Search results for " Cells"

showing 10 items of 6636 documents

A receptor-antibody hybrid hampering MET-driven metastatic spread

2021

AbstractBackgroundThe receptor encoded by the MET oncogene and its ligand Hepatocyte Growth Factor (HGF) are at the core of the invasive-metastatic behavior. In a number of instances genetic alterations result in ligand-independent onset of malignancy (METaddiction). More frequently, ligand stimulation of wild-type MET contributes to progression toward metastasis (METexpedience). Thus, while MET inhibitors alone are effective in the first case, combination therapy with ligand inhibitors is required in the second condition.MethodsIn this paper, we generated hybrid molecules gathering HGF and MET inhibitory properties. This has been achieved by ‘head-to-tail’ or ‘tail-to-head’ fusion of a sin…

0301 basic medicineCancer ResearchImmunoconjugatesmedicine.medical_treatmentMice SCIDEpitopeFusion proteins; HGF; MET; Metastasis; Targeted therapy; A549 Cells; Animals; Binding Sites Antibody; Cell Line Tumor; Cell Proliferation; Female; Hepatocyte Growth Factor; Humans; Immunoconjugates; Immunoglobulin Fab Fragments; Mice; Mice SCID; Neoplasm Metastasis; Neoplasms; Proto-Oncogene Proteins c-met; Rats; Rats Sprague-Dawley; Recombinant Proteins; Xenograft Model Antitumor AssaysMetastasisTargeted therapyMetastasisRats Sprague-DawleyTargeted therapyMice0302 clinical medicineNeoplasmsHGFNeoplasm MetastasisReceptorTumorHepatocyte Growth FactorChemistryProto-Oncogene Proteins c-metlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensRecombinant ProteinsOncology030220 oncology & carcinogenesisMETFemaleHepatocyte growth factormedicine.drugSCIDlcsh:RC254-282Cell LineImmunoglobulin Fab Fragments03 medical and health sciencesCell Line TumorPancreatic cancermedicineAnimalsHumansAntibodyCell ProliferationBinding SitesResearchmedicine.diseaseXenograft Model Antitumor AssaysFusion proteinRatsFusion proteins030104 developmental biologyA549 CellsCancer cellCancer researchBinding Sites AntibodySprague-DawleyJournal of Experimental & Clinical Cancer Research
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Targeting the MET oncogene by concomitant inhibition of receptor and ligand via an antibody-"decoy" strategy

2018

MET, a master gene sustaining "invasive growth," is a relevant target for cancer precision therapy. In the vast majority of tumors, wild-type MET behaves as a "stress-response" gene and relies on the ligand (HGF) to sustain cell "scattering," invasive growth and apoptosis protection (oncogene "expedience"). In this context, concomitant targeting of MET and HGF could be crucial to reach effective inhibition. To test this hypothesis, we combined an anti-MET antibody (MvDN30) inducing "shedding" (i.e., removal of MET from the cell surface), with a "decoy" (i.e., the soluble extracellular domain of the MET receptor) endowed with HGF-sequestering ability. To avoid antibody/decoy interaction-and …

0301 basic medicineCancer ResearchLung NeoplasmsCellContext (language use)ApoptosisMice SCIDLigands03 medical and health sciencesMice0302 clinical medicineMice Inbred NODanti-HGF therapy; antibodies; decoy; MET oncogene; MET target therapyMET oncogeneExtracellularmedicineTumor Cells CulturedantibodiesAnimalsHumansdecoyCell ProliferationOncogenebiologyMET target therapyChemistryAntibodies MonoclonalProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysIn vitro030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer cellColonic NeoplasmsCancer researchbiology.proteinanti-HGF therapyFemaleAntibodyDecoyGlioblastoma
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Trabectedin Overrides Osteosarcoma Differentiative Block and Reprograms the Tumor Immune Environment Enabling Effective Combination with Immune Check…

2016

Abstract Purpose: Osteosarcoma, the most common primary bone tumor, is characterized by an aggressive behavior with high tendency to develop lung metastases as well as by multiple genetic aberrations that have hindered the development of targeted therapies. New therapeutic approaches are urgently needed; however, novel combinations with immunotherapies and checkpoint inhibitors require suitable preclinical models with intact immune systems to be properly tested. Experimental Design: We have developed immunocompetent osteosarcoma models that grow orthotopically in the bone and spontaneously metastasize to the lungs, mimicking human osteosarcoma. These models have been used to test the effica…

0301 basic medicineCancer ResearchLung Neoplasmsmedicine.medical_treatmentCellular differentiationT-LymphocytesProgrammed Cell Death 1 ReceptorBone NeoplasmsCore Binding Factor Alpha 1 SubunitDioxolesBiology03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorTetrahydroisoquinolinesmedicineTumor MicroenvironmentHumansTrabectedinTumor microenvironmentOsteosarcomaCancerCell DifferentiationImmunotherapymedicine.diseaseCellular ReprogrammingPrimary tumor030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer researchOsteosarcomaImmunotherapyOsteosarcoma Trabectedin tumor mouse models immune cells immune checkpoint inhibitors.Tumor Suppressor Protein p53medicine.drugTrabectedinClinical cancer research : an official journal of the American Association for Cancer Research
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Dual Constant Domain-Fab: A novel strategy to improve half-life and potency of a Met therapeutic antibody

2016

The kinase receptor encoded by the Met oncogene is a sensible target for cancer therapy. The chimeric monovalent Fab fragment of the DN30 monoclonal antibody (MvDN30) has an odd mechanism of action, based on cell surface removal of Met via activation of specific plasma membrane proteases. However, the short half-life of the Fab, due to its low molecular weight, is a severe limitation for the deployment in therapy. This issue was addressed by increasing the Fab molecular weight above the glomerular filtration threshold through the duplication of the constant domains, in tandem (DCD-1) or reciprocally swapped (DCD-2). The two newly engineered molecules showed biochemical properties comparable…

0301 basic medicineCancer ResearchMice SCIDCancer targeted therapy0302 clinical medicineMice Inbred NODEpidermal growth factor receptorPhosphorylationbiologyChemistryImmunoglobulin Fab FragmentsAntibodies MonoclonalGeneral MedicineArticlesProto-Oncogene Proteins c-metHalf-lifeCell biologyOncology030220 oncology & carcinogenesisColonic NeoplasmsMetMolecular MedicineFemalemedicine.symptomSignal transductionAntibodySignal Transductionmedicine.drug_classColonAntibody; Cancer targeted therapy; Fab; Half-life; Met; Protein engineering; Cancer Research; Genetics; Molecular MedicineAntineoplastic AgentsMonoclonal antibody03 medical and health sciencesImmunoglobulin Fab FragmentsProtein DomainsCell Line TumormedicineGeneticsAnimalsHumansFabAntibodyCell growthMolecular biology030104 developmental biologyHEK293 CellsMechanism of actionHepatocyte Growth Factor ReceptorA549 Cellsbiology.proteinProtein engineering
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DNA methylation of shelf, shore and open sea CpG positions distinguish high microsatellite instability from low or stable microsatellite status colon…

2019

Aim: To investigate the genome-wide methylation of genetically characterized colorectal cancer stem cell (CR-CSC) lines. Materials & methods: Eight CR-CSC lines were isolated from primary colorectal cancer (CRC) tissues, cultured and characterized for aneuploidy, mutational status of CRC-related genes and microsatellite instability (MSI). Genome-wide DNA methylation was assessed by MethylationEPIC microarray. Results: We describe a distinctive methylation pattern that is maintained following in vivo passages in immune-compromised mice. We identified an epigenetic CR-CSC signature associated with MSI. We noticed that the preponderance of the differentially methylated positions do not re…

0301 basic medicineCancer ResearchMicroarrayColorectal cancercolon cancer stem cellsSocio-culturaleBiologyEpigenesis Genetic03 medical and health sciencesMice0302 clinical medicineGeneticsmedicineAnimalsHumansEpigeneticsneoplasmsMSIMSSMicrosatellite instabilityMethylationcolon cancer stem cells DNA methylation MSI MSSDNA Methylationmedicine.diseasedigestive system diseases030104 developmental biologyCpG siteDrug Resistance Neoplasm030220 oncology & carcinogenesisDNA methylationColonic NeoplasmsCancer researchNeoplastic Stem CellsMicrosatelliteHeterograftsCpG IslandsMicrosatellite Instabilitycolon cancer stem cellEpigenomics
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Myeloid Cell-Derived Reactive Oxygen Species Induce Epithelial Mutagenesis

2017

Increased oxidative stress has been suggested to initiate and promote tumorigenesis by inducing DNA damage and to suppress tumor development by triggering apoptosis and senescence. The contribution of individual cell types in the tumor microenvironment to these contrasting effects remains poorly understood. We provide evidence that during intestinal tumorigenesis, myeloid cell-derived H2O2 triggers genome-wide DNA mutations in intestinal epithelial cells to stimulate invasive growth. Moreover, increased reactive oxygen species (ROS) production in myeloid cells initiates tumor growth in various organs also in the absence of a carcinogen challenge in a paracrine manner. Our data identify an i…

0301 basic medicineCancer ResearchMyeloidDNA damageApoptosismedicine.disease_causeMice03 medical and health sciencesParacrine signallingmedicineAnimalsMyeloid Cellschemistry.chemical_classificationReactive oxygen speciesTumor microenvironmentChemistryEpithelial CellsHydrogen PeroxideCell BiologyMice Mutant StrainsCell biologyOxidative Stress030104 developmental biologymedicine.anatomical_structureOncologyMutagenesisMutationTumor necrosis factor alphaReactive Oxygen SpeciesCarcinogenesisOxidative stressDNA DamageSignal TransductionCancer Cell
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Transcriptional Profiles and Stromal Changes Reveal Bone Marrow Adaptation to Early Breast Cancer in Association with Deregulated Circulating microRN…

2020

Abstract The presence of a growing tumor establishes a chronic state of inflammation that acts locally and systemically. Bone marrow responds to stress signals by expanding myeloid cells endowed with immunosuppressive functions, further fostering tumor growth and dissemination. How early in transformation the cross-talk with the bone marrow begins and becomes detectable in blood is unknown. Here, gene expression profiling of the bone marrow along disease progression in a spontaneous model of mammary carcinogenesis demonstrates that transcriptional modifications in the hematopoietic compartment occurred as early as preinvasive disease stages. The transcriptional profile showed downregulation…

0301 basic medicineCancer ResearchMyeloidStromal cellInflammationApoptosisBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaCXCR403 medical and health sciencesMice0302 clinical medicineBone MarrowmedicineBiomarkers TumorTumor Cells CulturedAnimalsHumansCirculating MicroRNACell ProliferationMice Inbred BALB CInnate immune systemGene Expression ProfilingAcquired immune systemAdaptation PhysiologicalXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticHaematopoiesis030104 developmental biologymedicine.anatomical_structureOncologyTrascriptional profiles early brest cancer microRNAs030220 oncology & carcinogenesisCancer researchFemaleBone marrowmedicine.symptomStromal CellsTranscriptomeCancer research
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Nicotinamide Phosphoribosyltransferase Acts as a Metabolic Gate for Mobilization of Myeloid-Derived Suppressor Cells

2019

Abstract Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow. NAMPT inhibits CXCR4 through a NAD/Sirtuin 1–mediated inactivation of HIF1α-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide. Pharmacologic inhibition or myeloid-specific ablation …

0301 basic medicineCancer ResearchMyeloidmedicine.medical_treatmentNudeNicotinamide phosphoribosyltransferaseApoptosisColorectal NeoplasmInbred C57BLMicechemistry.chemical_compound0302 clinical medicineTumor Cells CulturedHematopoiesiNicotinamide PhosphoribosyltransferaseInbred BALB CMice Inbred BALB CCulturedbiologySarcomaTumor CellsHaematopoiesismedicine.anatomical_structureOncology030220 oncology & carcinogenesisSirtuinFemaleSarcoma ExperimentalColorectal NeoplasmsAnimals; Apoptosis; Cell Proliferation; Colorectal Neoplasms; Female; Hematopoiesis; Humans; Mammary Neoplasms Experimental; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Mice Nude; Myeloid-Derived Suppressor Cells; NAD; Nicotinamide Phosphoribosyltransferase; Sarcoma Experimental; Signal Transduction; Tumor Cells Cultured; Xenograft Model Antitumor AssaysHumanSignal TransductionMice NudeExperimental03 medical and health sciencesmedicineMyeloid-Derived Suppressor CellAnimalsHumansCell ProliferationAnimalMyeloid-Derived Suppressor CellsMammary NeoplasmsApoptosiMammary Neoplasms ExperimentalImmunotherapyNADXenograft Model Antitumor AssaysHematopoiesisMice Inbred C57BL030104 developmental biologychemistrybiology.proteinCancer researchMyeloid-derived Suppressor CellNAD+ kinaseBone marrowCancer Research
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Parthenolide and DMAPT exert cytotoxic effects on breast cancer stem-like cells by inducing oxidative stress, mitochondrial dysfunction and necrosis

2016

Triple-negative breast cancers (TNBCs) are aggressive forms of breast carcinoma associated with a high rate of recidivism. In this paper, we report the production of mammospheres from three lines of TNBC cells and demonstrate that both parthenolide (PN) and its soluble analog dimethylaminoparthenolide (DMAPT) suppressed this production and induced cytotoxic effects in breast cancer stem-like cells, derived from dissociation of mammospheres. In particular, the drugs exerted a remarkable inhibitory effect on viability of stem-like cells. Such an effect was suppressed by N-acetylcysteine, suggesting a role of reactive oxygen species (ROS) generation in the cytotoxic effect. Instead z-VAD, a ge…

0301 basic medicineCancer ResearchNecrosismedicine.disease_causeCancer -- Treatmentchemistry.chemical_compoundOnium CompoundsMedicineCytotoxic T cellBreast -- CancerMembrane Potential Mitochondrialchemistry.chemical_classificationSuperoxideMitochondrial DNAMitochondriaNeoplastic Stem CellsFemaleOriginal Articlemedicine.symptomOligopeptidesSesquiterpenesCell SurvivalNF-E2-Related Factor 2ImmunologyBreast NeoplasmsReal-Time Polymerase Chain Reaction03 medical and health sciencesCellular and Molecular NeuroscienceDownregulation and upregulationCell Line TumorHumansParthenolideparthenolide cancer stem cell triple-negative breast cancer reactive oxygen species nuclear factor erythroid 2-related factor 2Fluorescent DyesReactive oxygen speciesbusiness.industryAcetophenonesNADPH OxidasesCell BiologyCell nuclei -- AbnormalitiesOxidative Stress030104 developmental biologychemistryApocyninImmunologyCancer researchReactive Oxygen SpeciesbusinessOxidative stressTranscription FactorsCell Death & Disease
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Isolation, culture and analysis of adult subependymal neural stem cells

2016

Individual cells dissected from the subependymal neurogenic niche of the adult mouse brain proliferate in medium containing basic fibroblast growth factor (bFGF) and/or epidermal growth factor (EGF) as mitogens, to produce multipotent clonal aggregates called neurospheres. These cultures constitute a powerful tool for the study of neural stem cells (NSCs) provided that they allow the analysis of their features and potential capacity in a controlled environment that can be modulated and monitored more accurately than in vivo. Clonogenic and population analyses under mitogen addition or withdrawal allow the quantification of the self-renewing and multilineage potency of these cells and the id…

0301 basic medicineCancer ResearchNeurogenesisCellular differentiationBasic fibroblast growth factorPopulationCell Culture TechniquesBiologyMice03 medical and health scienceschemistry.chemical_compoundNeural Stem CellsEpendymaNeurosphereSubependymal zoneAnimalsHumanseducationMolecular BiologyNeuronseducation.field_of_studyNeurogenesisCell DifferentiationCell BiologyNeural stem cellCell biologyAdult Stem Cells030104 developmental biologychemistryImmunologyDevelopmental BiologyAdult stem cellDifferentiation
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