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1. 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
The Journal of clinical investigation, ISSN 0021-9738, 09/2008, Volume 118, Issue 9, pp. 3038 - 3050
Life Sciences & Biomedicine | Medicine, Research & Experimental | Science & Technology | Research & Experimental Medicine | 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 | Prevention | Leukemia | Index Medicus | Abridged Index Medicus
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2. 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
Life Sciences & Biomedicine | Oncology | Science & Technology | Biological and medical sciences | Medical sciences | Antineoplastic agents | Chromosome aberrations | Pharmacology. Drug treatments | Medical genetics | 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 | Index Medicus
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3. Full Text Chemical proteomic profiles of the BCR-ABL inhibitors imatinib, nilotinib, and dasatinib reveal novel kinase and nonkinase targets
by Rix, Uwe and Hantschel, Oliver and Dürnberger, Gerhard and Remsing Rix, Lily L and Planyavsky, Melanie and Fernbach, Nora V and Kaupe, Ines and Bennett, Keiryn L and Valent, Peter and Colinge, Jacques and Köcher, Thomas and Superti-Furga, Giulio
Blood, ISSN 0006-4971, 12/2007, Volume 110, Issue 12, pp. 4055 - 4063
Life Sciences & Biomedicine | Hematology | Science & Technology | Hematologic and hematopoietic diseases | Chemotherapy | Pharmacology. Drug treatments | Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis | Biological and medical sciences | Medical sciences | Antineoplastic agents | Protein-Tyrosine Kinases - metabolism | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Drug Resistance, Neoplasm | Neoplasm Proteins - antagonists & inhibitors | Piperazines - chemistry | Thiazoles - therapeutic use | Neoplasm Proteins - metabolism | Pyrimidines - chemistry | Dose-Response Relationship, Drug | Protein Kinase Inhibitors - chemistry | Fusion Proteins, bcr-abl | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Dasatinib | Quinone Reductases - metabolism | Piperazines - therapeutic use | Discoidin Domain Receptor 1 | Pyrimidines - pharmacology | Receptor Protein-Tyrosine Kinases - metabolism | Imatinib Mesylate | Piperazines - pharmacology | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Quinone Reductases - antagonists & inhibitors | K562 Cells | Proteomics | Thiazoles - chemistry | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Benzamides | Drug Screening Assays, Antitumor | Protein-Tyrosine Kinases - antagonists & inhibitors | Index Medicus | Abridged Index Medicus
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4. 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, Frank and Adrian, Lauren T and Zhou, Tianjun 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 Wang, Yihan and Sundaramoorthi, Raji and Thomas, Mathew and Zhou, Dong 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
CHEMBIO | HUMDISEASE | Oncology | Life Sciences & Biomedicine | Science & Technology | Cell Biology | 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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5. Full Text Twins with different personalities: STAT5B—but not STAT5A—has a key role in BCR/ABL-induced leukemia
by Kollmann, Sebastian and Grundschober, Eva and Maurer, Barbara and Warsch, Wolfgang and Grausenburger, Reinhard and Edlinger, Leo and Huuhtanen, Jani and Lagger, Sabine and Hennighausen, Lothar and Valent, Peter and Decker, Thomas and Strobl, Birgit and Mueller, Mathias and Mustjoki, Satu and Hoelbl-Kovacic, Andrea and Sexl, Veronika
Leukemia, ISSN 0887-6924, 2019, Volume 33, Issue 7, pp. 1583 - 1597
Oncology | Life Sciences & Biomedicine | Hematology | Science & Technology | Leukemia, Large Granular Lymphocytic - drug therapy | Cell Proliferation | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | STAT5 Transcription Factor - genetics | STAT5 Transcription Factor - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Tumor Suppressor Proteins - genetics | Antineoplastic Agents - pharmacology | Leukemia, Large Granular Lymphocytic - pathology | Tumor Suppressor Proteins - metabolism | Interferons - pharmacology | Survival Rate | Mice, SCID | Cell Transformation, Neoplastic - metabolism | Mice, Knockout | Xenograft Model Antitumor Assays | Fusion Proteins, bcr-abl - genetics | Animals | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Leukemia, Large Granular Lymphocytic - metabolism | Mice, Inbred NOD | Mice | Cell Transformation, Neoplastic - drug effects | Mutation | Cell Transformation, Neoplastic - pathology | Fusion Proteins, bcr-abl - metabolism | RNA sequencing | Usage | Gene mutations | Leukemia | Development and progression | Genetic aspects | Cellular signal transduction | Research | BCR protein | Biotechnology | Transformation | Deregulation | Transcription factors | Profiling | Transcription | Abl gene | BCR gene | Kinases | Gene sequencing | α-Interferon | Signal transduction | Janus kinase | Transducers | Cell survival | Colonies | Inhibition (psychology) | Stat5 protein | Ribonucleic acid--RNA | Disease control | Survival | Hemopoiesis | Lymphocytes B | γ-Interferon | Leukemogenesis | Interferon | Tumors | Index Medicus | Cell signalling | Acute lymphocytic leukaemia
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6. Full Text HDAC inhibitors potentiate the activity of the BCR/ABL kinase inhibitor KW-2449 in imatinib-sensitive or -resistant BCR/ABL+ leukemia cells in vitro and in vivo
by Nguyen, Tri and Dai, Yun and Attkisson, Elisa and Kramer, Lora and Jordan, Nicholas and Nguyen, Nguyen and Kolluri, Nikhil and Muschen, Markus and Grant, Steven
Clinical cancer research, ISSN 1078-0432, 05/2011, Volume 17, Issue 10, pp. 3219 - 3232
Life Sciences & Biomedicine | Oncology | Science & Technology | Biological and medical sciences | Medical sciences | Antineoplastic agents | Chromosome aberrations | Pharmacology. Drug treatments | Medical genetics | Piperazines - administration & dosage | Humans | Histone Deacetylase Inhibitors - administration & dosage | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Indazoles - administration & dosage | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Adult | Piperazines - therapeutic use | Mice, SCID | Imatinib Mesylate | Piperazines - pharmacology | Drug Synergism | Indazoles - pharmacology | Xenograft Model Antitumor Assays | Protein Kinase Inhibitors - administration & dosage | Animals | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Pyrimidines - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Histone Deacetylase Inhibitors - pharmacology | Mice | Mice, Inbred BALB C | Protein Kinase Inhibitors - pharmacology | Benzamides | Fusion Proteins, bcr-abl - metabolism | Drug Resistance, Neoplasm - drug effects | Index Medicus
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7. Full Text Targeting BCR-ABL+ stem/progenitor cells and BCR-ABL-T315I mutant cells by effective inhibition of the BCR-ABL-Tyr177-GRB2 complex
by Chen, Min and Turhan, Ali G and Ding, Hongxia and Lin, Qingcong and Meng, Kun and Jiang, Xiaoyan
Oncotarget, ISSN 1949-2553, 2017, Volume 8, Issue 27, pp. 43662 - 43677
BCR-ABL+ human leukemia | Icaritin (SNG162 and SNG1153) | ERa36 | Leukemic stem cells | Tyrosine kinase inhibitors | Oncology | Life Sciences & Biomedicine | Science & Technology | Cell Biology | Cell Membrane | Phosphorylation | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics | Chromans - pharmacology | Neoplastic Stem Cells - metabolism | Estrogen Receptor alpha - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - mortality | Gene Expression | Protein Transport | Fusion Proteins, bcr-abl - genetics | Estrogen Receptor alpha - genetics | Models, Biological | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Protein Binding | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Mutation | GRB2 Adaptor Protein - metabolism | Fusion Proteins, bcr-abl - metabolism | Amino Acid Substitution | Index Medicus
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8. Full Text Disruption of the Bcr-Abl Hsp90 protein complex: a possible mechanism to inhibit Bcr-Abl-positive human leukemic blasts by novobiocin
by Wu, L.X and Xu, J.H and Zhang, K.Z and Lin, Q and Huang, X.W and Wen, C.X and Chen, Y.Z
Leukemia, ISSN 0887-6924, 07/2008, Volume 22, Issue 7, pp. 1402 - 1409
Oncology | Life Sciences & Biomedicine | Hematology | Science & Technology | Hematologic and hematopoietic diseases | Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis | Biological and medical sciences | Medical sciences | Chromosome aberrations | Medical genetics | Blast Crisis - drug therapy | Caspase 9 - metabolism | Immunoprecipitation | Leukemia - pathology | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | Leukemia - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Novobiocin - pharmacology | Cytochromes c - metabolism | Leukemia - drug therapy | Pyrimidines - pharmacology | Lactams, Macrocyclic - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Proteasome Endopeptidase Complex - physiology | Benzoquinones - pharmacology | Fusion Proteins, bcr-abl - analysis | HSP90 Heat-Shock Proteins - antagonists & inhibitors | K562 Cells | HL-60 Cells | HSP90 Heat-Shock Proteins - metabolism | Cell Proliferation - drug effects | Benzamides | Fusion Proteins, bcr-abl - metabolism | Care and treatment | Heat shock proteins | Genetic aspects | Acute lymphocytic leukemia | Diagnosis | Health aspects | Philadelphia chromosome | Index Medicus
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9. Full Text Combined inhibition of β-catenin and Bcr–Abl synergistically targets tyrosine kinase inhibitor-resistant blast crisis chronic myeloid leukemia blasts and progenitors in vitro and in vivo
by Zhou, H and Mak, P.Y and Mu, H and Mak, D.H and Zeng, Z and Cortes, J and Liu, Q and Andreeff, M and Carter, B.Z
Leukemia, ISSN 0887-6924, 04/2017, Volume 31, Issue 10, pp. 2065 - 2074
Oncology | Life Sciences & Biomedicine | Hematology | Science & Technology | RNA, Small Interfering - genetics | Blast Crisis - drug therapy | Coculture Techniques | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Neoplasm Proteins - antagonists & inhibitors | Molecular Targeted Therapy | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Mesenchymal Stromal Cells - cytology | Leukemia, Myeloid, Accelerated Phase - pathology | RNA Interference | Bridged Bicyclo Compounds, Heterocyclic - therapeutic use | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Female | Pyrimidinones - pharmacology | Tumor Cells, Cultured | Neoplasm Proteins - genetics | Leukemia, Myeloid, Accelerated Phase - drug therapy | Blast Crisis - pathology | Neoplasm Proteins - biosynthesis | Pyrimidinones - therapeutic use | Pyrimidines - pharmacology | Random Allocation | Mice, SCID | beta Catenin - genetics | Mice, Knockout | Drug Synergism | Xenograft Model Antitumor Assays | Bridged Bicyclo Compounds, Heterocyclic - pharmacology | Animals | Wnt Signaling Pathway - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Pyrimidines - therapeutic use | beta Catenin - antagonists & inhibitors | Fusion Proteins, bcr-abl - antagonists & inhibitors | Mice, Inbred NOD | Drug Resistance, Neoplasm - drug effects | Index Medicus | Original
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10. Full Text Flying under the radar: the new wave of BCR-ABL inhibitors
by Kantarjian, Hagop and Cortes, Jorge and Quintás-Cardama, Alfonso
Nature reviews. Drug discovery, ISSN 1474-1776, 10/2007, Volume 6, Issue 10, pp. 834 - 848
Pharmacology & Pharmacy | Life Sciences & Biomedicine | Biotechnology & Applied Microbiology | Science & Technology | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Models, Molecular | Antineoplastic Agents - therapeutic use | Clinical Trials as Topic | Antineoplastic Agents - chemistry | Point Mutation | Drug Resistance, Neoplasm - genetics | Protein Kinase Inhibitors - chemistry | Protein-Tyrosine Kinases - genetics | Animals | Fusion Proteins, bcr-abl | Protein Kinase Inhibitors - therapeutic use | Drug Design | Protein Binding | Antineoplastic Agents - pharmacology | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects | Protein-Tyrosine Kinases - antagonists & inhibitors | Development and progression | Care and treatment | Prognosis | Chronic myeloid leukemia | Index Medicus
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