Search results for " MICE"

showing 10 items of 558 documents

Prevention of chemotherapy-induced anemia and thrombocytopenia by constant administration of stem cell factor.

2011

Abstract Purpose: Chemotherapy-induced apoptosis of immature hematopoietic cells is a major cause of anemia and thrombocytopenia in cancer patients. Although hematopoietic growth factors such as erythropoietin and colony-stimulating factors cannot prevent the occurrence of drug-induced myelosuppression, stem cell factor (SCF) has been previously shown to protect immature erythroid and megakaryocytic cells in vitro from drug-induced apoptosis. However, the effect of SCF in vivo as a single myeloprotective agent has never been elucidated. Experimental Design: The ability of SCF to prevent the occurrence of chemotherapy-induced anemia and thrombocytopenia was tested in a mouse model of cisplat…

Cancer ResearchAnemiamedicine.medical_treatmentSCF Bcl-2/Bcl-XL–positiveStem cell factorAntineoplastic AgentsBone Marrow CellsInbred C57BLDrug Administration ScheduleMiceSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsCisplatinErythroid Precursor CellsChemotherapyStem Cell Factorbusiness.industryAnemiamedicine.diseaseAnemia; Animals; Antineoplastic Agents; Bone Marrow Cells; Cisplatin; Drug Administration Schedule; Erythroid Precursor Cells; Female; Megakaryocytes; Mice; Mice Inbred C57BL; Stem Cell Factor; Thrombocytopenia; Oncology; Cancer ResearchThrombocytopeniaMice Inbred C57BLHaematopoiesisCytokinemedicine.anatomical_structureOncologyErythropoietinImmunologyCancer researchFemaleBone marrowCisplatinbusinessMegakaryocytesmedicine.drugClinical cancer research : an official journal of the American Association for Cancer Research
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In vivo targeting of human neutralizing antibodies against CD55 and CD59 to lymphoma cells increases the antitumor activity of rituximab.

2007

AbstractAn in vivo model of human CD20+ B-lymphoma was established in severe combined immunodeficiency mice to test the ability of human neutralizing miniantibodies to CD55 and CD59 (MB55 and MB59) to enhance the therapeutic effect of rituximab. The miniantibodies contained single-chain fragment variables and the hinge-CH2-CH3 domains of human IgG1. LCL2 cells were selected for the in vivo study among six B-lymphoma cell lines for their high susceptibility to rituximab-dependent complement-mediated killing enhanced by MB55 and MB59. The cells injected i.p. primarily colonized the liver and spleen, leading to the death of the animals within 30 to 40 days. Thirty percent of mice receiving bio…

Cancer ResearchLymphoma B-Cellmedicine.drug_classmedicine.medical_treatmentAntineoplastic AgentsCD59 AntigensAntigens CD59Mice SCIDPharmacologyMonoclonal antibodyAntigens CD55Antineoplastic AgentAntibodies Monoclonal Murine-DerivedMicerituximabIn vivomedicineAnimalsHumansantibodies against CD55 and CD59CD20Severe combined immunodeficiencyMice Inbred BALB CbiologyCD55 AntigensAnimalAntibody-Dependent Cell CytotoxicityAntibodies MonoclonalImmunotherapyrituximab; antibodies against CD55 and CD59medicine.diseaseDisease Models AnimalOncologyAnimals; Antibodies Monoclonal; Antibodies Monoclonal Murine-Derived; Antibody-Dependent Cell Cytotoxicity; Antigens CD55; Antigens CD59; Antineoplastic Agents; Disease Models Animal; Female; Humans; Lymphoma B-Cell; Mice; Mice Inbred BALB C; Mice SCID; Rituximab; Cancer Research; OncologyMonoclonalImmunologybiology.proteinRituximabFemaleAntibodymedicine.drugHuman
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Bispecific antibodies targeting tumor-associated antigens and neutralizing complement regulators increase the efficacy of antibody-based immunotherap…

2015

The efficacy of antibody-based immunotherapy is due to the activation of apoptosis, the engagement of antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity (CDC). We developed a novel strategy to enhance CDC using bispecific antibodies (bsAbs) that neutralize the C-regulators CD55 and CD59 to enhance C-mediated functions. Two bsAbs (MB20/55 and MB20/59) were designed to recognize CD20 on one side. The other side neutralizes CD55 or CD59. Analysis of CDC revealed that bsAbs could kill 4-25 times more cells than anti-CD20 recombinant antibody in cell lines or cells isolated from patients with chronic lymphocytic leukemia. The pharmacokinetics of the bsAbs was evaluate…

Cancer ResearchLymphomaMacrophageChronic lymphocytic leukemiamedicine.medical_treatmentAntibodieCell SeparationMice SCIDMiceAntibodies BispecificCloning MolecularCytotoxicityCD20LeukemiabiologyCD55 AntigensMedicine (all)HematologyFlow CytometryBurkitt LymphomaKiller Cells NaturalLeukemiaOncologyFemaleImmunotherapyAntibodybispecific antibodiesExperimental Lymphoma Mice MiceHumanComplement System ProteinCD59 AntigensEnzyme-Linked Immunosorbent AssayAntigens CD59Antigens CD55AntibodiesExperimentalAntigenbispecific antibodies; Leukemia; Experimental Lymphoma Mice Mice; complement systemmedicineAnimalsHumanscomplement systemAnimalMacrophagesAntibody-Dependent Cell CytotoxicityImmunotherapyComplement System Proteinsmedicine.diseaseAntigens CD20Complement systembispecific antibodieDisease Models AnimalAnesthesiology and Pain MedicineMicroscopy FluorescenceImmunologybiology.protein
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SOCS2 controls proliferation and stemness of hematopoietic cells under stress conditions and its deregulation marks unfavorable acute leukemias

2015

Abstract Hematopoietic stem cells (HSC) promptly adapt hematopoiesis to stress conditions, such as infection and cancer, replenishing bone marrow–derived circulating populations, while preserving the stem cell reservoir. SOCS2, a feedback inhibitor of JAK–STAT pathways, is expressed in most primitive HSC and is upregulated in response to STAT5-inducing cytokines. We demonstrate that Socs2 deficiency unleashes HSC proliferation in vitro, sustaining STAT5 phosphorylation in response to IL3, thrombopoietin, and GM-CSF. In vivo, SOCS2 deficiency leads to unrestricted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC function along serial bone marro…

Cancer ResearchMyeloidSuppressor of Cytokine Signaling ProteinsMice TransgenicNeoplasm ProteinMiceBone MarrowSuppressor of Cytokine Signaling ProteinmedicineAnimalsHumansMEF2 Transcription FactorThrombopoietinSTAT5Cell ProliferationRegulation of gene expressionABLLeukemiabiologyMEF2 Transcription FactorsAnimalMedicine (all)Animals; Bone Marrow; Cell Differentiation; Cell Proliferation; Fluorouracil; Gene Expression Regulation Neoplastic; Hematopoietic Stem Cells; Humans; Leukemia; MEF2 Transcription Factors; Mice; Mice Transgenic; Neoplasm Proteins; Neoplastic Stem Cells; Suppressor of Cytokine Signaling Proteins; Cancer Research; Oncology; Medicine (all)breakpoint cluster regionCell DifferentiationHematopoietic Stem CellHematopoietic Stem CellsNeoplasm ProteinsGene Expression Regulation NeoplasticHaematopoiesismedicine.anatomical_structureOncologyImmunologybiology.proteinCancer researchNeoplastic Stem CellsFluorouracilNeoplastic Stem CellStem cellHuman
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Mast Cells Infiltrating Inflamed or Transformed Gut Alternatively Sustain Mucosal Healing or Tumor Growth.

2015

Abstract Mast cells (MC) are immune cells located next to the intestinal epithelium with regulatory function in maintaining the homeostasis of the mucosal barrier. We have investigated MC activities in colon inflammation and cancer in mice either wild-type (WT) or MC-deficient (KitW-sh) reconstituted or not with bone marrow-derived MCs. Colitis was chemically induced with dextran sodium sulfate (DSS). Tumors were induced by administering azoxymethane (AOM) intraperitoneally before DSS. Following DSS withdrawal, KitW-sh mice showed reduced weight gain and impaired tissue repair compared with their WT littermates or KitW-sh mice reconstituted with bone marrow-derived MCs. MCs were localized i…

Cancer ResearchPathologyColorectal cancerCell CountAnimals; Animals Congenic; Azoxymethane; Carcinoma; Cell Count; Cell Transformation Neoplastic; Cells Cultured; Colitis; Colonic Neoplasms; Dextran Sulfate; Epithelial Cells; Humans; Inflammatory Bowel Diseases; Interleukin-33; Intestinal Mucosa; Mast Cells; Mice; Mice Inbred C57BL; Mice Knockout; Models Biological; Proto-Oncogene Proteins c-kit; Receptors Interleukin; Regeneration; Serine Endopeptidases; Species Specificity; Specific Pathogen-Free Organisms; Cancer Research; Oncology; Medicine (all)chemistry.chemical_compoundMiceAnimals CongenicMast CellMast CellsIntestinal MucosaCells CulturedMice KnockoutColonic NeoplasmMedicine (all)Dextran SulfateSerine EndopeptidasesColitisIntestinal epitheliumSpecific Pathogen-Free OrganismsSerine EndopeptidaseProto-Oncogene Proteins c-kitCell Transformation NeoplasticOncologyColonic Neoplasmsmedicine.symptomHumanmedicine.medical_specialtyAzoxymethaneInflammationModels BiologicalImmune systemSpecies SpecificitymedicineSpecific Pathogen-Free OrganismAnimalsHumansRegenerationColitisEpithelial CellAnimalAzoxymethanebusiness.industryInflammatory Bowel DiseaseCarcinomaEpithelial CellsReceptors Interleukinmedicine.diseaseInflammatory Bowel DiseasesInterleukin-33Interleukin-1 Receptor-Like 1 ProteinMice Inbred C57BLchemistrybusinessWound healingColitiHomeostasisCancer research
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Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells.

2011

Breast cancer is the most common cancer and the second leading cause of cancer death in industrialized countries. Systemic treatment of breast cancer is effective at the beginning of therapy. However, after a variable period of time, progression occurs due to therapy resistance. Artesunate, clinically used as anti-malarial agent, has recently revealed remarkable anti-tumor activity offering a role as novel candidate for cancer chemotherapy. We analyzed the anti-tumor effects of artesunate in metastasizing breast carcinoma in vitro and in vivo. Unlike as expected, artesunate induced resistance in highly metastatic human breast cancer cells MDA-MB-231. Likewise acquired resistance led to abol…

Cancer ResearchPhytochemistryPhytopharmacologyCancer TreatmentArtesunateApoptosisElectrophoretic Mobility Shift AssayDrug resistanceNude MiceMetastasischemistry.chemical_compoundMiceMolecular Cell BiologyDrug DiscoveryBreast TumorsBasic Cancer ResearchMedicinebcl-2-Associated X ProteinMultidisciplinaryQRNF-kappa BArtemisininsChemistryOncologyMedicineFemaleMatrix Metalloproteinase 1Breast carcinomamedicine.drugResearch Article570Drugs and DevicesDrug Research and DevelopmentCell SurvivalScienceMice Nude570 Life SciencesBreast NeoplasmsTumor Cell Line610 Medical Sciences MedicineBreast cancerComplementary and Alternative MedicineCell Line TumorAnimalsHumansDoxorubicinBiologyNeoplasm Drug Resistancebusiness.industryCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseaseXenograft Model Antitumor AssaysTranscription Factor AP-1chemistryTumor progressionArtesunateDrug Resistance NeoplasmCancer cellImmunologyEthnopharmacologyCancer researchbusinessPloS one
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Efficacy of CAR-T immunotherapy in MET overexpressing tumors not eligible for anti-MET targeted therapy

2022

Abstract Background Aberrant activation of the MET receptor in cancer is sustained by genetic alterations or, more frequently, by transcriptional upregulations. A fraction of MET-amplified or mutated tumors are sensible to MET targeting agents, but their responsiveness is typically short-lasting, as secondary resistance eventually occurs. Since in the absence of genetic alterations MET is usually not a tumor driver, MET overexpressing tumors are not/poorly responsive to MET targeted therapies. Consequently, the vast majority of tumors exhibiting MET activation still represent an unmet medical need. Methods Here we propose an immunotherapy strategy based on T lymphocytes expressing a Chimeri…

Cancer ResearchReceptors Chimeric AntigenTumorTargeted therapy.T-LymphocytesChimeric AntigenXenograft Model Antitumor AssaysCARCell LineTargeted therapyMiceOncologyCell Line TumorMET oncogeneReceptorsHumansAnimalsHeterograftsImmunotherapyCAR; Gastric cancer; Immunotherapy; MET oncogene; Targeted therapy; Humans; Mice; Animals; Immunotherapy; T-Lymphocytes; Cell Line Tumor; Heterografts; Xenograft Model Antitumor Assays; Receptors Chimeric AntigenGastric cancer
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hOA-DN30: a highly effective humanized single-arm MET antibody inducing remission of ‘MET-addicted’ cancers

2022

Abstract Background The tyrosine kinase receptor encoded by the MET oncogene is a major player in cancer. When MET is responsible for the onset and progression of the transformed phenotype (MET-addicted cancers), an efficient block of its oncogenic activation results in potent tumor growth inhibition. Methods Here we describe a molecular engineered MET antibody (hOA-DN30) and validate its pharmacological activity in MET-addicted cancer models in vitro and in vivo. Pharmacokinetics and safety profile in non-human primates have also been assessed. Results hOA-DN30 efficiently impaired MET activation and the intracellular signalling cascade by dose and time dependent removal of the receptor fr…

Cancer ResearchTumorCorrectionProto-Oncogene Proteins c-metCell LineTargeted therapyMiceAntibody; Gastric cancer; MET oncogene; Targeted therapy; Animals; Cell Line Tumor; Cell Proliferation; Humans; Mice; Signal Transduction; Proto-Oncogene Proteins c-met; Stomach NeoplasmsOncologyStomach NeoplasmsCell Line TumorMET oncogeneAnimalsHumansGastric cancerAntibodyCell ProliferationSignal TransductionJournal of Experimental & Clinical Cancer Research
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Mast cells boost myeloid-derived suppressor cell activity and contribute to the development of tumor-favoring microenvironment

2014

Abstract Inflammation plays crucial roles at different stages of tumor development and may lead to the failure of immune surveillance and immunotherapy. Myeloid-derived suppressor cells (MDSC) are one of the major components of the immune-suppressive network that favors tumor growth, and their interaction with mast cells is emerging as critical for the outcome of the tumor-associated immune response. Herein, we showed the occurrence of cell-to-cell interactions between MDSCs and mast cells in the mucosa of patients with colon carcinoma and in the colon and spleen of tumor-bearing mice. Furthermore, we demonstrated that the CT-26 colon cancer cells induced the accumulation of CD11b+Gr1+ imma…

Cancer Researchmedicine.medical_treatmentCD40 LigandImmunologyInflammationCell CommunicationBiologyNitric OxideProinflammatory cytokineInterferon-gammaMiceImmune systemAntigens CD40Animals; Antigens CD40; CD40 Ligand; Cell Line Tumor; Colonic Neoplasms; Humans; Inflammation; Interferon-gamma; Mast Cells; Mice; Mice Inbred BALB C; Mice Knockout; Myeloid Cells; Nitric Oxide; Tumor Microenvironment; Cell Communication; Cancer Research; Immunology; Medicine (all)Cell Line TumormedicineMast cell; Myeloid-Derived Suppressor Cell; tumor microenvironment; colon cancerTumor MicroenvironmentAnimalsHumansMyeloid-Derived Suppressor CellMast CellMyeloid CellsMast CellsCD40 AntigensMyeloid CellInflammationMice KnockoutTumor microenvironmentColonic NeoplasmMice Inbred BALB CCD40AnimalMedicine (all)ImmunotherapyMast cellmedicine.anatomical_structurecolon cancerImmunologyColonic NeoplasmsCancer researchMyeloid-derived Suppressor Cellbiology.proteinmedicine.symptomHuman
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Influence of temperature on the behaviour of small linear peptides in capillary electrochromatography

2000

The influence of temperature, T, on the retention times, peak widths, peak symmetry coefficients and theoretical plate numbers of two small linear peptides, [Met5]enkephalin and [Leu5]enkephalin, has been studied with capillary electrochromatography (CEC) capillary columns of 100 microm I.D. and 250 mm packed length with a total length of 335 mm, containing 3 microm Hypersil n-octadecyl bonded silica. With increasing column temperature from 15 to 60 degrees C, the electroosmotic flow (EOF) and the column efficiencies increased, whereas the retention coefficients (Kcec) of both peptides decreased. A linear relationship was found between the EOF value and the square root of the temperature ov…

Capillary electrochromatographyChromatographyChemistryCapillary actionOrganic ChemistryTemperatureAnalytical chemistryElectro-osmosisGeneral MedicineReversed-phase chromatographyAtmospheric temperature rangeBiochemistryAnalytical ChemistryColumn chromatographyElectrochromatographyTheoretical platePeptidesChromatography Micellar Electrokinetic CapillaryJournal of Chromatography A
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