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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 | Index Medicus | Abridged Index Medicus
Journal Article
Cellular Signalling, ISSN 0898-6568, 04/2013, Volume 25, Issue 4, pp. 931 - 938
The interleukin-6 (IL-6)/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway mediates cell proliferation and migration.... 
Cytoskeleton | p27 | Gastric cancer | Migration | Invasion | Signal transducer and activator of transcription 3 | P27 | ACTIVATION | E-CADHERIN | BETA-CATENIN | INTERLEUKIN-6 | IL-6 | CELL BIOLOGY | OVEREXPRESSION | SIGNALING PATHWAY | SKP2 | CARCINOMA | CYCLE | Up-Regulation | Cell Proliferation | Cadherins - metabolism | Humans | Stomach Neoplasms - metabolism | Sp1 Transcription Factor - metabolism | Stomach Neoplasms - pathology | rhoA GTP-Binding Protein - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - antagonists & inhibitors | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Matrix Metalloproteinase 9 - metabolism | Microtubules - metabolism | RNA Interference | Janus Kinase 2 - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Focal Adhesion Kinase 1 - metabolism | Interleukin-6 - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Signal Transduction | Matrix Metalloproteinase 2 - metabolism | Down-Regulation | S-Phase Kinase-Associated Proteins - metabolism | Cell Adhesion | GPI-Linked Proteins - metabolism | Cell Line, Tumor | STAT3 Transcription Factor - antagonists & inhibitors | Stathmin - metabolism | Cyclin-Dependent Kinase Inhibitor p27 - genetics | RNA, Small Interfering - metabolism | Phosphates | Enzymes | Cysteine | Analysis | Fluorescein | Cancer cells | Tubulins | Stomach cancer | Enzyme-linked immunosorbent assay | Cancer | Index Medicus
Journal Article
Oncogene, ISSN 0950-9232, 07/2007, 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 | Index Medicus
Journal Article
American Journal of Surgical Pathology, ISSN 0147-5185, 09/2009, Volume 33, Issue 9, pp. 1401 - 1408
Gastrointestinal stromal tumors (GISTs), KIT or platelet derived growth factor receptor alpha (PDGFRA) signaling driven mesenchymal tumors of the... 
PDGFRA | Chloride channel protein | Sarcoma | DOG1 | KIT | Mutation | Gastrointestinal stromal tumor | PDGFRA MUTATIONS | GASTRIC TUMORS | SURGERY | sarcoma | MARKER | KINASE-C-THETA | MONOCLONAL-ANTIBODY | PATHOLOGY | mutation | chloride channel protein | gastrointestinal stromal tumor | TERM-FOLLOW-UP | EXPRESSION | PKC-THETA | MORPHOLOGY | Immunohistochemistry | Myenteric Plexus - pathology | Predictive Value of Tests | Anoctamin-1 | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - pathology | Humans | Stomach Neoplasms - metabolism | Leiomyoma - metabolism | Myenteric Plexus - metabolism | Neoplasm Proteins - metabolism | Proto-Oncogene Proteins c-kit - metabolism | Esophageal Neoplasms - pathology | Leiomyoma - pathology | Chloride Channels | Gastrointestinal Stromal Tumors - diagnosis | Esophageal Neoplasms - metabolism | Mesenchymoma - diagnosis | Biomarkers, Tumor - metabolism | Membrane Proteins - metabolism | Intestinal Neoplasms - diagnosis | Colorectal Neoplasms - metabolism | Peritoneal Neoplasms - pathology | Mesenchymoma - metabolism | Diagnosis, Differential | Stomach Neoplasms - diagnosis | Intestinal Neoplasms - metabolism | Sarcoma, Synovial - metabolism | Peritoneal Neoplasms - metabolism | Gastrointestinal Stromal Tumors - metabolism | Mesenchymoma - secondary | Colorectal Neoplasms - pathology | Sarcoma, Synovial - pathology | Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 9/2011, 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 | Pathogens | Gram-negative bacteria | Rodents | Index Medicus | Adhesins | Histone H2A | Mesenchyme | Gastric mucosa | Carcinogenesis | Risk factors | Mammalian cells | Metaphase | genomics | Blood groups | Chromosomes | Gastric cancer | Gel electrophoresis | virulence factors | Infection | Cytotoxins | gamma -Glutamyltransferase | Molecular modelling | Microscopy | pathogenicity islands | Ataxia telangiectasia mutated protein | Chromosome aberrations | Biological Sciences
Journal Article
Nature Medicine, ISSN 1078-8956, 10/2002, 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 | Index Medicus
Journal Article
Cancer Cell, ISSN 1535-6108, 12/2015, 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 | Index Medicus
Journal Article
American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, 08/2011, Volume 301, Issue 2, pp. G260 - G268
Bondzio A, Gabler C, Badewien-Rentzsch B, Schulze P, Martens H, Einspanier R. Identification of differentially expressed proteins in ruminal epithelium in... 
Mrna expression | Sheep | Protein markers | Proteomics | protein markers | PHYSIOLOGY | proteomics | PHOSPHOLIPID-METABOLISM | ACTIVE-SITE | S-ADENOSYLHOMOCYSTEINE-HYDROLASE | mRNA expression | DAIRY-COWS | CARBONIC-ANHYDRASE-I | COLORECTAL-CANCER | ANNEXIN-V | GENE-EXPRESSION | RUMEN MUCOSA | GASTROENTEROLOGY & HEPATOLOGY | sheep | FATTY-ACID ABSORPTION | Adaptation, Physiological | Up-Regulation | Protein Disulfide-Isomerases - metabolism | Methyltransferases - metabolism | Two-Dimensional Difference Gel Electrophoresis | Male | Carbonic Anhydrase I - metabolism | RNA, Messenger - metabolism | Peroxiredoxin VI - metabolism | Proton-Translocating ATPases - metabolism | ATP Synthetase Complexes - metabolism | Actin-Related Protein 3 - metabolism | Female | Stomach, Ruminant - physiology | Gene Expression | Epithelium - metabolism | Down-Regulation | Adenosylhomocysteinase - metabolism | Stomach, Ruminant - metabolism | Random Allocation | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Annexin A5 - metabolism | Animals | Proteins - metabolism | Annexin A1 - metabolism | Isocitrate Dehydrogenase - metabolism | Epithelium - physiology | Thiolester Hydrolases - metabolism | Dietary Supplements | Proteome - metabolism | Cellular proteins | Messenger RNA | Dietary supplements | Physiological aspects | Genetic aspects | Research | Biological markers | Health aspects | Proteins | Gene amplification | Diet | Metabolism | 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 | Index Medicus
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 0950-9232, 09/2013, 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
Gastroenterology, ISSN 0016-5085, 2007, Volume 132, Issue 3, pp. 1066 - 1076
Background & Aims: FHL2 (4-1/2 LIM protein 2) is an adapter and modifier in protein interactions that is expressed mainly in the heart and ovary. It functions... 
Gastroenterology and Hepatology | CANCER CELLS | COLORECTAL-CANCER | LIM-ONLY PROTEIN | E-CADHERIN EXPRESSION | HUMAN-MELANOMA | TRANSCRIPTIONAL COACTIVATOR | BETA-CATENIN | C-JUN | GASTROENTEROLOGY & HEPATOLOGY | DOMAIN PROTEIN | ACTIN-BUNDLING PROTEIN | Up-Regulation | Colonic Neoplasms - genetics | Cell Proliferation | Cadherins - metabolism | Homeodomain Proteins - metabolism | Humans | RNA, Messenger - metabolism | Colonic Neoplasms - metabolism | Carcinoembryonic Antigen - metabolism | Telomerase - genetics | RNA Interference | Time Factors | Cell Transformation, Neoplastic - genetics | Cyclooxygenase 2 - genetics | Telomerase - metabolism | Transcription, Genetic | Cell Differentiation | Neoplasm Proteins - genetics | Inhibitor of Apoptosis Proteins | Membrane Proteins - genetics | Muscle Proteins - genetics | Mice, Nude | Cell Line, Tumor | Mice | RNA, Small Interfering - metabolism | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Actins - metabolism | Stomach Neoplasms - metabolism | Stomach Neoplasms - pathology | Transplantation, Heterologous | Neoplasm Proteins - metabolism | Transcription Factor AP-1 - metabolism | Transfection | Cell Shape | Muscle Proteins - metabolism | Membrane Proteins - metabolism | Stomach Neoplasms - genetics | Proto-Oncogene Proteins c-jun - genetics | Transcription Factors - genetics | Cell Transformation, Neoplastic - metabolism | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Animals | Proto-Oncogene Proteins c-jun - metabolism | Colonic Neoplasms - pathology | RNA, Antisense - metabolism | Cyclooxygenase 2 - metabolism | LIM-Homeodomain Proteins | Cell Transformation, Neoplastic - pathology | Colon cancer | Index Medicus | Abridged Index Medicus
Journal Article