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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
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
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2011, Volume 108, Issue 36, pp. 14944 - 14949
The bacterial pathogen Helicobacter pylori chronically infects the human gastric mucosa and is the leading risk factor for the development of gastric cancer.... 
Helicobacter pylori | Epithelial cells | DNA damage | DNA | Cell nucleus | Cell lines | Bacteria | Cultured cells | Infections | Mice | Chromosome breaks | DNA damage signaling | Gastric tumorigenesis | Genomic instability | CYTOLETHAL DISTENDING TOXIN | MULTIDISCIPLINARY SCIENCES | RISK | MISMATCH REPAIR | COLONIZATION | GENETIC INSTABILITY | EPITHELIAL-CELLS | chromosome breaks | GASTRIC-CANCER | INFLAMMATION | INFECTION | MICE | genomic instability | gastric tumorigenesis | Phosphorylation | Epithelial Cells - metabolism | Humans | Stomach Neoplasms - metabolism | Helicobacter Infections - complications | Stomach Neoplasms - pathology | Intracellular Signaling Peptides and Proteins - metabolism | Antigens, Bacterial - genetics | DNA Breaks, Double-Stranded | Helicobacter Infections - pathology | DNA-Binding Proteins - metabolism | Tumor Suppressor Proteins - genetics | Trans-Activators - genetics | Cell Cycle Proteins - genetics | Helicobacter Infections - metabolism | Nuclear Proteins - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Stomach Neoplasms - genetics | Tumor Suppressor Proteins - metabolism | Chromosomal Proteins, Non-Histone - metabolism | Bacterial Proteins - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Genomic Islands | Epithelial Cells - pathology | Nuclear Proteins - metabolism | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Chromosomal Proteins, Non-Histone - genetics | Bacterial Adhesion | Stomach Neoplasms - microbiology | Animals | Histones - genetics | Helicobacter pylori - metabolism | Epithelial Cells - microbiology | Chromosome Aberrations | Cell Line, Tumor | Bacterial Proteins - metabolism | Trans-Activators - metabolism | Histones - metabolism | Tumor Suppressor p53-Binding Protein 1 | Antigens, Bacterial - metabolism | Carcinogens | Cocarcinogens | Physiological aspects | Genetic aspects | Research | Health aspects | Cells | Biological Sciences
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. Here, we show that Mist1 expression marks quiescent stem cells in... 
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
Nature medicine, ISSN 1546-170X, 2002, Volume 8, Issue 10, pp. 1089 - 1097
The intracellular signaling mechanisms that specify tissue-specific responses to the interleukin-6 (IL-6) family of cytokines are not well understood. Here, we... 
MEDICINE, RESEARCH & EXPERIMENTAL | HEPATIC CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL BIOLOGY | INTESTINAL INFLAMMATION | RESPONSES | INTERLEUKIN-6 FAMILY | COLITIS | IN-VIVO | DISEASE | CYTOKINE RECEPTORS | TRANSGENIC MICE | SIGNAL TRANSDUCER | Protein Tyrosine Phosphatase, Non-Receptor Type 11 | Membrane Glycoproteins - metabolism | Transcriptional Activation | Peptides - genetics | Neuropeptides | Protein Tyrosine Phosphatases - metabolism | Wound Healing | Antigens, CD - genetics | Antigens, CD - metabolism | Growth Substances - genetics | Peptides - metabolism | Digestive System Physiological Phenomena | Protein Phosphatase 2 | Interleukin-6 - metabolism | Cytokine Receptor gp130 | Colon - pathology | Interleukin-11 - metabolism | Mice, Transgenic | Spleen - cytology | Colon - metabolism | STAT1 Transcription Factor | Mice | Intestinal Mucosa - pathology | Intestinal Mucosa - metabolism | Homeostasis | Stomach Neoplasms - metabolism | Stomach Neoplasms - pathology | Stomach - metabolism | Adenoma - metabolism | DNA-Binding Proteins - metabolism | Muscle Proteins | Trefoil Factor-3 | Trefoil Factor-2 | Cell Line | Stomach - pathology | Gene Expression Regulation | Intracellular Signaling Peptides and Proteins | Membrane Glycoproteins - genetics | Proteins - genetics | Animals | Proteins - metabolism | Spleen - metabolism | Mucins | Stomach - cytology | Adenoma - pathology | Signal Transduction - physiology | Trans-Activators - metabolism | Growth Substances - metabolism | Mitogen-Activated Protein Kinases - metabolism
Journal Article
Gastroenterology, ISSN 0016-5085, 2008, Volume 134, Issue 7, pp. 1842 - 1860
Recent milestones in the understanding of gastric acid secretion and treatment of acid-peptic disorders include the (1) discovery of histamine H2 -receptors... 
Gastroenterology and Hepatology | RABBIT PARIETAL-CELLS | PERFUSED RAT STOMACH | COMMUNITY-ACQUIRED PNEUMONIA | ATRIAL-NATRIURETIC-PEPTIDE | HELICOBACTER-PYLORI INFECTION | GASTROESOPHAGEAL-REFLUX DISEASE | PROTON PUMP INHIBITORS | ENTEROCHROMAFFIN-LIKE CELLS | SOMATOSTATIN RECEPTOR SCINTIGRAPHY | GASTROENTEROLOGY & HEPATOLOGY | GLYCINE-EXTENDED GASTRINS | Gastrointestinal Diseases - physiopathology | Gastroesophageal Reflux - physiopathology | Humans | Acetylcholine - metabolism | Stomach - metabolism | Gastric Mucosa - metabolism | Gastrointestinal Diseases - microbiology | Gastric Acid - secretion | Histamine - metabolism | Helicobacter pylori | Gastrointestinal Diseases - drug therapy | Helicobacter Infections - metabolism | Duodenal Ulcer - metabolism | Stomach - innervation | Stomach - drug effects | Somatostatin - metabolism | Helicobacter Infections - physiopathology | Anti-Ulcer Agents - therapeutic use | Eating | Proton Pump Inhibitors - adverse effects | Gastroesophageal Reflux - metabolism | Stomach Ulcer - metabolism | H(+)-K(+)-Exchanging ATPase - metabolism | Paracrine Communication | Anti-Ulcer Agents - adverse effects | Histamine H2 Antagonists - adverse effects | Digestion | Duodenal Ulcer - physiopathology | Gastrins - metabolism | Proton Pump Inhibitors - therapeutic use | Histamine H2 Antagonists - therapeutic use | Stomach Ulcer - physiopathology | Animals | Gastrointestinal Diseases - metabolism | Ion Channels - metabolism | Gastric Mucosa - secretion | Stomach - enzymology | Stomach - microbiology | Gastroesophageal reflux | Polypeptides | Gastrin
Journal Article
by Liu, Z and Li, Q and Li, K and Chen, L and Li, W and Hou, M and Liu, T and Yang, J and Lindvall, C and Björkholm, M and Jia, J and Xu, D
Oncogene, ISSN 1476-5594, 2012, Volume 32, Issue 36, pp. 4203 - 4213
Telomerase activation through induction of telomerase reverse transcriptase (hTERT) contributes to malignant transformation by stabilizing telomeres. Clinical... 
hTERT | gastric cancer | EMT | CSCs | SURVIVAL | METASTASIS | INDUCED APOPTOSIS | BIOCHEMISTRY & MOLECULAR BIOLOGY | BETA-CATENIN | TUMOR-INITIATING CELLS | CELL BIOLOGY | ONCOLOGY | GASTRIC-CANCER | GROWTH | GENETICS & HEREDITY | EXPRESSION | CARCINOMA | SNAIL | Neoplasms - metabolism | Vimentin - metabolism | Humans | Transforming Growth Factor beta1 - metabolism | Gene Expression Regulation, Neoplastic | Stomach Neoplasms - metabolism | Stomach Neoplasms - pathology | Epithelial-Mesenchymal Transition - genetics | Cell Nucleus - metabolism | Telomerase - genetics | Neoplasms - genetics | Neoplastic Stem Cells - metabolism | RNA Interference | Cell Transformation, Neoplastic - genetics | Vimentin - genetics | Hyaluronan Receptors - metabolism | Telomerase - metabolism | Transcription, Genetic | Catalysis | Snail Family Transcription Factors | Biomarkers - metabolism | Stomach Neoplasms - genetics | Promoter Regions, Genetic | Gene Expression | Signal Transduction | Neoplasm Invasiveness | Transcription Factors - genetics | Cell Transformation, Neoplastic - metabolism | beta Catenin - metabolism | Protein Transport | Transcription Factors - metabolism | Animals | Cell Line, Tumor | Protein Binding | Mice | Neoplasms - pathology | Quantitative Trait Loci | Neoplastic processes | Cellular control mechanisms | Cancer cells | Research | Properties | Observations | Telomerase | Proteins | Signal transduction | Gene expression | Stomach cancer | Stem cells | Index Medicus
Journal Article
Molecular Cell, ISSN 1097-2765, 04/2013, Volume 50, Issue 2, pp. 185 - 199
Tissue-specific differentiation programs become dysregulated during cancer evolution. The transcription factor Nkx2-1 is a master regulator of pulmonary... 
FOXA1 | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENE-EXPRESSION | NUCLEAR FACTOR 4-ALPHA | ENHANCERS | EPIGENETIC SIGNATURES | CANCER | ORGANOGENESIS | EGFR | THYROID TRANSCRIPTION FACTOR-1 | P53 | CELL BIOLOGY | Thyroid Nuclear Factor 1 | Adenocarcinoma - pathology | Cell Proliferation | Proto-Oncogene Proteins p21(ras) - genetics | Humans | Lung Neoplasms - metabolism | Transcriptional Activation | Gene Expression Regulation, Neoplastic | Transcriptome | Lung Neoplasms - pathology | Stomach - metabolism | Mutation, Missense | Respiratory Mucosa - pathology | Adenocarcinoma - metabolism | Pulmonary Alveoli - metabolism | Cell Differentiation | Lung - metabolism | Nuclear Proteins - genetics | Binding Sites | Hyperplasia - metabolism | Proto-Oncogene Proteins p21(ras) - metabolism | Hepatocyte Nuclear Factor 3-beta - metabolism | Hepatocyte Nuclear Factor 4 - metabolism | Lung - pathology | Transcription Factors - physiology | Pulmonary Alveoli - pathology | Stomach - pathology | Mice, Transgenic | Nuclear Proteins - metabolism | Hepatocyte Nuclear Factor 4 - genetics | Transcription Factors - genetics | Tumor Burden | Organ Specificity | Hepatocyte Nuclear Factor 3-alpha - metabolism | Transcription Factors - metabolism | Animals | Cell Transformation, Neoplastic | Protein Binding | Mice | Nuclear Proteins - physiology | Respiratory Mucosa - metabolism | Adenocarcinoma | Chromosomal proteins | Lung cancer | Genomics | Tumors
Journal Article