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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2010, Volume 107, Issue 28, pp. 12611 - 12616
Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells. Asbestos is cytotoxic... 
Actinomycin | Asbestos | Cell death | Secretion | Plasma cells | Inflammation | Macrophages | Carcinogenesis | Necrosis | Apoptosis | Mesothelioma | Biomarker | Tumor necrosis factor-alpha | Chemoprevention | TRANSFORMATION | POLY(ADP-RIBOSE) POLYMERASE | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | CROCIDOLITE ASBESTOS | HMGB1 | biomarker | MAMMALIAN-CELLS | tumor necrosis factor-alpha | PATHOGENESIS | chemoprevention | NECROTIC CELLS | carcinogenesis | TNF-ALPHA | INHIBITORS | mesothelioma | Tumor Necrosis Factor-alpha - metabolism | Asbestos - metabolism | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Humans | Reactive Oxygen Species - pharmacology | Adenosine Diphosphate Ribose - metabolism | Adenosine Diphosphate Ribose - pharmacology | Carcinogens - metabolism | Asbestos - pharmacology | Pleural Neoplasms - metabolism | Inflammation - metabolism | Carcinogens - pharmacology | Cell Nucleus - metabolism | HMGB Proteins - pharmacology | HMGB1 Protein - pharmacology | HMGB1 Protein - metabolism | Cell Death | Mesocricetus | Female | HMGB Proteins - metabolism | Poly Adenosine Diphosphate Ribose - pharmacology | Epithelium - drug effects | Cricetinae | Cytokines - metabolism | Epithelium - metabolism | Hydrogen Peroxide - pharmacology | Necrosis - metabolism | Hydrogen Peroxide - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Macrophages - metabolism | Poly(ADP-ribose) Polymerases - metabolism | Animals | Mesothelioma - metabolism | Poly(ADP-ribose) Polymerases - pharmacology | Cells - metabolism | Mice | Mice, Inbred BALB C | Cytokines - pharmacology | Prevention | Mesothelium | Chromosomal proteins | Research | Chemical properties | Health aspects | Proteins | Carcinogens | Cytokines | Oncology | Biochemistry | Cells | Index Medicus | Reactive oxygen species | Transformation | Deposits | Hydrogen peroxide | Cytotoxicity | HMGB1 protein | Nuclei | Tumor necrosis factor-a | ATP | Cytoplasm | Biological Sciences
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
Molecular Cancer, ISSN 1476-4598, 09/2011, Volume 10, Issue 1, pp. 117 - 117
Journal Article
British Journal of Cancer, ISSN 0007-0920, 02/2018, Volume 118, Issue 3, pp. 428 - 434
Background: Periodontal pathogens have been linked to oral and gastrointestinal (orodigestive) carcinogenesis. However, the exact mechanisms remain unknown.... 
chymotrypsin-like proteinase | Treponema denticola | periodontopathogen | COLLAGENASE-2 MMP-8 | PORPHYROMONAS-GINGIVALIS | PANCREATIC-CANCER | TISSUE INHIBITORS | PERIODONTAL-DISEASE | METALLOPROTEINASES | ONCOLOGY | gastrointestinal cancer | ALPHA-1-ANTITRYPSIN | EXPRESSION | oral cancer | HUMAN NEUTROPHIL | PROGRESSION | Digestive System Neoplasms - metabolism | Pancreatic Neoplasms - chemistry | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - pathology | Humans | Treponema denticola - enzymology | Mouth Neoplasms - metabolism | Stomach Neoplasms - pathology | Tonsillar Neoplasms - chemistry | Complement C1q - metabolism | Colonic Neoplasms - metabolism | Head and Neck Neoplasms - metabolism | Esophageal Neoplasms - pathology | Tonsillar Neoplasms - metabolism | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Tissue Inhibitor of Metalloproteinase-2 - metabolism | Head and Neck Neoplasms - chemistry | Matrix Metalloproteinase 9 - metabolism | Adenocarcinoma - metabolism | Matrix Metalloproteinase 8 - metabolism | Esophageal Neoplasms - metabolism | Digestive System Neoplasms - pathology | Colonic Neoplasms - chemistry | Stomach Neoplasms - chemistry | Adenocarcinoma - chemistry | Esophageal Neoplasms - chemistry | Tonsillar Neoplasms - pathology | Pancreatic Neoplasms - pathology | Carcinoma, Squamous Cell - chemistry | Mouth Neoplasms - chemistry | Head and Neck Neoplasms - pathology | Cell Transformation, Neoplastic - immunology | Digestive System Neoplasms - chemistry | alpha 1-Antichymotrypsin - metabolism | Colonic Neoplasms - pathology | Chymases - analysis | Mouth Neoplasms - pathology | Immunohistochemistry | Proteinase | Virulence | Tissue inhibitor of metalloproteinase 2 | Tissues | Tissue inhibitor of metalloproteinase 1 | Carcinogenesis | Proteins | Carcinogens | Pancreatic carcinoma | Bacteria | Colon | Pancreas | Gastric cancer | Squamous cell carcinoma | Tonsil | Immunomodulation | Teeth | Proteinase inhibitors | Esophagus | Complement component C1q | Chymotrypsin | Periodontitis | Neutrophil collagenase | Tumors | Index Medicus | Molecular Diagnostics
Journal Article
Cancer Research, ISSN 0008-5472, 07/2013, Volume 73, Issue 14, pp. 4212 - 4221
VEGF-C and VEGF-D were identified as lymphangiogenic growth factors and later shown to promote tumor metastasis, but their effects on carcinogenesis are poorly... 
VESSELS | ANGIOGENESIS | SPECIFICITY | ONCOLOGY | TUMOR LYMPHANGIOGENESIS | MOUSE | SQUAMOUS-CELL CARCINOMA | FACTOR RECEPTOR-3 | CANCER | LYMPHATIC METASTASIS | ENDOTHELIAL GROWTH-FACTOR | Inflammation - pathology | Leukocytes - pathology | Skin Neoplasms - drug therapy | Skin - metabolism | Carcinogenesis - chemically induced | Carcinoma, Squamous Cell - metabolism | Carcinoma, Squamous Cell - pathology | Carcinoma, Squamous Cell - chemically induced | Carcinogenesis - metabolism | Neovascularization, Pathologic - pathology | Carcinogens | Inflammation - metabolism | Inflammation - drug therapy | Female | Skin - pathology | Skin Neoplasms - pathology | Epidermis - metabolism | Epidermis - pathology | Vascular Endothelial Growth Factor D - antagonists & inhibitors | Cytokines - metabolism | Macrophages - pathology | Epidermis - drug effects | Mice, Transgenic | Skin Neoplasms - chemically induced | Vascular Endothelial Growth Factor Receptor-3 - metabolism | Skin Neoplasms - metabolism | Carcinogenesis - drug effects | Keratinocytes - pathology | Macrophages - metabolism | Vascular Endothelial Growth Factor D - metabolism | Animals | Carcinoma, Squamous Cell - drug therapy | Vascular Endothelial Growth Factor C - antagonists & inhibitors | Keratinocytes - drug effects | Keratinocytes - metabolism | Neovascularization, Pathologic - drug therapy | Vascular Endothelial Growth Factor C - metabolism | Leukocytes - drug effects | Macrophages - drug effects | Cell Proliferation - drug effects | Mice | Neovascularization, Pathologic - metabolism | Leukocytes - metabolism | Skin - drug effects | Index Medicus
Journal Article
Neoplasia, ISSN 1476-5586, 01/2010, Volume 12, Issue 1, pp. 39,IN5 - 50,IN5
Constitutive activation of signal transducer and activator of transcription 3 (STAT3) signaling is frequently detected in cancer, promoting its emergence as a... 
RNA INTERFERENCE | TRANSFORMATION | APOPTOSIS | ONCOLOGY | CONSTITUTIVELY-ACTIVATED STAT3 | COLONY FORMATION | GENE-REGULATION | TRANSCRIPTION-3 | TARGETS | EXPRESSION | SIGNAL TRANSDUCER | Anthraquinones - metabolism | Neoplasms - metabolism | Cyclin D1 - metabolism | Pancreatic Neoplasms - metabolism | Microtubule-Associated Proteins - genetics | Apoptosis - drug effects | Microtubule-Associated Proteins - metabolism | Humans | Caspase 3 - metabolism | Male | STAT3 Transcription Factor - chemistry | Breast Neoplasms - metabolism | Antineoplastic Agents - metabolism | Proto-Oncogene Proteins c-bcl-2 - metabolism | Glioblastoma - genetics | Female | Glioblastoma - metabolism | Antineoplastic Agents - pharmacology | Phosphorylation - drug effects | STAT3 Transcription Factor - metabolism | Cell Line | Inhibitor of Apoptosis Proteins | Sulfonamides - chemistry | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Survivin | Antineoplastic Agents - chemistry | Reverse Transcriptase Polymerase Chain Reaction | Sulfonamides - pharmacology | Blotting, Western | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Poly(ADP-ribose) Polymerases - metabolism | Animals | Breast Neoplasms - genetics | Cyclin D1 - genetics | Breast Neoplasms - pathology | Mice, Nude | Glioblastoma - pathology | Sulfonamides - metabolism | Cell Line, Tumor | Protein Binding | Anthraquinones - pharmacology | Cell Proliferation - drug effects | Mice | Anthraquinones - chemistry | Neoplasms - pathology | Proto-Oncogene Proteins c-bcl-2 - genetics | Index Medicus
Journal Article
Cell, ISSN 0092-8674, 2007, Volume 130, Issue 6, pp. 1005 - 1018
Heat shock factor 1 (HSF1) is the master regulator of the heat shock response in eukaryotes, a very highly conserved protective mechanism. HSF1 function... 
PROTEINS | HUMDISEASE | PROTEIN-KINASE-A | CELLS | APOPTOSIS | TARGETED DISRUPTION | PROTECTION | TRANSCRIPTION FACTOR-1 | MOLECULAR CHAPERONES | BIOCHEMISTRY & MOLECULAR BIOLOGY | IN-VIVO | INHIBITORS | EXPRESSION | CELL BIOLOGY | ras Proteins - genetics | Protein Biosynthesis | Tetradecanoylphorbol Acetate | Cell Proliferation | Skin - metabolism | Humans | Transcription Factors - deficiency | Gene Expression Regulation, Neoplastic | Methylnitronitrosoguanidine | ras Proteins - metabolism | DNA-Binding Proteins - deficiency | Tumor Suppressor Protein p53 - genetics | Heat Shock Transcription Factors | DNA-Binding Proteins - metabolism | Carcinogens | RNA Interference | Time Factors | Cell Transformation, Neoplastic - genetics | Skin - pathology | Fibroblasts - metabolism | Skin Neoplasms - pathology | Proto-Oncogene Proteins c-sis - genetics | Transduction, Genetic | Proto-Oncogene Proteins c-sis - metabolism | Cell Survival | Tumor Suppressor Protein p53 - metabolism | Genotype | Signal Transduction - genetics | Skin Neoplasms - chemically induced | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Fibroblasts - pathology | Cell Transformation, Neoplastic - metabolism | Mice, Knockout | Skin Neoplasms - metabolism | Transcription Factors - metabolism | Phenotype | Animals | Skin Neoplasms - genetics | Cell Line, Tumor | Glucose - metabolism | 9,10-Dimethyl-1,2-benzanthracene | Mice | Mice, Inbred BALB C | Mutation | Cell Transformation, Neoplastic - pathology | RNA, Small Interfering - metabolism | Heat shock proteins | Knowledge-based systems | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2015, Volume 10, Issue 4, pp. e0124000 - e0124000
Inhibition of carcinogenesis may be a consequence of attenuation of oxidative stress via activation of antioxidant defence system, restoration and... 
NRF2-MEDIATED ANTIOXIDANT | QUINONE OXIDOREDUCTASE-1 | GROWTH-FACTOR-BETA | LYMPHOMA-BEARING MICE | NAD(P)H-QUINONE OXIDOREDUCTASE-1 | TGF-BETA | NITRIC-OXIDE SYNTHASE | MULTIDISCIPLINARY SCIENCES | IN-VIVO | SMOOTH-MUSCLE-CELLS | GLUTATHIONE-S-TRANSFERASE | Consensus Sequence | Glutathione Reductase - metabolism | Antioxidants - metabolism | Male | NAD(P)H Dehydrogenase (Quinone) - genetics | RNA, Messenger - metabolism | Lymphoma, T-Cell - prevention & control | Glutathione Reductase - genetics | Lymphoma, T-Cell - metabolism | Glutathione Transferase - genetics | Liver - drug effects | Cyclooxygenase 2 - genetics | Protein Binding - drug effects | Inflammation Mediators - metabolism | NF-E2-Related Factor 2 - genetics | Anticarcinogenic Agents - pharmacology | Tumor Microenvironment - drug effects | Liver - metabolism | RNA, Messenger - genetics | Curcumin - pharmacology | Tumor Suppressor Protein p53 - metabolism | Glutathione Transferase - metabolism | Transforming Growth Factor beta1 - genetics | Lymphoma, T-Cell - drug therapy | Animals | Nitric Oxide Synthase Type II - genetics | Signal Transduction - drug effects | NF-E2-Related Factor 2 - metabolism | Cyclooxygenase 2 - metabolism | NAD(P)H Dehydrogenase (Quinone) - metabolism | Mice | Mice, Inbred AKR | Nitric Oxide Synthase Type II - metabolism | Prevention | Antioxidants | Patient outcomes | Development and progression | Genetic aspects | Research | Non-Hodgkin's lymphomas | Transforming growth factors | Tumor proteins | Risk factors | Oxidative stress | Regulations | Laboratories | Zoology | Liver | p53 Protein | Smooth muscle | Biochemistry | Lymphocytes T | Activation | Metastasis | Carcinogenesis | Bearing | Proteins | Signal transduction | Angiogenesis | Carcinogens | Metabolites | Restoration | Rodents | Modulation | Cell cycle | Attenuation | Curcumin | Inhibition | Growth factors | Deoxyribonucleic acid--DNA | Enzymes | Inflammation | Gene expression | Lymphoma | Nitric-oxide synthase | Signaling | Phytochemicals | Hepatocytes | Nitric oxide | Glycolysis | Lymphomas | Cyclooxygenase-2 | Molecular biology | T-cell lymphoma | Cancer | Apoptosis | Tumors | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article