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PLoS ONE, ISSN 1932-6203, 01/2017, Volume 12, Issue 1, p. e0169899
Journal Article
PloS one, ISSN 1932-6203, 2014, Volume 9, Issue 4, p. e94621
The cell surface proteins CD133, CD24 and CD44 are putative markers for cancer stem cell populations in colon cancer, associated with aggressive cancer types and poor prognosis... 
EPITHELIAL-MESENCHYMAL TRANSITION | BREAST-CANCER | INITIATING CELLS | SIGNALING PATHWAYS | SURVIVAL PATHWAY | CARCINOMA CELLS | COLORECTAL-CANCER | MULTIDISCIPLINARY SCIENCES | LARGE GENE LISTS | LYN KINASE | EXPRESSION | CD24 Antigen - metabolism | HCT116 Cells | Humans | Glycoproteins - metabolism | AC133 Antigen | Colonic Neoplasms - metabolism | Antigens, CD - metabolism | HT29 Cells | Peptides - metabolism | Protein Isoforms - metabolism | Neoplastic Stem Cells - metabolism | Hyaluronan Receptors - metabolism | Cell Line, Tumor | Oncogene Protein v-akt - metabolism | Physiological aspects | Care and treatment | Glycoproteins | Colon cancer | Research | Cancer cells | Mesenchyme | Laboratories | Genes | Colorectal cancer | Radiation | Science | AKT protein | Oncology | Radioresistance | Systematic review | Metastasis | Kinases | Cancer therapies | Cell surface | E-cadherin | Cell adhesion & migration | Proteins | CD44 antigen | Cell adhesion | Cell cycle | Colon | Growth factors | γ Radiation | AKT1 protein | Sensitivity analysis | Epidermal growth factor receptors | Markers | AKT2 protein | T cell receptors | Breast cancer | Gene expression | Gamma rays | Gamma radiation | Molecular modelling | Medical prognosis | Isoforms | Stem cells | Radiation tolerance | Snail protein | Cancer | Apoptosis
Journal Article
PloS one, ISSN 1932-6203, 2016, Volume 11, Issue 6, p. e0157830
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2017, Volume 12, Issue 7, p. e0181183
.... Previous studies have shown that ursodeoxycholic acid (UDCA) suppresses the proliferation of colon cancer cells... 
DEOXYCHOLIC-ACID | APOPTOSIS | INFLAMMATORY-BOWEL-DISEASE | MULTIDISCIPLINARY SCIENCES | ULCERATIVE-COLITIS | CHEMOPREVENTIVE AGENT | RISK | CYCLE PROGRESSION | NF-KAPPA-B | PRIMARY SCLEROSING CHOLANGITIS | SUSTAINED ERK PHOSPHORYLATION | Neoplastic Stem Cells - cytology | Cyclin-Dependent Kinases - metabolism | Reactive Oxygen Species - metabolism | Neoplastic Stem Cells - drug effects | HCT116 Cells | Humans | RNA, Messenger - metabolism | Colonic Neoplasms - metabolism | HT29 Cells | Cyclin-Dependent Kinase Inhibitor p27 - metabolism | Ursodeoxycholic Acid - pharmacology | Cyclin-Dependent Kinase Inhibitor p21 - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Neoplastic Stem Cells - metabolism | Cell Cycle Checkpoints - drug effects | Colonic Neoplasms - pathology | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Cell Proliferation - drug effects | p38 Mitogen-Activated Protein Kinases - metabolism | Oxidative Stress - drug effects | Cyclin-Dependent Kinases - genetics | Real-Time Polymerase Chain Reaction | Cyclin-Dependent Kinase Inhibitor p27 - genetics | Mitogen-Activated Protein Kinase 1 - metabolism | Cell proliferation | Oxidative stress | Reactive oxygen species | Colon cancer | Growth | Analysis | Cancer cells | Ursodiol | Research | Fluorescein isothiocyanate | Cell culture | Flow cytometry | Regulations | Biotechnology | GTP-binding protein | Phosphorylation | Colorectal cancer | Fluorescence | Staining | Bromodeoxyuridine | mRNA | Cancer therapies | Phase transitions | Cyclin-dependent kinase 4 | Western blotting | Ursodeoxycholic acid | Cell growth | Rodents | Gastroenterology | Cell cycle | Colon | Inhibition | Immunoglobulins | Oxygen | Internal medicine | Extracellular signal-regulated kinase | Isothiocyanate | Tumor cell lines | Cell counters | Cyclin-dependent kinase 2 | Polymerase chain reaction | Medicine | Inhibitors | Microscopy | Fluorescein | Intracellular | Cancer
Journal Article
PloS one, ISSN 1932-6203, 2018, Volume 13, Issue 1, p. e0191358
Natural killer cells harnessed from healthy individuals can be expanded ex vivo using various platforms to produce large doses for adoptive transfer into cancer patients... 
GROWTH-FACTOR-BETA | NKG2D | VIVO | MULTIDISCIPLINARY SCIENCES | EXPANSION | THROMBOPOIETIN | CYTOTOXICITY | SMALL-MOLECULE INHIBITOR | TGF-BETA-1 | Immunotherapy, Adoptive - methods | Signal Transduction | Humans | Cytotoxicity, Immunologic - physiology | Colonic Neoplasms - metabolism | Killer Cells, Natural - physiology | Xenograft Model Antitumor Assays | Animals | Receptor, Transforming Growth Factor-beta Type II | Receptors, Transforming Growth Factor beta - metabolism | Models, Biological | Cell Line, Tumor | Transforming Growth Factor beta - antagonists & inhibitors | Liver Neoplasms - pathology | Mice | Killer Cells, Natural - metabolism | Transforming Growth Factor beta - metabolism | Protein-Serine-Threonine Kinases - metabolism | Killer cells | Colon cancer | Physiological aspects | Development and progression | Genetic aspects | Research | Transforming growth factors | Therapy | Cell culture | Animal models | Target recognition | Toxicity | Leukemia | Liver | Transforming growth factor-b | Colorectal cancer | Cytotoxicity | Oncology | Metastasis | Kinases | Cancer therapies | Adoptive transfer | Metastases | NKG2 antigen | Biocompatibility | Colon | Inhibition | Natural killer cells | Growth factors | Antigens | Hematology | Myeloid leukemia | Stroma | T cell receptors | Tumor cell lines | Signaling | Immunosuppression | CD16 antigen | Hospitals | Acute myeloid leukemia | Cancer
Journal Article
Cell death and differentiation, ISSN 1476-5403, 2012, Volume 19, Issue 12, pp. 2003 - 2014
...) switches TRAIL-induced apoptosis to regulated necrosis (or necroptosis) in human HT29 colon and HepG2 liver cancer cells... 
RIPK1/RIPK3 | TRAIL | hepatitis | concanavalin A | colon cancer | necroptosis | APOPTOSIS | MITOCHONDRIAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | INVOLVEMENT | PROGRAMMED NECROSIS | IDENTIFICATION | CELL-DEATH | CELL BIOLOGY | TUMOR-NECROSIS-FACTOR | INHIBITION | LIGAND | T-CELLS | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | Hepatocytes - metabolism | TNF-Related Apoptosis-Inducing Ligand - pharmacology | RNA Interference | Adenosine Triphosphate - metabolism | Killer Cells, Natural - immunology | Indoles - pharmacology | Hepatocytes - drug effects | Disease Models, Animal | Cell Line | Imidazoles - pharmacology | Poly(ADP-ribose) Polymerase Inhibitors | Hep G2 Cells | HT29 Cells | Phenanthrenes - pharmacology | Poly(ADP-ribose) Polymerases - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Killer Cells, Natural - drug effects | Mice | Killer Cells, Natural - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Hydrogen-Ion Concentration | RNA, Small Interfering - metabolism | Killer Cells, Natural | Poly(ADP-ribose) Polymerases | Reactive Oxygen Species | Receptor-Interacting Protein Serine-Threonine Kinases | Biochemistry, Molecular Biology | Adenosine Triphosphate | Life Sciences | Phenanthrenes | Imidazoles | TNF-Related Apoptosis-Inducing Ligand | Hepatocytes | RNA, Small Interfering | Indoles | Apoptosis | RIPK3 | Original Paper | RIPK1
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2013, Volume 8, Issue 2, p. e56082
Cancer stem cells (CSCs), a rare population in any type of cancers, including colon cancer, are tumorigenic... 
SURVIVAL | INVASION | CARCINOMA CELLS | COLORECTAL-CANCER | MULTIDISCIPLINARY SCIENCES | TUMOR | PROLIFERATION | DIFFERENTIATION | TRANSCRIPTION FACTOR KLF4 | KRUPPEL-LIKE-FACTOR-4 | EXPRESSION | Oncogene Proteins - genetics | Colonic Neoplasms - genetics | Receptors, G-Protein-Coupled - metabolism | Humans | Retinal Dehydrogenase - metabolism | Glycoproteins - metabolism | Peptides - genetics | Spheroids, Cellular - pathology | Transplantation, Heterologous | Fetal Proteins - metabolism | Antigens, CD - genetics | Cell Movement - genetics | Antigens, CD - metabolism | Peptides - metabolism | Neoplastic Stem Cells - metabolism | RNA Interference | Cell Transformation, Neoplastic - genetics | Isoenzymes - metabolism | Neoplastic Stem Cells - pathology | Female | Cell Adhesion Molecules, Neuronal - metabolism | Glycoproteins - genetics | Isoenzymes - genetics | HCT116 Cells | Spheroids, Cellular - metabolism | Retinal Dehydrogenase - genetics | Reverse Transcriptase Polymerase Chain Reaction | AC133 Antigen | Blotting, Western | Cell Adhesion Molecules, Neuronal - genetics | HT29 Cells | Animals | Mice, Nude | Colonic Neoplasms - pathology | Cell Line, Tumor | Fetal Proteins - genetics | Mice | Mice, Inbred BALB C | Receptors, G-Protein-Coupled - genetics | Kruppel-Like Transcription Factors - genetics | Microscopy, Fluorescence | Mesenchyme | Embryo cells | Colorectal cancer | Science | Metastasis | Drug resistance | Cancer therapies | Metastases | Serum-free medium | Colon cancer | KLF4 protein | Surgery | Colon | Tumorigenicity | Gene expression | Ribonucleic acid--RNA | Studies | Somatic cells | Medical prognosis | Stem cells | Biomarkers | Laboratory animals | Pluripotency | Cell migration | Tumors | Cancer | Apoptosis | RNA | Ribonucleic acid
Journal Article
Oncogene, ISSN 1476-5594, 2018, Volume 38, Issue 11, pp. 1951 - 1965
Cancer stem cells (CSCs) are inherently resistant to chemotherapy, and CSCs in chemotherapy-failed recurrent tumors are enriched... 
POPULATION | STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | ENVIRONMENT | SELF-RENEWAL | BETA-CATENIN | FIBROBLASTS | CELL BIOLOGY | HETEROGENEITY | ONCOLOGY | EQUILIBRIUM | GENETICS & HEREDITY | EXPRESSION | PROGRESSION | Exosomes - drug effects | Exosomes - metabolism | Fibroblasts - physiology | Neoplastic Stem Cells - drug effects | Humans | Wnt Signaling Pathway - physiology | Exosomes - pathology | Colorectal Neoplasms - drug therapy | Neoplastic Stem Cells - pathology | Female | Antineoplastic Agents - pharmacology | Colorectal Neoplasms - metabolism | Neoplastic Stem Cells - physiology | Cell Dedifferentiation - drug effects | Cells, Cultured | Fibroblasts - pathology | Mice, SCID | HT29 Cells | Xenograft Model Antitumor Assays | Drug Resistance, Neoplasm - genetics | Oxaliplatin - pharmacology | Animals | Wnt Signaling Pathway - drug effects | Paracrine Communication - drug effects | Mice, Inbred NOD | Cell Proliferation - drug effects | Fluorouracil - pharmacology | Mice | Pyridines - pharmacology | Colorectal Neoplasms - pathology | Pyrazines - pharmacology | Cell Dedifferentiation - genetics | Drug Resistance, Neoplasm - drug effects | Chemotherapy | Usage | Care and treatment | Cancer cells | Colorectal cancer | Cellular signal transduction | Research | Drug resistance | Cell differentiation | Cancer | Wnt protein | Colorectal carcinoma | Stem cells | Chemoresistance | Fibroblasts | Cell interactions | Exosomes | Tumors | Cell biology | Cancer therapeutic resistance | Cancer stem cells | Cancer microenvironment
Journal Article