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Gastroenterology, ISSN 0016-5085, 2008, Volume 134, Issue 2, pp. 511 - 522
Background & Aims: Loss of gastric parietal cells is a critical precursor to gastric metaplasia and neoplasia. However, the origin of metaplasia remains... 
Gastroenterology and Hepatology | OXYNTIC ATROPHY | LOCALIZATION | COMPLEX | ZYMOGENIC CELLS | ADENOCARCINOMA | RISK | INFECTION | DEFICIENT MICE | TISSUES | GASTROENTEROLOGY & HEPATOLOGY | CANCER | Metaplasia - metabolism | Humans | Parietal Cells, Gastric - metabolism | Stomach Neoplasms - metabolism | Gastric Mucosa - pathology | Precancerous Conditions - metabolism | Stomach Neoplasms - pathology | beta-Defensins | Fetal Proteins - metabolism | Gastric Mucosa - metabolism | Stomach Neoplasms - physiopathology | Minichromosome Maintenance Complex Component 3 | Atrophy | DNA-Binding Proteins - metabolism | Peptides - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Mucins - metabolism | Muscle Proteins - metabolism | Precancerous Conditions - pathology | Trefoil Factor-2 | Gastric Fundus - metabolism | Chief Cells, Gastric - metabolism | Mice, Inbred C57BL | Cell Cycle Proteins - metabolism | Microtubule-Associated Proteins | Nuclear Proteins - metabolism | Gastrins - metabolism | Cell Transformation, Neoplastic - metabolism | Metaplasia - pathology | Mice, Knockout | Animals | Carrier Proteins - metabolism | Parietal Cells, Gastric - pathology | Epididymal Secretory Proteins - metabolism | Chief Cells, Gastric - pathology | Mice | Cell Transformation, Neoplastic - pathology | Gastric Fundus - pathology | Intrinsic Factor - metabolism | Vasoactive intestinal peptides | Analysis | Polypeptides
Journal Article
Molecular cell, ISSN 1097-2765, 2010, Volume 39, Issue 4, pp. 493 - 506
A transient inflammatory signal can initiate an epigenetic switch from nontransformed to cancer cells via a positive feedback loop involving NF-κB, Lin28,... 
RNA | HUMDISEASE | SIGNALING | Signaling | Humdisease | BREAST-CANCER | MICRORNA MIR-21 | TARGET | TRANSFORMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | EMBRYONIC STEM-CELLS | LET-7 | IDENTIFICATION | NF-KAPPA-B | EXPRESSION | BINDING | CELL BIOLOGY | Colonic Neoplasms - genetics | Cell Proliferation | Epigenesis, Genetic | Humans | Transcriptional Activation | MicroRNAs - metabolism | NF-kappa B - metabolism | Colonic Neoplasms - metabolism | Inflammation - metabolism | Adenocarcinoma - metabolism | RNA Interference | Cell Transformation, Neoplastic - genetics | Proto-Oncogene Proteins c-akt - metabolism | Binding Sites | Colonic Neoplasms - therapy | Tumor Suppressor Proteins - metabolism | Signal Transduction | HCT116 Cells | Computational Biology | Mammary Glands, Human - pathology | Tumor Burden | Breast Neoplasms - genetics | Adenocarcinoma - therapy | Mice, Nude | Mice | Proto-Oncogene Proteins c-myc - genetics | Kinetics | Cell Movement | Deubiquitinating Enzyme CYLD | Gene Expression Regulation, Neoplastic | Mammary Glands, Human - metabolism | Breast Neoplasms - metabolism | Transfection | Tumor Suppressor Proteins - genetics | Inflammation Mediators - metabolism | Female | Adenocarcinoma - genetics | STAT3 Transcription Factor - metabolism | Promoter Regions, Genetic | Receptors, Estrogen - genetics | Neoplasm Invasiveness | PTEN Phosphohydrolase - metabolism | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | HT29 Cells | Xenograft Model Antitumor Assays | Algorithms | Animals | Breast Neoplasms - pathology | Inflammation - genetics | Cell Transformation, Neoplastic - pathology | Genes, src | Medical colleges | Inflammation | Colon cancer | Cancer | Adenocarcinoma | microRNAs | cancer | transformation | transcription factors | inflammation | STAT3
Journal Article
Oncogene, ISSN 1476-5594, 2007, Volume 26, Issue 32, pp. 4617 - 4626
Infection with Helicobacter pylori cagA-positive strains is associated with gastric adenocarcinoma. Intestinal metaplasia is a precancerous lesion of the... 
β-catenin | Gastric adenocarcinoma | Helicobacter pylori CagA | E-cadherin | Intestinal metaplasia | beta-catenin | TARGET | ACTIVATION | PROTEIN | CDX1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | CANCER | CELL BIOLOGY | gastric adenocarcinoma | GENE | ONCOLOGY | intestinal metaplasia | WNT PATHWAY | ATROPHIC GASTRITIS | GENETICS & HEREDITY | INFECTION | EXPRESSION | Intestinal Mucosa - metabolism | Phosphorylation | Adenocarcinoma - pathology | Cadherins - metabolism | beta Catenin - analysis | Adenocarcinoma - etiology | Homeodomain Proteins - metabolism | Humans | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Stomach Neoplasms - metabolism | Cytoplasm - metabolism | Gastric Mucosa - pathology | Precancerous Conditions - metabolism | Stomach Neoplasms - pathology | Bacterial Proteins - analysis | Gastric Mucosa - metabolism | Adenocarcinoma - metabolism | Cell Nucleus - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Cell Transformation, Neoplastic - genetics | Mucins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Precancerous Conditions - pathology | Stomach Neoplasms - etiology | Cytoplasm - chemistry | Cell Line | Cadherins - analysis | Cell Transformation, Neoplastic - metabolism | Precancerous Conditions - genetics | beta Catenin - metabolism | Homeodomain Proteins - genetics | Mucin-2 | Tyrosine - metabolism | Antigens, Bacterial - analysis | Bacterial Proteins - metabolism | Cell Nucleus - chemistry | Cell Transformation, Neoplastic - pathology | Antigens, Bacterial - metabolism | Intestinal Mucosa - pathology
Journal Article
The Journal of cell biology, ISSN 1540-8140, 2011, Volume 192, Issue 5, pp. 767 - 780
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 06/2013, Volume 210, Issue 6, pp. 1137 - 1151
Journal Article
Gastroenterology, ISSN 0016-5085, 2014, Volume 146, Issue 7, pp. 1784 - 1794.e6
Background & Aims Premalignant lesions and early stage tumors contain immunosuppressive microenvironments that create barriers for cancer vaccines. Kras G12D/+... 
Gastroenterology and Hepatology | Tumor Microenvironment | Pancreatic Cancer | Listeria Vaccine | Immunity | MONOCYTOGENES | DUCTAL ADENOCARCINOMA | ONCOGENIC KRAS | CANCER | TUMORS | ADOPTIVE TRANSFER | IMMUNOTHERAPY | MOUSE MODEL | TC17 CELLS | SUPPRESSOR-CELLS | GASTROENTEROLOGY & HEPATOLOGY | Pancreatic Neoplasms - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Homeodomain Proteins - metabolism | Humans | Carcinoma, Pancreatic Ductal - metabolism | Interferon-gamma - metabolism | Mice, 129 Strain | Carcinoma, Pancreatic Ductal - genetics | T-Lymphocytes, Regulatory - immunology | Cancer Vaccines - therapeutic use | Carcinoma in Situ - genetics | Time Factors | Forkhead Transcription Factors - metabolism | Listeria monocytogenes - metabolism | Disease Models, Animal | Carcinoma in Situ - pathology | Antibodies, Monoclonal - pharmacology | Pancreatic Neoplasms - pathology | Mice, Transgenic | Disease Progression | Interleukin-17 - metabolism | Cyclophosphamide - pharmacology | Pancreatic Neoplasms - immunology | Mice | Mutation | Carcinoma in Situ - metabolism | T-Lymphocytes, Regulatory - metabolism | Carcinoma in Situ - drug therapy | Carcinoma in Situ - immunology | Listeria monocytogenes - immunology | Tumor Suppressor Protein p53 - genetics | Pancreatic Neoplasms - drug therapy | Inflammation Mediators - metabolism | Trans-Activators - genetics | Integrases - metabolism | Carcinoma, Pancreatic Ductal - immunology | Proto-Oncogene Proteins p21(ras) - metabolism | Mice, Inbred C57BL | Receptors, Chemokine - metabolism | Tumor Suppressor Protein p53 - metabolism | Pancreatic Neoplasms - genetics | Carcinoma, Pancreatic Ductal - pathology | Homeodomain Proteins - genetics | Cancer Vaccines - immunology | Carcinoma, Pancreatic Ductal - drug therapy | Animals | Listeria monocytogenes - genetics | Trans-Activators - metabolism | CD11b Antigen - metabolism | Integrases - genetics | Medical colleges | Vaccines | Listeria | Developmental biology | Pancreatic cancer | Contamination
Journal Article
Nature (London), ISSN 1476-4687, 2014, Volume 510, Issue 7504, pp. 283 - 287
Deregulation of lysine methylation signalling has emerged as a common aetiological factor in cancer pathogenesis, with inhibitors of several histone lysine... 
LUNG-CANCER | ACTIVATION | PROTEIN | K-RAS | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | KINASE | PANCREATIC INTRAEPITHELIAL NEOPLASIA | GROWTH-FACTOR | HISTONE METHYLTRANSFERASE | PROGRESSION | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Adenocarcinoma of Lung | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Oncogene Protein p21(ras) - metabolism | MAP Kinase Kinase Kinases - chemistry | Adenocarcinoma - metabolism | Cell Transformation, Neoplastic - genetics | MAP Kinase Kinase Kinase 2 - chemistry | Adenocarcinoma - genetics | Lysine - metabolism | Disease Models, Animal | Lung Neoplasms - genetics | MAP Kinase Kinase Kinase 2 - metabolism | Lung Neoplasms - enzymology | Protein Phosphatase 2 - antagonists & inhibitors | Signal Transduction | Pancreatic Neoplasms - pathology | Adenocarcinoma - enzymology | Pancreatic Neoplasms - enzymology | Pancreatic Neoplasms - genetics | MAP Kinase Kinase Kinases - metabolism | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins A-raf - metabolism | Animals | Histone-Lysine N-Methyltransferase - metabolism | Protein Phosphatase 2 - metabolism | Cell Line, Tumor | Mice | Cell Transformation, Neoplastic - pathology | Methylation | Mitogen-Activated Protein Kinases - metabolism | Oncogene Protein p21(ras) - genetics | Physiological aspects | Research | Lysine | Oncology, Experimental | Cancer | DNA methylation | Peptides | Kinases | Rodents | Tumors
Journal Article
Cancer cell, ISSN 1535-6108, 2012, Volume 21, Issue 6, pp. 836 - 847
Stromal responses elicited by early stage neoplastic lesions can promote tumor growth. However, the molecular mechanisms that underlie the early recruitment of... 
COLONY-STIMULATING FACTORS | T-CELL RESPONSES | TUMOR PROGRESSION | P21 RAS | ONCOLOGY | DUCTAL ADENOCARCINOMA | INFLAMMATION | MOUSE | MICE | SUPPRESSOR-CELLS | CANCER | CELL BIOLOGY | Immunohistochemistry | Adenocarcinoma - pathology | Epithelial Cells - metabolism | Pancreatic Neoplasms - metabolism | Granulocyte-Macrophage Colony-Stimulating Factor - metabolism | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Carcinoma, Pancreatic Ductal - metabolism | Immunoblotting | Green Fluorescent Proteins - genetics | Pancreatic Ducts - metabolism | Carcinoma, Pancreatic Ductal - genetics | Adenocarcinoma - metabolism | RNA Interference | HEK293 Cells | CD8-Positive T-Lymphocytes - metabolism | Adenocarcinoma - genetics | Proto-Oncogene Proteins p21(ras) - metabolism | Green Fluorescent Proteins - metabolism | Pancreatic Ducts - cytology | Mice, Inbred C57BL | Pancreatic Neoplasms - pathology | Receptors, Chemokine - metabolism | Cells, Cultured | Mice, Transgenic | Pancreatic Neoplasms - genetics | Carcinoma, Pancreatic Ductal - pathology | Granulocyte-Macrophage Colony-Stimulating Factor - genetics | Animals | Cell Transformation, Neoplastic | Myeloid Cells - metabolism | Mice | CD11b Antigen - metabolism | Microscopy, Fluorescence | T cells | Tumors | granulocyte-macrophage colony stimulating factor | immunosuppression | Kras | cancer | inflammation | pancreas
Journal Article
Cell (Cambridge), ISSN 0092-8674, 2014, Volume 158, Issue 1, pp. 185 - 197
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 0027-8424, 2/2014, Volume 111, Issue 7, pp. 2554 - 2559
Journal Article