Search results for "Cell Proliferation"

showing 10 items of 1056 documents

Aza-isoindolo and isoindolo-azaquinoxaline derivatives with antiproliferative activity

2015

Abstract Three new ring systems, pyrido[2′,3′:3,4]pyrrolo[1,2- a ]quinoxalines, pyrido[3′,2′:3,4]pyrrolo[1,2- a ]quinoxalines and pyrido[2′,3′:5,6]pyrazino[2,1- a ]isoindoles, were synthesized through an aza-substitution on the already active isoindolo-quinoxaline system and in particular in the position 7 or 4 of the isoindole moiety and in position 5 of the quinoxaline portion. All new compounds were screened by the National Cancer Institute (Bethesda, MD) against a panel of 60 human tumor cell lines. Biological results of the most active derivatives, with pGI 50 values between 7.09 and 7.27, confirmed the importance of the presence of methoxy substituents for biological activity. The ant…

QuinoxalineIsoindolesAzaisoindolo-quinoxalinesStereochemistryAntiproliferative activity; Apoptosis; Azaisoindolo-quinoxalines; DNA interaction; Isoindolo-azaquinoxalines; Quinoxalines; Antineoplastic Agents; Apoptosis; Aza Compounds; Cell Line Tumor; Cell Proliferation; Dose-Response Relationship Drug; Drug Screening Assays Antitumor; Humans; Isoindoles; Molecular Structure; Quinoxalines; Structure-Activity Relationship; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; Pharmacology; Medicine (all)ApoptosisAntineoplastic AgentsAntiproliferative activityIsoindolesRing (chemistry)Drug Screening AssaysCell LineDose-Response Relationshipchemistry.chemical_compoundStructure-Activity RelationshipQuinoxalineCell Line TumorQuinoxalinesDrug DiscoverymedicineMoietyHumansAntiproliferative activity; Apoptosis; Azaisoindolo-quinoxalines; DNA interaction; Isoindolo-azaquinoxalines; Quinoxalines; Drug Discovery3003 Pharmaceutical Science; Organic Chemistry; PharmacologyCell ProliferationPharmacologyAza CompoundsAzaisoindolo-quinoxalineTumorDose-Response Relationship DrugMolecular StructureDrug Discovery3003 Pharmaceutical ScienceMedicine (all)Organic ChemistryApoptosiBiological activityGeneral MedicineAntitumorCell cycleSettore CHIM/08 - Chimica FarmaceuticaDNA interactionSettore ING-IND/22 - Scienza E Tecnologia Dei MaterialiMechanism of actionchemistryIsoindolo-azaquinoxalineDrug Screening Assays Antitumormedicine.symptomDrugIsoindoleIsoindolo-azaquinoxalines
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Peripheral artery disease: potential role of ACE-inhibitor therapy

2008

Giuseppe Coppola, Giuseppe Romano, Egle Corrado, Rosa Maria Grisanti, Salvatore NovoDepartment of Internal Medicine, Cardiovascular and Nephro-Urological Diseases, Chair of Cardiovascular Disease, University of Palermo, Palermo, ItalyAbstract: Subjects with peripheral arterial disease (PAD) of the lower limbs are at high risk for cardiovascular and cerebrovascular events and the prevalence of coronary artery disease in such patients is elevated. Recent studies have shown that regular use of cardiovascular medications, such as therapeutic and preventive agents for PAD patients, seems to be promising in reducing long-term mortality and morbidity. The angiotensin-converting-enzyme (ACE) system…

Ramiprillcsh:Diseases of the circulatory (Cardiovascular) systemmedicine.medical_specialtyPathologyACE inhibitorsEndocrinology Diabetes and MetabolismBradykininAngiotensin-Converting Enzyme InhibitorsReviewDiseaseendothelial dysfunctionCoronary artery diseasechemistry.chemical_compoundperipheral arterial diseaseInternal medicineHumansMedicinePharmacology (medical)Endothelial dysfunctionCell ProliferationSubclinical infectionPeripheral Vascular Diseasesbusiness.industryFibrinolysisPublic Health Environmental and Occupational HealthCardiovascular AgentsPeripheral artery disease ACE-inhibitorintermittent claudicationHematologyGeneral Medicinemedicine.diseaseSettore MED/11 - Malattie Dell'Apparato Cardiovascolareperipheral arterial disease.Oxidative StressTreatment OutcomeLower ExtremitychemistryCardiovascular Diseaseslcsh:RC666-701ACE-inhibitorsACE inhibitorCardiovascular agentCardiologyEndothelium VascularatherosclerosisCardiology and Cardiovascular Medicinebusinessmedicine.drugVascular Health and Risk Management
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PDGFRα-Positive B Cells Are Neural Stem Cells in the Adult SVZ that Form Glioma-like Growths in Response to Increased PDGF Signaling

2006

Neurons and oligodendrocytes are produced in the adult brain subventricular zone (SVZ) from neural stem cells (B cells), which express GFAP and have morphological properties of astrocytes. We report here on the identification B cells expressing the PDGFRalpha in the adult SVZ. Specifically labeled PDGFRalpha expressing B cells in vivo generate neurons and oligodendrocytes. Conditional ablation of PDGFRalpha in a subpopulation of postnatal stem cells showed that this receptor is required for oligodendrogenesis, but not neurogenesis. Infusion of PDGF alone was sufficient to arrest neuroblast production and induce SVZ B cell proliferation contributing to the generation of large hyperplasias wi…

Receptor Platelet-Derived Growth Factor alphaAdolescentNeuroscience(all)Subventricular zoneMice TransgenicDEVBIOBiologyMOLNEUROMiceNeuroblastLateral VentriclesmedicineAnimalsHumansCell ProliferationAged 80 and overNeuronsPlatelet-Derived Growth FactorStem CellsGeneral NeuroscienceNeurogenesisGliomaMiddle AgedSTEMCELLOligodendrocyteNeural stem cellCell biologymedicine.anatomical_structurenervous systemNeuronStem cellNeuroscienceSignal TransductionAdult stem cellNeuron
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Regulatory T cells selectively preserve immune privilege of self-antigens during viral central nervous system infection.

2012

Abstract Regulatory T cells (Tregs) are important for the attenuation of immune reactions. During viral CNS infections, however, an indiscriminate maintenance of CNS immune privilege through Treg-mediated negative regulation could prevent autoimmune sequelae but impair the control of viral replication. We analyzed in this study the impact of Tregs on the development of acute viral encephalomyelitis, T cell-mediated antiviral protection, and prevention of CNS autoimmunity following intranasal infection with the gliatropic mouse hepatitis virus strain A59. To assess the contribution of Tregs in vivo, we specifically depleted CD4+Foxp3+ T cells in a diphtheria toxin-dependent manner. We found …

Receptors CXCR3T cellImmunologychemical and pharmacologic phenomenaAutoimmunityBiologyCD8-Positive T-Lymphocytesmedicine.disease_causeCXCR3Lymphocyte ActivationAutoantigensT-Lymphocytes RegulatoryLymphocyte DepletionAutoimmunity03 medical and health sciencesMice0302 clinical medicineCentral Nervous System InfectionsImmune privilegeImmunitymedicineImmunology and AllergyAnimalsHumansEncephalomyelitisAdministration Intranasal030304 developmental biologyCell Proliferation0303 health sciencesImmunity CellularMice Inbred BALB CMurine hepatitis virusFOXP3hemic and immune systemsForkhead Transcription Factors3. Good healthmedicine.anatomical_structureViral replicationImmunologyAcute DiseaseCD4 AntigensLymph NodesCoronavirus InfectionsCD8030215 immunologyJournal of immunology (Baltimore, Md. : 1950)
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Requirement of Retinoic Acid Receptor Isotypes α, β, and γ during the Initial Steps of Neural Differentiation of PCC7 Cells

2005

Retinoic acid (RA) is indispensable for morphogenesis and differentiation of several tissues, including the nervous system. The requirement of the RA receptor (RAR) isotypes alpha, beta, and gamma and the putative role of retinoid X receptor-(RXR) signaling in RA-induced neural differentiation, was analyzed. For this compound-selective retinoids and the murine embryonal carcinoma cell line PCC7, a model system for RA-dependent neural differentiation was used. The present paper shows that proliferating PCC7 cells primarily express RXRalpha and RARalpha, lower levels of RXRbeta, and barely detectable amounts of RARbeta, RARgamma, and RXRgamma. At receptor-selective concentrations, only a RARa…

Receptors Retinoic AcidRetinoic acidReceptors Cytoplasmic and NuclearApoptosisLigandsMicechemistry.chemical_compoundEndocrinologyGenes ReporterNuclear Receptor Subfamily 6 Group A Member 1Protein IsoformsRetinoidReceptorGlutathione TransferaseNeuronsCell DeathReverse Transcriptase Polymerase Chain ReactionCell DifferentiationGeneral MedicineImmunohistochemistryUp-RegulationCell biologyDNA-Binding ProteinsBiochemistrySignal transductionPlasmidsProtein BindingSignal Transductionmedicine.drugTranscriptional ActivationDNA Complementarymedicine.drug_classRecombinant Fusion ProteinsBlotting WesternDown-RegulationTretinoinRetinoid X receptorBiologyTransfectionCell LineTretinoinCell Line TumormedicineAnimalsHumansMolecular BiologyCell ProliferationKineticsRetinoic acid receptorRetinoid X ReceptorschemistryNuclear receptorRNAOctamer Transcription Factor-3Transcription FactorsMolecular Endocrinology
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Macrophage migration inhibitory factor is critically involved in basal and fluoxetine-stimulated adult hippocampal cell proliferation and in anxiety,…

2011

Intensive research is devoted to unravel the neurobiological mechanisms mediating adult hippocampal neurogenesis, its regulation by antidepressants, and its behavioral consequences. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that is expressed in the CNS, where its function is unknown. Here, we show, for the first time, the relevance of MIF expression for adult hippocampal neurogenesis. We identify MIF expression in neurogenic cells (in stem cells, cells undergoing proliferation, and in newly proliferated cells undergoing maturation) in the subgranular zone of the rodent dentate gyrus. A causal function for MIF in cell proliferation was shown using genetic (M…

Receptors SteroidStem-Cellsanimal diseasesmedicine.medical_treatmentHippocampusExpressionHippocampal formationHippocampusSubgranular zonememoryMice0302 clinical medicineConditioning PsychologicalCyclin D2Rat Dentate GyrusMice KnockoutNeurons0303 health sciencesMicroscopy ConfocalChronic StressMifNeurogenesisBrainFearrespiratory systemanxietyPsychiatry and Mental healthC-Reactive ProteinCytokinemedicine.anatomical_structuredepressionAntidepressive Agents Second-GenerationStem cellPsychologyAnimal-ModelNeurogenesisSpatial BehaviorNerve Tissue Proteinschemical and pharmacologic phenomena03 medical and health sciencesCellular and Molecular Neurosciencemedicineotorhinolaryngologic diseasesAnimalsRats WistarMaze LearningMacrophage Migration-Inhibitory FactorsMolecular BiologyCell Proliferation030304 developmental biologyMemory DisordersDentate gyrusfluoxetineFactor Mifbiological factorsRatsDisease Models AnimalAcoustic StimulationBromodeoxyuridineMacrophage migration inhibitory factorCorticosteroneNeuroscience030217 neurology & neurosurgery
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Intercellular communication and human hepatocellular carcinoma.

2005

We have previously reported that gap junction-mediated intercellular communication (GJIC) can be restored in junctionally deficient human prostate epithelial cells, also suggesting that GJIC activity is regulated by estrogen. In the present work, we report studies on sex steroid regulation of GJIC and proliferative activity in both nontumoral (Chang liver, CL) and malignant (HepG2, Huh7) human liver cells. Junctional activity and liver cell growth were measured using the scrape-loading/dye-transfer (SL/DT) and the MTS assay, respectively. Using the SL/DT, only Huh7 cells exhibited a moderate degree of Junctional activity in basic conditions, while neither CL nor HepG2 cells showed functiona…

Receptors SteroidTime FactorsProliferationCell Communicationchemistry.chemical_compoundNeoplasmsReceptorTumorGeneral NeuroscienceLiver cellLiver NeoplasmsGap JunctionsGap junction-mediated intercellular communication (GJIC)ImmunohistochemistryLiverLiver NeoplasmReceptors AndrogenGap JunctionReceptors ProgesteroneHumanmedicine.medical_specialtyCell signalingCarcinoma HepatocellularTime Factormedicine.drug_classEstroneBiologyGeneral Biochemistry Genetics and Molecular BiologyCell LineHistory and Philosophy of ScienceInternal medicineCell Line TumormedicineCarcinomaEstrogen Receptor betaHumansHepatocellular carcinoma (HCC)SteroidCell ProliferationBiochemistry Genetics and Molecular Biology (all)Cell growthEstrogen Receptor alphamedicine.diseasedigestive system diseasesEndocrinologychemistryEstrogenCell cultureCancer researchNeoplasmAnnals of the New York Academy of Sciences
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Tumor cells convert immature myeloid dendritic cells into TGF-β–secreting cells inducing CD4+CD25+ regulatory T cell proliferation

2005

The mechanisms through which regulatory T cells accumulate in lymphoid organs of tumor-bearing hosts remain elusive. Our experiments indicate that the accumulation of CD4+CD25+ regulatory T cells (T reg cells) expressing FoxP3 and exhibiting immunosuppressive function originates from the proliferation of naturally occurring CD25+ T cells and requires signaling through transforming growth factor (TGF)–β receptor II. During tumor progression, a subset of dendritic cells (DCs) exhibiting a myeloid immature phenotype is recruited to draining lymph nodes. This DC subset selectively promotes the proliferation of T reg cells in a TGF-β–dependent manner in mice and rats. Tumor cells are necessary a…

Regulatory T cellImmunologychemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryArticleMiceInterleukin 21Transforming Growth Factor betaCell Line TumorNeoplasmsmedicineAnimalsImmunology and AllergyCytotoxic T cellIL-2 receptorAntigen-presenting cellCell ProliferationDNA PrimersInterleukin 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationForkhead Transcription FactorsRats Inbred Strainshemic and immune systemsDendritic CellsNatural killer T cellImmunohistochemistryMolecular biologyRatsCell biologymedicine.anatomical_structureBromodeoxyuridineInterleukin 12Receptors Transforming Growth Factor betaSignal TransductionJournal of Experimental Medicine
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Mast cells counteract regulatory T-cell suppression through interleukin-6 and OX40/OX40L axis toward Th17-cell differentiation

2009

Abstract The development of inflammatory diseases implies inactivation of regulatory T (Treg) cells through mechanisms that still are largely unknown. Here we showed that mast cells (MCs), an early source of inflammatory mediators, are able to counteract Treg inhibition over effector T cells. To gain insight into the molecules involved in their interplay, we set up an in vitro system in which all 3 cellular components were put in contact. Reversal of Treg suppression required T cell–derived interleukin-6 (IL-6) and the OX40/OX40L axis. In the presence of activated MCs, concomitant abundance of IL-6 and paucity of Th1/Th2 cytokines skewed Tregs and effector T cells into IL-17–producing T cel…

Regulatory T cellmedicine.medical_treatmentCellular differentiationImmunologyPriming (immunology)chemical and pharmacologic phenomenaMice TransgenicMast cell; T regulatory cell; Immune responseBiologyLymphocyte ActivationT-Lymphocytes RegulatoryBiochemistryImmune toleranceMiceMice CongenicmedicineImmune ToleranceMast CellT regulatory cellImmune responseCells CulturedCell ProliferationAnimalInterleukin-6Experimental autoimmune encephalomyelitisInterleukin-17hemic and immune systemsCell DifferentiationT lymphocyteT-Lymphocytes Helper-InducerHematologyCell BiologyReceptors OX40medicine.diseaseCell biologyMice Inbred C57BLmedicine.anatomical_structureCytokineImmunologyAnimals; Cell Differentiation; Cell Proliferation; Cells Cultured; Immune Tolerance; Interleukin-17; Interleukin-6; Lymphocyte Activation; Mast Cells; Membrane Glycoproteins; Mice; Mice Congenic; Mice Inbred C57BL; Mice Transgenic; Receptors OX40; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Tumor Necrosis Factors; Hematology; Biochemistry; Cell Biology; ImmunologyInterleukin 17Membrane GlycoproteinTumor Necrosis FactorSignal Transduction
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Ki-67 assessment of pancreatic neuroendocrine neoplasms: Systematic review and meta-analysis of manual vs. digital pathology scoring

2022

Ki-67 assessment is a key step in the diagnosis of neuroendocrine neoplasms (NENs) from all anatomic locations. Several challenges exist related to quantifying the Ki-67 proliferation index due to lack of method standardization and inter-reader variability. The application of digital pathology coupled with machine learning has been shown to be highly accurate and reproducible for the evaluation of Ki-67 in NENs. We systematically reviewed all published studies on the subject of Ki-67 assessment in pancreatic NENs (PanNENs) employing digital image analysis (DIA). The most common advantages of DIA were improvement in the standardization and reliability of Ki-67 evaluation, as well as its spee…

Reproducibility of ResultsBreast NeoplasmsCarcinoid TumorPathology and Forensic MedicinePancreatic Neoplasmsneuroendocrine neoplasms pancreasNeuroendocrine TumorsKi-67 AntigenGastroenteropancreatic Neuroendocrine TumorBiomarkers TumorImage Processing Computer-AssistedHumansGastroenteropancreatic Neuroendocrine Tumor; Cancer; Carcinoid TumorFemaleCell ProliferationCancer
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