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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 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 ed.), ISSN 1433-7851, 01/2016, Volume 55, Issue 2, pp. 807 - 810
inhibitors | cancer | drug design | E3 ubiquitin ligases | protein degradation | 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 | Index Medicus | Drug Design
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4. Full Text Regulation of the c-Abl and Bcr-Abl tyrosine kinases
by Superti-Furga, Giulio and Hantschel, Oliver
Nature reviews. Molecular cell biology, ISSN 1471-0072, 01/2004, Volume 5, Issue 1, pp. 33 - 44
Life Sciences & Biomedicine | Science & Technology | Cell Biology | Amino Acid Sequence | Phosphorylation | Proto-Oncogene Proteins c-abl - genetics | src-Family Kinases | Gene Expression Regulation - genetics | Protein-Tyrosine Kinases - metabolism | Humans | Proto-Oncogene Proteins c-abl - chemistry | Molecular Sequence Data | src Homology Domains | Sequence Homology, Amino Acid | Point Mutation | Fusion Proteins, bcr-abl - genetics | Protein-Tyrosine Kinases - genetics | Sequence Alignment | Animals | Protein-Tyrosine Kinases - chemistry | Proto-Oncogene Proteins c-abl - metabolism | Protein Conformation | Catalysis | Binding Sites | Fusion Proteins, bcr-abl - metabolism | Leukemia - genetics | Index Medicus
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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 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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7. 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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8. 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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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 (London), ISSN 0028-0836, 01/2010, Volume 463, Issue 7280, pp. 501 - 506
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Fundamental and applied biological sciences. Psychology | Biological and medical sciences | Molecular and cellular biology | 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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