Search results for "STAT5 Transcription Factor"

showing 10 items of 28 documents

Reduced numbers of IL-7 receptor (CD127) expressing immune cells and IL-7-signaling defects in peripheral blood from patients with breast cancer

2007

Interleukin-7-receptor-signaling plays a pivotal role in T-cell development and maintenance of T-cell memory. We studied IL-7Ralpha (CD127) expression in PBMCs obtained from patients with breast cancer and examined IL-7 receptor-mediated downstream effects defined by STAT5 phosphorylation (p-STAT5). Reduced numbers of IL-7Ralpha-positive cells were identified in CD4+ T-cells as well as in a CD8+ T-cell subset defined by CD8alpha/alpha homodimer expression in patients with breast cancer. PBMCs obtained from healthy donors (n = 19) and from patients with breast cancer (n = 19) exhibited constitutive p-STAT5 expression in the range of 0-6.4% in CD4+ T-cells and 0-4% in CD8+ T-cells. Stimulatio…

CD4-Positive T-LymphocytesCancer Researchmedicine.medical_specialtyT-Lymphocytesmedicine.medical_treatmentBreast NeoplasmsCD8-Positive T-LymphocytesPeripheral blood mononuclear cellchemistry.chemical_compoundImmune systemBreast cancerInternal medicineSTAT5 Transcription FactormedicineHumansPhosphorylationInterleukin-7 receptorSTAT5Receptors Interleukin-7biologybusiness.industryInterleukin-7Flow Cytometrymedicine.diseaseRecombinant ProteinsCytokineEndocrinologyOncologychemistryIonomycinLeukocytes Mononuclearbiology.proteinCytokinesFemalebusinessCD8Signal TransductionInternational Journal of Cancer
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Nitric oxide enhances Th9 cell differentiation and airway inflammation

2014

International audience; Th9 cells protect hosts against helminthic infection but also mediate allergic disease. Here we show that nitric oxide (NO) promotes Th9 cell polarization of murine and human CD4(+) T cells. NO de-represses the tumour suppressor gene p53 via nitrosylation of Mdm2. NO also increases p53-mediated IL-2 production, STAT5 phosphorylation and IRF4 expression, all essential for Th9 polarization. NO also increases the expression of TGFβR and IL-4R, pivotal to Th9 polarization. OVA-sensitized mice treated with an NO donor developed more severe airway inflammation. Transferred Th9 cells induced airway inflammation, which was exacerbated by NO and blocked by anti-IL-9 antibody.…

CD4-Positive T-LymphocytesInterleukin 2[SDV]Life Sciences [q-bio]Cellular differentiationNitric Oxide Synthase Type IIGeneral Physics and AstronomyMice TransgenicInflammationCell SeparationNitric OxideArticleGeneral Biochemistry Genetics and Molecular BiologyNitric oxideMicechemistry.chemical_compoundEosinophiliaSTAT5 Transcription FactormedicineAnimalsHumansInterleukin 9Cells CulturedInflammationMice Inbred BALB CMultidisciplinarybiologyNitrosylationInterleukin-9Cell DifferentiationGeneral Chemistryrespiratory systemFlow Cytometry3. Good healthCell biologyMice Inbred C57BLchemistryInterferon Regulatory FactorsImmunologyLeukocytes Mononuclearbiology.proteinInterleukin-2Mdm2Tumor Suppressor Protein p53medicine.symptomAntibodymedicine.drugNature Communications
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STAT5 and STAT5 Inhibitors in Hematological Malignancies

2019

The JAK-STAT pathway is an important physiologic regulator of different cellular functions including proliferation, apoptosis, differentiation, and immunological responses. Out of six different STAT proteins, STAT5 plays its main role in hematopoiesis and constitutive STAT5 activation seems to be a key event in the pathogenesis of several hematological malignancies. This has led many researchers to develop compounds capable of inhibiting STAT5 activation or interfering with its functions. Several anti-STAT5 molecules have shown potent STAT5 inhibitory activity in vitro. However, compared to the large amount of clinical studies with JAK inhibitors that are currently widely used in the clini…

Cancer ResearchFLT3-ITDAntineoplastic Agents03 medical and health sciences0302 clinical medicineMyeloproliferative DisordersCancer stem cellSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesSTAT5 Transcription FactormedicineAnimalsHumansBCR-ABLSTAT5030304 developmental biologyPharmacology0303 health sciencesSTAT transcription factorbiologybusiness.industryfood and beveragesCancerHematopoietic stem cellMyeloid leukemiamedicine.diseaseSTAT5 inhibitorleukemia.Leukemiamedicine.anatomical_structureHematologic Neoplasms030220 oncology & carcinogenesisJak2V617Fbiology.proteinCancer researchSettore BIO/14 - FarmacologiaMolecular MedicinebusinessTyrosine kinase
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The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistan…

2013

The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules. Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells. Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells. Moreover, it showed a…

Cancer ResearchFusion Proteins bcr-ablApoptosisPiperazinesSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundhemic and lymphatic diseasesSTAT5 Transcription FactorCytotoxic T cellPharmacology (medical)Cyclin D1STAT5biologyDrug SynergismCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiaOncologyProto-Oncogene Proteins c-bcl-2BenzamidesImatinib MesylateGrowth inhibitionmedicine.drugbcl-X ProteinDown-RegulationAntineoplastic AgentsBone Marrow CellsResting Phase Cell CycleColony-Forming Units AssayBenzophenonesNecrosisCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansneoplasmsBenzofuransPharmacologyG1 PhaseImatinibBCR-ABL chronic myeloid leukemia imatinib resistance STAT5 tyrosine kinase inhibitorsmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGenes bcl-1Genes bcl-2PyrimidineschemistryApoptosisDrug Resistance NeoplasmSettore BIO/14 - FarmacologiaCancer researchbiology.proteinK562 CellsK562 cells
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STAT5 is crucial to maintain leukemic stem cells in acute myelogenous leukemias induced by MOZ-TIF2.

2012

Abstract MOZ-TIF2 is a leukemogenic fusion oncoprotein that confers self-renewal capability to hematopoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone marrow transplantation assays. Here, we report that FLT3-ITD transforms hematopoietic cells in cooperation with MOZ-TIF2 in vitro and in vivo. Coexpression of FLT3-ITD confers growth factor independent survival/proliferation, shortens disease latency, and results in an increase in the number of leukemic stem cells (LSC). We show that STAT5, a major effector of aberrant FLT3-ITD signal transduction, is both necessary and sufficient for this cooperative effect. In addition, STAT5 signaling is essent…

Cancer ResearchMyeloidOncogene Proteins Fusionmedicine.medical_treatmentArticleMyelogenousMicehemic and lymphatic diseasesmedicineSTAT5 Transcription FactorAnimalsSTAT5Mice Inbred BALB CbiologyGrowth factormedicine.diseaseFlow CytometryHaematopoiesisLeukemiaBlotting SouthernLeukemia Myeloid Acutemedicine.anatomical_structureCell Transformation NeoplasticOncologyCancer researchbiology.proteinNeoplastic Stem CellsSignal transductionStem cellSignal TransductionCancer research
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In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.

2003

In BCR-ABL-positive cells, the transcription factor STAT-5 is constitutively activated by tyrosine phosphorylation. STAT-5 activation results in upregulation of bcl-X(L) and increased resistance to induction of apoptosis. Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells. Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts. In contrast to JAK-2 and PI-3-kinase inhibition, exposure of K562 cells to imatinib mesylate resulted in obvious suppression of proliferation. R…

Cancer ResearchProgrammed cell deathBlotting WesternFusion Proteins bcr-ablDown-RegulationAntineoplastic AgentsApoptosisBiologyPiperazineschemistry.chemical_compoundDownregulation and upregulationhemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineIn Situ Nick-End LabelingSTAT5 Transcription FactorHumansEnzyme InhibitorsPhosphorylationCell growthCytarabineImatinibTyrosine phosphorylationDrug SynergismHematologyDNAU937 CellsProtein-Tyrosine KinasesMilk ProteinsPrecipitin TestsDNA-Binding ProteinsImatinib mesylatePyrimidinesOncologychemistryApoptosisCaspasesBenzamidesCancer researchImatinib MesylateTrans-ActivatorsTyrosinePoly(ADP-ribose) PolymerasesK562 CellsCell Divisionmedicine.drugK562 cellsSignal TransductionLeukemia
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Platelet-derived growth factor alpha mediates the proliferation of peripheral T-cell lymphoma cells via an autocrine regulatory pathway.

2014

Peripheral T-cell lymphomas not otherwise specified (PTCL/NOS) are very aggressive tumors characterized by consistent aberrant expression of platelet-derived growth factor receptor alpha (PDGFRA). In this study, we aimed to identify the determinants of PDGFRA activity in PTCL/NOS and to elucidate the biological consequences of its activation. We observed overexpression of the PDGFRA gene by gene expression profiling in most of the tested PTCLs and confirmed the expression of PDGFRA and phospho-PDGFRA using immunohistochemistry. The integrity of the PDFGRA locus was demonstrated using several different approaches, including massive parallel sequencing and Sanger sequencing. PDGF-AA was found…

Cancer ResearchReceptor Platelet-Derived Growth Factor alphamedicine.medical_treatmentT celltumor cell proliferationPDGFRAGrowth factor receptorCell Line TumormedicinePDFGRASTAT5 Transcription FactorHumansAutocrine signallingExtracellular Signal-Regulated MAP KinasesSTAT5PTCL/NOS; PDFGRA; tumor cell proliferationCell ProliferationPlatelet-Derived Growth FactorbiologyCell growthExtracellular Signal-Regulated MAP KinaseGrowth factorLymphoma T-Cell PeripheralHematologyPTCL/NOSdigestive system diseasesGene expression profilingAutocrine Communicationmedicine.anatomical_structureAnesthesiology and Pain MedicineSTAT1 Transcription FactorOncologyCancer researchbiology.proteinT-cell lymphomaProto-Oncogene Proteins c-aktHuman
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In Activated Murine Mast Cells, NFATc2 Is Critical for the Production of Autocrine IL-3, Thereby Promoting the Expression of IL-9

2019

Abstract IL-9 has lent its numerical designation to the Th9 subset of CD4+ Th cells, although it is also produced by additional cell types, including mast cells. It is a pleiotropic cytokine involved in allergic reactions, parasitic infections, autoimmune inflammation, and cancer immunity. In this article, we provide evidence that NFATc2 has contradictory functions in the expression of IL-9 in murine Th9 cells and bone marrow–derived mast cells (BMMC). The basis for this is our observation that the production of IL-9 in NFATc2-deficient Th9 cells is increased, whereas it is decreased in BMMC devoid of NFATc2. In addition, NFATc2 deficiency almost completely abrogates the expression of IL-3 …

Cell typeNFATC2medicine.medical_treatmentImmunologyCellAutocrine CommunicationMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationSTAT5 Transcription FactormedicineAnimalsImmunology and AllergyMast CellsAutocrine signallingCells CulturedSTAT5Feedback PhysiologicalMice KnockoutMice Inbred BALB CNFATC Transcription FactorsbiologyChemistryInterleukin-9T-Lymphocytes Helper-InducerUp-RegulationCell biologyMice Inbred C57BLAutocrine CommunicationCytokinemedicine.anatomical_structurebiology.proteinInterleukin-3030215 immunologyThe Journal of Immunology
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Inhibition of activated STAT5 in Bcr/Abl expressing leukemia cells with new pimozide derivatives.

2014

STATs are transcription factors acting as intracellular signaling after stimulation with cytokines, growth factors and hormones. STAT5 is also constitutively active in many forms of cancers, including chronic myelogenous leukemia, acute lymphoblastic leukemia and Hodgkin's lymphoma. Recently, literature reported that the neuroleptic drug pimozide inhibits STAT5 phosphorylation inducing apoptosis in CML cells. We undertook an investigation from pimozide structure, obtaining simple derivatives with cytotoxic and STAT5-inhibitory activity, two of them markedly more potent than pimozide.

Clinical BiochemistryFusion Proteins bcr-ablPharmaceutical ScienceApoptosisBiochemistrySettore MED/15 - Malattie Del SangueCell LineStructure-Activity RelationshipPimozideSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesDrug DiscoverymedicineSTAT5 Transcription FactorCytotoxic T cellHumansPhosphorylationMolecular BiologyTranscription factorSTAT5Cell ProliferationbiologyDose-Response Relationship DrugMolecular StructureChemistrySTAT5 inhibitorsPimozideBCR/ABL expressing leukemia ApoptosisCell growth inhibitionOrganic ChemistryCell CyclePimozidemedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaLeukemiaApoptosisCancer researchbiology.proteinSettore BIO/14 - FarmacologiaMolecular MedicinePhosphorylationK562 Cellsmedicine.drugChronic myelogenous leukemia
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Expression analysis and functional activity of interleukin-7 splice variants.

2008

Alternative splicing results in multiple protein isoforms derived from a single gene. The magnitude of this process ranges from a complete loss of function to gain of new function. We examined, as a paradigm, alternative splicing of the non-redundant human cytokine, interleukin-7 (IL-7). We show that extensive IL-7 splicing in human tissues of different histology, including MTB+ granuloma lesions, transformed tissue and tumor cell lines. IL-7 splice variants were expressed as recombinant proteins. A differentially spliced IL-7 isoform, lacking exon 5, leads to STAT-5 phosphorylation in CD4+ and CD8+ T cells, promotes thymocyte maturation and T-cell survival. Human tumor lesions show aberran…

Gene isoformCD4-Positive T-LymphocytesCell SurvivalImmunologyBiologyCD8-Positive T-LymphocytesExonCell Line TumorGeneticsSTAT5 Transcription FactorHumansProtein IsoformssplicePhosphorylationGenetics (clinical)GranulomaInterleukin-7Alternative splicingInterleukinExonsMolecular biologyRecombinant ProteinsCell biologyThymocyteAlternative SplicingOrgan SpecificityRNA splicingCD8Genes and immunity
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