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Nature communications, ISSN 2041-1723, 2018, Volume 9, Issue 1, pp. 424 - 15
Transition from pluripotency to differentiation is a pivotal yet poorly understood developmental step. Here, we show that the tumour suppressor RASSF1A is a... 
GATA FACTORS | DNA METHYLATION DYNAMICS | ZYGOTIC GENE-EXPRESSION | TGF-BETA | PROTEIN | PATHWAY | MULTIDISCIPLINARY SCIENCES | EMBRYONIC STEM-CELLS | TRANSCRIPTION | SELF-RENEWAL | PREIMPLANTATION MOUSE DEVELOPMENT | Embryonic Stem Cells - cytology | Humans | Tumor Protein p73 - genetics | Male | Phosphoproteins - metabolism | Wnt Proteins - metabolism | Tumor Protein p73 - metabolism | DNA-Binding Proteins - metabolism | Octamer Transcription Factor-3 - genetics | Basic Helix-Loop-Helix Transcription Factors - metabolism | Gene Expression Regulation, Developmental | Tumor Suppressor Proteins - genetics | Mice, Inbred CBA | Female | Cell Differentiation | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | Signal Transduction | Mice, Inbred C57BL | Protein-Serine-Threonine Kinases - genetics | Phosphoproteins - genetics | beta Catenin - metabolism | Embryonic Stem Cells - physiology | Transcription Factors - metabolism | Animals | Octamer Transcription Factor-3 - metabolism | Adaptor Proteins, Signal Transducing - genetics | Adaptor Proteins, Signal Transducing - metabolism | Cell Cycle Proteins | Wnt protein | Quaternary | Oct-4 protein | Yes-associated protein | GATA-1 protein | β-catenin | Demethylation | Signaling | Cell fate | Stem cells | Differentiation | Pluripotency | Tumors
Journal Article
Cancer research (Chicago, Ill.), ISSN 1538-7445, 2017, Volume 77, Issue 8, pp. 1997 - 2007
.... Through proteomics and informatic analyses of PEAK1-depleted PDAC cells, we defined protein translation, cytoskeleton organization, and cell-cycle regulatory pathways as major pathways controlled by PEAK1... 
BREAST-CANCER | OCT4 | CARCINOGENESIS | ONCOLOGY | DUCTAL ADENOCARCINOMA | SELF-RENEWAL | YAP | KRAS | TAZ | TRANSLATION FACTOR EIF5A | NANOG EXPRESSION | RNA-Binding Proteins - genetics | Pancreatic Neoplasms - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Carcinoma, Pancreatic Ductal - metabolism | Octamer Transcription Factor-3 - biosynthesis | Phosphoproteins - metabolism | RNA, Messenger - metabolism | Peptide Initiation Factors - biosynthesis | Carcinoma, Pancreatic Ductal - genetics | Octamer Transcription Factor-3 - genetics | RNA-Binding Proteins - biosynthesis | Protein-Tyrosine Kinases - genetics | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Protein-Tyrosine Kinases - biosynthesis | Phosphoproteins - biosynthesis | Signal Transduction | Pancreatic Neoplasms - pathology | RNA, Messenger - genetics | Pancreatic Neoplasms - genetics | Transcription Factors - biosynthesis | Phosphoproteins - genetics | Transcription Factors - genetics | Carcinoma, Pancreatic Ductal - pathology | Peptide Initiation Factors - metabolism | Transcription Factors - metabolism | Peptide Initiation Factors - genetics | Adaptor Proteins, Signal Transducing - genetics | Cell Cycle - physiology | Cell Line, Tumor | Cytoskeleton - metabolism | Adaptor Proteins, Signal Transducing - biosynthesis | Adaptor Proteins, Signal Transducing - metabolism | RNA-Binding Proteins - metabolism | Adenocarcinoma | Translation | Transcription factors | Oct-4 protein | c-Myc protein | Translation initiation | Tumorigenicity | Myc protein | Kinases | Adhesion | K-Ras protein | Proteins | Yes-associated protein | Signal transduction | Signaling | Pathways | Pancreatic cancer | Proteomics | Interrogation | Stem cells | Cytoskeleton | Protein expression | Focal adhesion kinase | Cancer | YAP1 | PEAK1 | pancreatic ductal adenocarcinoma | eIF5A
Journal Article
PloS one, ISSN 1932-6203, 2019, Volume 14, Issue 2, p. e0211980
... (Shh) signaling pathway and its downstream transcription factors gli are considered as one of these mechanisms [1-3]. The gli1, gli2 and gli3 proteins are required... 
PROTEIN-KINASE-A | STEM-CELLS | GLIOBLASTOMA | MESSENGER-RNA | CELL SELF-RENEWAL | SIGNALING PATHWAY | SPLICE VARIANT | MULTIDISCIPLINARY SCIENCES | KRUPPEL FAMILY | EXPRESSION | SONIC-HEDGEHOG | Neoplastic Stem Cells - drug effects | Humans | Brain Neoplasms - metabolism | Repressor Proteins - antagonists & inhibitors | Gene Knockdown Techniques | Glioma - metabolism | Glioma - genetics | Neoplastic Stem Cells - metabolism | Zinc Finger Protein Gli2 - antagonists & inhibitors | Zinc Finger Protein GLI1 - antagonists & inhibitors | Gene Expression Regulation, Neoplastic - drug effects | Nuclear Proteins - genetics | Zinc Finger Protein Gli2 - genetics | Cell Survival - drug effects | Nerve Tissue Proteins - antagonists & inhibitors | Zinc Finger Protein GLI1 - genetics | Zinc Finger Protein Gli3 - antagonists & inhibitors | Brain Neoplasms - genetics | Repressor Proteins - genetics | Pyrimidines - pharmacology | Nerve Tissue Proteins - genetics | Zinc Finger Protein Gli3 - genetics | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Forkhead Box Protein M1 - genetics | Pyridines - pharmacology | HeLa Cells | Research | DNA binding proteins | Gene expression | Gliomas | Cell death | Stem cells | Brain | Biotechnology | Transformation | Transcription factors | Dehydrogenases | Brain cancer | Genes | Oct-4 protein | Differentiation (biology) | Kinases | Tissues | Cell adhesion & migration | Proteins | Demethylation | Signal transduction | Embryogenesis | Glioma cells | Cell cycle | Deoxyribonucleic acid--DNA | Cell survival | siRNA | Cell differentiation | Survival | Embryonic growth stage | Brain research | Cell lines | Ligands | Nuclear physics | Deoxyribonucleic acid | DNA
Journal Article
PloS one, ISSN 1932-6203, 2010, Volume 5, Issue 11, p. e14060
... from excising the aberrant gemcitabine nucleotide [4], [5]. Incorporated gemcitabine can be recognized by p53 and DNA dependent protein kinase, which may induce apoptosis... 
EXCISION-REPAIR | METHYLATION | MECHANISM | CISPLATIN | HUMAN-CELLS | BIOLOGY | MISMATCH REPAIR | DRUG-RESISTANCE | CANCER | DAMAGE | 2',2'-DIFLUORODEOXYCYTIDINE | Xenopus | MutL Protein Homolog 1 | Xenopus Proteins - genetics | Humans | Deoxycytidine - pharmacology | HEK293 Cells | Cell Cycle Proteins - genetics | Oocytes - drug effects | Antimetabolites, Antineoplastic - pharmacology | Female | Epigenesis, Genetic - drug effects | Nuclear Proteins - genetics | DNA Repair - drug effects | Oocytes - metabolism | HCT116 Cells | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Gene Expression Regulation - drug effects | Animals | Adaptor Proteins, Signal Transducing - genetics | Cell Line, Tumor | Xenopus Proteins - metabolism | Adaptor Proteins, Signal Transducing - metabolism | DNA Methylation - drug effects | Deoxycytidine - analogs & derivatives | Epigenetic inheritance | Care and treatment | Gemcitabine | Analysis | Genes | DNA | Genetic engineering | Methylation | Health aspects | DNA repair | Cells | Cancer | Camptothecin | Leukemia | Oct-4 protein | Cytotoxicity | Kinases | Drug resistance | Cancer therapies | Base excision repair | Neurogenesis | Oocytes | Mammalian cells | Proteins | Demethylation | Embryology | Reporter gene | DNA methylation | Inhibition | Repair | Deoxyribonucleic acid--DNA | Enzymes | MLH1 protein | DNA topoisomerase | Polymerization | Nucleotide excision repair | DNA biosynthesis | Gene silencing | Chemotherapy | Gadd45A protein | Plasmids | Epigenetics | GADD45 protein | Tumors | Deoxyribonucleic acid
Journal Article
PloS one, ISSN 1932-6203, 09/2013, Volume 8, Issue 9, p. e73940
Stem cell pluripotency, angiogenesis and epithelial-mesenchymal transition (EMT) have been shown to be significantly upregulated in pancreatic ductal... 
EPITHELIAL-MESENCHYMAL TRANSITION | STEM-CELLS | INHIBITION | REPROGRAMMING FACTOR LIN28 | MULTIDISCIPLINARY SCIENCES | DOWN-REGULATION | LET-7 | TUMOR-GROWTH | EXPRESSION | EGF RECEPTOR | FEEDBACK LOOP | Pancreatic Neoplasms - metabolism | RNA Processing, Post-Transcriptional | Humans | Pancreatic Neoplasms - pathology | Gene Expression Regulation, Neoplastic | Gene Silencing | Protein-Serine-Threonine Kinases - genetics | MicroRNAs - metabolism | Pancreatic Neoplasms - genetics | Intracellular Signaling Peptides and Proteins - metabolism | DNA-Binding Proteins - genetics | Epithelial-Mesenchymal Transition - genetics | DNA-Binding Proteins - metabolism | Xenograft Model Antitumor Assays | Animals | Neoplastic Stem Cells - metabolism | Cell Line, Tumor | Neovascularization, Pathologic - genetics | Tumor Burden - genetics | Mice | MicroRNAs - genetics | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Disease Models, Animal | MicroRNA | Analysis | Pancreatic cancer | Stem cells | Development and progression | DNA binding proteins | Metastasis | Vascular endothelial growth factor | Health aspects | Adenocarcinoma | Post-transcription | Health sciences | Animal models | Transcription factors | Mesenchyme | Veterans | Oct-4 protein | Gene regulation | c-Myc protein | Homeostasis | Myc protein | Kinases | K-Ras protein | Metastases | Angiogenesis | Allografts | KLF4 protein | Intestine | Xenografts | miRNA | siRNA | Gene expression | Ribonucleic acid--RNA | Ablation | Medicine | MicroRNAs | Tumor suppressor genes | Poly(lactide-co-glycolide) | Snail protein | Polyps | Pluripotency | Tumors | Cancer | RNA | Ribonucleic acid
Journal Article
PloS one, ISSN 1932-6203, 2010, Volume 5, Issue 11, p. e13952
... Sox genes are expressed throughout embryogenesis and encode a subclass of high mobility group (HMG) box proteins driving cell fate decisions by acting... 
PLURIPOTENT STEM-CELLS | DOUBLE-STRANDED-RNA | CELL SELF-RENEWAL | MULTIDISCIPLINARY SCIENCES | TROPHOBLAST DEVELOPMENT | GENE-EXPRESSION | PRIMITIVE ENDODERM | NANOG | TRANSCRIPTIONAL REGULATION | PROTEIN TRANSDUCTION | MOUSE EMBRYO | Immunohistochemistry | Embryonic Stem Cells - metabolism | Embryonic Stem Cells - cytology | Homeodomain Proteins - metabolism | Apoptosis - genetics | Male | Morula - metabolism | Phosphoproteins - metabolism | RNA, Messenger - metabolism | SOXB1 Transcription Factors - metabolism | DNA-Binding Proteins - metabolism | Octamer Transcription Factor-3 - genetics | Cell Differentiation - genetics | RNA Interference | SOXB1 Transcription Factors - genetics | Gene Expression Regulation, Developmental | Muscle Proteins - metabolism | Female | Trophoblasts - cytology | Cell Lineage - genetics | Trophoblasts - metabolism | RNA, Messenger - genetics | Blastocyst - metabolism | Cells, Cultured | Blastocyst - cytology | Morula - cytology | Phosphoproteins - genetics | Transcription Factors - genetics | DNA-Binding Proteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Homeodomain Proteins - genetics | Muscle Proteins - genetics | Transcription Factors - metabolism | Microscopy, Confocal | Animals | Octamer Transcription Factor-3 - metabolism | Adaptor Proteins, Signal Transducing - genetics | Mice | Adaptor Proteins, Signal Transducing - metabolism | CDX2 Transcription Factor | Embryonic development | Embryo | Fibroblast growth factors | Genetic transcription | RNA | Genes | Neurosciences | Transcription factors | Oct-4 protein | Neurobiology | CDX2 protein | Trophectoderm | Proteins | Embryogenesis | Restoration | Developmental stages | Cell fate | Life sciences | Trends | Growth factors | Fibroblast growth factor receptor 2 | Sox2 protein | RNA-mediated interference | Markers | Zebrafish | Implantation | Blastocysts | siRNA | Mammals | Gene expression | Ribonucleic acid--RNA | Embryos | Cavitation | Fibroblast growth factor 4 | Yes-associated protein | Stem cells | Pluripotency | Apoptosis | Ribonucleic acid
Journal Article
Cancer Letters, ISSN 0304-3835, 2017, Volume 401, pp. 53 - 62
Abstract Tumor-initiating cells (TICs) play an important role in tumorigenesis and development for many various tissue origin cancers including non-small cell... 
Hematology, Oncology and Palliative Medicine | c-Myc | NDRG1 | Skp2 | Cancer initiating cells | Lung cancer | SUPPRESSOR | PROTEIN | ANGIOGENESIS | PHOSPHORYLATION | PLURIPOTENCY | IDENTIFICATION | ONCOLOGY | DEGRADATION | INHIBITOR | Phosphorylation | Prognosis | Lung Neoplasms - mortality | Humans | Lung Neoplasms - metabolism | Middle Aged | Gene Expression Regulation, Neoplastic | Lung Neoplasms - pathology | Male | Intracellular Signaling Peptides and Proteins - metabolism | Ubiquitination | Transfection | Neoplastic Stem Cells - metabolism | RNA Interference | Proteolysis | Cell Cycle Proteins - genetics | Neoplastic Stem Cells - pathology | Adult | Female | Protein Stability | Tumor Cells, Cultured | Spheroids, Cellular | Intracellular Signaling Peptides and Proteins - genetics | Carcinoma, Non-Small-Cell Lung - pathology | Lung Neoplasms - genetics | A549 Cells | Cyclin-Dependent Kinase 2 - metabolism | Signal Transduction | Carcinoma, Non-Small-Cell Lung - genetics | Carcinoma, Non-Small-Cell Lung - metabolism | Cell Cycle Proteins - metabolism | S-Phase Kinase-Associated Proteins - metabolism | Carcinoma, Non-Small-Cell Lung - mortality | Proto-Oncogene Proteins c-myc - metabolism | Phenotype | Survival Analysis | Aged | Proto-Oncogene Proteins c-myc - genetics | Ubiquitin | Medical colleges | RNA | Analysis | Genes | Stem cells | Genetic aspects | Lung cancer, Non-small cell | Cancer | Cancer cells | Development and progression | Respiratory agents
Journal Article
Scientific reports, ISSN 2045-2322, 01/2015, Volume 5, Issue 1, p. 8081
The development of human induced pluripotent stem cell (iPSC) technology has revolutionized the regenerative medicine field. This technology provides a... 
DERIVATION | STEM-CELLS | HUMAN ES | VIRUS | MULTIDISCIPLINARY SCIENCES | GENERATION | MECHANISMS | EXPRESSION | VECTOR | Leukocytes, Mononuclear - metabolism | RNA-Binding Proteins - genetics | Tumor Suppressor Protein p53 - antagonists & inhibitors | Homeodomain Proteins - metabolism | Humans | Tumor Suppressor Protein p53 - genetics | Cellular Reprogramming | Codon | Karyotyping | Plasmids - genetics | Epstein-Barr Virus Nuclear Antigens - metabolism | Fibroblasts - metabolism | Nanog Homeobox Protein | Pluripotent Stem Cells - cytology | Epstein-Barr Virus Nuclear Antigens - genetics | Introns | Cells, Cultured | Transcription Factors - genetics | Immunity, Innate | Plasmids - metabolism | Proto-Oncogene Proteins c-myc - metabolism | Homeodomain Proteins - genetics | Pluripotent Stem Cells - metabolism | Transcription Factors - metabolism | Animals | Leukocytes, Mononuclear - cytology | Fibroblasts - cytology | Mice | Proto-Oncogene Proteins c-myc - genetics | Microscopy, Fluorescence | RNA-Binding Proteins - metabolism | RNA, Small Interfering - metabolism | Integration | p53 Protein | Oct-4 protein | Color | c-Myc protein | Leukocytes (mononuclear) | Genomes | Myc protein | Drug screening | Ribonucleic acid--RNA | Regeneration | Transfection | KLF4 protein | Rodents | Stem cells | Fibroblasts | Peripheral blood mononuclear cells | Pluripotency | Inhibitory postsynaptic potentials
Journal Article
PloS one, ISSN 1932-6203, 06/2013, Volume 8, Issue 6, p. e64877
.... Here we demonstrate that Akt phosphorylates special AT-rich sequences binding protein 1 (SATB1... 
OCT4 | F9 CELLS | SATB1 | PHOSPHORYLATION | LEUKEMIA-INITIATING CELLS | MULTIDISCIPLINARY SCIENCES | HEMATOPOIETIC STEM-CELLS | QUIESCENCE | GROWTH | PLURIPOTENCY | NANOG EXPRESSION | Phosphorylation | Homeodomain Proteins - metabolism | Humans | Phosphatidylinositol 3-Kinases - metabolism | Recombinant Fusion Proteins - metabolism | Proto-Oncogene Proteins c-akt - genetics | SOXB1 Transcription Factors - metabolism | Octamer Transcription Factor-3 - genetics | Proto-Oncogene Proteins c-bcl-2 - metabolism | SOXB1 Transcription Factors - genetics | Kruppel-Like Transcription Factors - metabolism | HEK293 Cells | Nestin - genetics | Cell Differentiation | Gene Expression Regulation, Neoplastic - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Tretinoin - pharmacology | Nanog Homeobox Protein | Matrix Attachment Region Binding Proteins - metabolism | Homeodomain Proteins - genetics | Nestin - metabolism | Phosphatidylinositol 3-Kinases - genetics | Animals | Signal Transduction - drug effects | Matrix Attachment Region Binding Proteins - genetics | Octamer Transcription Factor-3 - metabolism | Embryonal Carcinoma Stem Cells - pathology | Recombinant Fusion Proteins - genetics | Mice | Embryonal Carcinoma Stem Cells - metabolism | Kruppel-Like Transcription Factors - genetics | Proto-Oncogene Proteins c-bcl-2 - genetics | Embryonal Carcinoma Stem Cells - drug effects | Amino acids | Carcinoma | Genetic transcription | Stem cells | Protein binding | Cancer | Binding | Nestin | Transcription | Threonine | Laboratories | Oct-4 protein | Serine | Homeostasis | AKT protein | Activation | Insulin-like growth factors | Kinases | Gene expression | Substrates | 1-Phosphatidylinositol 3-kinase | Signaling | KLF4 protein | Rodents | Differentiation | Retinoic acid | Pluripotency | Apoptosis
Journal Article
PloS one, ISSN 1932-6203, 07/2015, Volume 10, Issue 7, p. e0132977
... (Brother of Regulator of Imprinted Sites) or CTCFL (CTCF-like) is a DNA-binding protein that is expressed in normal tissues only in germ cells and is re-activated in tumors... 
TESTIS ANTIGEN BORIS | HEPATOCELLULAR-CARCINOMA | SIDE POPULATION | IN-VITRO | INDUCED APOPTOSIS | TELOMERASE | MULTIDISCIPLINARY SCIENCES | IMPRINTED SITES | CTCF | IDENTIFICATION | TUMOR-INITIATING CELLS | ATP Binding Cassette Transporter, Sub-Family G, Member 2 | RNA, Small Interfering - genetics | Cell Proliferation | Epithelial Cells - metabolism | Polycomb Repressive Complex 1 - metabolism | Homeodomain Proteins - metabolism | Humans | Retinal Dehydrogenase - metabolism | Gene Expression Regulation, Neoplastic | Spheroids, Cellular - pathology | Epithelial-Mesenchymal Transition - genetics | Neoplasm Proteins - metabolism | SOXB1 Transcription Factors - metabolism | DNA-Binding Proteins - metabolism | Octamer Transcription Factor-3 - genetics | Polycomb Repressive Complex 1 - genetics | Telomerase - genetics | ATP-Binding Cassette Transporters - genetics | Neoplastic Stem Cells - metabolism | SOXB1 Transcription Factors - genetics | Isoenzymes - metabolism | Hyaluronan Receptors - metabolism | ATP-Binding Cassette Transporters - metabolism | Biomarkers, Tumor - metabolism | Neoplastic Stem Cells - pathology | Telomerase - metabolism | Neoplasm Proteins - genetics | DNA-Binding Proteins - antagonists & inhibitors | Nanog Homeobox Protein | Signal Transduction | Isoenzymes - genetics | Spheroids, Cellular - metabolism | Epithelial Cells - pathology | Retinal Dehydrogenase - genetics | DNA-Binding Proteins - genetics | Organ Specificity | Hyaluronan Receptors - genetics | Homeodomain Proteins - genetics | Phenotype | Octamer Transcription Factor-3 - metabolism | Cell Line, Tumor | Biomarkers, Tumor - genetics | Cell Movement | RNA, Small Interfering - metabolism | RNA | Genes | Colorectal cancer | Stem cells | Genetic aspects | Gene expression | Cancer | Protein binding | Neurosciences | Germ cells | Telomerase reverse transcriptase | Populations | Dyes | Mesenchyme | Oct-4 protein | Gene regulation | Oncology | Spheres | Drug resistance | Tissues | Metastases | DNA-binding protein | CD44 antigen | Cell cycle | Life sciences | Colon | Telomerase | Growth factors | Deoxyribonucleic acid--DNA | Medical research | Antigens | Cell survival | Tumor cells | Invasiveness | Cervix | Survival | Brain research | Molecular modelling | Medical prognosis | Epigenetics | Breast | Tumors | Deoxyribonucleic acid | DNA
Journal Article