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Gastroenterology, ISSN 0016-5085, 2014, Volume 147, Issue 5, pp. 1119 - 1133.e4
Background & Aims Although smoking is a leading risk factor for pancreatic ductal adenocarcinoma (PDAC), little is known about the mechanisms by which smoking... 
Gastroenterology and Hepatology | Metastasis | Pancreas | Progenitor Cells | Mouse Model | METFORMIN | STEM-CELLS | DUCTAL ADENOCARCINOMA | PROLIFERATION | EPITHELIAL-MESENCHYMAL TRANSITION | ADULT-MOUSE PANCREAS | ACETYLCHOLINE-RECEPTORS | K-RAS | GROWTH | DIFFERENTIATION | GASTROENTEROLOGY & HEPATOLOGY | Pancreatic Neoplasms - metabolism | Neoplastic Stem Cells - drug effects | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Carcinoma, Pancreatic Ductal - metabolism | Epithelial-Mesenchymal Transition - drug effects | Mice, 129 Strain | Carcinoma, Pancreatic Ductal - genetics | Neoplastic Stem Cells - metabolism | Time Factors | Cell Transformation, Neoplastic - genetics | Neoplastic Stem Cells - pathology | Pancreatic Neoplasms - chemically induced | Liver Neoplasms - secondary | Nicotinic Agonists - toxicity | Proto-Oncogene Proteins c-akt - metabolism | Neoplastic Cells, Circulating - drug effects | GATA6 Transcription Factor - deficiency | Liver Neoplasms - genetics | Pancreatic Neoplasms - pathology | Pancreas - pathology | alpha7 Nicotinic Acetylcholine Receptor - genetics | Pancreas - metabolism | Mice, Knockout | Acinar Cells - pathology | Signal Transduction - drug effects | Mice, Nude | Liver Neoplasms - metabolism | Cell Line, Tumor | alpha7 Nicotinic Acetylcholine Receptor - metabolism | Mutation | Carcinoma, Pancreatic Ductal - secondary | Carcinoma, Pancreatic Ductal - chemically induced | Neoplastic Cells, Circulating - pathology | Neoplastic Cells, Circulating - metabolism | Cell Transformation, Neoplastic - chemically induced | Extracellular Signal-Regulated MAP Kinases - metabolism | Carcinoma, Pancreatic Ductal - prevention & control | Tumor Suppressor Protein p53 - genetics | Transfection | Proto-Oncogene Proteins p21(ras) - deficiency | Gene Expression Regulation, Neoplastic - drug effects | Pancreatic Neoplasms - prevention & control | Tumor Cells, Cultured | Proto-Oncogene Proteins p21(ras) - metabolism | Acinar Cells - metabolism | Cell Dedifferentiation - drug effects | Metformin - pharmacology | Mice, Inbred C57BL | Tumor Suppressor Protein p53 - metabolism | Pancreas - drug effects | Pancreatic Neoplasms - genetics | Nicotine - toxicity | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | GATA6 Transcription Factor - metabolism | Animals | Acinar Cells - drug effects | GATA6 Transcription Factor - genetics | Cell Transformation, Neoplastic - pathology | Pancreatic cancer | Stem cells | Nicotine
Journal Article
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2012, 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... 
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 | Biological Sciences
Journal Article
Genes & development, ISSN 0890-9369, 2009, Volume 23, Issue 1, pp. 24 - 36
Journal Article
Cancer cell, ISSN 1535-6108, 2015, Volume 28, Issue 6, pp. 800 - 814
The regulation and stem cell origin of normal and neoplastic gastric glands are uncertain... 
CARCINOMA-CELLS | PROGENITOR CELLS | CHIEF CELLS | MAINTENANCE | ONCOLOGY | MOUSE STOMACH | INNATE LYMPHOID-CELLS | E-CADHERIN | BONE | INTRAEPITHELIAL NEOPLASIA | CANCER | CELL BIOLOGY | Epithelial Cells - metabolism | Cadherins - metabolism | Neoplastic Stem Cells - drug effects | Epithelial Cells - drug effects | Humans | Stomach Neoplasms - metabolism | Tumor Microenvironment | Gastric Mucosa - pathology | Male | Stomach Neoplasms - pathology | Wnt-5a Protein | Gastric Mucosa - metabolism | Wnt Proteins - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Neoplastic Stem Cells - metabolism | Time Factors | Cell Transformation, Neoplastic - genetics | Cellular Senescence | Bone Marrow Transplantation | Gastric Mucosa - drug effects | Neoplastic Stem Cells - pathology | Antineoplastic Agents - pharmacology | Wnt Signaling Pathway | Lymphocytes - metabolism | Stomach Neoplasms - genetics | Basic Helix-Loop-Helix Transcription Factors - genetics | Stem Cell Niche | Signal Transduction | Endothelial Cells - metabolism | Cell Communication | Epithelial Cells - pathology | Mice, Transgenic | Stomach Neoplasms - drug therapy | Cell Transformation, Neoplastic - metabolism | Receptors, CXCR4 - metabolism | Cell Lineage | Lymphocytes - pathology | Animals | Chemokine CXCL12 - metabolism | rho GTP-Binding Proteins - metabolism | Cell Line, Tumor | Anoikis | Mice | Cell Transformation, Neoplastic - pathology | Endothelial Cells - pathology | Antimitotic agents | Medical colleges | Antineoplastic agents | Liver | Stem cells | Microbiology
Journal Article
Molecular cell, ISSN 1097-2765, 2016, Volume 62, Issue 4, pp. 479 - 490
Journal Article
Nature (London), ISSN 1476-4687, 2009, Volume 463, Issue 7279, pp. 318 - 325
.... Two transcription factors (C/EBP beta and STAT3) emerge as synergistic initiators and master regulators of mesenchymal transformation... 
SURVIVAL | GROWTH-FACTOR RECEPTOR | MULTIDISCIPLINARY SCIENCES | C-MYC | MECHANISMS | PROLIFERATION | NEURAL STEM-CELL | DIFFERENTIATION | EXPRESSION | BINDING | GLIOGENESIS | 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
Journal Article
Nature (London), ISSN 1476-4687, 2012, Volume 483, Issue 7390, pp. 484 - 488
Journal Article
Oncogene, ISSN 1476-5594, 2014, Volume 34, Issue 37, pp. 4821 - 4833
Journal Article