Search results for "Myeloid"

showing 10 items of 538 documents

Chronic myelogenous leukaemia exosomes modulate bone marrow microenvironment through activation of epidermal growth factor receptor

2016

Abstract Chronic myelogenous leukaemia (CML) is a clonal myeloproliferative disorder. Recent evidence indicates that altered crosstalk between CML and mesenchymal stromal cells may affect leukaemia survival; moreover, vesicles released by both tumour and non‐tumour cells into the microenvironment provide a suitable niche for cancer cell growth and survival. We previously demonstrated that leukaemic and stromal cells establish an exosome‐mediated bidirectional crosstalk leading to the production of IL8 in stromal cells, thus sustaining the survival of CML cells. Human cell lines used are LAMA84 (CML cells), HS5 (stromal cells) and bone marrow primary stromal cells; gene expression and protei…

0301 basic medicineStromal cellchronic myeloid leukaemiaEGFRBone Marrow CellsexosomesBiologyInterleukin 8AmphiregulinBone Marrow Stromal Cell03 medical and health sciencesAmphiregulinSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineCell AdhesionHumansInterleukin 8Epidermal growth factor receptorRNA MessengerPhosphorylationRNA Small InterferingAnnexin A2SNAILMesenchymal stem cellInterleukin-8Cell BiologyOriginal ArticlesMicrovesiclesCell biologyErbB Receptors030104 developmental biologymedicine.anatomical_structureCellular MicroenvironmentMatrix Metalloproteinase 9Cancer cellChronic Myelogenous Leukemia Exosomes; Interleukin 8; Bone Marrow Stromal Cells; EGFRbiology.proteinMolecular MedicineOriginal ArticleBone marrowSnail Family Transcription FactorsChronic Myelogenous Leukemia ExosomeStromal Cellsepidermal growth factor receptor
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Targeting myeloid cells in the tumor sustaining microenvironment.

2017

Myeloid cells are the most abundant cells in the tumor microenvironment (TME). The tumor recruits and modulates endogenous myeloid cells to tumor-associated macrophages (TAM), dendritic cells (DC), myeloid-derived suppressor cells (MDSC) and neutrophils (TAN), to sustain an immunosuppressive environment. Pathologically overexpressed mediators produced by cancer cells like granulocyte-macrophage colony-stimulating- and vascular endothelial growth factor induce myelopoiesis in the bone marrow. Excess of myeloid cells in the blood, periphery and tumor has been associated with tumor burden. In cancer, myeloid cells are kept at an immature state of differentiation to be diverted to an immunosupp…

0301 basic medicineTumor microenvironmentImmunologyCancerTumor-associated macrophageDendritic cellBiologymedicine.disease03 medical and health sciences030104 developmental biologymedicine.anatomical_structureNeoplasmsCancer cellImmunologymedicineCancer researchTumor MicroenvironmentAnimalsHumansTumor promotionMyeloid CellsBone marrowMyelopoiesisImmunotherapyCellular immunology
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Loss of MCL1 function sensitizes the MDA-MB-231 breast cancer cells to rh-TRAIL by increasing DR4 levels.

2019

Triple-negative breast cancer (TNBC) is a form of BC characterized by high aggressiveness and therapy resistance probably determined by cancer stem cells. MCL1 is an antiapoptotic Bcl-2 family member that could limit the efficacy of anticancer agents as recombinant human tumor necrosis factor related apoptosis-inducing ligand (rh-TRAIL). Here, we investigated MCL1 expression in TNBC tissues and cells. We found MCL1 differentially expressed (upregulated or downregulated) in TNBC tissues. Furthermore, in comparison to the human mammary epithelial cells, we found that MDA-MB-231 cells show similar messenger RNA levels but higher MCL1 protein levels, whereas it resulted downregulated in MDA-MB-…

0301 basic medicinecancer stem cellIndolesPhysiologyCell SurvivalClinical BiochemistryCellPopulationApoptosisTNF-Related Apoptosis-Inducing Ligand03 medical and health sciences0302 clinical medicineCancer stem cellSettore BIO/10 - BiochimicaCell Line Tumormedicinerh-TRAILBiomarkers TumorGene silencingHumansViability assayGene SilencingeducationCell ShapeCell ProliferationMembrane Potential Mitochondrialeducation.field_of_studySulfonamidesChemistryCell growthCell CycleCell BiologyCell cycleRecombinant ProteinsGene Expression Regulation NeoplasticReceptors TNF-Related Apoptosis-Inducing Ligand030104 developmental biologymedicine.anatomical_structureMCL1ApoptosisDR4 receptor030220 oncology & carcinogenesisCancer researchtriple-negative breast cancerMyeloid Cell Leukemia Sequence 1 ProteinJournal of cellular physiology
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Genetics and Pathogenetic Role of Inflammasomes in Philadelphia Negative Chronic Myeloproliferative Neoplasms: A Narrative Review

2021

The last decade has been very important for the quantity of preclinical information obtained regarding chronic myeloproliferative neoplasms (MPNs) and the following will be dedicated to the translational implications of the new biological acquisitions. The overcoming of the mechanistic model of clonal evolution and the entry of chronic inflammation and dysimmunity into the new model are the elements on which to base a part of future therapeutic strategies. The innate immune system plays a major role in this context. Protagonists of the initiation and regulation of many pathological aspects, from cytokine storms to fibrosis, the NLRP3 and AIM2 inflammasomes guide and condition the natural hi…

0301 basic medicinechronic inflammationInflammasomesmyeloproliferative neoplasmAIM2Context (language use)DiseaseReviewBioinformaticsSomatic evolution in cancerCatalysismyeloproliferative neoplasmsLeukemia Myeloid Chronic Atypical BCR-ABL NegativeAutoimmune Diseaseslcsh:ChemistryInorganic ChemistryClonal Evolution03 medical and health sciencesAIM20302 clinical medicineNLRP3inflammasomeNLR Family Pyrin Domain-Containing 3 ProteinmedicineHumansPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyPhiladelphia negativeInflammationInnate immune systembusiness.industryOrganic ChemistryInflammasomeGeneral MedicineComputer Science ApplicationsNatural historyDNA-Binding Proteins030104 developmental biologylcsh:Biology (General)lcsh:QD1-999030220 oncology & carcinogenesisbusinessmedicine.drugInternational Journal of Molecular Sciences
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Structural and mechanistic insights into the interaction of the circadian transcription factor BMAL1 with the KIX domain of the CREB-binding protein

2019

JBC papers in press xx, 16604-16619 (2019). doi:10.1074/jbc.RA119.009845

0301 basic medicineendocrine systemCircadian clockTranscription factor complex610BiochemistryProtein Structure SecondaryProtein–protein interaction03 medical and health sciencesTransactivationMiceProto-Oncogene Proteins c-mybProtein DomainsX-Ray DiffractionCircadian ClocksScattering Small AngleAnimalsddc:610Amino Acid SequenceCREB-binding proteinMolecular BiologyTernary complexTranscription factorBinding Sites030102 biochemistry & molecular biologybiologyChemistryARNTL Transcription FactorsCell BiologyHistone-Lysine N-MethyltransferaseSurface Plasmon ResonanceCREB-Binding ProteinRecombinant ProteinsCell biologyProtein Structure Tertiary030104 developmental biologyStructural biologyProtein Structure and Foldingbiology.proteinMutagenesis Site-DirectedMyeloid-Lymphoid Leukemia ProteinProtein Binding
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Myeloid-Derived Suppressor Cells Specifically Suppress IFN-γ Production and Antitumor Cytotoxic Activity of Vδ2 T Cells.

2018

γδ T cells represent less than 5% of circulating T cells; they exert a potent cytotoxic function against tumor or infected cells and secrete cytokines like conventional αβ T cells. As αβ T cells γδ T cells reside in the typical T cell compartments (the lymph nodes and spleen), but are more widely distributed in tissues throughout the body. For these reasons, some investigators are exploring the possibility of immunotherapies aimed to expand and activate Vδ2 T cells, or using them as Chimeric Antigen Receptor carriers. However, the role of immunosuppressive microenvironment on Vδ2 T cells during infections and cancers has not been completely elucidated. In particular, the effects of myeloid-…

0301 basic medicinelcsh:Immunologic diseases. AllergyCytotoxicity Immunologicγmedicine.medical_treatmentT cellδImmunologyAntitumoral activityT cellsSpleenLymphocyte ActivationJurkat cellsγδ T cellsImmunophenotyping03 medical and health sciencesInterferon-gamma0302 clinical medicineT-Lymphocyte SubsetsCell Line TumorNeoplasmsmedicineMyeloid-derived suppressor cellImmunology and AllergyCytotoxic T cellHumansIFN-γantitumoral activityArginaseChemistryMyeloid-Derived Suppressor CellsDegranulationReceptors Antigen T-Cell gamma-deltaImmunotherapy030104 developmental biologymedicine.anatomical_structureCell cultureCancer researchMyeloid-derived Suppressor CellLeukocytes MononuclearCytokinesImmunotherapyimmunotherapylcsh:RC581-607Biomarkers030215 immunologyFrontiers in immunology
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Gliptins Suppress Inflammatory Macrophage Activation to Mitigate Inflammation, Fibrosis, Oxidative Stress, and Vascular Dysfunction in Models of Nona…

2017

Abstract Aims: Nonalcoholic steatohepatitis (NASH) is characterized by steatosis, panlobular inflammation, liver fibrosis, and increased cardiovascular mortality. Dipeptidyl peptidase-4 inhibitors (gliptins) are indirect glucagon-like peptide 1 agonists with antidiabetic and anti-inflammatory activity, used for the treatment of type 2 diabetes. Their potential and underlying mechanisms to treat metabolic liver inflammation and fibrosis as well as the associated vascular dysfunction remain to be explored. Results: In the methionine/choline-deficient (MCD) diet and Mdr2−/− models of NASH and liver fibrosis, treatment with sitagliptin and linagliptin significantly decreased parameters of steat…

0301 basic medicinemedicine.medical_specialtyPhysiologyClinical BiochemistryAnti-Inflammatory AgentsGene ExpressionInflammationType 2 diabetes030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryAntioxidantsProinflammatory cytokineMice03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisInternal medicinemedicineAnimalsMyeloid CellsMolecular BiologyDipeptidyl peptidase-4General Environmental ScienceInflammationMice KnockoutDipeptidyl-Peptidase IV Inhibitorsbusiness.industryMacrophagesCell BiologyMacrophage Activationmedicine.diseaseFibrosisDietDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyLiverNADPH Oxidase 2General Earth and Planetary SciencesTumor necrosis factor alphaSteatosismedicine.symptomReactive Oxygen SpeciesbusinessBiomarkersOxidative stressAntioxidants & Redox Signaling
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Reproducibility Issues: Avoiding Pitfalls in Animal Inflammation Models

2017

In light of an enhanced awareness of ethical questions and ever increasing costs when working with animals in biomedical research, there is a dedicated and sometimes fierce debate concerning the (lack of) reproducibility of animal models and their relevance for human inflammatory diseases. Despite evident advancements in searching for alternatives, that is, replacing, reducing, and refining animal experiments-the three R's of Russel and Burch (1959)-understanding the complex interactions of the cells of the immune system, the nervous system and the affected tissue/organ during inflammation critically relies on in vivo models. Consequently, scientific advancement and ultimately novel therape…

0301 basic medicinemedicine.medical_specialtyResearch assessmentbusiness.industryPhysiologyInflammation03 medical and health sciences030104 developmental biologyMyeloid cellsJournal Articlemedicinemedicine.symptomIntensive care medicinebusiness
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Management of Ponatinib in Patients with Chronic Myeloid Leukemia with Cardiovascular Risk Factors

2019

Cardiovascular (CV) adverse events are considered common complications of ponatinib treatment. Recently, it has been demonstrated that ponatinib dose reductions in definite settings can obtain optimal responses and lower ponatinib-related CV events. In this study, we describe the management of 5 patients with chronic myeloid leukemia treated with ponatinib, from second to fourth line of tyrosine kinase inhibitor therapy, carrying high pre-ponatinib CV risk, who obtained optimal molecular response and developed no CV adverse event during follow-up. Among these 5 patients, 2 had diagnosis of ischemic heart disease and underwent percutaneous angioplasty, 2 had type 2 diabetes and arterial hype…

0301 basic medicinemedicine.medical_specialtymedicine.drug_class030106 microbiologyCardiovascular risk factorsType 2 diabetesDiseaseTyrosine-kinase inhibitorSettore MED/15 - Malattie Del Sangue03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineDrug DiscoverymedicinePharmacology (medical)In patientAdverse effectPharmacologybusiness.industryPonatinibChronic myeloid leukemiaMyeloid leukemiaGeneral Medicinemedicine.diseaseCardiovascular riskInfectious DiseasesOncologychemistry030220 oncology & carcinogenesisPonatinibbusiness
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Leukemia-associated activating mutation of Flt3 expands dendritic cells and alters T cell responses

2016

Lau et al. show that the FLT3-ITD mutation directly affects dendritic cell development in preleukemic mice, indirectly modulating T cell homeostasis and supporting the expansion of regulatory T cells.

0301 basic medicinemedicine.medical_treatmentT cellT-LymphocytesImmunologyDown-RegulationBiologyCD8-Positive T-LymphocytesArticle03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesGene DuplicationmedicineImmunology and AllergyAnimalsHomeostasisCell LineageProgenitor cellResearch ArticlesCell ProliferationLeukemiaCell growthGene Expression Regulation LeukemicMyeloid leukemiaMembrane Proteinshemic and immune systemsDendritic CellsCell biologyImmunosurveillanceMice Inbred C57BLHaematopoiesis030104 developmental biologyCytokinemedicine.anatomical_structureImmunologyMutationCD8030215 immunologySignal TransductionThe Journal of Experimental Medicine
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