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Gastroenterology, ISSN 0016-5085, 2017, Volume 152, Issue 4, pp. 880 - 894.e6
Background & Aims Hepatocellular adenomas (HCAs) are benign liver tumors that can be assigned to molecular subtypes based on inactivating mutations in... 
Gastroenterology and Hepatology | HCC | SHH | Tumor Progression | Benign | HEDGEHOG PATHWAY | FOLLOW-UP | CANCER | TUMORS | SOMATIC MUTATIONS | INACTIVATION | INHIBITION | THERAPEUTIC TARGETS | GASTROENTEROLOGY & HEPATOLOGY | LIVER ADENOMATOSIS | ACTIVATING MUTATIONS | Liver Neoplasms - classification | Hepatocyte Nuclear Factor 1-alpha - genetics | Adenoma - genetics | Cytokine Receptor gp130 - genetics | Humans | Middle Aged | Transcriptome | Hedgehog Proteins - metabolism | Male | Liver Neoplasms - chemistry | GTP-Binding Protein alpha Subunits, Gs - genetics | Young Adult | Protein-Tyrosine Kinases - genetics | Telomerase - genetics | Cell Transformation, Neoplastic - genetics | Carcinoma, Hepatocellular - genetics | Hemorrhage - etiology | Aged, 80 and over | Adult | Chromogranins - genetics | Female | Carcinoma, Hepatocellular - chemistry | Inhibin-beta Subunits - genetics | Neoplasm Proteins - genetics | Child | STAT3 Transcription Factor - genetics | Liver Neoplasms - genetics | Signal Transduction | Zinc Finger Protein GLI1 - genetics | Risk Factors | Janus Kinase 2 - genetics | Gene Fusion | Adenoma - chemistry | beta Catenin - genetics | Sequence Analysis, RNA | Adenoma - classification | Adolescent | Carcinoma, Hepatocellular - pathology | Aged | Mutation | Liver cancer | Liver | Risk factors | Adenoma | Index Medicus | Abridged Index Medicus | Life Sciences | Human health and pathology | Santé publique et épidémiologie | Hépatology and Gastroenterology | Tissues and Organs
Journal Article
by Palles, Claire and Cazier, Jean-Baptiste and Howarth, Kimberley M and Domingo, Enric and Jones, Angela M and Broderick, Peter and Kemp, Zoe and Spain, Sarah L and Almeida, Estrella Guarino and Salguero, Israel and Sherborne, Amy and Chubb, Daniel and Carvajal-Carmona, Luis G and Ma, Yusanne and Kaur, Kulvinder and Dobbins, Sara and Barclay, Ella and Gorman, Maggie and Martin, Lynn and Kovac, Michal B and Humphray, Sean and Lucassen, Anneke and Holmes, Christopher H and Bentley, David and Donnelly, Peter and Taylor, Jenny and Petridis, Christos and Roylance, Rebecca and Sawyer, Elinor J and Kerr, David J and Clark, Susan and Grimes, Jonathan and Kearsey, Stephen E and Thomas, Huw J.W and McVean, Gilean and Houlston, Richard S and Tomlinson, Ian and Thomas, Huw J.W and Maher, Eamonn and Evans, Gareth and Cummings, Carole and Stevens, Margaret and Walker, Lisa and Halliday, Dorothy and Armstrong, Ruth and Paterson, Joan and Hodgson, Shirley and Homfray, Tessa and Side, Lucy and Izatt, Louise and Donaldson, Alan and Tomkins, Susan and Morrison, Patrick and Goodman, Selina and Brewer, Carole and Henderson, Alex and Davidson, Rosemarie and Murday, Victoria and Cook, Jaqueline and Haites, Nneva and Bishop, Timothy and Sheridan, Eamonn and Green, Andrew and Marks, Christopher and Carpenter, Sue and Broughton, Mary and Greenhalge, Lynn and Suri, Mohnish and Bell, John and Ratcliffe, Peter and Wilkie, Andrew and Broxholme, John and Buck, David and Cornall, Richard and Gregory, Lorna and Knight, Julian and Lunter, Gerton and Kingsbury, Zoya and Grocock, Russell and Hatton, Edouard and Holmes, Christopher C and Hughes, Linda and Humburg, Peter and Kanapin, Alexander and Murray, Lisa and Rimmer, Andy and WGS500 Consortium and CORGI Consortium and The WGS500 Consortium and The CORGI Consortium
Nature Genetics, ISSN 1061-4036, 02/2013, Volume 45, Issue 2, pp. 136 - 143
Journal Article
Gut, ISSN 0017-5749, 01/2017, Volume 66, Issue 1, pp. 97 - 106
Objective Sessile serrated adenomas (SSAs) are the precursors of at least 15% of colorectal carcinomas, but their biology is incompletely understood. We... 
COLONIC POLYPS | COLON CARCINOGENESIS | COLORECTAL CANCER GENES | COLONIC NEOPLASMS | ISLAND METHYLATOR PHENOTYPE | COLON-CANCER | COLONOSCOPY | HYPERPLASTIC POLYPS | EARLY NEOPLASTIC PROGRESSION | BRAF MUTATION | PATHWAY | COLORECTAL-CANCER | MICROSATELLITE INSTABILITY | POOR SURVIVAL | GASTROENTEROLOGY & HEPATOLOGY | Adenoma - genetics | Proto-Oncogene Proteins p21(ras) - genetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | Male | Tumor Suppressor Protein p14ARF - analysis | Carcinoma - chemistry | Young Adult | Colonic Polyps - genetics | Cell Transformation, Neoplastic - genetics | Aged, 80 and over | Neoplastic Syndromes, Hereditary - genetics | Wnt Signaling Pathway | Brain Neoplasms - genetics | Tumor Burden | DNA Repair Enzymes - analysis | Phenotype | MutL Protein Homolog 1 - genetics | CpG Islands | Carcinoma - genetics | Mutation | Age Factors | beta Catenin - analysis | Colonic Polyps - pathology | DNA Repair Enzymes - genetics | Colorectal Neoplasms - chemistry | Tumor Suppressor Protein p53 - genetics | Tumor Suppressor Protein p53 - analysis | Tumor Suppressor Proteins - genetics | Adult | Female | Carcinoma - pathology | DNA Modification Methylases - analysis | Cross-Sectional Studies | Gene Silencing | Adenoma - chemistry | Colonic Polyps - chemistry | beta Catenin - genetics | MutL Protein Homolog 1 - analysis | DNA Modification Methylases - genetics | Proto-Oncogene Proteins B-raf - genetics | Sex Factors | Adenoma - pathology | Aged | Tumor Suppressor Protein p14ARF - genetics | Cell Transformation, Neoplastic - pathology | Colorectal Neoplasms - pathology | Tumor Suppressor Proteins - analysis | Dysplasia | Usage | Carcinoma | Diagnosis | Clinical pathology | Cancer | DNA methylation | Bias | Deoxyribonucleic acid--DNA | Tumors | Index Medicus | Abridged Index Medicus
Journal Article
American Journal of Surgical Pathology, ISSN 0147-5185, 09/2011, Volume 35, Issue 9, pp. 1274 - 1286
Abundant recent data suggest that sessile serrated adenoma/polyp (SSA/P) is an early precursor lesion in the serrated pathway of carcinogenesis. It is believed... 
dysplasia | serrated adenoma | cancer | polyp | pathology | SURGERY | CPG ISLAND METHYLATION | MICROSATELLITE INSTABILITY | PHENOTYPE | PREVALENCE | KRAS MUTATIONS | BRAF MUTATION | PATHWAY | EXPRESSION | ADENOMAS | MutL Protein Homolog 1 | United States - epidemiology | Proto-Oncogene Proteins p21(ras) | Adenoma - genetics | Colorectal Neoplasms - genetics | Humans | Hyperplasia | Middle Aged | Male | Young Adult | Colonic Polyps - genetics | Cadherins - genetics | Intestinal Polyps - ethnology | Genes, p16 | Intestinal Polyps - pathology | Mutation | Adenoma - ethnology | ras Proteins - genetics | Microsatellite Instability | Colonic Polyps - pathology | Asian Continental Ancestry Group - genetics | DNA Repair Enzymes - genetics | Gene Expression Regulation, Neoplastic | Rectal Diseases - pathology | Colonic Polyps - ethnology | Genes, APC | Rectal Diseases - ethnology | DNA Methylation | Intestinal Polyps - genetics | Chromatin Immunoprecipitation | Tumor Suppressor Proteins - genetics | Polymerase Chain Reaction | Adult | Female | Nuclear Proteins - genetics | Rectal Diseases - genetics | Republic of Korea - epidemiology | Colorectal Neoplasms - ethnology | Linear Models | Proto-Oncogene Proteins - genetics | Chi-Square Distribution | Nerve Tissue Proteins - genetics | Carrier Proteins - genetics | DNA Modification Methylases - genetics | Proto-Oncogene Proteins B-raf - genetics | Adaptor Proteins, Signal Transducing - genetics | Adenoma - pathology | Aged | Colorectal Neoplasms - pathology | Index Medicus
Journal Article
PLoS Genetics, ISSN 1553-7390, 02/2009, Volume 5, Issue 2, pp. e1000384 - e1000384
Journal Article
Nature Genetics, ISSN 1061-4036, 12/2014, Volume 47, Issue 1, pp. 31 - 38
Cushing's disease is caused by corticotroph adenomas of the pituitary. To explore the molecular mechanisms of endocrine autonomy in these tumors, we performed... 
UBPY | ENDOSOMES | DOMAIN | PROTEIN | EPIDERMAL-GROWTH-FACTOR | GENETICS & HEREDITY | UBIQUITYLATION | DEGRADATION | RECEPTOR DOWN-REGULATION | ENDOCYTIC TRAFFICKING | PITUITARY-ADENOMAS | Adenoma - genetics | Humans | Neoplasm Proteins - physiology | Gene Expression Regulation, Neoplastic | Cercopithecus aethiops | Endosomal Sorting Complexes Required for Transport - genetics | Molecular Sequence Data | Pituitary Neoplasms - complications | ACTH-Secreting Pituitary Adenoma - complications | Pituitary ACTH Hypersecretion - genetics | ACTH-Secreting Pituitary Adenoma - genetics | Receptor, Epidermal Growth Factor - metabolism | Pituitary Neoplasms - secretion | Neoplasm Proteins - genetics | Pro-Opiomelanocortin - genetics | Amino Acid Sequence | ACTH-Secreting Pituitary Adenoma - metabolism | Pituitary Neoplasms - genetics | Ubiquitin Thiolesterase - physiology | Pituitary Neoplasms - metabolism | Ubiquitin Thiolesterase - genetics | 14-3-3 Proteins - metabolism | Adrenocorticotropic Hormone - secretion | Sequence Homology, Amino Acid | Exome - genetics | Sequence Alignment | Animals | Endopeptidases - genetics | ACTH-Secreting Pituitary Adenoma - secretion | Pro-Opiomelanocortin - biosynthesis | Mutation | COS Cells | Endosomal Sorting Complexes Required for Transport - physiology | Endopeptidases - physiology | Gene mutations | Cushing syndrome | Physiological aspects | Genetic aspects | Research | Ubiquitin-proteasome system | Health aspects | Risk factors | Pituitary gland | Kinases | Rodents | Genes | Tumors | Index Medicus
Journal Article
Gastroenterology, ISSN 0016-5085, 2012, Volume 142, Issue 2, pp. 248 - 256
Journal Article
Science, ISSN 0036-8075, 3/2009, Volume 323, Issue 5922, pp. 1747 - 1750
Journal Article
Hepatology, ISSN 0270-9139, 01/2007, Volume 45, Issue 1, pp. 42 - 52
Hepatocellular carcinomas (HCCs) are a heterogeneous group of tumors that differ in risk factors and genetic alterations. We further investigated... 
OVEREXPRESSION | CELLS | FACTOR-II | PRIMARY LIVER-CANCER | HEPATITIS-B VIRUS | HUMAN HEPATOCELLULAR CARCINOMAS | BETA-CATENIN MUTATIONS | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | TUMORS | HEPATOCARCINOGENESIS | Multigene Family | Liver Neoplasms - classification | Adenoma - genetics | Genes, Neoplasm | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Phosphatidylinositol 3-Kinases - metabolism | Wnt Proteins - metabolism | Proto-Oncogene Proteins c-akt - genetics | Tumor Suppressor Protein p53 - genetics | Adenoma - metabolism | Nuclear Pore Complex Proteins - genetics | Carcinoma, Hepatocellular - drug therapy | Wnt Proteins - genetics | Carcinoma, Hepatocellular - genetics | Adenoma - drug therapy | Cell Cycle Proteins - genetics | Female | Transcription, Genetic | Proto-Oncogene Proteins c-akt - metabolism | Carcinoma, Hepatocellular - classification | Liver Neoplasms - genetics | Nuclear Pore Complex Proteins - metabolism | Cell Cycle Proteins - metabolism | Liver Neoplasms - drug therapy | Tumor Suppressor Protein p53 - metabolism | Signal Transduction - genetics | Mutation - genetics | Phosphatidylinositol 3-Kinases - genetics | Class I Phosphatidylinositol 3-Kinases | Adenoma - classification | Liver Neoplasms - metabolism | DNA, Neoplasm - genetics | Carcinoma, Hepatocellular - metabolism | Index Medicus
Journal Article
Genes Chromosomes and Cancer, ISSN 1045-2257, 2009, Volume 49, Issue 12, pp. 1114 - 1124
The diagnosis of myoepithelial (ME) tumors outside salivary glands remains challenging, especially in unusual clinical presentations, such as bone or visceral... 
ONCOLOGY | CHORDOMA | GENETICS & HEREDITY | IN-SITU HYBRIDIZATION | DEFINES | SALIVARY-GLANDS | MUCOEPIDERMOID CARCINOMA | EXPRESSION | ADENOMAS | POU5F1 | RNA-Binding Proteins - genetics | Salivary Gland Neoplasms - genetics | Soft Tissue Neoplasms - diagnosis | Humans | Middle Aged | Biomarkers, Tumor | Octamer Transcription Factor-3 - genetics | Young Adult | Molecular Diagnostic Techniques | Oncogene Fusion | Skin Neoplasms - diagnosis | Adult | Bone Neoplasms - genetics | Cytogenetic Analysis | Pre-B-Cell Leukemia Transcription Factor 1 | Child | Soft Tissue Neoplasms - genetics | Calmodulin-Binding Proteins - genetics | Myoepithelioma - diagnosis | Gene Expression | Zinc Fingers | Bone Neoplasms - diagnosis | RNA-Binding Protein FUS - genetics | Immunophenotyping | In Situ Hybridization, Fluorescence | Proto-Oncogene Proteins - genetics | DNA-Binding Proteins - genetics | Myoepithelioma - genetics | Salivary Gland Neoplasms - diagnosis | Oncogene Proteins, Fusion - genetics | Gene Rearrangement | Skin Neoplasms - genetics | Adolescent | Aged | RNA-Binding Protein EWS | Pediatrics | Lung | Benign | Cytology | FUS gene | Salivary gland | Bone tumors | EWSR1 gene | FLI-1 protein | Soft tissues | Clear cells | FUS protein | Fluorescence in situ hybridization | Skin | Children | gene rearrangement | Differentiation | Tumors | Index Medicus
Journal Article