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Cancer cell, ISSN 1535-6108, 2002
Journal
International journal of cancer, ISSN 0020-7136, 2018, Volume 143, Issue 8, pp. 1994 - 2007
...‐associated inflammation, including macrophage infiltration. But knowledge of early interactions between neoplastic epithelium and macrophages in PDA carcinogenesis is limited... 
macrophage | PEDF | KRAS | pancreas cancer | CELLS | ONCOGENIC KRAS | IFN-GAMMA | RECEPTOR | CANCER | PIGMENT-EPITHELIUM | INDUCED EXPRESSION | ONCOLOGY | INFLAMMATION | NITRIC-OXIDE | TUMOR-ASSOCIATED MACROPHAGES | Epithelial Cells - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Carcinoma, Pancreatic Ductal - genetics | Cell Transformation, Neoplastic - genetics | Female | Precancerous Conditions - pathology | Cell Proliferation - genetics | Macrophages - pathology | Pancreatic Neoplasms - pathology | Carcinogenesis - genetics | Pancreas - pathology | Epithelial Cells - pathology | Pancreatic Neoplasms - genetics | Pancreas - metabolism | Mice, SCID | Mutation - genetics | Carcinoma, Pancreatic Ductal - pathology | Precancerous Conditions - genetics | Carcinogenesis - pathology | Macrophages - metabolism | Animals | Cell Line, Tumor | Mice, Inbred NOD | RAW 264.7 Cells | Mice | Cell Transformation, Neoplastic - pathology | Antimitotic agents | Medical research | Pancreatic cancer | Analysis | Genes | Genomics | Medicine, Experimental | Genetic aspects | Antineoplastic agents | Macrophages | Gene expression | Financial disclosure | Cell proliferation | Adenocarcinoma | Phenotypes | Transformation | Epithelial cells | Genomes | Epithelium | Carcinogenesis | Metastases | Genotype & phenotype | Carcinogens | Organoids | Infiltration | Mutation | Pancreas | Cancer | Tumors | Index Medicus | Pancreas cancer
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
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
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
The EMBO journal, ISSN 1460-2075, 2015, Volume 34, Issue 7, pp. 856 - 880
Journal Article