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Nature (London), ISSN 1476-4687, 2015, Volume 520, Issue 7547, pp. 368 - 372
Drug resistance invariably limits the clinical efficacy of targeted therapy with kinase inhibitors against cancer(1,2... 
CNS CELL-TYPES | MELANOMA | METASTASIS | MICROENVIRONMENT | TRANSLATIONAL PROFILING APPROACH | MULTIDISCIPLINARY SCIENCES | RAF INHIBITOR RESISTANCE | ACQUIRED-RESISTANCE | KINASE INHIBITORS | DRUG-RESISTANCE | CANCER CHEMORESISTANCE | Lung Neoplasms - drug therapy | Adenocarcinoma - pathology | Clone Cells - drug effects | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Proto-Oncogene Proteins c-fos - deficiency | Adenocarcinoma - metabolism | Anaplastic Lymphoma Kinase | Neoplasm Metastasis - drug therapy | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Female | Proto-Oncogene Proteins c-akt - metabolism | Melanoma - metabolism | Tumor Microenvironment - drug effects | Cell Survival - drug effects | ErbB Receptors - antagonists & inhibitors | Melanoma - pathology | Down-Regulation - drug effects | Enzyme Activation - drug effects | Adenocarcinoma - drug therapy | Disease Progression | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Cell Movement - drug effects | Animals | Clone Cells - pathology | Metabolome - drug effects | Signal Transduction - drug effects | Neoplasm Metastasis - pathology | Protein Kinase Inhibitors - therapeutic use | Melanoma - drug therapy | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects | Antimitotic agents | Pharmaceutical research | Care and treatment | Oncology, Experimental | Dosage and administration | Research | Drug therapy | Drug resistance | Antineoplastic agents | Tumors | Cancer | Melanoma | Mutation | Metastasis | Kinases | Cancer therapies
Journal Article
Journal of aerosol medicine and pulmonary drug delivery, ISSN 1941-2711, 2008
Journal
PLoS ONE, ISSN 1932-6203, 04/2013, Volume 8, Issue 4, p. e62082
Some potent chemotherapy drugs including tubulin-binding agents had been developed from nature plants, such as podophyllotoxin and paclitaxel... 
MITOSIS | ANTIMITOTIC ACTIVITY | MICROTUBULES | NATURAL-PRODUCTS | MULTIDISCIPLINARY SCIENCES | DRUG DISCOVERY | RESISTANCE | TUBULIN | BINDING AGENTS | EXPRESSION | KINASES | Lung Neoplasms - drug therapy | Podophyllotoxin - pharmacology | Apoptosis - drug effects | Humans | Lung Neoplasms - metabolism | Apoptosis - genetics | Endoplasmic Reticulum Stress - genetics | Microtubules - metabolism | Podophyllotoxin - toxicity | Drug Evaluation, Preclinical | Disease Models, Animal | DNA Damage - drug effects | Lung Neoplasms - genetics | M Phase Cell Cycle Checkpoints - drug effects | Endoplasmic Reticulum Stress - drug effects | Antineoplastic Agents, Phytogenic - toxicity | Xenograft Model Antitumor Assays | Animals | Mitosis - drug effects | Signal Transduction - drug effects | Tumor Burden - drug effects | Cell Cycle Checkpoints - drug effects | Models, Biological | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Antineoplastic Agents, Phytogenic - pharmacology | Protein Multimerization - drug effects | Podophyllotoxin - analogs & derivatives | Chemotherapy | Podophyllotoxin | Analysis | Lung cancer | Polymerization | Stress (Physiology) | Tubulins | Health aspects | Apoptosis | Cancer | Drugs | Flow cytometry | Toxicity | Mitosis | Leukemia | DNA damage | Cytotoxicity | Selectivity | Biochemistry | Drug development | Kinases | Cancer therapies | Anticancer properties | Metastases | Proteins | Signal transduction | Tubulin | Paclitaxel | Xenografts | Cell cycle | Inhibition | Stains | Deoxyribonucleic acid--DNA | Stresses | Plants (botany) | Hematology | Injection | Survivin | Tumor cell lines | Gene expression | Stress | Aurora B protein | Signaling | Side effects | Colonization | Deoxyribonucleic acid | DNA
Journal Article
Nature (London), ISSN 1476-4687, 2016, Volume 534, Issue 7605, pp. 129 - 132
..., an allosteric inhibitor that targets selected drug-resistant EGFR mutants but spares the wild-type receptor. The crystal structure shows that the compound binds... 
CELL LUNG-CANCER | EGFR KINASE | GROWTH-FACTOR RECEPTOR | TARGETED THERAPIES | GEFITINIB | ACTIVATION | MECHANISM | MULTIDISCIPLINARY SCIENCES | MUTATIONS | AZD9291 | Lung Neoplasms - drug therapy | Drug Resistance, Multiple - drug effects | Protein Conformation - drug effects | ErbB Receptors - genetics | Lung Neoplasms - pathology | Antineoplastic Agents - pharmacology | Benzeneacetamides - pharmacology | Mutant Proteins - antagonists & inhibitors | Disease Models, Animal | Allosteric Regulation - drug effects | Carcinoma, Non-Small-Cell Lung - pathology | Drug Resistance, Multiple - genetics | ErbB Receptors - antagonists & inhibitors | ErbB Receptors - metabolism | Lung Neoplasms - enzymology | Allosteric Site - drug effects | Mutant Proteins - genetics | Cetuximab - pharmacology | Mutant Proteins - metabolism | Drug Synergism | Drug Resistance, Neoplasm - genetics | Animals | ErbB Receptors - chemistry | Mutant Proteins - chemistry | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Protein Multimerization - drug effects | Drug Resistance, Neoplasm - drug effects | Studies | Phosphorylation | Nuclear magnetic resonance--NMR | Epidermal growth factor | Mutation | Kinases | Enzyme kinetics | Tumors
Journal Article
Pulmonary pharmacology, ISSN 0952-0600, 1988
Journal
International journal of molecular sciences, ISSN 1422-0067, 2017, Volume 18, Issue 7, p. 1414
.... Mechanisms of anticancer effects of HDAC inhibitors are not uniform; they may be different and depend on the cancer type, HDAC inhibitors, doses, etc... 
Histone deacetylase inhibitors | Anti-angiogenic effect | Cell cycle arrest | Drug combinations | Histone deacetylases | Autophagy | Apoptosis | Cancer | HDAC INHIBITORS | autophagy | SUBEROYLANILIDE HYDROXAMIC ACID | HUMAN LEUKEMIA-CELLS | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | TUMOR-SUPPRESSOR GENES | apoptosis | VALPROIC ACID | cell cycle arrest | anti-angiogenic effect | CHEMISTRY, MULTIDISCIPLINARY | drug combinations | CELL LUNG-CANCER | EPITHELIAL-MESENCHYMAL TRANSITION | PHASE-II TRIAL | LONG NONCODING RNA | histone deacetylases | cancer | histone deacetylase inhibitors | Immunomodulation - drug effects | Apoptosis - drug effects | Humans | Angiogenesis Inhibitors - pharmacology | Antineoplastic Combined Chemotherapy Protocols - adverse effects | Antineoplastic Agents - therapeutic use | Clinical Trials as Topic | Autophagy - drug effects | Acetylation - drug effects | Animals | Signal Transduction - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Cell Cycle Checkpoints - drug effects | Angiogenesis Inhibitors - therapeutic use | Histone Deacetylase Inhibitors - pharmacology | Antineoplastic Agents - pharmacology | Epigenesis, Genetic - drug effects | Histone Deacetylase Inhibitors - therapeutic use | Gene Expression Regulation, Neoplastic - drug effects | Drug Evaluation, Preclinical
Journal Article
Nature medicine, ISSN 1546-170X, 2016, Volume 22, Issue 3, pp. 262 - 269
Journal Article
Aging cell, ISSN 1474-9718, 2015, Volume 14, Issue 4, pp. 644 - 658
...‐related chronic diseases. Here, we describe the rationale for identification and validation of a new class of drugs termed senolytics, which selectively kill senescent cells... 
dasatinib | plasminogen‐activated inhibitor | dependence receptors | quercetin | ephrins | PI3K delta | p21 | Dasatinib | Dependence receptors | Ephrins | Plasminogen-activated inhibitor | Quercetin | P21 | ENDOTHELIAL DYSFUNCTION | PLASMINOGEN-ACTIVATOR INHIBITOR-1 | EXPRESSION PROFILES | plasminogen-activated inhibitor | CELLULAR SENESCENCE | CANCER-THERAPY | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | LUNG-CANCER | SET ENRICHMENT ANALYSIS | GENE-EXPRESSION | IONIZING-RADIATION | TUMOR-GROWTH | Carotid Arteries - drug effects | Endonucleases - genetics | Plasminogen Activator Inhibitor 2 - genetics | Transcriptome | Gene Expression Profiling | Adipocytes - drug effects | Aging - genetics | Osteoporosis - metabolism | Ephrins - metabolism | Plasminogen Activator Inhibitor 2 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Osteoporosis - genetics | Intervertebral Disc - pathology | Fibroblasts - metabolism | Endothelial Cells - metabolism | Intervertebral Disc - chemistry | Fibroblasts - pathology | Mesenchymal Stem Cells - pathology | Mice, Knockout | Dasatinib - pharmacology | Osteoporosis - pathology | Ephrins - genetics | Fibroblasts - drug effects | Mice | Endothelial Cells - pathology | bcl-X Protein - metabolism | Aging - metabolism | Aging - drug effects | bcl-X Protein - genetics | Cellular Senescence - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Endonucleases - metabolism | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Mesenchymal Stem Cells - drug effects | Mesenchymal Stem Cells - metabolism | Heart - physiopathology | Cellular Senescence - genetics | Osteoporosis - prevention & control | DNA-Binding Proteins - genetics | Adipocytes - pathology | Aging - pathology | Phosphatidylinositol 3-Kinases - genetics | Animals | Quercetin - pharmacology | Adipocytes - metabolism | Heart - drug effects | Carotid Arteries - pathology | Intervertebral Disc - drug effects | Drug Combinations | Endothelial Cells - drug effects | Original
Journal Article
RNA, ISSN 1355-8382, 2012, Volume 18, Issue 7, pp. 1373 - 1384
The recruitment of ribosomes to eukaryotic cellular mRNAs requires the activity of two prototypic RNA helicases, eukaryotic initiation factor (eIF) 4AI and... 
Translation | eIF4AI | eIF4AII | DEAD-box RNA helicase | Hippuristanol | Translational control | RNA helicase | MAMMALIAN TRANSLATION | FACTOR EIF-4A | BIOCHEMISTRY & MOLECULAR BIOLOGY | BINDING-PROTEIN | CROSS-LINKING | translational control | 5' END | EUKARYOTIC TRANSLATION INITIATION | MESSENGER-RNA | translation | hippuristanol | DEGRADATION | INHIBITS TRANSLATION | RNA HELICASE EIF4A | Transcription, Genetic - drug effects | Testis - metabolism | Humans | Fetus - metabolism | Male | Muscle, Skeletal - metabolism | Spleen - drug effects | Prostate - metabolism | Testis - drug effects | Brain - metabolism | Kidney - metabolism | Protein Isoforms - metabolism | Liver - drug effects | Muscle, Skeletal - drug effects | Myocardium - metabolism | Prostate - drug effects | Adult | Female | Ovary - drug effects | Lung - metabolism | Thymus Gland - metabolism | Ovary - metabolism | Sterols - pharmacology | Cell Line | Kidney - drug effects | Liver - metabolism | Pancreas - drug effects | Pancreas - metabolism | Thymus Gland - drug effects | Eukaryotic Initiation Factor-4A - antagonists & inhibitors | Brain - drug effects | Fetus - drug effects | Placenta - drug effects | Placenta - metabolism | Pregnancy | Transcription, Genetic - physiology | Spleen - metabolism | Lung - drug effects | Eukaryotic Initiation Factor-4A - metabolism
Journal Article
Molecular Oncology, ISSN 1574-7891, 08/2016, Volume 10, Issue 7, pp. 949 - 965
Development of therapeutic resistance is responsible for most prostate cancer (PCa) related mortality. Resistance has been attributed to an acquired or... 
Anticancer drugs | Mitochondria | Combination therapy | Prostate cancer | Unfolded protein response | Apoptosis | STEM-CELLS | STRESS-RESPONSE | DNA-DAMAGE | ESTRAMUSTINE PHOSPHATE | CELL-CYCLE ARREST | TUMOR-CELLS | PACLITAXEL | EPITHELIAL-MESENCHYMAL TRANSITION | LUNG-CANCER | ONCOLOGY | ENDOPLASMIC-RETICULUM | Cell Death - radiation effects | Prostatic Neoplasms - radiotherapy | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Membrane Potential, Mitochondrial - radiation effects | Neoplastic Stem Cells - drug effects | Humans | Unfolded Protein Response - radiation effects | Male | Interferon-gamma - metabolism | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Interleukin-8 - metabolism | Phosphorylation - drug effects | Prostatic Neoplasms - drug therapy | G2 Phase - radiation effects | Cytoskeleton - radiation effects | beta Catenin - metabolism | Cell Cycle Checkpoints - radiation effects | G1 Phase - radiation effects | Cell Cycle Checkpoints - drug effects | X-Rays | Cell Line, Tumor | Cytoskeleton - metabolism | Peptides, Cyclic - therapeutic use | Thapsigargin - pharmacology | Thapsigargin - therapeutic use | Prostatic Neoplasms - metabolism | Apoptosis - radiation effects | Peptides, Cyclic - pharmacology | G1 Phase - drug effects | Membrane Potential, Mitochondrial - drug effects | G2 Phase - drug effects | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Caspases - metabolism | Paclitaxel | Mitochondria - radiation effects | Cell Death - drug effects | Neoplastic Stem Cells - radiation effects | Prostatic Neoplasms - pathology | Unfolded Protein Response - drug effects | Mitochondria - metabolism | Mitochondria - drug effects | Enzyme Activation - drug effects | HSP70 Heat-Shock Proteins - metabolism | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Matrix Metalloproteinases - metabolism | Transforming Growth Factor beta - metabolism | Cytoskeleton - drug effects | Care and treatment | Mortality | Oncology, Experimental | Mitochondrial DNA | Research | Drug resistance | Transforming growth factors | Nuclear radiation | Stem cells | Bone morphogenetic proteins | Germany | Cancer | Histone deacetylase | Phenotypes | Immunoglobulins | Transforming growth factor-b | Caspase | Metastasis | Cancer therapies | Cell adhesion & migration | Adenomatous polyposis coli | Thapsigargin | Androgens | Protein folding | CD44 antigen | Cell cycle | Cytoskeleton
Journal Article