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American Journal of Pathology, The, ISSN 0002-9440, 2012, Volume 181, Issue 6, pp. 2188 - 2201
Journal Article
Gastroenterology, ISSN 0016-5085, 2011, Volume 141, Issue 1, pp. 279 - 291.e5
...; we investigated genes associated with stem cell–like features of colorectal cancer (CRC) cells. Methods We isolated colonospheres from primary CRC tissues and cell lines and characterized their gene expression patterns by microarray analysis... 
Gastroenterology and Hepatology | Gene Regulation | Tumor Development | Systems Biology | Colon Cancer | A33 ANTIGEN | TRANSCRIPTION FACTOR SNAIL | E-CADHERIN | NECK-CANCER | TUMOR-INITIATING CELLS | EPITHELIAL-MESENCHYMAL TRANSITION | HUMAN COLON-CANCER | PROSTATE-CANCER | GENE-EXPRESSION | GASTROENTEROLOGY & HEPATOLOGY | PROGRESSION | Interleukin-8 - genetics | Oligonucleotide Array Sequence Analysis | Neoplastic Stem Cells - drug effects | Colorectal Neoplasms - genetics | Humans | Middle Aged | Radiation Tolerance | Drug Resistance, Neoplasm | Epithelial-Mesenchymal Transition - drug effects | Fetal Proteins - metabolism | Antigens, CD - metabolism | Neoplastic Stem Cells - metabolism | Time Factors | Colorectal Neoplasms - drug therapy | Hyaluronan Receptors - metabolism | Aged, 80 and over | Neoplastic Stem Cells - pathology | Antimetabolites, Antineoplastic - pharmacology | Interleukin-8 - metabolism | Signal Transduction - radiation effects | Binding Sites | Carcinoma - drug therapy | Colorectal Neoplasms - immunology | Signal Transduction - drug effects | Mice, Nude | Carcinoma - genetics | Fluorouracil - pharmacology | Mice | Interleukin-8 - immunology | Dose-Response Relationship, Radiation | Gene Expression Regulation, Neoplastic | Neoplastic Stem Cells - immunology | Dose-Response Relationship, Drug | Transfection | Adult | Cell Adhesion Molecules, Neuronal - metabolism | Tumor Cells, Cultured | Carcinoma - pathology | Spheroids, Cellular | Snail Family Transcription Factors | Colorectal Neoplasms - metabolism | Neoplastic Stem Cells - radiation effects | Carcinoma - immunology | Gene Expression Profiling - methods | Transcription Factors - genetics | E-Box Elements | Antibodies - pharmacology | HT29 Cells | Transcription Factors - metabolism | Xenograft Model Antitumor Assays | Animals | Tumor Burden - drug effects | Aged | Cell Proliferation - drug effects | Carcinoma - metabolism | Colorectal Neoplasms - pathology | Antigen-antibody reactions | Developmental biology | Antibodies | Development and progression | Viral antibodies | Anopheles | Colon cancer | Epidermal growth factor | Interleukins | Stem cells | Genetic research | Fibroblast growth factors | Universities and colleges | Tumors
Journal Article
PloS one, ISSN 1932-6203, 2011, Volume 6, Issue 8, p. e24099
...) and HDAC inhibitor Vorinostat (SAHA). Methodology/ Principal Findings: Re-expression of miR-34a in human pancreatic cancer stem cells (CSCs... 
BIOMARKERS | NERVOUS-SYSTEM | APOPTOSIS | TRAIL | SIGNALING PATHWAY | P53 PROTEIN | MULTIDISCIPLINARY SCIENCES | NOTCH | TUMOR-SUPPRESSOR | MICRORNAS | EXPRESSION | 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 | 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 | miRNA | Inducers | Departments | Caspase | Pharmacology | Breast cancer | Tumor cell lines | Ribonucleic acid--RNA | Medicine | Cyclin-dependent kinase inhibitor p21 | Medical prognosis | Reagents | Epigenetics | Cyclin-dependent kinase inhibitor p27 | Prostate cancer | RNA | Ribonucleic acid
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 4, p. e18784
Background: The aggressiveness of melanoma tumors is likely to rely on their well-recognized heterogeneity and plasticity. Melanoma comprises... 
INITIATING CELLS | IN-VITRO | ACTIVATION | METASTASIS | MULTIDISCIPLINARY SCIENCES | B-16 MELANOMA | PHENOTYPE | LIGAND | EXPRESSION | CANCER STEM-CELLS | MHC CLASS-II | Embryonic Stem Cells - metabolism | Immunomodulation - drug effects | Transcription, Genetic - drug effects | Neoplastic Stem Cells - drug effects | Genes, Neoplasm | Humans | Neural Crest - pathology | Spheroids, Cellular - pathology | Gene Expression Profiling | Cell Lineage - drug effects | Neural Crest - metabolism | Neoplastic Stem Cells - metabolism | Melanoma - genetics | Neoplastic Stem Cells - pathology | Spheroids, Cellular - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Tumor Cells, Cultured | Neoplasm Invasiveness | Spheroids, Cellular - metabolism | Melanoma - pathology | Neural Crest - drug effects | Pluripotent Stem Cells - metabolism | Transcription Factors - metabolism | Cell Movement - drug effects | Phenotype | Embryonic Stem Cells - drug effects | Cell Differentiation - drug effects | Melanoma - immunology | Pluripotent Stem Cells - drug effects | Culture Media - pharmacology | Cell Proliferation - drug effects | Metastasis | T cells | Gene expression | Analysis | Stem cells | Cancer | Cell proliferation | Transcription factors | Mesenchyme | Oct-4 protein | Lymphocytes T | Activation | Assaying | Immunity | Metastases | Skin cancer | Heterogeneity | Genotype & phenotype | Cell activation | KLF4 protein | Lymphocytes | Mathematical models | Immune system | Subpopulations | Antigens | Aggressive behavior | Cytokines | Immunomodulation | Tumor cells | Invasiveness | Melanoma | Tumorigenicity | Neural crest | Embryos | Spheroids | Studies | Ligands | Prostate cancer | Cell migration | Chemokines | Tumors | Apoptosis | Cell Proliferation | Gene Expression Regulation, Neoplastic | Neoplastic Stem Cells | Cellular Biology | Neural Crest | Life Sciences | Cell Lineage | Pluripotent Stem Cells | Culture Media | Transcription, Genetic | Cell Differentiation | Transcription Factors | Embryonic Stem Cells | Spheroids, Cellular | Cell Movement
Journal Article
Biomaterials, ISSN 0142-9612, 2012, Volume 33, Issue 5, pp. 1462 - 1476
.... However, the role of miRNAs in GBM-associated CSCs remains mostly unclear. In this study, our miRNA/mRNA-microarray and RT-PCR analysis showed that the expression of miR145... 
Advanced Basic Science | Dentistry | miR145 | Drug-resistance | Polyurethane-short branch polyethylenimine | Glioblastoma | MiR145 | LUNG | MATERIALS SCIENCE, BIOMATERIALS | ENGINEERING, BIOMEDICAL | GLIOMA | TRANSFECTION EFFICIENCY | IDENTIFICATION | SOX2 | OCT4 | RESISTANCE | CHEMORESISTANCE | EXPRESSION | CD133 | Dacarbazine - therapeutic use | Neoplastic Stem Cells - drug effects | Humans | Middle Aged | 3' Untranslated Regions - genetics | Molecular Sequence Data | Polyurethanes - chemical synthesis | Male | MicroRNAs - metabolism | Gene Expression Profiling | Glioblastoma - radiotherapy | SOXB1 Transcription Factors - metabolism | Glioblastoma - genetics | Neoplastic Stem Cells - metabolism | Dacarbazine - pharmacology | Base Sequence | Polyethyleneimine - chemistry | Dacarbazine - analogs & derivatives | Neoplastic Stem Cells - pathology | Female | Gene Expression Regulation, Neoplastic - drug effects | Polyethyleneimine - chemical synthesis | Gene Transfer Techniques | Polyurethanes - chemistry | Down-Regulation - drug effects | Down-Regulation - genetics | Radiation Tolerance - drug effects | Polyethyleneimine - analogs & derivatives | Glioblastoma - pathology | Octamer Transcription Factor-3 - metabolism | Aged | MicroRNAs - genetics | Cell Transformation, Neoplastic - drug effects | Cell Transformation, Neoplastic - pathology | Glioblastoma - drug therapy | Drug Resistance, Neoplasm - drug effects | Medical colleges | Care and treatment | Biological products | Brain tumors | Genes | Drug resistance | Prevention | MicroRNA | Gliomas | Nuclear radiation | Analysis | Stem cells | Cancer
Journal Article
PLoS ONE, ISSN 1932-6203, 01/2015, Volume 10, Issue 1, p. e0116747
Cellular mechanisms of multidrug resistance (MDR) are related to ABC transporters, apoptosis, antioxidation, drug metabolism, DNA repair and cell proliferation... 
EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER CELLS | STEM-CELLS | MDR1 | TRANSPORTERS | MULTIDISCIPLINARY SCIENCES | DOWN-REGULATION | MUTANT P53 | TUMOR-SUPPRESSOR PROTEIN | DRUG-RESISTANCE | OVARIAN-CANCER | Apoptosis - drug effects | Neoplastic Stem Cells - drug effects | Drug Resistance, Multiple - drug effects | Genes, Neoplasm | Humans | Apoptosis - genetics | Epithelial-Mesenchymal Transition - drug effects | Gene Expression Profiling | DNA Repair - genetics | Epithelial-Mesenchymal Transition - genetics | Neoplasm Proteins - metabolism | Dose-Response Relationship, Drug | MCF-7 Cells | Neoplastic Stem Cells - metabolism | Inhibitory Concentration 50 | Gene Expression Regulation, Neoplastic - drug effects | Neoplasm Proteins - genetics | DNA Repair - drug effects | Drug Resistance, Multiple - genetics | Tumor Suppressor Protein p53 - metabolism | Signal Transduction - genetics | Down-Regulation - drug effects | Cell Shape - drug effects | Up-Regulation - drug effects | Drug Resistance, Neoplasm - genetics | Breast Neoplasms - genetics | Signal Transduction - drug effects | Doxorubicin - pharmacology | Drug Resistance, Neoplasm - drug effects | Physiological aspects | Drug resistance in microorganisms | Anthracyclines | Tumor proteins | Intermediate filament proteins | Genes | Cell proliferation | Transcription | Bcl-2 protein | Mesenchyme | Gene regulation | Cytology | AKT protein | Cytotoxicity | Drug resistance | Kinases | DNA repair | Cancer therapies | Doxorubicin | Cell surface | E-cadherin | Cell morphology | Proteins | MDR1 protein | Clonal deletion | CD44 antigen | Rodents | Cell cycle | Drug metabolism | Repair | Drug dosages | Pharmaceutical sciences | Deoxyribonucleic acid--DNA | Glutathione | Enzymes | Ploidy | BRCA1 protein | Multidrug resistance | Breast cancer | Gene expression | Metabolism | 1-Phosphatidylinositol 3-kinase | Medicine | Hypotheses | Chemotherapy | Gene amplification | Pharmacy | Stem cells | Mutation | Codons | Surface markers | Apoptosis | Tumors | Deoxyribonucleic acid | DNA
Journal Article
Nature (London), ISSN 1476-4687, 2015, Volume 529, Issue 7584, pp. 110 - 114
...). Genomic alterations that remove CTCF-associated boundaries allow aberrant enhancer-gene interactions and alter gene expression (17). Since CTCF binding is methylation... 
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
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2013, Volume 8, Issue 11, p. e80883
.... This effect was associated with reduced expressions of MMP-2 and TIMP-2 mRNA and protein levels... 
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 | Plant-based foods | Food | Kaempferol | Activator protein 1 | Melanoma | Extracellular signal-regulated kinase | c-Jun protein | Plant protection | Breast cancer | Gene expression | Gelatinase A | Signaling | Bone cancer | Chemotherapy | Flavonoids | Hospitals | Molecular modelling | Cell migration | Apoptosis
Journal Article
Toxicology and applied pharmacology, ISSN 0041-008X, 2015, Volume 282, Issue 1, pp. 9 - 19
The incidence of lung diseases, including cancer, caused by cigarette smoke is increasing, but the molecular mechanisms of gene regulation induced by cigarette smoke remain unclear... 
lncRNAs | Epithelial-mesenchymal transition (EMT) | Inflammation | Cancer stem cells (CSCs) | Carcinogenesis | Cigarette smoke extract (CSE) | LncRNAs | BLADDER-CANCER | HUMAN-DISEASE | METASTASIS | STAT3 | IL-6 SECRETION | EMT | LUNG-CANCER | SIGNALING PATHWAY | POOR-PROGNOSIS | IncRNAs | PHARMACOLOGY & PHARMACY | TOXICOLOGY | EXPRESSION | Smoking - adverse effects | Up-Regulation | Epithelial Cells - metabolism | Neoplastic Stem Cells - drug effects | Epithelial Cells - drug effects | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Epithelial-Mesenchymal Transition - drug effects | Lung Neoplasms - pathology | Autocrine Communication - drug effects | Dose-Response Relationship, Drug | Transfection | Lung Neoplasms - etiology | Neoplastic Stem Cells - metabolism | RNA Interference | Time Factors | Cell Transformation, Neoplastic - genetics | Neoplastic Stem Cells - pathology | Female | Lung - metabolism | Interleukin-6 - metabolism | STAT3 Transcription Factor - metabolism | Lung Neoplasms - genetics | Lung - pathology | Smoke - adverse effects | Epithelial Cells - pathology | RNA, Long Noncoding - genetics | Cell Transformation, Neoplastic - metabolism | Animals | Signal Transduction - drug effects | Mice, Nude | Lung - drug effects | Mice | Cell Transformation, Neoplastic - pathology | RNA, Long Noncoding - metabolism | Cell Line, Transformed | Antisense RNA | Stem cells | Cancer | Smoking | Index Medicus | ANTIBODIES | TOBACCO SMOKES | CARCINOGENESIS | NEOPLASMS | RNA | CELL CULTURES | INFLAMMATION | LUNGS | STEM CELLS | GENE REGULATION | 60 APPLIED LIFE SCIENCES
Journal Article