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Oncogene, ISSN 0950-9232, 07/2012, Volume 31, Issue 28, pp. 3322 - 3332
The molecular mechanisms that contribute to the initiation and progression of head and neck squamous cell carcinoma (HNSCC) have not been completely... 
cancer mouse model | TGF-β | conditional knockout | head and neck squamous cell carcinoma | PI3K/Akt | PATHWAYS | APOPTOSIS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MAMMARY-CARCINOMA | FACTOR-KAPPA-B | MODEL | CELL BIOLOGY | COLON-CANCER | TGF-beta | GROWTH-FACTOR-BETA | ONCOLOGY | GENETICS & HEREDITY | TUMOR-SUPPRESSOR | TUMORIGENESIS | Cell Proliferation | Epithelial Cells - metabolism | Carcinoma, Squamous Cell - genetics | Carcinoma, Squamous Cell - pathology | Cell Count | Humans | Transforming Growth Factor beta1 - metabolism | Apoptosis - genetics | Phosphatidylinositol 3-Kinases - metabolism | Inflammation - complications | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Proto-Oncogene Proteins c-akt - metabolism | Cellular Senescence - genetics | PTEN Phosphohydrolase - genetics | PTEN Phosphohydrolase - deficiency | PTEN Phosphohydrolase - metabolism | Epithelial Cells - pathology | Penetrance | Signal Transduction - genetics | Transforming Growth Factor beta1 - genetics | Gene Knockout Techniques | Head and Neck Neoplasms - pathology | Animals | Carcinoma, Squamous Cell - complications | Cell Line, Tumor | Head and Neck Neoplasms - complications | Head and Neck Neoplasms - genetics | Mice | Myeloid Cells - pathology | Index Medicus | Cell proliferation | Animal models | Senescence | Transformation | biomarkers | AKT protein | Inflammation | Transforming growth factor- beta | Suppressor cells | Carcinogenesis | 1-Phosphatidylinositol 3-kinase | Metastases | Angiogenesis | Signal transduction | Cell activation | Molecular modelling | Stem cells | Head and neck | Head and neck cancer | Microenvironments | PTEN protein | Apoptosis | Tumors | squamous cell carcinoma | Head and Neck Squamous Cell Carcinoma (HNSCC) | Akt | PI3K | Conditional Knockout | Cancer Mouse Model
Journal Article
Journal Article
International Journal of Cancer, ISSN 0020-7136, 04/2014, Volume 134, Issue 7, pp. 1669 - 1682
The role of IL‐33/ST2 pathway in antitumor immunity is unclear. Using 4T1 breast cancer model we demonstrate time‐dependent increase of endogenous IL‐33 at... 
IL‐33 | NK cells | dendritic cells | T regs | myeloid‐derived suppressor cells | innate lymphoid cells | 4T1 mammary carcinoma | IL-33 | myeloid-derived suppressor cells | TUMOR | ST2 | MYELOID SUPPRESSOR-CELLS | PROGNOSTIC-FACTOR | ONCOLOGY | INFLAMMATION | CYTOKINE IL-33 | EXPRESSION | T-CELLS | Interleukin-1 Receptor-Like 1 Protein | Mammary Neoplasms, Experimental - immunology | Cell Growth Processes - immunology | Spleen - immunology | Breast Neoplasms - immunology | Immunity, Innate - genetics | Killer Cells, Natural - pathology | Mammary Neoplasms, Experimental - metabolism | Interleukins - metabolism | Mammary Neoplasms, Experimental - genetics | Breast Neoplasms - metabolism | T-Lymphocytes, Cytotoxic - pathology | Receptors, Interleukin - metabolism | Interleukins - genetics | Neoplasm Metastasis | Lymphocytes - immunology | Interleukins - immunology | Mammary Neoplasms, Experimental - pathology | CD8-Positive T-Lymphocytes - metabolism | Killer Cells, Natural - immunology | Female | Cell Growth Processes - genetics | Spleen - pathology | Lymphocytes - metabolism | T-Lymphocytes, Cytotoxic - immunology | Receptors, Interleukin - immunology | Interleukin-33 | Receptors, Interleukin - genetics | Disease Progression | Immunity, Innate - immunology | Lymphocytes - pathology | Animals | Breast Neoplasms - genetics | Spleen - metabolism | T-Lymphocytes, Cytotoxic - metabolism | Breast Neoplasms - pathology | Cell Line, Tumor | Mice | Mice, Inbred BALB C | Killer Cells, Natural - metabolism | CD8-Positive T-Lymphocytes - immunology | Phosphates | RNA | Dendritic cells | Growth | Development and progression | Breast cancer | Metastasis | Transforming growth factors | T cells | Interleukins | Analysis | Bone morphogenetic proteins | Neovascularization | Cytokines | Rodents | Immunotherapy | Immune system | Tumors | Index Medicus
Journal Article
Advances in experimental medicine and biology, ISSN 0065-2598, 2013, Volume 734, pp. 145 - 179
Increasing evidence suggests that tumor dormancy represents an important mechanism underlying the observed failure of existing therapeutic modalities to fully... 
Progression | CYTOKERATIN-POSITIVE CELLS | INITIATING CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | Recurrence | Relapse | Animal models | Angiogenic switch | MAMMARY-CARCINOMA CELLS | Disseminated tumor cell | Antitumor immunity | Metastasis | MALIGNANT-MELANOMA | Epidemiology | BREAST-CANCER | Angiogenesis | Therapy resistance | REGULATORY T-CELLS | BONE-MARROW | Cancer stem cell | Minimal residual disease | Tumor initiation | SELF-RENEWAL | Tumorigenicity | Immune evasion | Immunoescape | ACUTE MYELOID-LEUKEMIA | Tumor dormancy | Quiescence | ONCOLOGY | CLASS-I EXPRESSION | Circulating tumor cell | Apoptosis | Neoplasm, Residual - pathology | Tumor Escape | Cell Proliferation | Humans | Neoplastic Stem Cells - immunology | Tumor Microenvironment | Drug Resistance, Neoplasm | Neovascularization, Pathologic - pathology | Neoplasm Recurrence, Local - immunology | Neoplasm Recurrence, Local - pathology | Neoplasm Metastasis - immunology | Cell Death | Neoplastic Stem Cells - pathology | Neoplasm, Residual - immunology | Antineoplastic Agents - pharmacology | Neovascularization, Pathologic - immunology | Neovascularization, Pathologic - therapy | Neoplasm Metastasis - therapy | Signal Transduction | Neoplasm Recurrence, Local - blood supply | Neoplasm Recurrence, Local - therapy | Cell Communication | Disease Progression | Cell Cycle Checkpoints | Cell Transformation, Neoplastic - immunology | Neoplasm Metastasis - pathology | Combined Modality Therapy - methods | Cell Transformation, Neoplastic - pathology | Neoplasm, Residual - therapy | Cell Movement
Journal Article
Cell, ISSN 0092-8674, 2007, Volume 129, Issue 4, pp. 723 - 733
Transcriptional activation of the nuclear receptor RAR by retinoic acid (RA) often leads to inhibition of cell growth. However, in some tissues, RA promotes... 
ACUTE-PROMYELOCYTIC-LEUKEMIA | PPAR-BETA | BREAST-CANCER CELLS | TERATOCARCINOMA STEM-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | MAMMARY-CARCINOMA | SYMPATHETIC NEURONS | E-FABP | FATTY-ACIDS | TARGET GENE | BINDING PROTEIN-II | CELL BIOLOGY | Active Transport, Cell Nucleus - physiology | Apoptosis - drug effects | Humans | Transcriptional Activation - drug effects | Cell Survival - genetics | Apoptosis - genetics | Mammary Neoplasms, Experimental - physiopathology | Fatty Acid-Binding Proteins - metabolism | Mammary Neoplasms, Experimental - metabolism | Mammary Neoplasms, Experimental - genetics | Receptors, Retinoic Acid - genetics | Cell Nucleus - metabolism | Mammary Neoplasms, Animal - physiopathology | Female | Gene Expression Regulation, Neoplastic - physiology | Mammary Neoplasms, Animal - genetics | Tretinoin - pharmacology | Receptors, Retinoic Acid - drug effects | Cell Survival - drug effects | PPAR-beta - metabolism | Keratinocytes | Receptors, Retinoic Acid - metabolism | Cell Transformation, Neoplastic - metabolism | Fatty Acid-Binding Proteins - genetics | Animals | PPAR-beta - drug effects | Active Transport, Cell Nucleus - drug effects | Mammary Neoplasms, Animal - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Transcriptional Activation - physiology | Cell Transformation, Neoplastic - drug effects | Cell Nucleus - drug effects | Growth | Tretinoin | Index Medicus
Journal Article
Oncogene, ISSN 0950-9232, 04/2008, Volume 27, Issue 18, pp. 2542 - 2551
Tumor microenvironment in carcinomas recruits mesenchymal cells with an abnormal proangiogenic and invasive phenotype. It is not clear whether mesenchymal... 
Angiogenesis | HER-2/neu | Mammary carcinoma | Reactive stromal cells | Mesenchymal stem cells | Molecular signature | reactive stromal cells | POSTNATAL NEOVASCULARIZATION | angiogenesis | BIOCHEMISTRY & MOLECULAR BIOLOGY | BONE-MARROW | ACUTE MYELOID-LEUKEMIA | IDENTIFICATION | CELL BIOLOGY | BREAST-CANCER CELLS | HUMAN ADIPOSE-TISSUE | IN-VITRO | ONCOLOGY | mammary carcinoma | mesenchymal stem cells | ENDOTHELIAL-CELLS | GENETICS & HEREDITY | STROMAL FIBROBLASTS | molecular signature | Neoplasm Transplantation | Stromal Cells - pathology | Gene Expression Regulation, Neoplastic | Mesenchymal Stem Cell Transplantation - adverse effects | Neovascularization, Pathologic - pathology | Neoplastic Stem Cells - metabolism | Neoplastic Stem Cells - pathology | Transcription, Genetic | Angiogenic Proteins - biosynthesis | Ischemia - pathology | Fibroblasts - metabolism | Stromal Cells - metabolism | Ischemia - metabolism | Ischemia - therapy | Mesenchymal Stromal Cells - metabolism | Rats | Fibroblasts - pathology | Transplantation, Isogeneic | Mammary Neoplasms, Animal - pathology | Animals | Mammary Neoplasms, Animal - metabolism | Cell Line, Tumor | Mice | Neovascularization, Pathologic - metabolism | Mesenchymal Stromal Cells - pathology | Cancer cells | Stem cells | Physiological aspects | Breast cancer | Genetic aspects | Research | Risk factors | Genotype & phenotype | Oncology | Genetics | Cellular biology | Tumors | Index Medicus
Journal Article
Stem Cells, ISSN 1066-5099, 03/2010, Volume 28, Issue 3, pp. 620 - 632
Emerging evidence suggests that myeloid-derived suppressor cells (MDSCs) have great potential as a novel immune intervention modality in the fields of... 
Graft-versus-host disease | Differentiation | Mouse hematopoietic stem/progenitor cells | Myeloid-derived suppressor cells | Mouse embryonic stem cells | TOLERANCE | DEPENDENT TUMOR ANGIOGENESIS | CANCER | MAMMARY CARCINOMAS | CELL & TISSUE ENGINEERING | CELL BIOLOGY | BEARING HOST | IN-VITRO | ARGINASE-I | ONCOLOGY | IMMUNE SUPPRESSION | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | EXPANSION | REGULATORY T-CELLS | HEMATOLOGY | Myeloid Cells - cytology | Embryonic Stem Cells - metabolism | Cell Proliferation | Embryonic Stem Cells - cytology | Immune Tolerance - physiology | Immunosuppression - methods | Graft vs Host Disease - immunology | Hematopoietic Stem Cells - immunology | Myeloid Cells - immunology | Immunity, Cellular - physiology | Antigens, Surface - metabolism | Interleukin-10 - metabolism | Cell Culture Techniques | Embryonic Stem Cells - immunology | Cell Line | Mice, Inbred C57BL | Hematopoietic Stem Cells - metabolism | Cell Differentiation - immunology | Graft vs Host Disease - surgery | Stem Cell Transplantation - methods | Animals | Adoptive Transfer - methods | Hematopoietic Stem Cells - cytology | Cell Line, Tumor | Myeloid Cells - metabolism | Graft vs Host Disease - prevention & control | T-Lymphocytes - immunology | Mice | Nitric Oxide - metabolism | Index Medicus | progenitor cells | Mouse hematopoietic stem
Journal Article
Journal Article
Journal Article