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世界胃肠病学杂志:英文版(电子版), ISSN 1007-9327, 2014, Volume 20, Issue 29, pp. 10050 - 10061
AIM:To investigate insulin-like growth factor 2(IGF2)differentially methylated region(DMR)0 hypomethylation in relation to clinicopathological and molecular... 
BRAF | polyp | Colorectal | Colon | Colorectum | neoplasia | Long interspersed nucleotide element-1 | Colon polyp | Serrated pathway | Microsatellite instability | Genome | Insulin-like growth factor | Colorectal neoplasia | EARLY NEOPLASTIC PROGRESSION | LINE-1 HYPOMETHYLATION | PROXIMAL COLON | COLON-CANCER | POLYPOSIS SYNDROME | BRAF MUTATION | PATHWAY | COLORECTAL-CANCER | POOR-PROGNOSIS | GASTROENTEROLOGY & HEPATOLOGY | ADENOMAS | Multivariate Analysis | MutL Protein Homolog 1 | ras Proteins - genetics | Microsatellite Instability | Proto-Oncogene Proteins p21(ras) | Prognosis | Adenoma - genetics | Adenoma - mortality | Colorectal Neoplasms - genetics | Humans | Middle Aged | DNA Repair Enzymes - genetics | Gene Expression Regulation, Neoplastic | Colorectal Neoplasms - chemistry | Male | DNA Methylation | Insulin-Like Growth Factor II - analysis | Insulin-Like Growth Factor II - genetics | Tumor Suppressor Proteins - genetics | Female | Nuclear Proteins - genetics | Colorectal Neoplasms - mortality | Genetic Predisposition to Disease | Biomarkers, Tumor - analysis | Kaplan-Meier Estimate | Logistic Models | Proto-Oncogene Proteins - genetics | Adenoma - chemistry | Chi-Square Distribution | Phosphatidylinositol 3-Kinases - genetics | DNA Modification Methylases - genetics | Phenotype | Class I Phosphatidylinositol 3-Kinases | Long Interspersed Nucleotide Elements | Proto-Oncogene Proteins B-raf - genetics | Adaptor Proteins, Signal Transducing - genetics | Adenoma - pathology | Aged | Biomarkers, Tumor - genetics | Colorectal Neoplasms - pathology | Index Medicus | Original
Journal Article
Journal of the National Cancer Institute, ISSN 0027-8874, 09/2015, Volume 107, Issue 9, p. djv170
Background: Inheritance of a germline mutation in one of the DNA mismatch repair (MMR) genes MLH1, MSH2, MSH6, and PMS2 causes a high risk of colorectal and... 
BREAST-CANCER | COLON-CANCER | REPAIR GENE MUTATION | RANDOMIZED-TRIALS | ONCOLOGY | NONSTEROIDAL ANTIINFLAMMATORY DRUGS | RESISTANT STARCH | PREVENTION | FAMILIAL ADENOMATOUS POLYPOSIS | CARRIERS | RECTAL ADENOMAS | MutL Protein Homolog 1 | United States - epidemiology | Prevalence | Bias | Colorectal Neoplasms - genetics | Humans | Middle Aged | DNA Repair Enzymes - genetics | Male | DNA Mismatch Repair - genetics | Aspirin - administration & dosage | Anticarcinogenic Agents - administration & dosage | Germ-Line Mutation | Adult | Female | Registries | Mismatch Repair Endonuclease PMS2 | Nuclear Proteins - genetics | Colorectal Neoplasms - epidemiology | Colorectal Neoplasms, Hereditary Nonpolyposis - genetics | Proportional Hazards Models | Colorectal Neoplasms - prevention & control | Ibuprofen - administration & dosage | MutS Homolog 2 Protein - genetics | DNA-Binding Proteins - genetics | Confounding Factors (Epidemiology) | Adaptor Proteins, Signal Transducing - genetics | Anti-Inflammatory Agents, Non-Steroidal - administration & dosage | Heterozygote | Adenosine Triphosphatases - genetics | Aged | Prevention | Aspirin | Gene mutations | Ibuprofen | Colorectal cancer | Health aspects | Risk factors | Cancer | Genetic susceptibility | Oncology, Experimental | Genetic research | Genetic aspects | Research | Index Medicus
Journal Article
Journal of Gastroenterology, ISSN 0944-1174, 10/2016, Volume 51, Issue 10, pp. 971 - 984
Journal Article
Journal Article
Journal Article
American Journal of Gastroenterology, ISSN 0002-9270, 02/2016, Volume 111, Issue 2, pp. 275 - 284
OBJECTIVES: Hereditary biallelic mismatch repair deficiency (BMMRD) is caused by biallelic mutations in the mismatch repair (MMR) genes and manifests features... 
TURCOT-SYNDROME | GENE-MUTATIONS | BRAIN-TUMOR | LYNCH-SYNDROME | COLORECTAL-CANCER | GERMLINE MUTATIONS | EARLY-ONSET | MSH6 MUTATIONS | GASTROENTEROLOGY & HEPATOLOGY | PMS2 MUTATIONS | CHILDHOOD | Colorectal Neoplasms - surgery | Melanoma - etiology | MutL Protein Homolog 1 | Adenoma - surgery | Prospective Studies | Brain Neoplasms - etiology | Adenoma - genetics | Glioma - etiology | Adenocarcinoma - etiology | Colorectal Neoplasms - genetics | Humans | Brain Neoplasms - physiopathology | DNA Repair Enzymes - genetics | Child, Preschool | Male | Brain Neoplasms - complications | Young Adult | Colorectal Neoplasms - etiology | Leukemia - etiology | Kidney Neoplasms - etiology | Germ-Line Mutation | Adult | Female | Adenocarcinoma - genetics | Mismatch Repair Endonuclease PMS2 | Neoplastic Syndromes, Hereditary - genetics | Retrospective Studies | Nuclear Proteins - genetics | Child | Intestinal Neoplasms - genetics | Intestinal Neoplasms - surgery | Brain Neoplasms - genetics | Adenoma - etiology | Intestinal Neoplasms - etiology | DNA-Binding Proteins - genetics | Colorectal Neoplasms - physiopathology | Phenotype | Intestine, Small - surgery | Lymphoma - etiology | Adaptor Proteins, Signal Transducing - genetics | Adolescent | Alleles | Neoplastic Syndromes, Hereditary - complications | Wilms Tumor - etiology | Neoplastic Syndromes, Hereditary - physiopathology | Adenosine Triphosphatases - genetics | Colorectal Neoplasms - complications | Adenocarcinoma - surgery | Index Medicus
Journal Article
JAMA, ISSN 0098-7484, 11/2005, Volume 294, Issue 19, pp. 2465 - 2473
CONTEXT Significant proportions of patients with hamartomatous polyposis or with hyperplastic/mixed polyposis remain without specific clinical and molecular... 
KRAS MUTATIONS | MEDICINE, GENERAL & INTERNAL | METHYLATION | SERRATED ADENOMAS | ENDOGLIN | COLORECTAL-CANCER | ENDOTHELIAL-CELLS | DISEASE | JUVENILE POLYPOSIS | EXPRESSION | BETA | Peutz-Jeghers Syndrome - pathology | Prospective Studies | Peutz-Jeghers Syndrome - classification | Humans | Middle Aged | Receptors, Cell Surface | Endoglin | Intestinal Polyps - genetics | Smad4 Protein - genetics | Germ-Line Mutation | Hamartoma Syndrome, Multiple - classification | Adult | Vascular Cell Adhesion Molecule-1 - genetics | Proto-Oncogene Proteins | Child | PTEN Phosphohydrolase - genetics | Genetic Predisposition to Disease | Hamartoma Syndrome, Multiple - genetics | Hamartoma Syndrome, Multiple - pathology | Intestinal Polyposis - pathology | Intestinal Polyposis - genetics | Protein-Serine-Threonine Kinases - genetics | Bone Morphogenetic Protein Receptors, Type I - genetics | Intestinal Polyposis - classification | Peutz-Jeghers Syndrome - genetics | Syndrome | Proteins - genetics | Intestinal Polyps - classification | Proto-Oncogene Proteins B-raf - genetics | Adolescent | Intestinal Polyps - pathology | Mutation | Tumor Suppressor Proteins | Antigens, CD | Diagnosis | Intestinal polyps | Comparative analysis | Peutz-Jeghers syndrome | Health risk assessment | Genes | Deoxyribonucleic acid--DNA | Cancer | Index Medicus | Abridged Index Medicus
Journal Article
ONCOGENE, ISSN 0950-9232, 08/2010, Volume 29, Issue 32, pp. 4567 - 4575
Somatically acquired, activating mutations of GNAS, the gene encoding the stimulatory G-protein Gsa subunit, have been identified in kidney, thyroid,... 
colorectal cancer | HUMAN BREAST | A33 ANTIGEN | BIOCHEMISTRY & MOLECULAR BIOLOGY | STIMULATORY G-PROTEIN | CELL-GROWTH | cAMP | MCCUNE-ALBRIGHT-SYNDROME | ADRENAL-HYPERPLASIA | CELL BIOLOGY | K-RAS | ONCOLOGY | COLORECTAL-CANCER | GENETICS & HEREDITY | GNAS | EXPRESSION | GTP-Binding Protein alpha Subunits, Gs - metabolism | Up-Regulation | Intestinal Mucosa - metabolism | Cell Proliferation | Epithelial Cells - metabolism | Adenoma - genetics | Colorectal Neoplasms - genetics | Humans | Gene Expression Regulation, Neoplastic | Genetic Loci - genetics | Substrate Specificity | Male | Stem Cells - metabolism | Wnt Proteins - metabolism | Promoter Regions, Genetic - genetics | Adenoma - metabolism | MAP Kinase Signaling System | GTP-Binding Protein alpha Subunits, Gs - genetics | Cell Differentiation - genetics | Adenoma - enzymology | Chromogranins | Female | Cyclic AMP - metabolism | Colorectal Neoplasms - metabolism | Colorectal Neoplasms - enzymology | Phosphoric Diester Hydrolases - metabolism | Mutant Proteins - genetics | Epithelial Cells - pathology | Mutant Proteins - metabolism | Organ Specificity | Disease Progression | Membrane Glycoproteins - genetics | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Adenomatous Polyposis Coli Protein - metabolism | Alleles | Adenoma - pathology | Stem Cells - pathology | Mice | Mutation | Colorectal Neoplasms - pathology | Intestinal Mucosa - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus
Journal Article
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 2014, Volume 289, Issue 29, pp. 20102 - 20119
Endoplasmic reticulum (ER) stress and ER stress-associated unfolded protein response (UPR) can promote cancer cell survival, but it remains unclear whether... 
CELLS | CARCINOGENESIS | INHIBITION | BIOCHEMISTRY & MOLECULAR BIOLOGY | SIGNALING NETWORK | TRANSCRIPTION | INDUCED SKIN TUMORIGENESIS | DIFFERENTIATION | EXPRESSION | CANCER | LIGAND ACTIVATION | RNA, Small Interfering - genetics | Colonic Neoplasms - genetics | TOR Serine-Threonine Kinases - metabolism | Adenoma - genetics | Humans | Colonic Neoplasms - metabolism | Adenoma - metabolism | Gene Knockdown Techniques | Heat-Shock Proteins - genetics | Genes, p53 | Cell Transformation, Neoplastic - genetics | Proto-Oncogene Proteins c-akt - metabolism | PPAR delta - genetics | Skin Neoplasms - pathology | Cellular Senescence - genetics | Gene Expression | PPAR delta - deficiency | PPAR-beta - metabolism | Signal Transduction | Cells, Cultured | Activating Transcription Factor 4 - genetics | Cellular Senescence - physiology | Keratinocytes - cytology | Transcription Factors - genetics | DNA-Binding Proteins - genetics | PPAR-beta - genetics | Unfolded Protein Response | Cell Transformation, Neoplastic - metabolism | PPAR-beta - deficiency | Regulatory Factor X Transcription Factors | Skin Neoplasms - metabolism | Animals | Keratinocytes - metabolism | Models, Biological | Colonic Neoplasms - pathology | Endoplasmic Reticulum Stress | Skin Neoplasms - genetics | Adenoma - pathology | Mice | PPAR delta - metabolism | Genes, ras | Index Medicus | Molecular Bases of Disease | Cancer Therapy | Keratinocyte | Cancer Biology | H-RAS-induced Senescence | Tumor Suppressor Gene | Peroxisome Proliferator-activated Receptor β | Cancer | Oncogene-induced Endoplasmic Reticulum Stress
Journal Article
The American Journal of Surgical Pathology, ISSN 0147-5185, 09/2014, Volume 38, Issue 9, pp. 1290 - 1297
Journal Article
Anticancer Research, ISSN 0250-7005, 11/2013, Volume 33, Issue 11, pp. 4779 - 4784
Journal Article