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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
Journal Article
Science, ISSN 0036-8075, 4/2011, Volume 332, Issue 6029, pp. 600 - 603
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2016, Volume 11, Issue 10, p. e0165210
A significant number of children with T-lineage acute lymphoblastic leukemia (T-ALL) fail to respond to therapy and experience early relapse. CD99 has been... 
B-ALL | THERAPY | MULTIDISCIPLINARY SCIENCES | FLOW-CYTOMETRIC DETECTION | UKALL 2003 | POPULATIONS | RISK | RANDOMIZED CONTROLLED-TRIAL | INDUCTION | MINIMAL RESIDUAL DISEASE | REMISSION | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology | Antigens, CD34 - metabolism | Cell Proliferation | Humans | Child, Preschool | Male | Flow Cytometry | T-Lymphocytes - metabolism | Female | Child | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - metabolism | Receptors, Antigen, T-Cell - metabolism | Bone Marrow Cells - cytology | Cells, Cultured | In Situ Hybridization, Fluorescence | Hematopoietic Stem Cells - metabolism | 12E7 Antigen - metabolism | Animals | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - diagnosis | T-Lymphocytes - cytology | Hematopoietic Stem Cells - cytology | Adolescent | Mice, Inbred NOD | Mice | Receptors, Antigen, T-Cell - genetics | Bone Marrow Cells - metabolism | Karyotype | Acute lymphocytic leukemia | T cells | Comparative analysis | Health aspects | Stem cells | Flow cytometry | Pediatrics | Leukemia | Stem cell transplantation | Lymphocytes T | Genomes | T-cell receptor | Lymphocytes | Early experience | Children | Blast cells | CD34 antigen | Subpopulations | Antigens | Acute lymphatic leukemia | Therapeutic applications | Cloning | Transplants | Lymphatic leukemia | Gene expression | Patients | CD99 antigen | Medicine
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 04/2013, Volume 368, Issue 16, pp. 1509 - 1518
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2016, Volume 11, Issue 3, p. e0149919
The most relevant therapeutic approaches to treat CML rely on the administration of tyrosine kinase inhibitors (TKIs) like Imatinib, which are able to... 
CHRONIC MYELOGENOUS LEUKEMIA | STEM-CELLS | SELECTIVE INHIBITOR | IN-VITRO | SONIC HEDGEHOG | SIGNALING PATHWAY | TYROSINE KINASE | MULTIDISCIPLINARY SCIENCES | BCR-ABL | STEM/PROGENITOR CELLS | HEDGEHOG PATHWAY ACTIVATION | Receptors, G-Protein-Coupled - metabolism | Apoptosis - drug effects | Imatinib Mesylate - pharmacology | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Hedgehog Proteins - metabolism | MicroRNAs - metabolism | Autophagy - drug effects | Neoplastic Stem Cells - metabolism | Signal Transduction - drug effects | Smoothened Receptor | K562 Cells | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Blast Crisis - metabolism | Fusion Proteins, bcr-abl - metabolism | Drug Resistance, Neoplasm - drug effects | Protein-Tyrosine Kinases - antagonists & inhibitors | Development and progression | Research | Chronic myeloid leukemia | Apoptosis | Tyrosine metabolism | BCR protein | Cell proliferation | Biotechnology | Leukemia | Antagonists | Kinases | Autophagy | Cancer therapies | Signal transduction | Cell cycle | Bone marrow | Blast crisis | Fusion protein | Protein-tyrosine kinase | Tyrosine | Imatinib | Gli1 protein | Life expectancy | Myeloid leukemia | Abl protein | Pharmacology | FDA approval | Ribonucleic acid--RNA | Patients | Survival | Signaling | Life span | Hedgehog protein | MicroRNAs | Pharmacy | Cell lines | Stem cells | Ligands | Hypoxia | Mutation | Phagocytosis | Binding sites | Cell Proliferation | Signal Transduction | Neurons and Cognition | Psychology and behavior | Receptors, G-Protein-Coupled | Neurobiology | Leukemia, Myelogenous, Chronic, BCR-ABL Positive | Drug Resistance, Neoplasm | Neoplastic Stem Cells | Imatinib Mesylate | Hedgehog Proteins | Life Sciences | Protein Kinase Inhibitors | Fusion Proteins, bcr-abl | Cognitive Sciences | Protein-Tyrosine Kinases | Blast Crisis | RNA | Ribonucleic acid
Journal Article
EMBO Molecular Medicine, ISSN 1757-4676, 06/2014, Volume 6, Issue 6, pp. 821 - 834
Development of novel therapies is critical for T ‐cell acute leukaemia ( T ‐ ALL ). Here, we investigated the effect of inhibiting the MAPK / MEK / ERK pathway... 
ALL | inflammation | stromal cells | 18 | Inflammation | T-ALL | IL-18 | Stromal cells | RHEUMATOID-ARTHRITIS | MEDICINE, RESEARCH & EXPERIMENTAL | NOTCH | OF-FUNCTION MUTATIONS | HUMAN GASTRIC-CANCER | GENE | MICROENVIRONMENT | ACUTE LYMPHOBLASTIC-LEUKEMIA | NF-KAPPA-B | EXPRESSION | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - pathology | Interleukin-18 - immunology | Cell Proliferation | Stromal Cells - pathology | Humans | T-Lymphocytes - metabolism | T-Lymphocytes - pathology | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - blood | Cell Line | Interleukin-18 - blood | Bone Marrow Cells - cytology | Stromal Cells - metabolism | Bone Marrow Cells - pathology | Gene Silencing | Stromal Cells - immunology | Gene Expression Regulation, Leukemic | Animals | MAP Kinase Signaling System - drug effects | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - genetics | Cell Line, Tumor | Mice, Inbred NOD | T-Lymphocytes - immunology | Mice | Precursor T-Cell Lymphoblastic Leukemia-Lymphoma - immunology | Interleukin-18 - genetics | Bone Marrow Cells - metabolism | Stromal Cells - cytology | DNA microarrays | Interleukins | T cells | Analysis | Cell proliferation | NF-κB protein | Cytokines | Transcription | Hematology | Leukemia | MEK inhibitors | Extracellular signal-regulated kinase | MAP kinase | Gene expression | Blast | Kinases | Interleukin 18 | Cell growth | Cell activation | Medical prognosis | Xenografts | Bone marrow | Mutation | Blast cells | Cancer | Life Sciences | Biochemistry, Molecular Biology
Journal Article