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eJournal
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
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
Cancer cell, ISSN 1535-6108, 2017, Volume 32, Issue 3, pp. 360 - 376.e6
We define how chronic cigarette smoke-induced time-dependent epigenetic alterations can sensitize human bronchial epithelial cells for transformation by a single oncogene... 
genetic | lung cancer | epigenetic | polycomb | addiction | DNA methylation | cigarette smoke exposure | Kras | human bronchial epithelial cells | oncogene | HBECs | LUNG-CANCER | TRANSLATIONAL IMPLICATIONS | GENOMIC LANDSCAPE | ONCOLOGY | DNA HYPERMETHYLATION | COLORECTAL-CANCER | EXPRESSION PROFILES | NEVER-SMOKERS | LARGE GENE LISTS | WNT | EPIGENETIC ALTERATIONS | CELL BIOLOGY | Sirtuin 1 - metabolism | Smoking - adverse effects | Chromatin - metabolism | Epithelial Cells - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Gene Expression Regulation, Neoplastic | Lung Neoplasms - pathology | Male | Epithelial-Mesenchymal Transition - genetics | Promoter Regions, Genetic - genetics | DNA (Cytosine-5-)-Methyltransferases - metabolism | Cell Transformation, Neoplastic - genetics | Bronchi - pathology | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Cell Proliferation - genetics | Enhancer of Zeste Homolog 2 Protein - metabolism | Epigenomics | Carcinoma, Non-Small-Cell Lung - genetics | DNA (Cytosine-5-)-Methyltransferase 1 | Epithelial Cells - pathology | Smoking - genetics | DNA Methylation - genetics | Signal Transduction - genetics | Mutation - genetics | Phenotype | Animals | Mice | DNA Damage | Cell Transformation, Neoplastic - pathology | Genome, Human | Epigenetic inheritance | Chromatin | Gene mutations | Stem cells | Genetic aspects | Lung cancer, Non-small cell | Methylation | Smoking | Medical colleges | Anopheles | Genes | Cellular signal transduction
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
Molecular cell, ISSN 1097-2765, 2016, Volume 62, Issue 4, pp. 479 - 490
Journal Article
by Alexandrov, Ludmil B and Nik-Zainal, Serena and Wedge, David C and Aparicio, Samuel A. J. R and Behjati, Sam and Biankin, Andrew V and Bignell, Graham R and Bolli, Niccolò and Borg, Ake and Børresen-Dale, Anne-Lise and Boyault, Sandrine and Burkhardt, Birgit and Butler, Adam P and Caldas, Carlos and Davies, Helen R and Desmedt, Christine and Eils, Roland and Eyfjörd, Jórunn Erla and Foekens, John A and Greaves, Mel and Hosoda, Fumie and Hutter, Barbara and Ilicic, Tomislav and Imbeaud, Sandrine and Imielinski, Marcin and Jäger, Natalie and Jones, David T. W and Jones, David and Knappskog, Stian and Kool, Marcel and Lakhani, Sunil R and López-Otín, Carlos and Martin, Sancha and Munshi, Nikhil C and Nakamura, Hiromi and Northcott, Paul A and Pajic, Marina and Papaemmanuil, Elli and Paradiso, Angelo and Pearson, John V and Puente, Xose S and Raine, Keiran and Ramakrishna, Manasa and Richardson, Andrea L and Richter, Julia and Rosenstiel, Philip and Schlesner, Matthias and Schumacher, Ton N and Span, Paul N and Teague, Jon W and Totoki, Yasushi and Tutt, Andrew N. J and Valdés-Mas, Rafael and van Buuren, Marit M and van ’t Veer, Laura and Vincent-Salomon, Anne and Waddell, Nicola and Yates, Lucy R and Zucman-Rossi, Jessica and Andrew Futreal, P and McDermott, Ultan and Lichter, Peter and Meyerson, Matthew and Grimmond, Sean M and Siebert, Reiner and Campo, Elías and Shibata, Tatsuhiro and Pfister, Stefan M and Campbell, Peter J and Stratton, Michael R and ICGC MMML-Seq Consortium and ICGC PedBrain and ICGC Breast Cancer Consortium and Australian Pancreatic Cancer Genome Initiative and ICGC Breast Canc Consortium and Australian Pancreatic Canc Genome
Nature (London), ISSN 1476-4687, 2013, Volume 500, Issue 7463, pp. 415 - 421
Journal Article