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Journal of Clinical Investigation, ISSN 0021-9738, 09/2012, Volume 122, Issue 9, pp. 3127 - 3144
The chemokine receptor CXCR2 is a key mediator of neutrophil migration that also plays a role in tumor development. However, CXCR2 influences tumors through... 
ATHEROSCLEROTIC LESIONS | COLON-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | TUMOR-NECROSIS-FACTOR | IMMUNE CELLS | INTESTINAL NEOPLASIA | PROSTATE-CANCER | SKIN CARCINOGENESIS | RECEPTOR D6 | MYELOID CELLS | BEARING MICE | Dextran Sulfate | Tetradecanoylphorbol Acetate | Adenocarcinoma - pathology | Colitis - pathology | Colonic Neoplasms - chemically induced | Mice, 129 Strain | Receptors, Interleukin-8B - antagonists & inhibitors | Receptors, Interleukin-8B - deficiency | Colonic Neoplasms - metabolism | Adenoma - metabolism | Adenocarcinoma - metabolism | Azoxymethane | Colitis - chemically induced | Statistics, Nonparametric | Papilloma - pathology | Precancerous Conditions - pathology | Neutrophils - metabolism | Papilloma - chemically induced | Papilloma - metabolism | Skin Neoplasms - pathology | Dermatitis, Contact - pathology | Gene Expression | Neutrophils - enzymology | Mice, Inbred C57BL | Skin Neoplasms - chemically induced | Tumor Burden | Chemokines, CXC - genetics | Chemokines, CXC - secretion | Mice, Knockout | Skin Neoplasms - metabolism | Animals | Cell Transformation, Neoplastic | Adenoma - secretion | Chemokines, CXC - metabolism | Receptors, Interleukin-8B - genetics | Animals, Inbred Strains | 9,10-Dimethyl-1,2-benzanthracene | Mice | Mice, Inbred BALB C | Precancerous Conditions - chemically induced | Colonic Neoplasms - secretion | Adenoma - chemically induced | Peroxidase - metabolism | Care and treatment | Cancer cells | Neutrophils | Papilloma | Genetic aspects | Diagnosis | Adenoma | Research | Gene expression
Journal Article
Journal Article
Immunity, ISSN 1074-7613, 12/2014, Volume 41, Issue 6, pp. 1052 - 1063
Interleukin-17A (IL-17A) is a pro-inflammatory cytokine linked to rapid malignant progression of colorectal cancer (CRC) and therapy resistance. IL-17A exerts... 
COLON-CANCER | APC INACTIVATION | GASTRIC-CANCER | IFN-GAMMA | MOUSE MODEL | COLITIS-ASSOCIATED CANCER | SUPPRESSOR-CELLS | IMMUNOLOGY | TUMOR-GROWTH | INTESTINAL EPITHELIAL-CELLS | T-CELLS | Colonic Neoplasms - drug therapy | Humans | Receptors, Interleukin-17 - immunology | Colonic Neoplasms - chemically induced | NF-kappa B - metabolism | Receptors, Interleukin-17 - genetics | Extracellular Signal-Regulated MAP Kinases - metabolism | Tamoxifen - administration & dosage | Antibodies, Blocking - administration & dosage | Aberrant Crypt Foci - genetics | Fluorouracil - administration & dosage | Colonic Neoplasms - immunology | Colorectal Neoplasms - drug therapy | p38 Mitogen-Activated Protein Kinases - metabolism | Receptors, Interleukin-17 - metabolism | Disease Models, Animal | Mice, Inbred C57BL | Carcinogenesis - genetics | Mice, Transgenic | Signal Transduction - genetics | Colorectal Neoplasms - chemically induced | Mice, Knockout | Carcinogenesis - drug effects | Interleukin-17 - metabolism | Animals | Colorectal Neoplasms - immunology | Enterocytes - drug effects | Signal Transduction - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Mice | Cell Line, Transformed | Drug Resistance, Neoplasm - drug effects | Enterocytes - physiology | Chemotherapy | Colon cancer | Interleukins | Gastrointestinal diseases | Development and progression | Cellular signal transduction | Tumors | Cancer | Science | Medical research | Rodents | Metabolic disorders | Colorectal cancer | Index Medicus
Journal Article
Cancer Research, ISSN 0008-5472, 11/2011, Volume 71, Issue 21, pp. 6888 - 6898
Despite the role of aerobic glycolysis in cancer, recent studies highlight the importance of the mitochondria and biosynthetic pathways as well. PPAR gamma... 
BREAST-CANCER | ESTROGEN-RELATED RECEPTOR | OXIDATIVE-PHOSPHORYLATION | FATTY-ACID SYNTHESIS | ONCOLOGY | ERR-ALPHA | NUCLEAR RECEPTORS | PGC-1 | PPAR-GAMMA | CELL-GROWTH | ENERGY-METABOLISM | Neoplasm Transplantation | Colonic Neoplasms - genetics | Colonic Neoplasms - prevention & control | Humans | Liver Neoplasms, Experimental - chemically induced | Colonic Neoplasms - chemically induced | Cell Line, Tumor - transplantation | Liver Neoplasms, Experimental - prevention & control | Acetyl-CoA Carboxylase - genetics | Trans-Activators - physiology | Fatty Acid Synthases - biosynthesis | Organic Anion Transporters - genetics | Lipogenesis - genetics | Cell Transformation, Neoplastic - genetics | Carcinoma, Hepatocellular - genetics | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Trans-Activators - genetics | Liver Neoplasms - pathology | Cell Line, Tumor - metabolism | Fatty Acid Synthases - genetics | Fatty Acids - metabolism | Gene Expression Regulation, Neoplastic - genetics | Liver Neoplasms - genetics | Oxidative Phosphorylation | Mitochondria - metabolism | Mice, SCID | Mice, Knockout | Citric Acid Cycle - genetics | Animals | Trans-Activators - deficiency | Colonic Neoplasms - pathology | Carcinoma, Hepatocellular - pathology | Acetyl-CoA Carboxylase - biosynthesis | Mice | Transcription Factors | Organic Anion Transporters - biosynthesis | Index Medicus | oxidative metabolism | Warburg Effect | lipogenesis | Cancer metabolism | transcriptional regulation
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 08/2010, Volume 207, Issue 8, pp. 1625 - 1636
Signaling through the adaptor protein myeloid differentiation factor 88 (MyD88) promotes carcinogenesis in several cancer models. In contrast, MyD88 signaling... 
EXPRESSION PATTERNS | MEDICINE, RESEARCH & EXPERIMENTAL | CHRONIC INTESTINAL INFLAMMATION | MUTANT MICE | SODIUM-SULFATE COLITIS | CELL LINES | COLITIS-ASSOCIATED CANCER | IMMUNOLOGY | BETA-CATENIN | TUMORIGENESIS | INNATE IMMUNITY | BOWEL-DISEASE | Colonic Neoplasms - genetics | Intestinal Mucosa - metabolism | Adenocarcinoma - pathology | Azoxymethane - pharmacology | Epithelial Cells - metabolism | Gene Expression - drug effects | Apoptosis - drug effects | Gene Expression - genetics | Adenocarcinoma - chemically induced | Colonic Polyps - pathology | Epithelial Cells - drug effects | Colon - drug effects | DNA Repair Enzymes - genetics | Apoptosis - genetics | Colonic Neoplasms - chemically induced | Gene Expression Profiling | Inflammatory Bowel Diseases - metabolism | Colonic Neoplasms - metabolism | Intestinal Mucosa - drug effects | Adenocarcinoma - metabolism | Cyclooxygenase 2 - genetics | Inflammatory Bowel Diseases - pathology | Inflammatory Bowel Diseases - genetics | Interleukin-18 Receptor alpha Subunit - genetics | Inflammatory Bowel Diseases - chemically induced | Adenocarcinoma - genetics | Phosphorylation - drug effects | STAT3 Transcription Factor - genetics | Dextran Sulfate - pharmacology | Genetic Predisposition to Disease - genetics | Specific Pathogen-Free Organisms | Colon - pathology | Mice, Inbred C57BL | Epithelial Cells - pathology | Mutation - genetics | Colon - metabolism | beta Catenin - genetics | Mice, Knockout | Animals | Colonic Neoplasms - pathology | Receptors, Interleukin-1 Type I - genetics | Signal Transduction - physiology | Cell Proliferation - drug effects | Mice | Interleukin-18 - genetics | Myeloid Differentiation Factor 88 - metabolism | Interleukin-18 - metabolism | Intestinal Mucosa - pathology | Index Medicus
Journal Article
Anticancer Research, ISSN 0250-7005, 01/2017, Volume 37, Issue 1, pp. 15 - 20
Background: Colorectal cancer (CRC) is one of the more intensively studied human malignancies. For many years, the general view has been that the vast majority... 
Conventional carcinoma pathway | Rats | Serrated carcinoma pathway | Colon cancer | Review | GALT carcinoma pathway | GLUTAMIC-ACID PYROLYSATE | INDUCTION | PATHOLOGY | 1,2-DIMETHYLHYDRAZINE | serrated carcinoma pathway | INTESTINAL TUMORS | ONCOLOGY | RECOMMENDATIONS | review | COLORECTAL-CANCER | LYMPHOID-TISSUE | conventional carcinoma pathway | DIMETHYLHYDRAZINE | rats | CARCINOMA | Colonic Neoplasms - genetics | Adenomatous Polyps - genetics | Adenomatous Polyps - pathology | Colonic Polyps - pathology | Gene Expression Regulation, Neoplastic | Colonic Neoplasms - chemically induced | Cell Transformation, Neoplastic - chemically induced | Neoplasms, Experimental - chemically induced | Colonic Polyps - metabolism | Colonic Neoplasms - metabolism | Neoplasms, Experimental - pathology | Colonic Polyps - genetics | Cell Transformation, Neoplastic - genetics | Neoplasms, Experimental - genetics | Biomarkers, Tumor - metabolism | Carcinoma - pathology | Signal Transduction | Colon - pathology | Adenomatous Polyps - chemically induced | Lymphoid Tissue - metabolism | Carcinoma - chemically induced | Cell Transformation, Neoplastic - metabolism | Rats, Sprague-Dawley | Colon - metabolism | Disease Progression | Colonic Polyps - chemically induced | Lymphoid Tissue - pathology | Animals | Colonic Neoplasms - pathology | Adenomatous Polyps - metabolism | Carcinoma - genetics | Biomarkers, Tumor - genetics | Carcinoma - metabolism | Neoplasms, Experimental - metabolism | Cell Transformation, Neoplastic - pathology
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 07/2012, Volume 287, Issue 30, pp. 25530 - 25540
Fas is a member of the death receptor family. Stimulation of Fas leads to induction of apoptotic signals, such as caspase 8 activation, as well as... 
CD95 | AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME | CANCER DEVELOPMENT | IFN-GAMMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | MOUSE MODEL | IN-VIVO | ALPHA-DEPENDENT APOPTOSIS | IKK-BETA | RECEPTOR | CELL-DEATH | Colonic Neoplasms - genetics | Fas Ligand Protein - metabolism | Humans | Caspase 8 - metabolism | Colonic Neoplasms - chemically induced | Neoplasms, Experimental - chemically induced | fas Receptor - metabolism | Promoter Regions, Genetic - genetics | Transcription Factor RelA - genetics | Colonic Neoplasms - metabolism | Embryo, Mammalian - metabolism | Caspase 8 - genetics | Sarcoma - chemically induced | NF-kappa B p52 Subunit - genetics | Tumor Suppressor Proteins - genetics | Neoplasms, Experimental - genetics | fas Receptor - genetics | Gene Expression Regulation, Neoplastic - drug effects | Sarcoma - genetics | Gene Expression Regulation, Neoplastic - genetics | Fibroblasts - metabolism | Tumor Suppressor Proteins - metabolism | Embryo, Mammalian - pathology | Fibroblasts - pathology | Sarcoma - pathology | Methylcholanthrene - toxicity | NF-kappa B p52 Subunit - metabolism | Mice, Knockout | Sarcoma - metabolism | Animals | Transcription Factor RelA - metabolism | Mice | Neoplasms, Experimental - metabolism | Fas Ligand Protein - genetics | Apoptosis | Molecular Bases of Disease | Cancer Tumor Promoter | Fas | NF-kappaB Transcription Factor | NF-kappaB | Cancer
Journal Article
Gastroenterology, ISSN 0016-5085, 12/2017, Volume 153, Issue 6, pp. 1621 - 1633.e6
Altered gut microbiota is implicated in development of colorectal cancer (CRC). Some intestinal bacteria have been reported to potentiate intestinal... 
Stool Transplantation | Germ-Free | Carcinogenesis | Colon Cancer | CELLS | MICROBIOME | COLON CARCINOGENESIS | PROLIFERATION | SEQUENCE | GENES | GASTROENTEROLOGY & HEPATOLOGY | TUMORIGENESIS | PROGRESSION | TOOLS | Cell Proliferation | Colonic Polyps - pathology | Humans | Gene Expression Regulation, Neoplastic | Ki-67 Antigen - metabolism | Male | Colonic Polyps - metabolism | Case-Control Studies | Th1 Cells - metabolism | Feces - microbiology | Azoxymethane | Colonic Polyps - microbiology | Th17 Cells - metabolism | Inflammation Mediators - metabolism | Lymphocytes, Tumor-Infiltrating - metabolism | Colorectal Neoplasms - metabolism | Disease Models, Animal | Colon - pathology | Mice, Inbred C57BL | Gastrointestinal Microbiome | Lymphocytes, Tumor-Infiltrating - microbiology | Colorectal Neoplasms - microbiology | Cell Transformation, Neoplastic - metabolism | Colorectal Neoplasms - chemically induced | Colon - metabolism | Colonic Polyps - chemically induced | Host-Pathogen Interactions | Th1 Cells - microbiology | Animals | Germ-Free Life | Colon - microbiology | Cell Transformation, Neoplastic - pathology | Colorectal Neoplasms - pathology | Th17 Cells - microbiology | Medical research | Cancer patients | Microbiota (Symbiotic organisms) | Analysis | Colorectal cancer | Medicine, Experimental | Mice | Index Medicus | Abridged Index Medicus
Journal Article
International Journal of Cancer, ISSN 0020-7136, 04/2016, Volume 138, Issue 7, pp. 1719 - 1731
Journal Article
Journal Article
Gastroenterology, ISSN 0016-5085, 2015, Volume 149, Issue 4, pp. 981 - 992.e11
Background & Aims Persistent activation of the inflammatory response contributes to the development of inflammatory bowel diseases, which increase the risk of... 
Gastroenterology and Hepatology | Chronic Inflammation | IL6 | IBD Progression | Mouse Model | TARGET | RISK | AKT | IDENTIFICATION | DNA ANEUPLOIDY | INFLAMMATORY-BOWEL-DISEASE | COLORECTAL-CANCER | SURVEILLANCE | MIR-21 | GASTROENTEROLOGY & HEPATOLOGY | NF-KAPPA-B | Dextran Sulfate | Colonic Neoplasms - genetics | Phosphorylation | Colonic Neoplasms - prevention & control | Humans | Colitis, Ulcerative - genetics | Gene Expression Regulation, Neoplastic | Colonic Neoplasms - chemically induced | MicroRNAs - metabolism | NF-kappa B - metabolism | LIM Domain Proteins - metabolism | Case-Control Studies | Colonic Neoplasms - metabolism | Azoxymethane | Transfection | RNA Interference | Inflammation Mediators - metabolism | Biomarkers, Tumor - metabolism | Transcription, Genetic | Tumor Cells, Cultured | Proto-Oncogene Proteins c-akt - metabolism | Interleukin-6 - metabolism | Colitis, Ulcerative - prevention & control | STAT3 Transcription Factor - metabolism | Disease Models, Animal | Cell Line | Signal Transduction | Colon - pathology | Colitis, Ulcerative - metabolism | PTEN Phosphohydrolase - metabolism | Colitis, Ulcerative - pathology | Colon - metabolism | Disease Progression | Animals | Colitis, Ulcerative - chemically induced | Colonic Neoplasms - pathology | Biomarkers, Tumor - genetics | Mice | MicroRNAs - genetics | RNAi Therapeutics | Adaptor Proteins, Signal Transducing - metabolism | Medical colleges | Colon cancer | MicroRNA | Inflammation | Cancer | Ulcerative colitis | Neurophysiology | Index Medicus | Abridged Index Medicus | mouse model | IBD progression | chronic inflammation
Journal Article
Cancer Science, ISSN 1347-9032, 11/2003, Volume 94, Issue 11, pp. 965 - 973
Journal Article