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Nature, ISSN 0028-0836, 01/2016, Volume 529, Issue 7584, pp. 110 - 114
Gain-of-function IDH mutations are initiating events that define major clinical and prognostic classes of gliomas(1,2). Mutant IDH protein produces a new... 
MAINTENANCE | METHYLATION | LANDSCAPE | DEMETHYLATION | MULTIDISCIPLINARY SCIENCES | INTEGRATED GENOMIC ANALYSIS | ARCHITECTURE | PHENOTYPE | EXPRESSION | 2-HYDROXYGLUTARATE | PRINCIPLES | Chromatin - metabolism | Up-Regulation | Humans | Glioma - genetics | Base Sequence | Glioma - pathology | Epigenesis, Genetic - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Binding Sites | Chromatin - drug effects | Repressor Proteins - metabolism | Oncogenes - genetics | Insulator Elements - genetics | Glioma - enzymology | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Cells, Cultured | Isocitrate Dehydrogenase - genetics | DNA Methylation - genetics | Down-Regulation - drug effects | Mutation - genetics | CRISPR-Cas Systems - genetics | Insulator Elements - drug effects | Phenotype | Isocitrate Dehydrogenase - chemistry | Receptor, Platelet-Derived Growth Factor alpha - genetics | CCCTC-Binding Factor | CpG Islands - genetics | Protein Binding | Isocitrate Dehydrogenase - metabolism | Cell Proliferation - drug effects | Enhancer Elements, Genetic - genetics | Glutarates - metabolism | Cell Transformation, Neoplastic - drug effects | Chromatin - genetics | DNA Methylation - drug effects | Glioma - drug therapy | Complications and side effects | Care and treatment | Platelet-derived growth factor | Gliomas | Analysis | Influence | Genetic aspects | Research | Methylation | Oncogenes | DNA methylation | Epigenetics | Genomes | Mutation | Gene expression | Binding sites | Deoxyribonucleic acid--DNA | Tumors | Index Medicus
Journal Article
American Journal of Pathology, The, ISSN 0002-9440, 2012, Volume 181, Issue 6, pp. 2188 - 2201
Journal Article
Nature, ISSN 0028-0836, 09/2015, Volume 525, Issue 7570, pp. 538 - 542
Bromodomain and extra terminal protein (BET) inhibitors are first-in-class targeted therapies that deliver a newtherapeutic opportunity by directly targeting... 
SELECTIVE-INHIBITION | ACCURATE | CHROMATIN | MECHANISM | MULTIDISCIPLINARY SCIENCES | ACUTE MYELOID-LEUKEMIA | DRUG-RESISTANCE | MUTATIONS | SEQUENCING DATA | CANCER | DISCOVERY | Chromatin - metabolism | Transcription, Genetic - drug effects | Clone Cells - drug effects | Neoplastic Stem Cells - drug effects | Epigenesis, Genetic | Humans | Leukemia, Myeloid, Acute - metabolism | Molecular Targeted Therapy | Neoplastic Stem Cells - metabolism | Leukemia, Myeloid, Acute - drug therapy | Neoplastic Stem Cells - pathology | Gene Expression Regulation, Neoplastic - drug effects | Hematopoietic Stem Cells - drug effects | Benzodiazepines - pharmacology | Leukemia, Myeloid, Acute - pathology | Cells, Cultured | Nuclear Proteins - metabolism | Transcription Factors - antagonists & inhibitors | Hematopoietic Stem Cells - metabolism | Clone Cells - metabolism | beta Catenin - metabolism | Azepines - pharmacology | Transcription Factors - metabolism | Triazoles - pharmacology | Drug Resistance, Neoplasm - genetics | Animals | Clone Cells - pathology | Wnt Signaling Pathway - drug effects | Genes, myc - genetics | Hematopoietic Stem Cells - cytology | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mice | Drug Resistance, Neoplasm - drug effects | Leukemia, Myeloid, Acute - genetics | Proteins | Leukemia | Cloning | Cell cycle | Stem cells | Epigenetics | Apoptosis | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2013, Volume 8, Issue 11, pp. e80883 - e80883
Background: Kaempferol has been proposed as a potential drug for cancer chemoprevention and treatment because it is a natural polyphenol contained in... 
MIGRATION | INACTIVATION | INVASION | COLORECTAL-CANCER | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | TISSUE INHIBITOR | FLAVONOIDS | PROGNOSTIC-SIGNIFICANCE | NF-KAPPA-B | CARCINOMA | Transcription, Genetic - drug effects | Protein Binding - genetics | Nitriles - pharmacology | DNA, Neoplasm - metabolism | Humans | Cell Survival - genetics | Extracellular Signal-Regulated MAP Kinases - metabolism | RNA, Messenger - metabolism | Transcription Factor AP-1 - metabolism | Cell Movement - genetics | Tissue Inhibitor of Metalloproteinase-2 - metabolism | Protein Binding - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Mouth Neoplasms - enzymology | Cell Survival - drug effects | Butadienes - pharmacology | Matrix Metalloproteinase 2 - metabolism | Neoplasm Invasiveness | RNA, Messenger - genetics | Signal Transduction - genetics | Down-Regulation - drug effects | Cell Movement - drug effects | Matrix Metalloproteinase 2 - genetics | Matrix Metalloproteinase Inhibitors - pharmacology | Signal Transduction - drug effects | Cell Line, Tumor | Mouth Neoplasms - pathology | Kaempferols - pharmacology | Prevention | Medical research | Care and treatment | Squamous cell carcinoma | RNA | Analysis | Medicine, Experimental | Metastasis | Cardiovascular diseases | Mouth cancer | Cancer | Biotechnology | Food plants | Transcription factors | Tongue | Phosphorylation | Transcription | Oral cancer | Laboratories | Gene regulation | Colorectal cancer | Otolaryngology | Biochemistry | Matrix metalloproteinase | Tissue inhibitor of metalloproteinase 2 | Cancer therapies | Metastases | Angiogenesis | Signal transduction | Cell cycle | Physiology | Metalloproteinase | Food | Kaempferol | Activator protein 1 | Melanoma | Extracellular signal-regulated kinase | c-Jun protein | Plant protection | Breast cancer | Gene expression | Gelatinase A | Studies | Signaling | Bone cancer | Chemotherapy | Flavonoids | Hospitals | Molecular modelling | Cell migration | Apoptosis | Index Medicus
Journal Article
Oncogene, ISSN 0950-9232, 03/2013, Volume 32, Issue 13, pp. 1616 - 1625
HOTAIR is a long intervening non-coding RNA (lincRNA) that associates with the Polycomb Repressive Complex 2 (PRC2) and overexpression is correlated with poor... 
HOTAIR | Cell cycle progression | Pro-oncogenic | Invasion | Prognostic | ACTIVATION | pro-oncogenic | PROTEIN | CHROMATIN | DUCTAL ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | MECHANISMS | CELL BIOLOGY | prognostic | INTERFERON | invasion | LONG NONCODING RNA | REPRESSION | ONCOLOGY | GENETICS & HEREDITY | GENE-EXPRESSION | cell cycle progression | MIRNAS | Prognosis | Pancreatic Neoplasms - diagnosis | Humans | Transplantation, Heterologous | RNA, Long Noncoding - physiology | Carcinoma, Pancreatic Ductal - genetics | Gene Knockdown Techniques | Cell Transformation, Neoplastic - genetics | Biomarkers, Tumor - metabolism | Carcinoma, Pancreatic Ductal - diagnosis | Female | Gene Expression Regulation, Neoplastic - drug effects | Gene Expression Regulation, Neoplastic - physiology | Pancreatic Neoplasms - pathology | RNA, Small Interfering - pharmacology | Pancreatic Neoplasms - genetics | Biomarkers, Tumor - physiology | RNA, Long Noncoding - genetics | Carcinoma, Pancreatic Ductal - pathology | Animals | Cell Line, Tumor | Biomarkers, Tumor - genetics | Cell Proliferation - drug effects | Mice | Cell Transformation, Neoplastic - drug effects | RNA, Long Noncoding - antagonists & inhibitors | RNA, Long Noncoding - metabolism | RNA | Pancreatic cancer | Physiological aspects | Genetic aspects | Research | Gene expression | Oncology | Cell cycle | Tumors | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 8, pp. e24099 - e24099
Background: MicroRNA-34a (miR-34a) is a transcriptional target of p53 and is down-regulated in pancreatic cancer. This study aimed to investigate the... 
BIOMARKERS | NERVOUS-SYSTEM | APOPTOSIS | TRAIL | P53 PROTEIN | MULTIDISCIPLINARY SCIENCES | TUMOR-SUPPRESSOR | NOTCH SIGNALING PATHWAY | MICRORNAS | EXPRESSION | TUMORIGENESIS | Cell Cycle - genetics | Chromatin - metabolism | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Humans | Spheroids, Cellular - pathology | Apoptosis - genetics | Epithelial-Mesenchymal Transition - drug effects | MicroRNAs - metabolism | Epithelial-Mesenchymal Transition - genetics | Pancreatic Neoplasms - drug therapy | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Epigenesis, Genetic - drug effects | Spheroids, Cellular - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Hydroxamic Acids - pharmacology | Tumor Stem Cell Assay | Neoplasm Invasiveness | Pancreatic Neoplasms - pathology | Spheroids, Cellular - metabolism | Pancreatic Neoplasms - genetics | Up-Regulation - genetics | Up-Regulation - drug effects | Azacitidine - pharmacology | Cell Movement - drug effects | Cell Line, Tumor | Hydroxamic Acids - therapeutic use | Cell Proliferation - drug effects | MicroRNAs - genetics | Cell Cycle - drug effects | Azacitidine - therapeutic use | Prevention | Epigenetic inheritance | Care and treatment | Chemotherapy | Chromatin | Pancreatic cancer | Stem cells | Development and progression | Tumor proteins | Cancer | Apoptosis | Bcl-2 protein | p53 Protein | Metastasis | Caspase-3 | Cancer therapies | Toxicology | Scholarships & fellowships | Cell growth | N-Cadherin | Restoration | Physiology | Tumorigenesis | Inhibition | MiRNA | Gene expression | SIRT1 protein | Pathology | Biomarkers | Notch protein | Mutation | Cell proliferation | Azacytidine | Histone deacetylase | Transcription | Mesenchyme | Laboratories | Leukemia | Gene regulation | Multiple myeloma | E-cadherin | Modulators | Cell cycle | Inducers | Departments | Caspase | Pharmacology | Breast cancer | Tumor cell lines | Ribonucleic acid--RNA | Medicine | Cyclin-dependent kinase inhibitor p21 | Medical prognosis | Reagents | Cell lines | Epigenetics | Cyclin-dependent kinase inhibitor p27 | Prostate cancer | Index Medicus | Migration | Ribonucleic acids
Journal Article
Cancer Cell, ISSN 1535-6108, 2011, Volume 19, Issue 1, pp. 58 - 71
Activation of the PI3K-AKT pathway in tumors is modulated by negative feedback, including mTORC1-mediated inhibition of upstream signaling. We now show that... 
RAPAMYCIN | TARGET | FORKHEAD TRANSCRIPTION FACTOR | CELLS | INSULIN-RECEPTOR | ACTIVATION | ONCOLOGY | SIGNALING PATHWAY | PHOSPHORYLATION | UPSTREAM | HUMAN CANCER | CELL BIOLOGY | RNA, Small Interfering - genetics | Receptor, IGF Type 1 - metabolism | Protein Binding - genetics | Receptor, ErbB-3 - metabolism | Humans | Forkhead Transcription Factors - metabolism | Protein Binding - drug effects | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Receptor, ErbB-2 - antagonists & inhibitors | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Quinoxalines - therapeutic use | Carcinoma, Non-Small-Cell Lung - metabolism | Receptor, ErbB-3 - genetics | Receptor Protein-Tyrosine Kinases - metabolism | Breast Neoplasms - drug therapy | Receptor, IGF Type 1 - genetics | Signal Transduction - drug effects | Mice, Nude | Models, Biological | Cell Line, Tumor | Mice | TOR Serine-Threonine Kinases | Feedback, Physiological - physiology | Quinazolines - pharmacology | Proteins - antagonists & inhibitors | Neoplasms - metabolism | Gene Expression - drug effects | Multiprotein Complexes | Receptor, ErbB-2 - metabolism | Promoter Regions, Genetic - genetics | Proto-Oncogene Proteins c-akt - genetics | Breast Neoplasms - metabolism | Mechanistic Target of Rapamycin Complex 1 | Quinoxalines - pharmacology | Receptor, Insulin - genetics | Female | Forkhead Transcription Factors - antagonists & inhibitors | Gene Expression Regulation, Neoplastic - drug effects | Drug Therapy, Combination | Gene Expression Regulation, Neoplastic - physiology | Carcinoma, Non-Small-Cell Lung - pathology | Up-Regulation - genetics | Forkhead Transcription Factors - genetics | Xenograft Model Antitumor Assays | Animals | Receptor Protein-Tyrosine Kinases - genetics | Breast Neoplasms - pathology | Protein Kinase Inhibitors - therapeutic use | Quinazolines - therapeutic use | Feedback, Physiological - drug effects | Receptor, Insulin - metabolism | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Benzylamines - pharmacology | Benzylamines - therapeutic use | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
Journal Article
Cell, ISSN 0092-8674, 2007, Volume 128, Issue 2, pp. 257 - 267
Assembly of the eIF4E/eIF4G complex has a central role in the regulation of gene expression at the level of translation initiation. This complex is regulated... 
FACTOR EIF-4E | HUMAN-DISEASE | MALIGNANT-TRANSFORMATION | CAP-DEPENDENT TRANSLATION | MESSENGER-RNA CAP | BIOCHEMISTRY & MOLECULAR BIOLOGY | BINDING PROTEIN EIF4E | EUKARYOTIC TRANSLATION | SECONDARY STRUCTURE | MTOR INHIBITORS | CANCER-THERAPY | CELL BIOLOGY | Protein Binding - genetics | Humans | Nitro Compounds - chemistry | Eukaryotic Initiation Factor-4E - metabolism | Peptide Fragments - pharmacology | Eukaryotic Initiation Factor-4G - drug effects | Eukaryotic Initiation Factor-4G - metabolism | Fluorescence Polarization Immunoassay - methods | Thiazoles - isolation & purification | Antineoplastic Agents - isolation & purification | Cell Transformation, Neoplastic - genetics | Protein Binding - drug effects | Nitro Compounds - pharmacology | Antineoplastic Agents - pharmacology | Protein Biosynthesis - genetics | Gene Expression Regulation, Neoplastic - drug effects | Eukaryotic Initiation Factor-4E - genetics | Peptide Fragments - genetics | Gene Expression Regulation, Neoplastic - genetics | RNA, Messenger - drug effects | Drug Evaluation, Preclinical - methods | Oncogenes - genetics | Peptide Fragments - metabolism | Jurkat Cells | RNA, Messenger - genetics | Hydrazones | Models, Molecular | Antineoplastic Agents - chemistry | Cell Transformation, Neoplastic - metabolism | Eukaryotic Initiation Factor-4E - drug effects | Nitro Compounds - isolation & purification | Animals | Cell Line, Tumor | Oncogenes - drug effects | Feedback, Physiological - drug effects | Protein Biosynthesis - drug effects | Thiazoles - chemistry | Eukaryotic Initiation Factor-4G - genetics | Mice | Thiazoles - pharmacology | Cell Transformation, Neoplastic - drug effects | Feedback, Physiological - physiology | Cell Line, Transformed | Index Medicus | Peptide Fragments | Protein Biosynthesis | Gene Expression Regulation, Neoplastic | Eukaryotic Initiation Factor-4E | Chemical Sciences | Fluorescence Polarization Immunoassay | Life Sciences | Thiazoles | Drug Evaluation, Preclinical | Feedback, Biochemical | Oncogenes | Analytical chemistry | Biochemistry, Molecular Biology | Antineoplastic Agents | Organic chemistry | Eukaryotic Initiation Factor-4G | Cell Transformation, Neoplastic | Nitro Compounds | Protein Binding | RNA, Messenger
Journal Article