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Nature (London), ISSN 1476-4687, 2018, Volume 562, Issue 7725, pp. 69 - 75
.... Here we show that the hepatic microenvironment epigenetically shapes lineage commitment in mosaic mouse models of liver tumorigenesis... 
PATHOGENESIS | HEPATOCELLULAR-CARCINOMA | READ ALIGNMENT | HEPATOCYTES | DNA | INFLAMMATION | PACKAGE | MULTIDISCIPLINARY SCIENCES | FRAMEWORK | BINDING | DISCOVERY | Humans | Tumor Microenvironment | Apoptosis - genetics | Hepatocytes - pathology | Male | Gene Expression Profiling | Genes, myc | Hepatocytes - metabolism | Proto-Oncogene Proteins c-akt - genetics | DNA-Binding Proteins - metabolism | Carcinoma, Hepatocellular - genetics | DNA Transposable Elements - genetics | Female | Liver Neoplasms - pathology | Cell Differentiation | Cell Lineage - genetics | Disease Models, Animal | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | Cytokines - metabolism | Liver Neoplasms - genetics | Carcinogenesis - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | T-Box Domain Proteins - genetics | T-Box Domain Proteins - metabolism | Transcription Factors - metabolism | Cholangiocarcinoma - pathology | Animals | Epigenesis, Genetic - genetics | Carcinoma, Hepatocellular - pathology | Cholangiocarcinoma - genetics | Mosaicism | Mice | Necrosis - genetics | Genes, ras | Liver cancer | Research | Carcinogenesis | Oncology, Experimental | Apoptosis | Cancer | Animal models | Cytokines | Liver | Hepatocellular carcinoma | Genomes | Metastasis | Risk analysis | Gene expression | Risk factors | Metastases | Hepatocytes | Morphology | DNA methylation | Tumorigenesis | Bioinformatics | Cholangiocarcinoma | Deoxyribonucleic acid--DNA | Tumors | T-Box Domain Proteins/metabolism | Hepatocytes/pathology | DNA-Binding Proteins/metabolism | Life Sciences | Cholangiocarcinoma/pathology | Transcription Factors/metabolism | Necrosis/genetics | Cytokines/metabolism | Epigenesis, Genetic/genetics | Cyclin-Dependent Kinase Inhibitor p16/deficiency | Carcinoma, Hepatocellular/pathology | DNA Transposable Elements/genetics | Cell Lineage/genetics | T-Box Domain Proteins/genetics | Transcription Factors/genetics | Apoptosis/genetics | Proto-Oncogene Proteins c-akt/genetics | Liver Neoplasms/genetics | Cholangiocarcinoma/genetics | Liver Neoplasms/pathology | DNA-Binding Proteins/genetics | Hepatocytes/metabolism | Carcinoma, Hepatocellular/genetics | Carcinogenesis/genetics
Journal Article
Journal of immunology research, ISSN 2314-7156, 2014, Volume 2014, pp. 1 - 19
Acute inflammation is a response to an alteration induced by a pathogen or a physical or chemical insult, which functions to eliminate the source of the damage... 
EPITHELIAL-MESENCHYMAL TRANSITION | ACTIVATED PROTEIN-KINASE | CARCINOMA-CELL-LINES | TGF-BETA | NITRIC-OXIDE SYNTHASE | NECROSIS-FACTOR-ALPHA | FACTOR-KAPPA-B | TNF-ALPHA | IMMUNOLOGY | ENDOTHELIAL GROWTH-FACTOR | PRIMARY SCLEROSING CHOLANGITIS | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Oxidative Stress | Colitis - genetics | Colorectal Neoplasms - genetics | Humans | Tumor Necrosis Factor-alpha - genetics | Colitis - complications | Colitis - pathology | Cholangiocarcinoma - metabolism | Inflammation - complications | Colorectal Neoplasms - etiology | Inflammation - metabolism | Bile Ducts, Intrahepatic - metabolism | Tumor Microenvironment - genetics | Interleukin-10 - metabolism | Bile Duct Neoplasms - genetics | Interleukin-6 - metabolism | Colorectal Neoplasms - metabolism | Bile Ducts, Intrahepatic - pathology | Gene Expression | Bile Duct Neoplasms - metabolism | Interleukin-6 - genetics | Carcinogenesis - genetics | Cholangiocarcinoma - pathology | Transforming Growth Factor beta - genetics | Interleukin-10 - genetics | Colitis - metabolism | Cholangiocarcinoma - genetics | Inflammation - genetics | Bile Duct Neoplasms - pathology | Colorectal Neoplasms - pathology | Chronic Disease | Transforming Growth Factor beta - metabolism | Free radicals | Cytokines | Disease | Mortality | Clinical trials | Metastasis | Cancer therapies | Proteins | Angiogenesis | Medical prognosis | Tumorigenesis | Nonsteroidal anti-inflammatory drugs | Chemokines | Immune system | Tumors | Cancer | Apoptosis | Review
Journal Article
Journal Article
Cancer research (Chicago, Ill.), ISSN 0008-5472, 08/2013, Volume 73, Issue 16, pp. 5016 - 5028
TGF-beta has limited effects on ovarian cancer cells, but its contributions to ovarian tumor growth might be mediated through elements of the tumor microenvironment... 
CROSS-TALK | MATRIX | STEM-CELLS | CONTRIBUTE | INHIBITION | ONCOLOGY | MEMBRANE | TRANSCRIPTION | STROMAL CELLS | EXPRESSION | FIBROBLASTS | Up-Regulation | Receptors, Transforming Growth Factor beta - genetics | Epithelial Cells - metabolism | Stromal Cells - pathology | Humans | Ovarian Neoplasms - pathology | Transcriptome | NF-kappa B - metabolism | Cell Movement - genetics | Ovarian Neoplasms - genetics | Matrix Metalloproteinase 9 - metabolism | Versicans - genetics | Tumor Microenvironment - genetics | Matrix Metalloproteinase 9 - genetics | Hyaluronan Receptors - metabolism | Female | Ovarian Neoplasms - metabolism | Extracellular Matrix Proteins - metabolism | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Signal Transduction | Neoplasm Invasiveness | Extracellular Matrix Proteins - genetics | Stromal Cells - metabolism | Protein-Serine-Threonine Kinases - genetics | Epithelial Cells - pathology | Smad Proteins - genetics | Fibroblasts - pathology | Hyaluronan Receptors - genetics | Disease Progression | Transforming Growth Factor beta - genetics | NF-kappa B - genetics | Receptors, Transforming Growth Factor beta - metabolism | Cell Line, Tumor | Versicans - metabolism | Smad Proteins - metabolism | Transforming Growth Factor beta - metabolism | cancer-associated fibroblast | TGF-β | versican | tumor microenvironment | ovarian cancer
Journal Article
Nature (London), ISSN 1476-4687, 2014, Volume 518, Issue 7537, pp. 107 - 110
Journal Article
Gut, ISSN 0017-5749, 09/2018, Volume 67, Issue 9, pp. 1692 - 1703
Journal Article