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Gastroenterology, ISSN 0016-5085, 2011, Volume 141, Issue 1, pp. 378 - 388.e4
...); 2 weeks later, some mice also received left and median bile duct ligation (LMBDL) and, then 1 week later, were fed DEN, in corn oil, weekly by oral gavage (DLD... 
Gastroenterology and Hepatology | Cell Cycle | Liver Disease | Carcinogenesis | Transcriptional Regulation | OVEREXPRESSION | INTRAHEPATIC CHOLANGIOCARCINOMA | CYCLIN D1 | LIVER | HYPOXIA | GASTROENTEROLOGY & HEPATOLOGY | Cholestasis - genetics | Cyclin D1 - metabolism | Liver - pathology | Cholestasis - complications | Cholestasis - metabolism | Hyperplasia | Gene Expression Regulation, Neoplastic | Male | MicroRNAs - metabolism | Cholangiocarcinoma - metabolism | Cholangiocarcinoma - etiology | Bile Ducts, Intrahepatic - metabolism | Ligation | Basic Helix-Loop-Helix Transcription Factors - metabolism | RNA Interference | Time Factors | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Diethylnitrosamine | Bile Duct Neoplasms - genetics | Repressor Proteins - metabolism | Disease Models, Animal | Bile Ducts, Intrahepatic - pathology | Bile Duct Neoplasms - metabolism | Signal Transduction | Liver - metabolism | Transcription Factors - genetics | Cholestasis - chemically induced | Proto-Oncogene Proteins c-myc - metabolism | Disease Progression | Bile Duct Neoplasms - etiology | Transcription Factors - metabolism | Cholestasis - pathology | Cholangiocarcinoma - pathology | Animals | Cholangiocarcinoma - genetics | Basic Helix-Loop-Helix Leucine Zipper Transcription Factors - metabolism | Mice | Mice, Inbred BALB C | Bile Duct Neoplasms - pathology | Bile Ducts, Intrahepatic - surgery | RNA-Binding Proteins - metabolism | Liver cancer | Chromatin | DNA binding proteins | Universities and colleges | RNA | carcinogenesis | cell cycle | transcriptional regulation | DNA binding | Liver disease
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 06/2009, Volume 119, Issue 6, pp. 1537 - 1545
...) in the embryonic liver caused hyperplasia of the biliary tree. Abnormal bile duct formation in Foxa1/2-deficient liver was due, at least in part, to activation of IL-6 expression, a proliferative signal for cholangiocytes... 
TRANSCRIPTION FACTORS | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATED PROTEIN-KINASE | LIVER MORPHOGENESIS | HEPATOCYTE GROWTH-FACTOR | GENE FAMILY | INTERLEUKIN-6-DEFICIENT MICE | BILIARY EPITHELIAL-CELLS | NF-KAPPA-B | EXPRESSION | CHOLANGIOCYTE PROLIFERATION | Bile Ducts - growth & development | Cell Proliferation | Hepatocyte Nuclear Factor 3-beta - genetics | Bile Ducts - metabolism | Receptors, Glucocorticoid - metabolism | Hepatocytes - metabolism | Fibrosis - metabolism | Bile Ducts - cytology | Hepatocytes - cytology | Hyperplasia - genetics | Bile Duct Diseases - metabolism | Cell Differentiation | Interleukin-6 - metabolism | Hyperplasia - metabolism | Hepatocyte Nuclear Factor 3-beta - metabolism | Microscopy, Electron, Transmission | Fibrosis - genetics | Interleukin-6 - genetics | Hepatocyte Nuclear Factor 3-alpha - deficiency | Liver - metabolism | Mice, Inbred C57BL | Bile Duct Diseases - genetics | Hepatocyte Nuclear Factor 3-alpha - genetics | Hepatocyte Nuclear Factor 3-alpha - metabolism | Mice, Knockout | Hyperplasia - pathology | Animals | Liver - cytology | Mice | Fibrosis - pathology | Bile Duct Diseases - pathology | Hepatocyte Nuclear Factor 3-beta - deficiency | Common bile duct | Growth | Bile ducts | Genes | Physiological aspects | Genetic aspects | Research | DNA binding proteins
Journal Article
Journal of immunology research, ISSN 2314-8861, 5/2014, Volume 2014, pp. 149185 - 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
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2017, Volume 114, Issue 19, pp. E3806 - E3815
Journal Article
Nature Medicine, ISSN 1078-8956, 08/2017, Volume 23, Issue 8, pp. 954 - 963
The treatment of common bile duct (CBD) disorders, such as biliary atresia or ischemic strictures, is restricted by the lack of biliary tissue from healthy donors suitable for surgical reconstruction... 
PLURIPOTENT STEM-CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | RAT | BIOCHEMISTRY & MOLECULAR BIOLOGY | LIVER | MICE | MODEL | CELL BIOLOGY | Gallbladder - injuries | Organoids - physiology | Biliary Tract - cytology | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Humans | Biliary Tract - physiology | Bile Ducts, Extrahepatic - physiology | Somatostatin - pharmacology | Tissue Scaffolds | Organoids - metabolism | Bile Ducts, Extrahepatic - injuries | Biliary Tract - injuries | Epithelial Cells - cytology | Tissue Engineering - methods | Organoids - cytology | Cell Transplantation | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | gamma-Glutamyltransferase - metabolism | Regeneration - physiology | Secretin - pharmacology | Animals | Keratin-7 - metabolism | Organoids - drug effects | Mice | Bile Ducts, Extrahepatic - cytology | In Vitro Techniques | Keratin-19 - metabolism | Gallbladder - physiology | Biodegradation | Bioengineering | Occlusion | Reconstruction | Biliary atresia | Biodegradability | Ducts | Tissue engineering | Reconstructive surgery | Stenosis | Transplantation | Epithelium | Regeneration (physiology) | Bile duct | Regeneration | Ischemia | Organoids | Surgery | Gallbladder | Tubes | Cholestasis | Bile | Kidney transplantation
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 08/2012, Volume 122, Issue 8, pp. 2911 - 2915
Journal Article
Oncotarget, ISSN 1949-2553, 2014, Volume 5, Issue 9, pp. 2839 - 2852
Journal Article
Development, ISSN 0950-1991, 12/2010, Volume 137, Issue 23, pp. 4061 - 4072
Journal Article
Journal Article