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Journal of Clinical Investigation, ISSN 0021-9738, 05/2009, Volume 119, Issue 5, pp. 1109 - 1123
Imatinib mesylate (IM), a potent inhibitor of the BCR/ABL tyrosine kinase, has become standard first-line therapy for patients with chronic myeloid leukemia... 
CHRONIC MYELOGENOUS LEUKEMIA | MEDICINE, RESEARCH & EXPERIMENTAL | MALIGNANT GLIOMA-CELLS | BLAST CRISIS | CLINICAL RESISTANCE | BCR-ABL MUTATIONS | ENDOPLASMIC-RETICULUM | CYTOCHROME-C RELEASE | CASPASE ACTIVATION | IMATINIB RESISTANCE | CHRONIC MYELOID-LEUKEMIA | Transcription Factor CHOP - genetics | Neoplastic Stem Cells - cytology | Gene Expression - drug effects | Calcium - metabolism | Gene Expression - genetics | Microtubule-Associated Proteins - metabolism | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Endoplasmic Reticulum - metabolism | Antineoplastic Agents - therapeutic use | Autophagy - physiology | Thiazoles - therapeutic use | Autophagy - drug effects | Chloroquine - pharmacology | Neoplastic Stem Cells - metabolism | RNA Interference | Endoplasmic Reticulum - drug effects | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Macrolides - pharmacology | Antineoplastic Agents - pharmacology | Cell Death - drug effects | Dasatinib | Chloroquine - therapeutic use | Piperazines - therapeutic use | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Mice, Inbred C3H | Xenograft Model Antitumor Assays | Fusion Proteins, bcr-abl - genetics | Animals | Cell Death - physiology | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Benzamides | Macrolides - therapeutic use | Protein-Tyrosine Kinases - antagonists & inhibitors | Causes of | Physiological aspects | Genetic aspects | Chronic myeloid leukemia | Research | Drug therapy | Phagocytosis | Index Medicus | Abridged Index Medicus
Journal Article
Nature, ISSN 0028-0836, 09/2015, Volume 525, Issue 7570, pp. 538 - 542
Bromodomain and extra terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a newtherapeutic opportunity by directly targeting... 
SELECTIVE-INHIBITION | ACCURATE | CHROMATIN | MECHANISM | MULTIDISCIPLINARY SCIENCES | ACUTE MYELOID-LEUKEMIA | DRUG-RESISTANCE | MUTATIONS | SEQUENCING DATA | CANCER | DISCOVERY | Chromatin - metabolism | Transcription, Genetic - drug effects | Clone Cells - drug effects | Neoplastic Stem Cells - drug effects | Epigenesis, Genetic | Humans | Leukemia, Myeloid, Acute - metabolism | Molecular Targeted Therapy | Neoplastic Stem Cells - metabolism | Leukemia, Myeloid, Acute - drug therapy | Neoplastic Stem Cells - pathology | Gene Expression Regulation, Neoplastic - drug effects | Hematopoietic Stem Cells - drug effects | Benzodiazepines - pharmacology | Leukemia, Myeloid, Acute - pathology | Cells, Cultured | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Hematopoietic Stem Cells - metabolism | Clone Cells - metabolism | beta Catenin - metabolism | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Clone Cells - pathology | Wnt Signaling Pathway - drug effects | Genes, myc - genetics | Hematopoietic Stem Cells - cytology | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mice | Drug Resistance, Neoplasm - drug effects | Leukemia, Myeloid, Acute - genetics | Proteins | Leukemia | Cloning | Cell cycle | Stem cells | Epigenetics | Apoptosis | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 10/2015, Volume 526, Issue 7571, pp. 131 - 135
Despite major advances in understanding the molecular and genetic basis of cancer, metastasis remains the cause of >90% of cancer-related mortality(1).... 
INHIBITION | COMMITMENT | MULTIDISCIPLINARY SCIENCES | GROWTH | GENES | MARKERS | IDENTIFICATION | FATE | TUMORS | TRANSCRIPTOME ANALYSIS | MAMMARY-GLAND | Neoplastic Stem Cells - drug effects | Epithelial Cells - drug effects | Humans | Gene Expression Profiling | Epithelial-Mesenchymal Transition - genetics | Cell Differentiation - genetics | Flow Cytometry | Neoplasm Metastasis - drug therapy | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Cyclin-Dependent Kinases - antagonists & inhibitors | Single-Cell Analysis | Disease Models, Animal | Cell Separation | Epithelial Cells - pathology | Mice, SCID | Breast Neoplasms - drug therapy | Disease Progression | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - genetics | Breast Neoplasms - pathology | Cell Differentiation - drug effects | Neoplasm Metastasis - pathology | Genes, myc - genetics | Cell Line, Tumor | Mice, Inbred NOD | Cell Proliferation - drug effects | Mesoderm - metabolism | Mice | Cell Transformation, Neoplastic - drug effects | Cell Cycle - drug effects | Cell Transformation, Neoplastic - pathology | Mesoderm - pathology | Stem cells | Cancer cells | Development and progression | Breast cancer | Metastasis | Observations | Health aspects | Bone marrow | Principal components analysis | Gene expression | Tumors | Apoptosis | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 506, Issue 7488, pp. 328 - 333
In acute myeloid leukaemia (AML), the cell of origin, nature and biological consequences of initiating lesions, and order of subsequent mutations remain poorly... 
BREAST-CANCER | RELAPSE | ACUTE NONLYMPHOCYTIC LEUKEMIA | MULTIDISCIPLINARY SCIENCES | ACUTE LYMPHOBLASTIC-LEUKEMIA | PANCREATIC-CANCER | DNA METHYLTRANSFERASE | CLONAL EVOLUTION | ACUTE MYELOID-LEUKEMIA | DNMT3A MUTATIONS | MYELODYSPLASTIC SYNDROMES | Clone Cells - cytology | Neoplasm Transplantation | Neoplastic Stem Cells - cytology | Neoplastic Stem Cells - drug effects | Humans | Hematopoietic Stem Cells - pathology | DNA (Cytosine-5-)-Methyltransferases - metabolism | Heterografts | Neoplastic Stem Cells - metabolism | T-Lymphocytes - metabolism | Hematopoiesis | Cell Division | Leukemia, Myeloid, Acute - drug therapy | Neoplastic Stem Cells - pathology | Female | Cell Differentiation | T-Lymphocytes - pathology | Nuclear Proteins - genetics | Hematopoietic Stem Cells - drug effects | Leukemia, Myeloid, Acute - pathology | Isocitrate Dehydrogenase - genetics | Hematopoietic Stem Cells - metabolism | Mice, SCID | Mutation - genetics | Clone Cells - metabolism | Remission Induction | Cell Lineage | DNA (Cytosine-5-)-Methyltransferases - genetics | Animals | Clone Cells - pathology | Leukemia, Myeloid, Acute - diagnosis | Hematopoietic Stem Cells - cytology | Mice, Inbred NOD | Mice | Drug Resistance, Neoplasm - drug effects | Leukemia, Myeloid, Acute - genetics | Acute leukemia | Genetic aspects | Diagnosis | Identification and classification | Hematopoietic stem cells | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 512, Issue 1, pp. 78 - 81
Myeloproliferative neoplasms (MPNs) are diseases caused by mutations in the haematopoietic stem cell (HSC) compartment. Most MPN patients have a common... 
TYROSINE KINASE JAK2 | JAK2-V617F | ACTIVATING MUTATION | POLYCYTHEMIA-VERA | BONE | MULTIDISCIPLINARY SCIENCES | Neuroprotective Agents - therapeutic use | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Sympathetic Nervous System - drug effects | Humans | Hematopoietic Stem Cells - pathology | Myeloproliferative Disorders - pathology | Sympathetic Nervous System - physiopathology | Adrenergic beta-3 Receptor Agonists - pharmacology | Neuroprotective Agents - pharmacology | Interleukin-1beta - metabolism | Neoplastic Stem Cells - pathology | Female | Sympathetic Nervous System - pathology | Schwann Cells - drug effects | Hematopoietic Stem Cells - drug effects | Nerve Fibers - pathology | Mesenchymal Stromal Cells - drug effects | Stem Cell Niche | Janus Kinase 2 - genetics | Nerve Fibers - drug effects | Schwann Cells - pathology | Myeloproliferative Disorders - drug therapy | Receptors, Adrenergic, beta-3 - metabolism | Disease Progression | Neoplasms - drug therapy | Nestin - metabolism | Adrenergic beta-3 Receptor Agonists - therapeutic use | Animals | Mice | Mesenchymal Stromal Cells - pathology | Neoplasms - pathology | Complications and side effects | Development and progression | Health aspects | Peripheral nerve diseases | Hematopoietic stem cells | Myeloproliferative disorders | Tumors | Studies | Mutation | Kinases | Rodents | Stem cells | Apoptosis | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 03/2017, Volume 543, Issue 7647, pp. 676 - 680
Journal Article
Cell Stem Cell, ISSN 1934-5909, 02/2017, Volume 20, Issue 2, pp. 233 - 246.e7
Journal Article
Journal Article
Cell Stem Cell, ISSN 1934-5909, 2010, Volume 6, Issue 6, pp. 603 - 615