Search results for "M-CSF"

showing 7 items of 7 documents

Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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The role of extracellular calcium in bone metastasis

2016

AbstractThis review summarizes the role of extracellular calcium, as found present in the bone tissue, in the process of bone metastasis.

0301 basic medicinelcsh:Diseases of the musculoskeletal systemIGF insulin-like growth factorPGE-2 prostaglandin E-2Bone tissueFibroblast growth factorM-CSF macrophage colony-stimulating factorPDGF platelet-derived growth factorBone remodelingSK3 small conductance calcium-activated potassium channel 30302 clinical medicineERK extracellular signal-regulated kinaseTGFβ transforming growth factor betaBMP's bone morphogenetic proteinsbiologyAKT AKT8 virus oncogene cellular homologBone metastasislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenshumanitiescAMP cyclic adenosine monophosphatemedicine.anatomical_structureOncologyRANKL030220 oncology & carcinogenesisIon channelsCaSR calcium-sensing receptorPTHrP parathyroid hormone-related proteinPlatelet-derived growth factor receptorResearch PaperTRP transient receptor potentialmedicine.medical_specialtychemistry.chemical_elementCalciumRANKL receptor activator of NF-κB ligandlcsh:RC254-28203 medical and health sciencesPLC phospholipase CInternal medicinemedicineExtracellularCaSRET-1 endothelin-1PTEN phosphatase and tensin homolog deleted on chromosome 10business.industryBone metastasismedicine.diseaseFGF fibroblast growth factor030104 developmental biologyEndocrinologyPSA prostate specific antigenchemistryCOPD chronic obstructive pulmonary diseasebiology.proteinCancer researchJNK jun N-terminal kinasePKA protein kinase ARANK receptor activator of NF-κBCalciumlcsh:RC925-935businessMAPK mitogen-activated protein kinaseJournal of Bone Oncology
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Comparative Antitumor Effect of Preventive versus Therapeutic Vaccines Employing B16 Melanoma Cells Genetically Modified to Express GM-CSF and B7.2 i…

2012

Cancer vaccines have always been a subject of gene therapy research. One of the most successful approaches has been working with genetically modified tumor cells. In this study, we describe our approach to achieving an immune response against a murine melanoma model, employing B16 tumor cells expressing GM-CSF and B7.2. Wild B16 cells were injected in C57BL6 mice to cause the tumor. Irradiated B16 cells transfected with GM-CSF, B7.2, or both, were processed as a preventive and therapeutic vaccination. Tumor volumes were measured and survival curves were obtained. Blood samples were taken from mice, and IgGs of each treatment group were also measured. The regulatory T cells (Treg) o…

Cytotoxicity Immunologicnon-viralHealth Toxicology and MutagenesisGenetic enhancementMelanoma Experimentallcsh:MedicineToxicologyTransfectionT-Lymphocytes RegulatoryImmunoglobulin GArticleMiceImmune systemCell Line TumormedicineAnimalsbiologylcsh:RGene Transfer TechniquesCancerGranulocyte-Macrophage Colony-Stimulating FactorGM-CSFTransfectionGenetic Therapymedicine.diseaseSurvival Analysisgene therapyGenetically modified organismVaccinationMice Inbred C57BLGranulocyte macrophage colony-stimulating factorB7.2Immunoglobulin GImmunologybiology.proteinB7-2 AntigenNeoplasm Transplantationcancer vaccinesmedicine.drugToxins
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Macrophage MerTK promotes profibrogenic cross-talk with hepatic stellate cells via soluble mediators

2022

Background & aims: Activation of Kupffer cells and recruitment of monocytes are key events in fibrogenesis. These cells release soluble mediators which induce the activation of hepatic stellate cells (HSCs), the main fibrogenic cell type within the liver. Mer tyrosine kinase (MerTK) signaling regulates multiple processes in macrophages and has been implicated in the pathogenesis of non-alcoholic steatohepatitis-related fibrosis. In this study, we explored if MerTK activation in macrophages influences the profibrogenic phenotype of HSCs. Methods: Macrophages were derived from THP-1 cells or differentiated from peripheral blood monocytes towards MerTK+/CD206+/CD163+/CD209- macrophages. Th…

HepatologyCM conditioned medium ECM extracellular matrix Gas-6 Gas-6 growth arrest-specific gene 6 HSC(s) hepatic stellate cells KC(s) Kupffer cell(s) M-CSF macrophage colony-stimulating factor M2c-like macrophages MerTK Myeloid-epithelial-reproductive tyrosine kinase NAFLD non-alcoholic fatty liver disease NASH NASH non-alcoholic steatohepatitis PMA phorbol 12-myristate 13-acetate TGFβ1 transforming growth factor-β1 THP-1 TIMP1 tissue inhibitor of metalloproteinase 1 VEGF-A vascular endothelial growth factor-A liver fibrosis siRNA small-interfering RNAGas-6; liver fibrosis; M2c-like macrophages; NASH; THP-1GastroenterologyInternal MedicineImmunology and AllergyJHEP Reports
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Role of the protein phosphatase CD45 and lipid rafts in the maintenance of acute myeloblastic leukemiaand development of a new therapeutic treatment

2017

CD45 is a pan-leukocyte protein with tyrosine phosphatase activity involved in the regulation of cytokinereceptors in hematopoiesis, such as the GM-CSF. We report here on new chemical compound,Pyrido[4,3-b]quinoxaline (PyQ), which is a plasma membrane disrupting agent, as a potential drug fortreatment of acute myeloid leukemia (AML). Indeed, we show that the hematopoietic cell lines aremore sensitive to PyQ, compared with non- hematopoietic cell lines. Using HOXA9-MEIS1-transformed blasts from a mouse model to study AML and human primary AML samples, wediscovered that CD45, which is mainly found within plasma-membrane lipid rafts, is rapidly delocalizedafter treatment with PyQ compound. The…

Lipid raftAcute myeloid leukemia[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyLeucémie aiguës myéloblastiquesRadeaux lipidiquesGM-CSFCD45
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Keratinocyte-Derived Granulocyte-Macrophage Colony Stimulating Factor Accelerates Wound Healing: Stimulation of Keratinocyte Proliferation, Granulati…

2001

Chronic, nonhealing wounds represent a major clinical challenge to practically all disciplines in modern medicine including dermatology, oncology, surgery, and hematology. In skin wounds, granulocyte-macrophage colony stimulating factor (GM-CSF) is secreted by keratinocytes shortly after injury and mediates epidermal cell proliferation in an autocrine manner. Many other cells involved in wound healing including macrophages, lymphocytes, fibroblasts, endothelial cells, and dendritic cells synthesize GM-CSF and/or are targets of this cytokine. Therefore, GM-CSF is a pleiotropic cytokine evoking complex processes during wound repair. Despite this complexity and the scarcity of mechanistic unde…

Macrophage colony-stimulating factorKeratinocytesMalemedicine.medical_treatmentGene ExpressionMitosisNeovascularization PhysiologicMice TransgenicDermatologytransgenic miceBiologyBiochemistryProinflammatory cytokineTransforming Growth Factor beta1MiceTransforming Growth Factor betamedicineAnimalsRNA MessengerAutocrine signallingMolecular BiologySkinWound Healingintegumentary systemGranulation tissueGranulocyte-Macrophage Colony-Stimulating FactorGM-CSFCell BiologyUp-RegulationCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyModels AnimalCancer researchCarcinogensGranulation TissueCytokinesTetradecanoylphorbol AcetateFemaleKeratinocyteWound healingmedicine.drugJournal of Investigative Dermatology
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GM-CSF Programs Hematopoietic Stem and Progenitor Cells During Candida albicans Vaccination for Protection Against Reinfection

2021

More mechanistic studies are needed to reveal the hidden details of in vivo-induced trained immunity. Here, using a Candida albicans live vaccine mouse model we show that vaccination protects mice against a secondary infection and increases the number of bone marrow, and especially, splenic trained monocytes. Moreover, vaccination expands and reprograms hematopoietic stem and progenitor cells (HSPCs) early during infection and mobilize them transiently to the spleen to produce trained macrophages. Trained HSPCs are not only primed for myeloid cell production but also reprogramed to produce a greater amount of proinflammatory cytokines in response to a second challenge. Additionally, their a…

MaleMacrophagesImmunologyVaccinationHSPCsGranulocyte-Macrophage Colony-Stimulating FactorGM-CSFmyelopoiesisRC581-607Hematopoietic Stem CellscandidiasisMice Inbred C57BLMicetrained immunityReinfectionCandida albicansImmunology and AllergyAnimalsCytokinesFemaleFungal VaccinesImmunologic diseases. AllergyOriginal ResearchFrontiers in Immunology
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