntland, Tove and Azam, Mohammad and Li, Allen G and Powers, John and Dierks, Christine and Strauss, André and Engen, John R and Cowan-Jacob, Sandra W and Wojciechowski, Amy and Liu, Yi and Fendrich, Gabriele and Iacob, Roxana E and Sim, Taebo and Sun, Fangxian and Vajpai, Navratna and Zhang, Jianming and Liu, Guoxun and Daley, George Q and Manley, Paul W and Choi, Yongmun
Nature, ISSN 0028-0836, 01/2010, Volume 463, Issue 7280, pp. 501 - 506
In an effort to find new pharmacological modalities to overcome resistance to ATP-binding-site inhibitors of Bcr-Abl, we recently reported the discovery of... 
CELL LUNG-CANCER | KINASE-INHIBITOR | SELECTIVE INHIBITOR | C-ABL | TYROSINE KINASE | MULTIDISCIPLINARY SCIENCES | DYNAMICS | MUTATIONS | LYMPHOBLASTIC-LEUKEMIA | IMATINIB RESISTANCE | CHRONIC MYELOID-LEUKEMIA | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Male | Transplantation, Heterologous | Piperazines - chemistry | Pyrimidines - chemistry | Pyrimidines - metabolism | Antineoplastic Agents - metabolism | Mass Spectrometry | Bone Marrow Transplantation | Inhibitory Concentration 50 | Female | Antineoplastic Agents - pharmacology | Binding Sites | Disease Models, Animal | Fusion Proteins, bcr-abl - chemistry | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Protein Structure, Tertiary | Crystallization | Antineoplastic Combined Chemotherapy Protocols | Models, Molecular | Pyrimidines - pharmacology | Antineoplastic Agents - chemistry | Mutation - genetics | Imatinib Mesylate | Piperazines - pharmacology | Fusion Proteins, bcr-abl - genetics | Animals | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Mice | Benzamides | Fusion Proteins, bcr-abl - metabolism | Drug Resistance, Neoplasm - drug effects | Nilotinib | Dasatinib | Drug resistance in microorganisms | Usage | Nuclear magnetic resonance spectroscopy | Research | Chronic myeloid leukemia | X-ray crystallography | Chromosome abnormalities | Gene mutations | Analysis | Genetic aspects | Diagnosis | Binding proteins | Drug therapy | Health aspects | Proteins | Studies | Competition | Enzymes | E coli | Kinases | Drug resistance | Crystal structure | 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
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11. 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
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12. 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 | Biological Sciences
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