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BMC Genomics, ISSN 1471-2164, 08/2013, Volume 14, Issue 1, pp. 589 - 589
Background: Qualitative alterations or abnormal expression of microRNAs (miRNAs) in colon cancer have mainly been demonstrated in primary tumors. Poorly... 
microRNA | Metastasis | Regulatory networks | Gene expression | Colorectal cancer | PROGNOSIS | ADENOCARCINOMA | CELL INVASION | EXPRESSION PROFILES | SIGNATURE | BREAST-CANCER | INVASIVENESS | INHIBITION | GASTRIC-CANCER | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | GENETICS & HEREDITY | PROMOTES | Oncogene Proteins - genetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Pyrophosphatases - genetics | Transcriptome | Male | MicroRNAs - metabolism | Gene Regulatory Networks | Liver Neoplasms - mortality | Carcinogenesis | Adenocarcinoma - metabolism | RNA Interference | Female | Adenocarcinoma - genetics | Liver Neoplasms - secondary | Colorectal Neoplasms - metabolism | Colorectal Neoplasms - mortality | Liver Neoplasms - genetics | Kaplan-Meier Estimate | Oncogene Proteins - metabolism | Adenocarcinoma - secondary | Disease Progression | Pyrophosphatases - metabolism | Liver Neoplasms - metabolism | Aged | MicroRNAs - genetics | Colorectal Neoplasms - pathology | Adenocarcinoma - mortality | Development and progression | Genetic aspects | Colon cancer | Research | Analysis | Liver | Biosynthesis | DNA binding proteins | Genetic transcription | Cluster analysis | Mortality | Oncology | Genomes | Patients | Studies | Survival analysis | Surgery | MicroRNAs | Colon | Tumors | Index Medicus
Journal Article
Gastroenterology, ISSN 0016-5085, 2017, Volume 152, Issue 6, pp. 1434 - 1448.e15
Background & Aims Intestinal tissues from patients with inflammatory bowel disease (IBD) and colorectal cancer have increased expression of microRNA-301a... 
Gastroenterology and Hepatology | Mouse model | Immune regulation | Crohn’s disease | Ulcerative colitis | Crohn's disease | TRANSLOCATION | APOPTOSIS | ACTIVATION | VITAMIN-D-RECEPTOR | CELL-PROLIFERATION | MICROBIOTA | TIGHT JUNCTION | BOWEL-DISEASE | MUCOSAL BARRIER | IMMUNE-SYSTEM | GASTROENTEROLOGY & HEPATOLOGY | Dextran Sulfate | Neoplasm Transplantation | Up-Regulation | Intestinal Mucosa - metabolism | Intestinal Mucosa - physiopathology | Colitis - genetics | Colorectal Neoplasms - genetics | Humans | Middle Aged | JNK Mitogen-Activated Protein Kinases - metabolism | Male | MicroRNAs - metabolism | Interleukin-1beta - genetics | Neoplasm Proteins - metabolism | RNA, Messenger - metabolism | Transcription Factor RelA - genetics | Case-Control Studies | Colorectal Neoplasms - etiology | Azoxymethane | Transfection | Interleukin-1beta - metabolism | Colitis - chemically induced | Inflammatory Breast Neoplasms - metabolism | Female | Cadherins - genetics | Neoplasm Proteins - genetics | Cell Proliferation - genetics | Gene Expression | Colon - pathology | Down-Regulation | HCT116 Cells | Mice, Inbred C57BL | Epithelial Cells | Signal Transduction - genetics | Inflammatory Breast Neoplasms - genetics | Tumor Burden | Colorectal Neoplasms - chemically induced | Mice, Knockout | Animals | Transcription Factor RelA - metabolism | Inflammatory Breast Neoplasms - complications | Aged | MicroRNAs - genetics | Colorectal Neoplasms - pathology | Intestinal Mucosa - pathology | Medical colleges | Medical research | MicroRNA | Gastrointestinal diseases | Colorectal cancer | Medicine, Experimental | Colitis | Cancer | Inflammation | Analysis | Index Medicus | Abridged Index Medicus
Journal Article
Journal Article
Cancer Letters, ISSN 0304-3835, 2015, Volume 371, Issue 1, pp. 99 - 106
Highlights • Higher expression of UCA1 is significantly associated with poorer survival time. • UCA1 overexpression enhanced the proliferation and colony... 
Hematology, Oncology and Palliative Medicine | UCA1 | lncRNA | ERBB4 | miR-193a-3p | Non-small cell lung cancer | LncRNA | MiR-193a-3p | BLADDER-CANCER | MARKER | CLASSIFICATION | TUMORS | LONG NONCODING RNA | ONCOLOGY | PATHWAY | COLORECTAL-CANCER | CARCINOMA-ASSOCIATED 1 | CONTRIBUTES | Receptor, ErbB-4 - metabolism | Multivariate Analysis | Up-Regulation | Cell Proliferation | Lung Neoplasms - mortality | Humans | Lung Neoplasms - metabolism | Middle Aged | Gene Expression Regulation, Neoplastic | Lung Neoplasms - pathology | Male | MicroRNAs - metabolism | Transfection | RNA Interference | Time Factors | Female | Retrospective Studies | Oncogenes | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | Carcinoma, Non-Small-Cell Lung - genetics | Risk Factors | Carcinoma, Non-Small-Cell Lung - metabolism | Kaplan-Meier Estimate | Proportional Hazards Models | Treatment Outcome | Lung Neoplasms - therapy | RNA, Long Noncoding - genetics | Chi-Square Distribution | Carcinoma, Non-Small-Cell Lung - mortality | Carcinoma, Non-Small-Cell Lung - therapy | Cell Line, Tumor | MicroRNAs - genetics | Receptor, ErbB-4 - genetics | RNA, Long Noncoding - metabolism | Lung cancer, Non-small cell | Lung cancer | Mortality | Manufacturers | Metastasis | Multivariate analysis | Gene expression | Proteins | Confidence intervals | Liver cancer | Cell growth | Chemotherapy | Medical prognosis | Binding sites | Index Medicus
Journal Article
Oncogene, ISSN 0950-9232, 11/2015, Volume 34, Issue 48, pp. 5890 - 5899
The retinoblastoma gene (Rb) is mutated at significant frequency in various human epithelial tumors, including colorectal cancer, and is strongly associated... 
PRB | BIOCHEMISTRY & MOLECULAR BIOLOGY | BETA-CATENIN | TUMORS | DEFICIENT CELLS | CELL BIOLOGY | ONCOLOGY | PROSTATE-CANCER | GENETICS & HEREDITY | MICE | MOLECULAR-BASIS | TUMORIGENESIS | EXPRESSION | Prostatic Neoplasms - metabolism | Adenocarcinoma - etiology | Humans | Lung Neoplasms - metabolism | Gene Expression Regulation, Neoplastic | Prostatic Neoplasms - etiology | Male | Immunoenzyme Techniques | Liver Neoplasms - etiology | Tumor Suppressor Protein p53 - physiology | Colorectal Neoplasms - etiology | Adenocarcinoma - metabolism | Lung Neoplasms - etiology | Lung Neoplasms - secondary | Female | Tumor Cells, Cultured | Liver Neoplasms - secondary | Retinoblastoma Protein - physiology | Colorectal Neoplasms - metabolism | Wnt Signaling Pathway | Disease Models, Animal | Neuroendocrine Tumors - metabolism | Intestinal Neoplasms - metabolism | Intestinal Neoplasms - etiology | Intestinal Neoplasms - secondary | Mutation - genetics | Adenocarcinoma - secondary | Mice, Knockout | Prostatic Neoplasms - secondary | Animals | Neuroendocrine Tumors - secondary | Liver Neoplasms - metabolism | Mice | Neuroendocrine Tumors - etiology | Colorectal Neoplasms - pathology | Gene mutations | Colorectal cancer | Development and progression | Tumor suppressor genes | Genetic aspects | Properties | Gene expression | Health aspects | Models | Genes | Rodents | Index Medicus | Rb | β-catenin | colorectal cancer | intestine | neuroendocrine | bladder
Journal Article
European Journal of Cancer, ISSN 0959-8049, 2016, Volume 68, pp. 1 - 10
Abstract Purpose We performed a multi-centre phase I study to assess the safety, pharmacokinetics (PK) and pharmacodynamics (PD) of the orally available small... 
Hematology, Oncology and Palliative Medicine | Pharmacodynamics | MEK inhibitor | Phase I | Optimal biological dose | Pharmacokinetics | BRAF-MUTATED MELANOMA | MULTICENTER | SELUMETINIB PLUS DOCETAXEL | SAFETY | TRAMETINIB | CELL LUNG-CANCER | TRIAL | DOSE-ESCALATION | ONCOLOGY | DOUBLE-BLIND | AZD6244 ARRY-142886 | Lung Neoplasms - drug therapy | Pancreatic Neoplasms - metabolism | Nausea - chemically induced | Allosteric Regulation | Humans | Lung Neoplasms - metabolism | Middle Aged | Male | Fatigue - chemically induced | Ribosomal Protein S6 Kinases, 70-kDa - drug effects | Protein Kinase Inhibitors - adverse effects | Colorectal Neoplasms - drug therapy | Chromatography, Liquid | Proto-Oncogene Proteins c-akt - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Bile Duct Neoplasms - metabolism | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Administration, Oral | Carcinoma, Non-Small-Cell Lung - metabolism | Neoplasms - drug therapy | Maximum Tolerated Dose | Mesothelioma - metabolism | Mitogen-Activated Protein Kinase 3 - metabolism | Anorexia - chemically induced | Glycogen Synthase Kinase 3 beta - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Neoplasms - metabolism | Phosphoproteins - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | Cholangiocarcinoma - metabolism | Chromatography, High Pressure Liquid | Diarrhea - chemically induced | Mitogen-Activated Protein Kinase 3 - drug effects | Pancreatic Neoplasms - drug therapy | Tandem Mass Spectrometry | Uterine Cervical Neoplasms - metabolism | Esophageal Neoplasms - metabolism | Adult | Female | Colorectal Neoplasms - metabolism | Bile Duct Neoplasms - drug therapy | Drug Eruptions - etiology | Abdominal Pain - chemically induced | Uterine Cervical Neoplasms - drug therapy | Glycogen Synthase Kinase 3 beta - metabolism | Mesothelioma - drug therapy | Cholangiocarcinoma - drug therapy | MAP Kinase Kinase 2 - antagonists & inhibitors | Protein Kinase Inhibitors - therapeutic use | Aged | Protein Kinase Inhibitors - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Esophageal Neoplasms - drug therapy | Proto-Oncogene Proteins c-akt - drug effects | Care and treatment | Protein kinases | Mitogens | Cells | Tumors | Index Medicus
Journal Article
Oncogene, ISSN 0950-9232, 10/2007, Volume 26, Issue 49, pp. 6979 - 6988
Epithelial to mesenchymal transition (EMT) is implicated in the progression of primary tumours towards metastasis andis likely caused by a pathological... 
Epithelial to mesenchymal transition | Transcription | Epithelial polarity | Invasion | Cell adhesion | epithelial polarity | DIFFERENTIATION PROGRAM | transcription | FACTOR SNAIL | BIOCHEMISTRY & MOLECULAR BIOLOGY | E-CADHERIN EXPRESSION | VITAMIN-D-RECEPTOR | BETA-CATENIN | CELL BIOLOGY | BREAST-CANCER | COLON-CANCER | LUNG-CANCER | invasion | ONCOLOGY | cell adhesion | MESENCHYMAL TRANSITIONS | GENETICS & HEREDITY | epithelial to mesenchymal transition | PROGRESSION | Cell Polarity | Colonic Neoplasms - genetics | Nucleoside-Phosphate Kinase - genetics | Cadherins - metabolism | Cytoskeletal Proteins - antagonists & inhibitors | Membrane Glycoproteins - metabolism | Oligonucleotide Array Sequence Analysis | Cytoskeletal Proteins - genetics | Homeodomain Proteins - metabolism | Humans | Middle Aged | Immunoblotting | Gene Expression Profiling | Colonic Neoplasms - metabolism | Breast Neoplasms - metabolism | Membrane Glycoproteins - antagonists & inhibitors | Chromatin Immunoprecipitation | Neoplasm Invasiveness - pathology | Adult | Cytoskeletal Proteins - metabolism | Cell Differentiation | Membrane Proteins - metabolism | Tumor Cells, Cultured | Snail Family Transcription Factors | Promoter Regions, Genetic | Epithelium - pathology | Epithelium - metabolism | Membrane Proteins - genetics | Down-Regulation | Nucleoside-Phosphate Kinase - antagonists & inhibitors | Transcription Factors - genetics | Reverse Transcriptase Polymerase Chain Reaction | Disease Progression | Homeodomain Proteins - genetics | Membrane Glycoproteins - genetics | Transcription Factors - metabolism | Breast Neoplasms - genetics | Membrane Proteins - antagonists & inhibitors | Breast Neoplasms - pathology | Colonic Neoplasms - pathology | Aged | Microscopy, Fluorescence | Nucleoside-Phosphate Kinase - metabolism | Zinc Finger E-box-Binding Homeobox 1 | Cancer cells | Physiological aspects | Genetic aspects | Research | DNA binding proteins | Health aspects | Proteins | Oncology | Gene expression | Colorectal cancer | Cell adhesion & migration | Tumors | Index Medicus
Journal Article
International Journal of Molecular Medicine, ISSN 1107-3756, 09/2017, Volume 40, Issue 3, pp. 587 - 606
Canonical WNT signaling through Frizzled and LRP5/6 receptors is transduced to the WNT/β-catenin and WNT/stabilization of proteins (STOP) signaling cascades to... 
regulatory T cells | FGF | angiogenesis | WNT5A | Notch | tumor microenvironment | cancer stem cells | Alzheimer's disease | myeloid-derived suppressor cells | epithelial-to-mesenchymal transition | Angiogenesis | Tumor microenvironment | Epithelial-to-mesenchymal transition | Myeloid-derived suppressor cells | Cancer stem cells | Regulatory T cells | MEDICINE, RESEARCH & EXPERIMENTAL | BONE-MINERAL DENSITY | NEURAL-TUBE DEFECTS | PLANAR CELL POLARITY | TCF SIGNALING PATHWAY | CANCER STEM-CELLS | DOMINANT ROBINOW SYNDROME | RECEPTOR TYROSINE KINASES | ACUTE LYMPHOBLASTIC-LEUKEMIA | FAMILIAL EXUDATIVE VITREORETINOPATHY | ENDOTHELIAL GROWTH-FACTOR | Prostatic Neoplasms - metabolism | Colorectal Neoplasms, Hereditary Nonpolyposis - genetics | Humans | Endometrial Neoplasms - metabolism | Male | Neoplasm Proteins - metabolism | Intellectual Disability - metabolism | Intellectual Disability - therapy | Prostatic Neoplasms - therapy | Colorectal Neoplasms, Hereditary Nonpolyposis - metabolism | Colorectal Neoplasms, Hereditary Nonpolyposis - therapy | Animals | Prostatic Neoplasms - genetics | Endometrial Neoplasms - genetics | Wnt Signaling Pathway - genetics | Endometrial Neoplasms - therapy | Female | Mutation | Neoplasm Proteins - genetics | Proteins | Tyrosine | Molecular genetics | Gene mutations | Colorectal cancer | Genetic aspects | Health aspects | Heparan sulfate | Phosphorylation | Pathogenesis | Genomics | Genes | Cardiovascular disease | Kinases | Defects | Cell adhesion & migration | Osteoporosis | Stem cells | Genetics | Ligands | Alzheimers disease
Journal Article