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PLoS ONE, ISSN 1932-6203, 11/2016, Volume 11, Issue 11, p. e0166500
Osteosarcoma (OS) is an aggressive bone malignancy with a high relapse rate despite combined treatment with surgery and multiagent chemotherapy. As for other... 
BREAST-CANCER | LUNG-CANCER | METASTASIS | MICROENVIRONMENT | PATHWAY | MULTIDISCIPLINARY SCIENCES | DOWN-REGULATION | GROWTH-FACTOR | KAPPA-B | INTERLEUKIN-6 | EXPRESSION | Inflammation - pathology | Cell Proliferation | Stromal Cells - pathology | Cell Count | Coculture Techniques | Humans | Stromal Cells - metabolism | Transforming Growth Factor beta1 - metabolism | Gene Expression Regulation, Neoplastic | Spheroids, Cellular - pathology | Mesenchymal Stromal Cells - metabolism | Cell Adhesion Molecules - metabolism | Interleukin-6 - secretion | Cell Movement - genetics | Neoplasm Metastasis | Neoplastic Stem Cells - metabolism | Models, Biological | Inflammation Mediators - metabolism | Biomarkers, Tumor - metabolism | Cell Line, Tumor | Neoplastic Stem Cells - pathology | Biomarkers, Tumor - genetics | Osteosarcoma - genetics | Osteosarcoma - pathology | Viral antibodies | Chemotherapy | Osteosarcoma | Stem cells | Antibodies | Development and progression | B cells | Metastasis | Transforming growth factors | Health aspects | Cancer | Mesenchyme | Lung cancer | Chemoresistance | Malignancy | Bone surgery | Metastases | Cell adhesion & migration | Anticancer properties | Interleukin 6 | Cell growth | Surgery | Biocompatibility | Growth factors | Multiagent systems | Cytokines | Intercellular adhesion molecule 1 | Tumor cells | Inflammation | Breast cancer | Medicine | Bone cancer | Stromal cells | Medical prognosis | Combined treatment | Tumors
Journal Article
Cancer Letters, ISSN 0304-3835, 2015, Volume 368, Issue 1, pp. 54 - 63
Highlights • NK cells ability to target osteosarcoma cells and the pathways involved were studied. • We explored NK cell elimination of osteosarcoma (OS) Tumor... 
Hematology, Oncology and Palliative Medicine | Natural killer cells | Immunotherapy | Osteosarcoma tumor initiating cells | NKG2D–NKG2DL interactions | NKG2D-NKG2DL interactions | RECEPTOR | MULTIPLE-MYELOMA CELLS | CANCER STEM-CELLS | THERAPY | NK CELLS | ONCOLOGY | LEUKEMIA-CELLS | PROGNOSTIC-SIGNIFICANCE | CYTOTOXICITY | NKG2D LIGAND EXPRESSION | T-CELLS | Cell Proliferation | Bone Neoplasms - therapy | Neoplastic Stem Cells - drug effects | Coculture Techniques | Humans | NK Cell Lectin-Like Receptor Subfamily K - immunology | Neoplastic Stem Cells - immunology | Bone Neoplasms - pathology | Bone Neoplasms - metabolism | Spironolactone - pharmacology | NK Cell Lectin-Like Receptor Subfamily K - metabolism | Neoplastic Stem Cells - metabolism | Time Factors | Neoplastic Stem Cells - pathology | Antineoplastic Agents - pharmacology | Osteosarcoma - metabolism | Immunotherapy, Adoptive - methods | Signal Transduction | Lymphocyte Activation | Killer Cells, Lymphokine-Activated - metabolism | Cell Communication | Bone Neoplasms - immunology | Mice, SCID | Killer Cells, Lymphokine-Activated - transplantation | Killer Cells, Lymphokine-Activated - immunology | Osteosarcoma - immunology | Animals | Cell Line, Tumor | Ligands | Mice, Inbred NOD | Osteosarcoma - therapy | Osteosarcoma - pathology | Cytotoxicity, Immunologic | Osteosarcoma | Killer cells | Tumors | Chemotherapy | Analysis | Stem cells | Metastasis | Protein binding | Cancer
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2016, Volume 11, Issue 11, pp. e0166027 - e0166027
Studies have shown that mesenchymal stem/stromal cells (MSCs) from bone marrow are involved in the growth and metastasis of solid tumors but the mechanism... 
MCT1 EXPRESSION | STEM-CELLS | PULMONARY METASTASIS | MULTIDISCIPLINARY SCIENCES | BONE-MARROW | GROWTH | DOWN-REGULATION | PROLIFERATION | TUMOR STROMA | CANCER | MICRORNA | Cell Proliferation | Oxidative Stress | Cell Survival | Extracellular Vesicles - pathology | Humans | Gene Expression Regulation, Neoplastic | Intercellular Signaling Peptides and Proteins - genetics | Cell Communication | Tumor Microenvironment | Culture Media, Conditioned | Mesenchymal Stromal Cells - cytology | Cell Line, Tumor | MicroRNAs - genetics | Osteosarcoma - pathology | Apoptosis | Cell Movement | MicroRNA | Osteosarcoma | Genes | Stem cells | Fibroblast growth factors | Metastasis | Cell proliferation | Fibroblast growth factor | Cell culture | Mesenchyme | Leukemia | Bone tumors | Biochemistry | Matrix metalloproteinase | Kinases | Assaying | Nutrient release | Metastases | Signal transduction | Penicillin | Bone marrow | Biocompatibility | Nutrients | miRNA | Metalloproteinase | Conditioning | Growth factors | Medical research | Wound healing | Cytokines | Tumor cells | Macromolecules | Gene expression | Metabolism | Fibroblast growth factor 7 | Adhesion | Studies | Polymerase chain reaction | Bone cancer | Stromal cells | MicroRNAs | Medical prognosis | Solid tumors | Mutation | Focal adhesion kinase | Cell migration | Tumors | Index Medicus
Journal Article
Oncogene, ISSN 0950-9232, 08/2014, Volume 34, Issue 25, pp. 3240 - 3250
Journal Article
Oncogene, ISSN 0950-9232, 10/2011, Volume 30, Issue 41, pp. 4261 - 4274
In the presence of sustained DNA damage occurring in S-phase or G2, normal cells arrest before mitosis and eventually become senescent. The checkpoint kinases... 
cyclin B1 | ATM | Chk2 | G2-M checkpoint | cell cycle | GENOTOXIC STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOTIC CATASTROPHE | TRANSCRIPTIONAL REPRESSION | G CHECKPOINT | CELL BIOLOGY | GENOMIC INSTABILITY | RETINOBLASTOMA PROTEIN | ONCOLOGY | GENETICS & HEREDITY | P53-DEFICIENT CELLS | CELL-CYCLE EXIT | IONIZING-RADIATION | ATAXIA-TELANGIECTASIA | Protein Kinases - metabolism | G2 Phase Cell Cycle Checkpoints - physiology | Phosphorylation | Protein Kinases - genetics | Tumor Suppressor Proteins - antagonists & inhibitors | Humans | Immunoblotting | Male | Cyclin B1 - metabolism | Pyrones - pharmacology | Tumor Suppressor Protein p53 - genetics | Cell Cycle Proteins - antagonists & inhibitors | DNA-Binding Proteins - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | G2 Phase Cell Cycle Checkpoints - drug effects | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Cycle Proteins - genetics | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Female | Antineoplastic Agents - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Tumor Suppressor Proteins - metabolism | DNA-Binding Proteins - antagonists & inhibitors | HCT116 Cells | Cell Cycle Proteins - metabolism | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Cyclin B1 - genetics | Morpholines - pharmacology | Signal Transduction - genetics | Ataxia Telangiectasia Mutated Proteins | DNA-Binding Proteins - genetics | Piperazines - pharmacology | G2 Phase Cell Cycle Checkpoints - genetics | Signal Transduction - drug effects | Cell Line, Tumor | Checkpoint Kinase 2 | Bleomycin - pharmacology | Checkpoint Kinase 1 | Signal Transduction - physiology | DNA Damage | HeLa Cells | Cell division | Oxidative stress | Signal transduction | DNA damage | Cyclin-dependent kinases | Cell cycle | CHK2 protein | Epithelial cells | Mitosis | CHK1 protein | G2 phase | Genotoxicity | Osteosarcoma cells | p53 protein | Cyclin-dependent kinase | Chemotherapy | Fibroblasts | Cancer
Journal Article
Oncogene, ISSN 0950-9232, 05/2012, Volume 31, Issue 18, pp. 2270 - 2282
Tumors are thought to be sustained by a reservoir of self-renewing cells, termed tumor-initiating cells or cancer stem cells. Osteosarcomas are high-grade... 
mesenchymal tumors | wnt signaling | differentiation | cancer stem cell | osteosarcoma | sarcosphere | PROGENITOR CELLS | OSTEOBLAST DIFFERENTIATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | BETA-CATENIN | CANCER STEM-CELLS | CELL BIOLOGY | ONCOLOGY | MOUSE MODEL | GROWTH | SARCOMA | GENETICS & HEREDITY | TRANSCRIPTION FACTOR SOX2 | WNT | LINEAGE | Cell Proliferation | Signal Transduction | Membrane Proteins - genetics | Humans | Antigens, Ly - genetics | Antigens, Surface - genetics | Bone Neoplasms - pathology | Cell Differentiation - genetics | Animals | Neoplastic Stem Cells - metabolism | SOXB1 Transcription Factors - genetics | Cell Transformation, Neoplastic - genetics | Antigens, Surface - metabolism | Cell Line, Tumor | Neoplastic Stem Cells - pathology | Antigens, Ly - metabolism | Bone Neoplasms - genetics | Membrane Proteins - metabolism | Mice | Osteosarcoma - genetics | Osteosarcoma - pathology | Wnt Signaling Pathway | Transcription factors | Osteosarcoma | Stem cells | Physiological aspects | Genetic aspects | Research | Risk factors | Signal transduction | Oncology | Gene expression | Tumors | Osteoprogenitor cells | Pediatrics | Mesenchyme | Sarcoma | Wnt protein | biomarkers | Data processing | survival factor | Malignancy | Tumorigenicity | Self | Osteosarcoma cells | Osteoblasts | Mutation | Cancer | Sox2 | Wnt signaling | tumor initiating cell
Journal Article
Oncogene, ISSN 0950-9232, 10/2010, Volume 29, Issue 42, pp. 5687 - 5699
The development of cancer is due to the growth and proliferation of transformed normal cells. Recent evidence suggests that the nature of oncogenic stress and... 
differentiation | animal model | osteosarcoma | PPARγ | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | OSTEOBLAST LINEAGE | PPAR gamma | CANCER | MESENCHYMAL STEM-CELLS | CELL BIOLOGY | PATHOGENESIS | GENE | ONCOLOGY | GENETICS & HEREDITY | MICE | TRANSCRIPTIONAL REGULATION | EXPRESSION | Immunohistochemistry | Stromal Cells - pathology | Humans | Immunoblotting | Male | Gene Expression Profiling | Stem Cells - metabolism | Adipogenesis - physiology | Bone Neoplasms - metabolism | Proto-Oncogene Proteins c-myc - biosynthesis | RNA Interference | Cell Transformation, Neoplastic - genetics | Cell Differentiation - physiology | Chondrocytes - metabolism | Osteosarcoma - metabolism | PPAR gamma - genetics | Chondrocytes - pathology | Cyclin-Dependent Kinase Inhibitor p16 - deficiency | Gene Expression | Mice, Inbred C57BL | Stromal Cells - metabolism | Bone Marrow Cells - pathology | Cyclin-Dependent Kinase Inhibitor p16 - genetics | Mesenchymal Stromal Cells - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Adipocytes - pathology | Cell Transformation, Neoplastic - metabolism | PPAR gamma - biosynthesis | Mice, Knockout | Animals | Adipocytes - metabolism | Stem Cells - pathology | Mice | Mesenchymal Stromal Cells - pathology | Osteosarcoma - genetics | Cell Transformation, Neoplastic - pathology | Bone Marrow Cells - metabolism | Adipose tissues | Care and treatment | Osteosarcoma | Stem cells | Genetic aspects | Research | Health aspects | Risk factors | Bone marrow | Bone cancer | Cellular biology | Gene expression | Rodents
Journal Article
Journal of Clinical Oncology, ISSN 0732-183X, 05/2015, Volume 33, Issue 15, pp. 1688 - 1696
Journal Article