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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2010, Volume 107, Issue 28, pp. 12611 - 12616
Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells. Asbestos is cytotoxic... 
Actinomycin | Asbestos | Cell death | Secretion | Plasma cells | Inflammation | Macrophages | Carcinogenesis | Necrosis | Apoptosis | Mesothelioma | Biomarker | Tumor necrosis factor-alpha | Chemoprevention | TRANSFORMATION | POLY(ADP-RIBOSE) POLYMERASE | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | CROCIDOLITE ASBESTOS | HMGB1 | biomarker | MAMMALIAN-CELLS | tumor necrosis factor-alpha | PATHOGENESIS | chemoprevention | NECROTIC CELLS | carcinogenesis | TNF-ALPHA | INHIBITORS | mesothelioma | Tumor Necrosis Factor-alpha - metabolism | Asbestos - metabolism | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Humans | Reactive Oxygen Species - pharmacology | Adenosine Diphosphate Ribose - metabolism | Adenosine Diphosphate Ribose - pharmacology | Carcinogens - metabolism | Asbestos - pharmacology | Pleural Neoplasms - metabolism | Inflammation - metabolism | Carcinogens - pharmacology | Cell Nucleus - metabolism | HMGB Proteins - pharmacology | HMGB1 Protein - pharmacology | HMGB1 Protein - metabolism | Cell Death | Mesocricetus | Female | HMGB Proteins - metabolism | Poly Adenosine Diphosphate Ribose - pharmacology | Epithelium - drug effects | Cricetinae | Cytokines - metabolism | Epithelium - metabolism | Hydrogen Peroxide - pharmacology | Necrosis - metabolism | Hydrogen Peroxide - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Macrophages - metabolism | Poly(ADP-ribose) Polymerases - metabolism | Animals | Mesothelioma - metabolism | Poly(ADP-ribose) Polymerases - pharmacology | Cells - metabolism | Mice | Mice, Inbred BALB C | Cytokines - pharmacology | Prevention | Mesothelium | Chromosomal proteins | Research | Chemical properties | Health aspects | Reactive oxygen species | Transformation | Deposits | Hydrogen peroxide | Cytokines | Cytotoxicity | HMGB1 protein | Nuclei | Carcinogens | Tumor necrosis factor-a | ATP | Cytoplasm | Biological Sciences
Journal Article
Journal Article
Pathology, ISSN 0031-3025, 02/2013, Volume 45, Issue 2, pp. 116 - 126
BAP1 (BRCA1-Associated Protein 1) was initially identified as a protein that binds to BRCA1. BAP1 is a tumour suppressor that is believed to mediate its... 
pathology | familial cancer | uveal melanoma | skin | diagnosis | inherited tumour susceptibility | melanoma | 3p21 loss syndrome | atypical Spitz tumour | germline mutation | BAP1 | Pathology | Inherited tumour susceptibility | Melanoma | Uveal melanoma | Atypical Spitz tumour | Familial cancer | Germline mutation | Skin | Diagnosis | PLEURAL MESOTHELIOMA | DNA-DAMAGE RESPONSE | BRCA1-ASSOCIATED PROTEIN-1 | RENAL-CELL CARCINOMA | BREAST-CANCER | POLYCOMB GROUP PROTEINS | SPITZ NEVI | HISTONE DEACETYLASE INHIBITORS | MALIGNANT MESOTHELIOMA | MYELODYSPLASTIC SYNDROMES | Neoplasms - metabolism | Carcinoma, Neuroendocrine - diagnosis | Melanoma - diagnosis | Humans | Lung Neoplasms - metabolism | Meningioma - genetics | Neoplasms - diagnosis | Paraganglioma - diagnosis | Adenocarcinoma - metabolism | Neoplasms - genetics | DNA Mutational Analysis | Melanoma - genetics | Gene Deletion | Nevus, Epithelioid and Spindle Cell - genetics | Skin Neoplasms - diagnosis | Tumor Suppressor Proteins - genetics | Biomarkers, Tumor - metabolism | Adenocarcinoma - genetics | Uveal Neoplasms - metabolism | Carcinoma, Neuroendocrine - metabolism | Lung Neoplasms - genetics | Melanoma - metabolism | Uveal Neoplasms - genetics | Genetic Predisposition to Disease | Meningioma - metabolism | Paraganglioma - genetics | Carcinoma, Neuroendocrine - genetics | Mesothelioma - diagnosis | Mesothelioma - genetics | Nevus, Epithelioid and Spindle Cell - metabolism | Ubiquitin Thiolesterase - genetics | Skin Neoplasms - metabolism | Immunohistochemistry - methods | Nevus, Epithelioid and Spindle Cell - diagnosis | Adenocarcinoma - diagnosis | Mesothelioma - metabolism | Paraganglioma - metabolism | Skin Neoplasms - genetics | Uveal Neoplasms - diagnosis | Biomarkers, Tumor - genetics | Meningioma - diagnosis | Mutation | Lung Neoplasms - diagnosis
Journal Article
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 11, p. e14110
Background: The role of estrogen and estrogen receptors in oncogenesis has been investigated in various malignancies. Recently our group identified estrogen... 
MOLECULAR-MECHANISM | BREAST-CANCER | CROSS-TALK | GROWTH-FACTOR RECEPTOR | LUNG-CANCER | TYROSINE KINASE | PROSTATE-CANCER CELLS | BIOLOGY | PHASE-II | ENDOCRINE THERAPY RESISTANCE | FACTOR SIGNALING PATHWAYS | Pleural Neoplasms - genetics | Cell Proliferation | Immunoprecipitation | Mesothelioma - pathology | Humans | Estrogen Receptor beta - metabolism | Pleural Neoplasms - metabolism | Receptor, Epidermal Growth Factor - metabolism | Estrogen Receptor beta - genetics | RNA Interference | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Pleural Neoplasms - pathology | Mesothelioma - genetics | Blotting, Western | Caveolin 1 - metabolism | Microscopy, Confocal | Mesothelioma - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Cell Line, Tumor | Protein Binding | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Protein Kinase Inhibitors - pharmacology | Epidermal Growth Factor - pharmacology | Quinazolines - pharmacology | Mitogen-Activated Protein Kinase 1 - metabolism | Cell proliferation | Caveolin-1 | Estrogens | Estrogen | Estrogen receptors | Mesothelioma | AKT protein | Activation | Kinases | Inactivation | Signal transduction | Receptors | Cell activation | Cell growth | Epidermal growth factor | Pathways | Rodents | Tumorigenesis | Gefitinib | Deactivation | Epidermal growth factor receptors | Caveolin | Pharmacology | Chemical compounds | Signaling | Molecular modelling | Internalization | Cell lines | Transduction | Tumors
Journal Article
Journal of Cellular and Molecular Medicine, ISSN 1582-1838, 11/2017, Volume 21, Issue 11, pp. 2663 - 2676
Malignant mesothelioma is an aggressive cancer that is resistant to current therapy. The poor prognosis of mesothelioma has been associated with elevated... 
YAP | therapeutic target | Hippo pathway | mesothelioma | MEDICINE, RESEARCH & EXPERIMENTAL | HIPPO SIGNALING CASCADE | CANCER STEM-CELLS | CELL BIOLOGY | TISSUE GROWTH-FACTOR | MELANOMA | TEAD | GENE | PATHWAY | DYSREGULATION | MUTATIONS | PROGRESSION | RNA, Small Interfering - genetics | Phosphorylation | Epithelial Cells - metabolism | Prognosis | Mesothelioma - pathology | Epithelial Cells - drug effects | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Spheroids, Cellular - pathology | Lung Neoplasms - pathology | rhoA GTP-Binding Protein - metabolism | Phosphoproteins - antagonists & inhibitors | rhoA GTP-Binding Protein - genetics | Phosphoproteins - metabolism | RNA, Messenger - metabolism | DNA-Binding Proteins - metabolism | rho-Associated Kinases - metabolism | Adaptor Proteins, Signal Transducing - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Spheroids, Cellular - drug effects | 3' Untranslated Regions | Nuclear Proteins - genetics | Genes, Reporter | Lung Neoplasms - genetics | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction | RNA, Messenger - genetics | Spheroids, Cellular - metabolism | rho-Associated Kinases - genetics | Epithelial Cells - pathology | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Mesothelioma - genetics | Phosphoproteins - genetics | Porphyrins - pharmacology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Transcription Factors - metabolism | Mesothelioma - metabolism | Nuclear Proteins - antagonists & inhibitors | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Adaptor Proteins, Signal Transducing - metabolism | RNA, Small Interfering - metabolism | Immunohistochemistry | Yuan (China) | Mesothelioma | RNA | Analysis | Biotechnology | Transcription | siRNA | Yes-associated protein | Proteins | Signaling | 3' Untranslated regions | Cell lines | Inhibition | Viability | Cancer | Original
Journal Article
European Journal of Cancer, ISSN 0959-8049, 2016, Volume 68, pp. 1 - 10
Abstract Purpose We performed a multi-centre phase I study to assess the safety, pharmacokinetics (PK) and pharmacodynamics (PD) of the orally available small... 
Hematology, Oncology and Palliative Medicine | Pharmacodynamics | MEK inhibitor | Phase I | Optimal biological dose | Pharmacokinetics | BRAF-MUTATED MELANOMA | MULTICENTER | SELUMETINIB PLUS DOCETAXEL | SAFETY | TRAMETINIB | CELL LUNG-CANCER | TRIAL | DOSE-ESCALATION | ONCOLOGY | DOUBLE-BLIND | AZD6244 ARRY-142886 | Lung Neoplasms - drug therapy | Pancreatic Neoplasms - metabolism | Nausea - chemically induced | Allosteric Regulation | Humans | Lung Neoplasms - metabolism | Middle Aged | Male | Fatigue - chemically induced | Ribosomal Protein S6 Kinases, 70-kDa - drug effects | Protein Kinase Inhibitors - adverse effects | Colorectal Neoplasms - drug therapy | Chromatography, Liquid | Proto-Oncogene Proteins c-akt - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Bile Duct Neoplasms - metabolism | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Administration, Oral | Carcinoma, Non-Small-Cell Lung - metabolism | Neoplasms - drug therapy | Maximum Tolerated Dose | Mesothelioma - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Anorexia - chemically induced | Glycogen Synthase Kinase 3 beta - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Neoplasms - metabolism | Phosphoproteins - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | Cholangiocarcinoma - metabolism | Chromatography, High Pressure Liquid | Diarrhea - chemically induced | Mitogen-Activated Protein Kinase 3 - drug effects | Pancreatic Neoplasms - drug therapy | Tandem Mass Spectrometry | Uterine Cervical Neoplasms - metabolism | Esophageal Neoplasms - metabolism | Adult | Female | Colorectal Neoplasms - metabolism | Bile Duct Neoplasms - drug therapy | Drug Eruptions - etiology | Abdominal Pain - chemically induced | Uterine Cervical Neoplasms - drug therapy | Glycogen Synthase Kinase 3 beta - metabolism | Mesothelioma - drug therapy | Cholangiocarcinoma - drug therapy | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Aged | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Esophageal Neoplasms - drug therapy | Proto-Oncogene Proteins c-akt - drug effects | Care and treatment | Protein kinases | Mitogens | Cells | Tumors
Journal Article
Cancer Letters, ISSN 0304-3835, 2017, Volume 393, pp. 52 - 59
Abstract Malignant mesothelioma remains an incurable cancer. We demonstrated that mesotheliomas expressed EGFR (79.2%), ErbB4 (49.0%) and HER2 (6.3%), but... 
Hematology, Oncology and Palliative Medicine | Mesothelioma | Chimeric antigen receptor | Lung cancer | Epidermal growth factor receptor | SURVIVAL | HEAD | PLEURAL MESOTHELIOMA | PHASE-II | PROLIFERATION | CANCER | DELIVERY | ONCOLOGY | EXPRESSION | MET | Mesothelioma - immunology | Receptor, ErbB-4 - metabolism | Pleural Neoplasms - genetics | Coculture Techniques | Humans | Lung Neoplasms - metabolism | Receptor, ErbB-2 - metabolism | Recombinant Fusion Proteins - metabolism | T-Lymphocytes - transplantation | Pleural Neoplasms - metabolism | Receptor, Epidermal Growth Factor - metabolism | T-Lymphocytes - metabolism | Time Factors | Lymphocytes, Tumor-Infiltrating - metabolism | Receptors, Antigen, T-Cell - immunology | Lung Neoplasms - genetics | Immunotherapy, Adoptive - methods | Mesothelioma - therapy | Pleural Neoplasms - immunology | ErbB Receptors - metabolism | Transduction, Genetic | Receptors, Antigen, T-Cell - metabolism | Interleukin-4 - metabolism | Lymphocytes, Tumor-Infiltrating - transplantation | Lung Neoplasms - therapy | Mesothelioma - genetics | Tumor Burden | Mice, SCID | Pleural Neoplasms - therapy | Xenograft Model Antitumor Assays | Interleukin-4 - immunology | Lung Neoplasms - immunology | Animals | Mesothelioma - metabolism | ErbB Receptors - immunology | Cell Line, Tumor | T-Lymphocytes - immunology | Receptors, Antigen, T-Cell - genetics | Genetic Therapy - methods | Lymphocytes, Tumor-Infiltrating - immunology | Interleukins | T cells | Immunotherapy | Genetically modified organisms | Antigens | Epidermal growth factor | Genetic engineering | Cytokines | Laboratories | Clinical trials | Histology | Kinases | Multivariate analysis | Patients | Medical prognosis | Tumors | Cancer
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 9/2006, Volume 103, Issue 38, pp. 14128 - 14133
Only a fraction of subjects exposed to asbestos develop malignant mesothelioma (MM), suggesting that additional factors may render some individuals more... 
Tumor cell line | Cocarcinogenesis | Phosphorylation | Asbestos | Cell lines | Small interfering RNA | Viruses | Infections | Hamsters | Tumors | Matrix metalloprotease | Activator protein-1 | ERK1/2 | Viral oncology | Environmental carcinogenesis | TRANSFORMATION | viral oncology | SIMIAN-VIRUS-40 | environmental carcinogenesis | activator protein-1 | MULTIDISCIPLINARY SCIENCES | BINDING-ACTIVITY | matrix metalloprotease | EPIDERMAL-GROWTH-FACTOR | C-JUN | MALIGNANT MESOTHELIOMA | ASSOCIATION | EXPRESSION | HUMAN TUMORS | HUMAN CANCER | Epithelial Cells - metabolism | Mesothelioma - pathology | Transcription Factor AP-1 - genetics | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Carcinogens - metabolism | Transcription Factor AP-1 - metabolism | Carcinogens - toxicity | Simian virus 40 - pathogenicity | Matrix Metalloproteinase 9 - metabolism | Asbestos, Crocidolite - metabolism | Matrix Metalloproteinase 9 - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Mesocricetus | Female | Epithelial Cells - cytology | Matrix Metalloproteinase 1 - genetics | Repressor Proteins - metabolism | Cricetinae | Epithelium - pathology | Epithelium - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Cells, Cultured | Proto-Oncogene Proteins c-fos - metabolism | Repressor Proteins - genetics | Asbestos, Crocidolite - toxicity | Gene Expression Regulation, Enzymologic | Animals | Mesothelioma - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Proto-Oncogene Proteins c-fos - genetics | Enzyme Activation | Matrix Metalloproteinase 1 - metabolism | Simian virus 40 - metabolism | Mesothelioma - etiology | Mitogen-Activated Protein Kinase 1 - metabolism | RNA, Small Interfering - metabolism | SV40 (Virus) | DNA binding proteins | Research | Carcinogenesis | Biological Sciences | ERK1
Journal Article
Cancer Cell, ISSN 1535-6108, 2008, Volume 13, Issue 3, pp. 261 - 271
Malignant mesothelioma is a devastating disease that has been associated with loss of Neurofibromatosis type 2 ( ) and genetic lesions affecting and pathways.... 
CELLCYCLE | SITE-SPECIFIC RECOMBINATION | ONCOLOGY | DEFICIENCY COOPERATE | CRE RECOMBINASE | NEUROFIBROMATOSIS TYPE-2 GENE | TUMOR-SUPPRESSOR PROTEIN | LARGE-T-ANTIGEN | CROCIDOLITE ASBESTOS | SARCOMATOID MESOTHELIOMA | SPINDLE-CELL NEOPLASMS | MUTANT NF2 PROTEIN | CELL BIOLOGY | Immunohistochemistry | Thoracic Cavity - pathology | Epithelial Cells - metabolism | Mesothelioma - pathology | Luminescent Measurements | Loss of Heterozygosity | Tumor Suppressor Protein p53 - genetics | Neoplasms, Experimental - pathology | Mixed Tumor, Malignant - pathology | Time Factors | Cell Transformation, Neoplastic - genetics | Recombination, Genetic | Neoplasms, Experimental - genetics | Adenoviridae - genetics | Integrases - metabolism | Neurofibromatosis 2 - metabolism | Mixed Tumor, Malignant - metabolism | Epithelioid Cells - pathology | Neoplasm Invasiveness | Thoracic Neoplasms - pathology | Tumor Suppressor Protein p53 - metabolism | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Epithelial Cells - pathology | Genotype | Mesothelioma - genetics | Neurofibromatosis 2 - genetics | Sarcoma - pathology | Cell Transformation, Neoplastic - metabolism | Thoracic Neoplasms - metabolism | Epithelioid Cells - metabolism | Mice, Knockout | Sarcoma - metabolism | Phenotype | Animals | Mesothelioma - metabolism | Thoracic Neoplasms - genetics | Cell Line, Tumor | Cyclin-Dependent Kinase Inhibitor p16 - metabolism | Mice | Neoplasms, Experimental - metabolism | Cell Transformation, Neoplastic - pathology | Genetic Vectors | Integrases - genetics | Thoracic Cavity - metabolism | Tumor proteins | Mesothelioma
Journal Article
Cancer Letters, ISSN 0304-3835, 2016, Volume 385, pp. 215 - 224
Abstract Malignant mesothelioma (MM) frequently exhibits Hippo signaling pathway inactivation (HPI) mainly due to NF2 and/or LATS2 mutations, which leads to... 
Hematology, Oncology and Palliative Medicine | Cancer stem cell | YAP | Malignant mesothelioma | Hippo pathway | Statin | CD44 | PLEURAL MESOTHELIOMA | ORGAN SIZE CONTROL | CANCER STEM-CELLS | BREAST-CANCER | ZOLEDRONIC ACID | ONCOLOGY | SIGNALING PATHWAY | DEUBIQUITINASE BAP1 | TUMOR-SUPPRESSOR | CANDIDATE ONCOGENE | MEVALONATE PATHWAY | Lung Neoplasms - drug therapy | Neurofibromin 2 - genetics | Phosphorylation | Fatty Acids, Monounsaturated - pharmacology | Mesothelioma - pathology | Neoplastic Stem Cells - drug effects | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Lung Neoplasms - pathology | Phosphoproteins - metabolism | Simvastatin - pharmacology | Dose-Response Relationship, Drug | Fluvastatin | Transfection | Neoplastic Stem Cells - metabolism | RNA Interference | Time Factors | Tumor Suppressor Proteins - genetics | Hyaluronan Receptors - metabolism | Neoplastic Stem Cells - pathology | Ubiquitin Thiolesterase - metabolism | Indoles - pharmacology | Transcription, Genetic | Antineoplastic Agents - pharmacology | Binding Sites | Neurofibromin 2 - metabolism | Protein-Serine-Threonine Kinases - metabolism | Lung Neoplasms - genetics | Promoter Regions, Genetic | Tumor Suppressor Proteins - metabolism | Neoplasm Invasiveness | Protein-Serine-Threonine Kinases - genetics | Mesothelioma - genetics | Phosphoproteins - genetics | Mevalonic Acid - metabolism | Ubiquitin Thiolesterase - genetics | Hyaluronan Receptors - genetics | Mesothelioma - drug therapy | Cell Movement - drug effects | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Mesothelioma - metabolism | Signal Transduction - drug effects | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Cell Proliferation - drug effects | Mutation | Adaptor Proteins, Signal Transducing - metabolism | Medical colleges | Mesothelioma | School construction | Statins | Stem cells | Medical research | Statistical analysis | Biosynthesis | Breast cancer | Metastasis | Gene expression | Experiments | Proteins | Insects | Medical prognosis | Cell cycle | Tumorigenesis | Tumors
Journal Article
Nature Genetics, ISSN 1061-4036, 03/2016, Volume 48, Issue 4, pp. 407 - 416
Journal Article