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Nature, ISSN 0028-0836, 2012, Volume 486, Issue 7405, pp. 114 - 118
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 1/2013, Volume 110, Issue 3, pp. 972 - 977
Metformin, the first-line drug for treating diabetes, inhibits cellular transformation and selectively kills cancer stem cells in breast cancer cell lines. In... 
T lymphocytes | Cell growth | Phosphorylation | Stem cells | Cell lines | Breast cancer | Diabetes | Heterologous transplantation | Tumors | Cancer | Cancer treatment | Cancer prevention | Inflammation | cancer treatment | RESPIRATORY-CHAIN | METABOLIC SYNDROME | ACTIVATION | cancer prevention | PROTEIN-KINASE | MULTIDISCIPLINARY SCIENCES | CYCLE ARREST | DECREASES | CHEMOTHERAPY | BREAST-CANCER | DIABETIC-PATIENTS | inflammation | AMPK | Inflammation - pathology | Neoplastic Stem Cells - drug effects | Humans | NF-kappa B - metabolism | Breast Neoplasms - metabolism | Inflammation - metabolism | Hypoglycemic Agents - administration & dosage | Neoplastic Stem Cells - metabolism | Anticarcinogenic Agents - administration & dosage | Neoplastic Stem Cells - pathology | Female | Stress, Physiological - drug effects | Metformin - administration & dosage | Anticarcinogenic Agents - pharmacology | STAT3 Transcription Factor - metabolism | Doxorubicin - administration & dosage | Cell Line | Metformin - pharmacology | Breast Neoplasms - drug therapy | Cell Transformation, Neoplastic - metabolism | Hypoglycemic Agents - pharmacology | Xenograft Model Antitumor Assays | Animals | Breast Neoplasms - pathology | Mice, Nude | Cell Line, Tumor | Feedback, Physiological - drug effects | Inflammation - prevention & control | Mice | Cell Transformation, Neoplastic - drug effects | Cell Transformation, Neoplastic - pathology | Prevention | Cancer cells | Physiological aspects | Dosage and administration | Hypoglycemic agents | Metformin | Research | Cell transformation | Health aspects | Signal transduction | Metabolism | Index Medicus | Biological Sciences
Journal Article
Nature, ISSN 0028-0836, 03/2012, Volume 483, Issue 7390, pp. 484 - 488
Journal Article
Nature, ISSN 0028-0836, 01/2010, Volume 463, Issue 7279, pp. 318 - 325
The inference of transcriptional networks that regulate transitions into physiological or pathological cellular states remains a central challenge in systems... 
SURVIVAL | GROWTH-FACTOR RECEPTOR | NEURAL STEM-CELLS | GLIOBLASTOMA | MULTIDISCIPLINARY SCIENCES | DISEASE | C-MYC | MECHANISMS | DIFFERENTIATION | EXPRESSION | BINDING | Neurons - pathology | Prognosis | Glioma - diagnosis | Humans | Brain Neoplasms - pathology | Gene Expression Regulation, Neoplastic | Gene Regulatory Networks | Glioma - genetics | Cell Differentiation - genetics | Cell Transformation, Neoplastic - genetics | Neoplasm Invasiveness - pathology | Glioma - pathology | Transcription, Genetic | Neurons - metabolism | Cellular Reprogramming - genetics | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Reproducibility of Results | Brain Neoplasms - diagnosis | CCAAT-Enhancer-Binding Protein-beta - genetics | Computational Biology | Brain Neoplasms - genetics | Mesenchymal Stromal Cells - metabolism | Mice, SCID | Cell Transformation, Neoplastic - metabolism | CCAAT-Enhancer-Binding Protein-beta - metabolism | Animals | Cell Line, Tumor | Mice, Inbred NOD | Mesoderm - metabolism | Mice | Mesenchymal Stromal Cells - pathology | Cell Transformation, Neoplastic - pathology | Neoplasm Invasiveness - genetics | Mesoderm - pathology | Transcription factors | Gliomas | Physiological aspects | Genetic aspects | Research | Genetic transcription | Risk factors | Proteins | Genotype & phenotype | Brain | Reverse engineering | Brain cancer | Regression analysis | Gene expression | Index Medicus
Journal Article
STEM CELLS, ISSN 1066-5099, 04/2014, Volume 32, Issue 4, pp. 983 - 997
Journal Article
Nature, ISSN 0028-0836, 07/2011, Volume 475, Issue 7354, pp. 106 - 110
Reactive oxygen species (ROS) are mutagenic and may thereby promote cancer(1). Normally, ROS levels are tightly controlled by an inducible antioxidant program... 
TRANSFORMATION | OXIDATIVE STRESS | ACTIVATION | INHIBITION | K-RAS | PATHWAY | MULTIDISCIPLINARY SCIENCES | PANCREATIC-CANCER | HEME OXYGENASE-1 | MUTATIONS | EXPRESSION | NIH 3T3 Cells | Cell Proliferation | Pancreatic Neoplasms - metabolism | Reactive Oxygen Species - metabolism | Cytoskeletal Proteins - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Antioxidants - metabolism | Humans | JNK Mitogen-Activated Protein Kinases - metabolism | Intracellular Signaling Peptides and Proteins - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Cell Transformation, Neoplastic - genetics | Cytoskeletal Proteins - metabolism | NF-E2-Related Factor 2 - genetics | Intracellular Signaling Peptides and Proteins - genetics | Kelch-Like ECH-Associated Protein 1 | Proto-Oncogene Proteins B-raf - metabolism | Fibroblasts - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Oncogenes - genetics | Oxidation-Reduction | Pancreatic Neoplasms - pathology | Cells, Cultured | Pancreatic Neoplasms - genetics | NF-E2-Related Factor 2 - deficiency | Cell Transformation, Neoplastic - metabolism | Animals | Proto-Oncogene Proteins B-raf - genetics | Genes, myc - genetics | NF-E2-Related Factor 2 - metabolism | Adaptor Proteins, Signal Transducing - genetics | Alleles | Cell Line, Tumor | Mice | Adaptor Proteins, Signal Transducing - metabolism | Cell Transformation, Neoplastic - pathology | Polymerase chain reaction | Usage | Reactive oxygen species | Physiological aspects | Research | Gene expression | Oncogenes | Studies | Mass spectrometry | Rodents | Evacuations & rescues | Cancer | Index Medicus
Journal Article
Genes and Development, ISSN 0890-9369, 01/2009, Volume 23, Issue 1, pp. 24 - 36
Journal Article
Journal Article