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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
Apoptosis, ISSN 1360-8185, 9/2007, Volume 12, Issue 9, pp. 1543 - 1568
Apoptosis has been accepted as a fundamental component in the pathogenesis of cancer, in addition to other human diseases including neurodegeneration, coronary... 
Biochemistry, general | TNFR | TRAF | Oncology | NFkB | Virology | Cell Biology | Biomedicine | Cancer Research | IAPs | Caspases | Smac | Knock out mice | Apoptosis | Cancer | X-LINKED INHIBITOR | MITOCHONDRIA-DERIVED ACTIVATOR | PROTEIN LIGASE ACTIVITY | BIOCHEMISTRY & MOLECULAR BIOLOGY | knock out mice | apoptosis | CELL-DEATH | CELL BIOLOGY | LUNG-CANCER | STRUCTURAL BASIS | PROSTATE-CANCER | cancer | SERINE-PROTEASE | CYTOCHROME-C RELEASE | caspases | CASPASE ACTIVATION | Caspases - physiology | Proto-Oncogene Proteins c-bcl-2 - physiology | Apoptosis - drug effects | Inhibitor of Apoptosis Proteins - genetics | Humans | Neoplasm Proteins - physiology | Serine Endopeptidases - physiology | Neoplasm Proteins - antagonists & inhibitors | Inhibitor of Apoptosis Proteins - physiology | X-Linked Inhibitor of Apoptosis Protein - antagonists & inhibitors | Neoplasms - genetics | Inhibitor of Apoptosis Proteins - antagonists & inhibitors | Oligonucleotides, Antisense - therapeutic use | Intracellular Signaling Peptides and Proteins - therapeutic use | Mitochondrial Proteins - therapeutic use | Peptide Termination Factors - physiology | Mitochondrial Proteins - physiology | Neoplasm Proteins - therapeutic use | Microtubule-Associated Proteins - antagonists & inhibitors | Caspase Inhibitors | High-Temperature Requirement A Serine Peptidase 2 | Neoplasms - drug therapy | Animals | Protein Kinases - physiology | Checkpoint Kinase 1 | Enzyme Activation | Genetic Vectors | Intracellular Signaling Peptides and Proteins - physiology | Proteins | Cancer therapies
Journal Article
Nature Cell Biology, ISSN 1465-7392, 09/2010, Volume 12, Issue 9, pp. 863 - 875
Accumulation of unwanted/misfolded proteins in aggregates has been observed in airways of patients with cystic fibrosis (CF), a life-threatening genetic... 
APOPTOSIS | UNFOLDED PROTEIN RESPONSE | BECLIN 1 | DOWN-REGULATION | ENDOPLASMIC-RETICULUM | MICE | GENE-TRANSFER | TISSUE TRANSGLUTAMINASE | NEURODEGENERATIVE DISEASES | CELL-DEATH | CELL BIOLOGY | Reactive Oxygen Species - metabolism | Respiratory Mucosa - drug effects | Sequestosome-1 Protein | Humans | Transglutaminases - genetics | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Autophagy - drug effects | Young Adult | Cystamine - therapeutic use | Inflammation - metabolism | Autophagy - genetics | Nasal Polyps - metabolism | Mice, Inbred CFTR | Respiratory Mucosa - cytology | Cystic Fibrosis - metabolism | Membrane Proteins - genetics | Mice, Transgenic | Protein Transport - genetics | Apoptosis Regulatory Proteins - metabolism | Reactive Oxygen Species - antagonists & inhibitors | Models, Biological | Cystic Fibrosis - genetics | Transglutaminases - metabolism | Adolescent | Cystic Fibrosis Transmembrane Conductance Regulator - genetics | Mice | GTP-Binding Proteins | Cystic Fibrosis - drug therapy | Protein Binding - physiology | Microtubule-Associated Proteins - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Salicylates - pharmacology | Epithelial Sodium Channels - genetics | Apoptosis Regulatory Proteins - genetics | Adult | Cystamine - pharmacology | Membrane Proteins - metabolism | Acetylcysteine - therapeutic use | Beclin-1 | Cystic Fibrosis Transmembrane Conductance Regulator - antagonists & inhibitors | Cell Line | Small Ubiquitin-Related Modifier Proteins - metabolism | Heat-Shock Proteins - metabolism | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | Antioxidants - pharmacology | Mice, Inbred Strains | Nasal Polyps - drug therapy | Antioxidants - therapeutic use | Animals | Acetylcysteine - pharmacology | Adaptor Proteins, Signal Transducing - genetics | Respiratory Mucosa - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Organometallic Compounds - pharmacology | Complications and side effects | Active oxygen | Gene mutations | Lung diseases | Physiological aspects | Cystic fibrosis | Genetic aspects | Research | Health aspects | Risk factors
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 10/2010, Volume 363, Issue 18, pp. 1693 - 1703
A small group of patients with non–small-cell lung cancer have genetic lesions that activate anaplastic lymphoma kinase (ALK). Crizotinib, an orally... 
ALK | MEDICINE, GENERAL & INTERNAL | GEFITINIB | EML4-ALK FUSION GENE | 2ND-LINE TREATMENT | PHASE-II | IDENTIFICATION | TUMORS | ACTIVATING MUTATIONS | EGFR | CHEMOTHERAPY | Lung Neoplasms - drug therapy | Pyrazoles - therapeutic use | Microtubule-Associated Proteins - genetics | Humans | Middle Aged | Receptors, Growth Factor - antagonists & inhibitors | Lung Neoplasms - pathology | Male | Protein Kinase Inhibitors - adverse effects | Protein-Tyrosine Kinases - genetics | Pyridines - adverse effects | Serine Endopeptidases - genetics | Cell Cycle Proteins - genetics | Adult | Female | Pyrazoles - adverse effects | Pyridines - therapeutic use | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Pyridines - administration & dosage | Administration, Oral | Carcinoma, Non-Small-Cell Lung - genetics | Proto-Oncogene Proteins c-met - antagonists & inhibitors | Kaplan-Meier Estimate | In Situ Hybridization, Fluorescence | Receptor Protein-Tyrosine Kinases | Disease Progression | Protein Kinase Inhibitors - administration & dosage | Pyrazoles - administration & dosage | Oncogene Proteins, Fusion - genetics | Protein Kinase Inhibitors - therapeutic use | Aged | Carcinoma, Non-Small-Cell Lung - drug therapy | Mutation | Protein-Tyrosine Kinases - antagonists & inhibitors | Tyrosine | Care and treatment | Lung cancer, Small cell | Genetic aspects | Diagnosis | Health aspects | Phosphotransferases | Lymphomas | Pharmaceutical industry | Lung cancer | Tumors
Journal Article
Biochemical Pharmacology, ISSN 0006-2952, 08/2017, Volume 138, pp. 150 - 162
[Display omitted] Autophagy is a cell survival mechanism hijacked by advanced tumors to endure a rough microenvironment. Late autophagy inhibitors such as... 
ATG4B | Benzotropolone | Colorectal tumor | Osmotic minipump | Autophagy | CARCINOMA-CELLS | ADVANCED SOLID TUMORS | MECHANISM | MTOR | RADIATION-THERAPY | BREAST-CANCER | HYDROXYCHLOROQUINE | PHASE-I TRIAL | THERAPEUTIC TARGET | RESISTANCE | PHARMACOLOGY & PHARMACY | Adenocarcinoma - pathology | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Colonic Neoplasms - drug therapy | Humans | Antineoplastic Agents - therapeutic use | Autophagy - drug effects | Cysteine Endopeptidases - metabolism | Forkhead Transcription Factors - metabolism | Drug Design | HEK293 Cells | Cysteine Proteinase Inhibitors - chemistry | Antineoplastic Agents - pharmacology | Autophagy-Related Proteins - genetics | Recombinant Proteins - metabolism | Cysteine Proteinase Inhibitors - therapeutic use | Jurkat Cells | Drug Stability | Tropolone - analogs & derivatives | Recombinant Proteins - chemistry | Mice, Transgenic | Microtubule-Associated Proteins - antagonists & inhibitors | Tropolone - pharmacology | Antineoplastic Agents - chemistry | Forkhead Transcription Factors - genetics | Adenocarcinoma - drug therapy | Mice, Knockout | HT29 Cells | Xenograft Model Antitumor Assays | Tropolone - therapeutic use | Animals | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Colonic Neoplasms - pathology | Cysteine Endopeptidases - genetics | Cysteine Proteinase Inhibitors - pharmacology | Tropolone - chemistry | Cell Proliferation - drug effects | Autophagy-Related Proteins - antagonists & inhibitors | Autophagy-Related Proteins - metabolism | Organoplatinum Compounds - therapeutic use | Chemotherapy | Cancer | Cysteine | Glutathione transferase | Gastrointestinal diseases | Colorectal cancer | Fluorescence | Cells | Index Medicus
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 10/2010, Volume 363, Issue 18, pp. 1734 - 1739
Journal Article
Virchows Archiv, ISSN 0945-6317, 2012, Volume 461, Issue 3, pp. 245 - 257
Journal Article