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BioImpacts, ISSN 2228-5660, 12/2018, Volume 8, Issue Suppl 1, pp. S1 - S129
Journal Article
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
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 06/2015, Volume 19, Issue 6, pp. 1262 - 1272
Emerging evidence shows that glioblastoma multiforme (GBM) originates from cancer stem cells (CSCs). Characterization of CSC‐specific signalling pathways would... 
glioblastoma multiforme | Oct4 | Sox2 | epidermal growth factor receptor | salinomycin | cancer stem cells | Nanog | EphB4 | Salinomycin | Cancer stem cells | Glioblastoma multiforme | Epidermal growth factor receptor | SURVIVAL | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | DELTA-LIKE-1 | GLIOMA | PROLIFERATION | BETA-CATENIN | CELL BIOLOGY | GENE-EXPRESSION | RECEPTOR TYROSINE KINASE | REVEALS | Receptor, Epidermal Growth Factor - genetics | Mitogens - pharmacology | Humans | Gene Expression Regulation, Neoplastic | Spheroids, Cellular - pathology | Cell Survival - genetics | Receptor, Epidermal Growth Factor - metabolism | Glioblastoma - genetics | Neoplastic Stem Cells - metabolism | Dacarbazine - pharmacology | Dacarbazine - analogs & derivatives | Neoplastic Stem Cells - pathology | Glioblastoma - metabolism | Cellular Reprogramming - genetics | Induced Pluripotent Stem Cells - metabolism | Induced Pluripotent Stem Cells - pathology | Cell Survival - drug effects | Cell Proliferation - genetics | Cellular Reprogramming Techniques - methods | Signal Transduction | Spheroids, Cellular - metabolism | Receptor, Notch1 - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Neural Stem Cells - pathology | beta Catenin - metabolism | Blotting, Western | Drug Resistance, Neoplasm - genetics | Glioblastoma - pathology | Cell Line, Tumor | Cell Proliferation - drug effects | Cell Dedifferentiation - genetics | Neural Stem Cells - metabolism | Physiological aspects | Growth | Mitogens | Stem cells | Cancer | Transcription factors | Chemotherapy | Rodents | Biotechnology | Target recognition | Wnt protein | Brain cancer | Oct-4 protein | Glioblastoma | Chemoresistance | Kinases | Cancer therapies | Signal transduction | Epidermal growth factor | Pathways | CD44 antigen | Transformed cells | Glioma cells | Neurospheres | Growth factors | Therapeutic applications | Cell division | Tumor cell lines | Radiation therapy | Cell differentiation | Signaling | Sensitivity | Temozolomide | Tumors | Original
Journal Article
JOURNAL OF NEUROSURGERY, ISSN 0022-3085, 12/2013, Volume 119, Issue 6, pp. 1415 - 1423
Journal Article
Journal Article
Colloids and Surfaces B: Biointerfaces, ISSN 0927-7765, 06/2015, Volume 130, pp. 48 - 52
Journal Article