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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
Journal Article
Science, ISSN 0036-8075, 11/2014, Volume 346, Issue 6212, pp. 1000 - 1003
Nucleoside reverse transcriptase inhibitors (NRTIs) are mainstay therapeutics for HIV that block retrovirus replication. Alu (an endogenous retroelement that... 
P2X7 RECEPTOR | PATHOGENESIS | INTERLEUKIN-18 | P2X RECEPTOR | INFLAMMASOME ACTIVATION | MULTIDISCIPLINARY SCIENCES | MACULAR DEGENERATION | NLRP3 INFLAMMASOME | ATP RELEASE | VERSUS-HOST-DISEASE | CASPASE-1 ACTIVATION | Retinal Pigment Epithelium - metabolism | Apoptosis - drug effects | NLR Family, Pyrin Domain-Containing 3 Protein | Reverse Transcriptase Inhibitors - pharmacology | Caspase 1 - metabolism | Geographic Atrophy - drug therapy | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | Hepatitis - drug therapy | Animals | Carrier Proteins - metabolism | Choroidal Neovascularization - drug therapy | Graft vs Host Disease - drug therapy | Inflammasomes - drug effects | Liver - drug effects | Anti-Inflammatory Agents, Non-Steroidal - therapeutic use | Retinal Pigment Epithelium - physiology | Receptors, Purinergic P2X7 - metabolism | Mice | Reverse Transcriptase Inhibitors - therapeutic use | Alu Elements | Disease Models, Animal | Retinal Pigment Epithelium - drug effects | Prevention | Genetic research | Genetic aspects | Genetic transcription | Research | HIV (Viruses) | Virus research | Macular degeneration | Inhibitor drugs | Drug therapy | Ribonucleic acid--RNA | Human immunodeficiency virus--HIV | Index Medicus | Atrophy | Drugs | Inhibitors | Ribonucleic acids | Blocking | Nucleosides | Activation | Grafting
Journal Article
BMC Medicine, ISSN 1741-7015, 03/2012, Volume 10, Issue 1, pp. 28 - 28
Background: The epidermal growth factor receptor (EGFR) is a validated therapeutic target in non-small cell lung cancer (NSCLC). However, current single agent... 
RNA interference | Lung cancer | Tyrosine kinase inhibitors (TKIs) | Proliferation | EGFR | Anti-EGFR monoclonal antibodies (mabs) | Apoptosis | GEFITINIB | ADVANCED SOLID TUMORS | proliferation | apoptosis | MONOCLONAL-ANTIBODY | COMBINATION | I DOSE-ESCALATION | tyrosine kinase inhibitors (TKIs) | lung cancer | PHASE-III TRIAL | MEDICINE, GENERAL & INTERNAL | MUTATION | RESISTANCE | EGFR MUTANTS | anti-EGFR monoclonal antibodies (mAbs) | ERLOTINIB | Caspase 7 - metabolism | Erlotinib Hydrochloride | Lung Neoplasms - drug therapy | RNA Interference - drug effects | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | Antibodies, Monoclonal - therapeutic use | Lung Neoplasms - pathology | Molecular Targeted Therapy | Antibodies, Monoclonal, Humanized | Receptor, Epidermal Growth Factor - metabolism | Transfection | Cetuximab | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - enzymology | Antibodies, Monoclonal - pharmacology | Down-Regulation - drug effects | Phenotype | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Quinazolines - pharmacology | RNA, Small Interfering - metabolism | Lung cancer, Non-small cell | Research | Kinases | Experiments | Cancer therapies | Manuscripts | Proteins | Studies | Angiogenesis | Signal transduction | Ligands | Mutation | Head & neck cancer | Tumors | Index Medicus
Journal Article
Journal Article
Journal Article
Journal of Pharmacology and Experimental Therapeutics, ISSN 0022-3565, 02/2012, Volume 340, Issue 2, pp. 248 - 255
Dipeptidyl peptidase (DPP) IV inhibitors are probably beneficial for preventing diabetic complication and modulating glucagon-like peptide-1 receptor (GLP-1R)... 
FIBROSIS | GROWTH-FACTOR-BETA | TGF-BETA | GLP-1 | GLUCAGON-LIKE PEPTIDE-1 | GLUCOSE-METABOLISM | BETA-CELL APOPTOSIS | RECEPTOR EXPRESSION | IMPROVES | PHARMACOLOGY & PHARMACY | NEPHROPATHY | Diabetes Mellitus, Experimental - drug therapy | Dipeptidyl Peptidase 4 - metabolism | Gene Expression - drug effects | Kidney - pathology | Gene Expression - genetics | Dipeptidyl-Peptidase IV Inhibitors - therapeutic use | Glycated Hemoglobin A - metabolism | Transforming Growth Factor beta1 - metabolism | Caspase 3 - metabolism | Body Weight - drug effects | Diabetic Nephropathies - drug therapy | Pyrrolidines - administration & dosage | Glucagon-Like Peptide 1 - blood | Male | Insulin - blood | Dipeptidyl-Peptidase IV Inhibitors - pharmacology | Pyrrolidines - pharmacology | Pyrrolidines - therapeutic use | Kidney - metabolism | Diabetic Nephropathies - physiopathology | Glomerular Basement Membrane - pathology | Adamantane - therapeutic use | Diabetes Mellitus, Experimental - complications | Adamantane - administration & dosage | Cyclic AMP - urine | Deoxyguanosine - analogs & derivatives | Kidney - physiopathology | Adamantane - analogs & derivatives | Diabetes Mellitus, Experimental - physiopathology | Receptors, Glucagon - genetics | Adamantane - pharmacology | Diabetic Nephropathies - pathology | Kidney - drug effects | Deoxyguanosine - urine | Diabetic Nephropathies - metabolism | Rats | Receptors, Glucagon - metabolism | Rats, Sprague-Dawley | Dipeptidyl-Peptidase IV Inhibitors - administration & dosage | Blood Glucose - drug effects | Eating - drug effects | Glomerular Basement Membrane - drug effects | Animals | Glucagon-Like Peptide-1 Receptor | Diabetes Mellitus, Experimental - pathology | Blood Glucose - metabolism | Index Medicus
Journal Article
Molecular and Cellular Biochemistry, ISSN 0300-8177, 10/2011, Volume 356, Issue 1, pp. 37 - 43
In this article we describe the preclinical characterization of 5-(3-chlorophenylamino) benzo[c][2,6]naphthyridine-8-carboxylic acid (CX-4945), the first... 
Life Sciences | Biochemistry, general | Oncology | Medical Biochemistry | CK2 | Cardiology | Non-oncogene | Prostate cancer | Kinase inhibitor | Cancer | CELLS | APOPTOSIS | THERAPY | PROTEIN-KINASE CK2 | NON-ONCOGENE ADDICTION | CELL BIOLOGY | Caspase 7 - metabolism | Immunohistochemistry | Small Molecule Libraries - pharmacology | Small Molecule Libraries - administration & dosage | Humans | Caspase 3 - metabolism | Male | Antineoplastic Agents - therapeutic use | Structure-Activity Relationship | Antineoplastic Agents - administration & dosage | Protein Kinase Inhibitors - chemistry | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | Prostatic Neoplasms - drug therapy | Naphthyridines - chemistry | Prostatic Neoplasms - pathology | Administration, Oral | Casein Kinase II - antagonists & inhibitors | Small Molecule Libraries - therapeutic use | Antineoplastic Agents - chemistry | Xenograft Model Antitumor Assays | Protein Kinase Inhibitors - administration & dosage | Small Molecule Libraries - chemistry | Animals | Protein Kinase Inhibitors - therapeutic use | Naphthyridines - therapeutic use | Cell Line, Tumor | Prostatic Neoplasms - enzymology | Mice | Protein Kinase Inhibitors - pharmacology | Cell Cycle - drug effects | Casein Kinase II - metabolism | Naphthyridines - pharmacology | Care and treatment | Chemical properties | Drug therapy | Health aspects | Apoptosis | Proteins | Molecular biology | Kinases | Cancer therapies | Index Medicus
Journal Article
Leukemia, ISSN 0887-6924, 2014, Volume 28, Issue 8, pp. 1636 - 1646
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 05/2009, Volume 119, Issue 5, pp. 1275 - 1285
The mechanism of mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, remains largely unknown. Here, we have... 
MEDICINE, RESEARCH & EXPERIMENTAL | BCL-2 PROTEIN FAMILY | ACUTE-RENAL-FAILURE | DEATH | MECHANISMS | FISSION | CYTOCHROME-C RELEASE | APOPTOTIC PATHWAYS | MAMMALIAN-CELLS | CISPLATIN NEPHROTOXICITY | DRP1 | Adenosine Triphosphate - deficiency | Kidney Tubular Necrosis, Acute - chemically induced | RNA, Small Interfering - genetics | Dynamins - metabolism | Microtubule-Associated Proteins - genetics | Apoptosis - drug effects | Male | GTP Phosphohydrolases - antagonists & inhibitors | Kidney Tubular Necrosis, Acute - prevention & control | Mitochondria - ultrastructure | Imaging, Three-Dimensional | Cell Line | Kidney Tubules, Proximal - cytology | Reperfusion Injury - pathology | Cytochromes c - metabolism | Mice, Inbred C57BL | Cells, Cultured | Enzyme Inhibitors - pharmacology | Dynamins - genetics | Rats | Mitochondria - metabolism | Cisplatin - pharmacology | Microtubule-Associated Proteins - antagonists & inhibitors | Mitochondria - pathology | Caspase Inhibitors | Enzyme Inhibitors - therapeutic use | Animals | Reperfusion Injury - prevention & control | GTP Phosphohydrolases - genetics | Mice | Proto-Oncogene Proteins c-bcl-2 - genetics | Sodium Azide - pharmacology | Kidney Tubular Necrosis, Acute - pathology | Cell culture | Complications and side effects | Physiological aspects | Models | Mitochondrial diseases | Research | Management | Kidney diseases | Drug therapy | Risk factors | Apoptosis | Index Medicus | Abridged Index Medicus
Journal Article
Nature Medicine, ISSN 1078-8956, 09/2006, Volume 12, Issue 9, pp. 1056 - 1064
Journal Article