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Journal Article
Nature, ISSN 0028-0836, 02/2018, Volume 554, Issue 7693, pp. 538 - 543
Most patients with colorectal cancer die as a result of the disease spreading to other organs. However, no prevalent mutations have been associated with... 
STEM-CELLS | GENE | COLORECTAL-CANCER | MULTIDISCIPLINARY SCIENCES | MOUSE | LEADS | RECEPTOR | MICE | GROWTH-FACTOR | TUMORIGENESIS | EXPRESSION | Intestines - drug effects | Colonic Neoplasms - genetics | Intestinal Mucosa - metabolism | Colonic Neoplasms - drug therapy | Humans | Male | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Stem Cells - metabolism | Th1 Cells - immunology | T-Lymphocytes, Cytotoxic - drug effects | Neoplasm Metastasis - drug therapy | Neoplasm Metastasis - immunology | Colonic Neoplasms - immunology | Immunotherapy | Transforming Growth Factor beta - antagonists & inhibitors | Female | Liver Neoplasms - secondary | Disease Models, Animal | T-Lymphocytes, Cytotoxic - immunology | Transforming Growth Factor beta - immunology | Tumor Microenvironment - drug effects | Th1 Cells - drug effects | Intestines - pathology | Liver Neoplasms - drug therapy | Liver Neoplasms - immunology | Drug Synergism | Tumor Microenvironment - immunology | Neoplasm Metastasis - genetics | Animals | Cell Differentiation - drug effects | Neoplasm Metastasis - pathology | Colonic Neoplasms - pathology | Alleles | Immune Evasion - drug effects | Stem Cells - drug effects | Stem Cells - pathology | Mice | Mutation | T-Lymphocytes, Cytotoxic - cytology | PD-1 protein | Liver | Colorectal carcinoma | Colorectal cancer | Stem cell transplantation | Cytotoxicity | Lymphocytes T | Metastasis | Metastases | Colon cancer | Intestine | Lymphocytes | Genetic analysis | Fibroblasts | Colon | Inhibition | Growth factors | Phenotypes | Data analysis | Liver diseases | Microsatellites | Organs | Gene expression | Patients | Signaling | Immune checkpoint | PD-L1 protein | Stem cells | Tumors | Cancer | Index Medicus
Journal Article
Genes and Development, ISSN 0890-9369, 06/2006, Volume 20, Issue 12, pp. 1569 - 1574
The tumor suppressor PTEN is frequently inactivated in human cancers. A major downstream effector of PTEN is Akt, which is hyperactivated via PTEN... 
Intestinal polyps | PIN | Endometrium carcinoma | Thyroid and adrenal tumors | Cancer therapy | AKT/PKB | GENETICALLY-ENGINEERED MICE | PTEN | DEVELOPMENTAL BIOLOGY | PHOSPHOINOSITIDE 3-KINASE | CANCER | CELL BIOLOGY | cancer therapy | PATHWAY | thyroid and adrenal tumors | NEOPLASIA | RELEVANCE | intestinal polyps | MUTATION | GENETICS & HEREDITY | endometrium carcinoma | Prostatic Intraepithelial Neoplasia - pathology | Thyroid Neoplasms - enzymology | Proto-Oncogene Proteins c-akt - deficiency | Male | Intestinal Polyps - enzymology | Proto-Oncogene Proteins c-akt - genetics | Adrenal Gland Neoplasms - enzymology | Prostatic Neoplasms - genetics | Endometrial Neoplasms - genetics | Neoplasms - genetics | Female | Pseudolymphoma - genetics | Pseudolymphoma - enzymology | Adrenal Gland Neoplasms - pathology | PTEN Phosphohydrolase - genetics | Prostatic Neoplasms - pathology | Endometrial Neoplasms - enzymology | Neoplasms - enzymology | PTEN Phosphohydrolase - metabolism | Pseudolymphoma - pathology | Thyroid Neoplasms - genetics | Animals | Prostatic Intraepithelial Neoplasia - enzymology | Intestinal Polyps - pathology | Prostatic Neoplasms - enzymology | Endometrial Neoplasms - pathology | Heterozygote | Mice | Prostatic Intraepithelial Neoplasia - genetics | Neoplasms - pathology | Adrenal Gland Neoplasms - genetics | Thyroid Neoplasms - pathology | Index Medicus | Research Communication
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2014, Volume 124, Issue 12, pp. 5368 - 5384
Growing evidence supports a link between inflammation and cancer; however, mediators of the transition between inflammation and carcinogenesis remain... 
INTESTINAL INFLAMMATION | MEDICINE, RESEARCH & EXPERIMENTAL | IN-VITRO | INFLAMMATORY-BOWEL-DISEASE | SPHINGOSINE KINASE 1 | EPITHELIAL-CELLS | GENE | INDUCED COLITIS | CELL-PROLIFERATION | PERSISTENT STAT3 ACTIVATION | CANCER | Lysophospholipids - metabolism | Colonic Neoplasms - genetics | Humans | Gene Expression Regulation, Neoplastic | Aldehyde-Lyases - biosynthesis | MicroRNAs - metabolism | Neoplasm Proteins - metabolism | Inflammatory Bowel Diseases - metabolism | RNA, Neoplasm - metabolism | Colonic Neoplasms - metabolism | Neoplasms, Experimental - pathology | Cell Transformation, Neoplastic - genetics | Gene Deletion | Inflammatory Bowel Diseases - genetics | Neoplasms, Experimental - genetics | Sphingosine - metabolism | Aldehyde-Lyases - genetics | Neoplasm Proteins - genetics | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Mice, Transgenic | Signal Transduction - genetics | Anion Transport Proteins - metabolism | Cell Transformation, Neoplastic - metabolism | Down-Regulation - genetics | Gene Expression Regulation, Enzymologic | Lysophospholipids - genetics | Sphingosine - analogs & derivatives | Animals | Biopsy | Colonic Neoplasms - pathology | RNA, Neoplasm - genetics | Sphingosine - genetics | Mice | MicroRNAs - genetics | Neoplasms, Experimental - metabolism | Anion Transport Proteins - genetics | Colon cancer | MicroRNA | Physiological aspects | Development and progression | Genetic aspects | Lyases | Research | Inflammatory bowel disease | Medical research | Kinases | Rodents | Colorectal cancer | Index Medicus | Abridged Index Medicus
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 5/2012, Volume 109, Issue 21, pp. 8253 - 8258
Autophagy is a lysosome-dependent degradative process that protects cancer cells from multiple stresses. In preclinical models, autophagy inhibition with... 
Cell death | Medical treatment | Cell lines | Lysosomes | Immunoblotting | Cytotoxicity | Dosage | Heterologous transplantation | Tumors | Cancer | Antimalarials | Cancer cell survival | Stress responses | Drug resistance | BISQUINOLINES | cancer cell survival | PROTEIN | cell death | MULTIDISCIPLINARY SCIENCES | TARGETING AUTOPHAGY | MOUSE | antimalarials | AKT | CELL-SURVIVAL | stress responses | NECROSIS | CANCER-TREATMENT | drug resistance | CYTOTOXICITY | Autophagy-Related Proteins | Colonic Neoplasms - genetics | Adenocarcinoma - pathology | Aminoquinolines - chemical synthesis | Antineoplastic Agents - chemical synthesis | Colonic Neoplasms - drug therapy | Humans | Brain Neoplasms - pathology | Aminoquinolines - toxicity | Drug Resistance, Neoplasm | Polyamines - toxicity | Intestinal Obstruction - chemically induced | Autophagy - drug effects | Antineoplastic Agents - toxicity | Glioblastoma - genetics | Adenocarcinoma - genetics | Antineoplastic Agents - pharmacology | Autophagy - genetics | Cell Death - drug effects | Aminoquinolines - pharmacology | Lysosomes - drug effects | Brain Neoplasms - genetics | Brain Neoplasms - drug therapy | Adenocarcinoma - drug therapy | Antimalarials - pharmacology | HT29 Cells | Xenograft Model Antitumor Assays | Carrier Proteins - genetics | Polyamines - pharmacology | Animals | Mice, Nude | Colonic Neoplasms - pathology | Glioblastoma - pathology | Hydroxychloroquine - pharmacology | Mice | Glioblastoma - drug therapy | Intestinal Obstruction - genetics | Polyamines - chemical synthesis | Autophagy (Cytology) | Phenotype | Genetic aspects | Dosage and administration | Enzyme inhibitors | Identification and classification | Genotype & phenotype | Genetics | Autophagy | Cells | Index Medicus | Biological Sciences
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
Nature, ISSN 0028-0836, 2009, Volume 457, Issue 7229, pp. 608 - 611
Journal Article
Gut, ISSN 0017-5749, 04/2017, Volume 66, Issue 4, pp. 633 - 643
Journal Article
Gut, ISSN 0017-5749, 12/2016, Volume 65, Issue 12, pp. 1973 - 1980
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