Search results for " CXC"

showing 10 items of 84 documents

The Expression and Prognostic Significance of VEGF and CXCR4 in Gastric Cancer: Correlation with Angiogenesis, Lymphangiogenesis and Progression

2022

The cellular response to hypoxia includes the expression of hypoxia-inducible factor-1 (HIF-1) and its target genes: vascular endothelial growth factor (VEGF) and CXC chemokine receptor 4 (CXCR4). The aim of this study was to investigate the expression and prognostic significance of VEGF and CXCR4, which are responsible for angiogenesis and progression in gastric cancer. Twenty-eight gastric cancer patients were analyzed. The mRNA expression was examined in primary tumors and corresponding normal gastric mucosa by RT-PCR. The protein level was examined by immunohistochemistry staining. The high expression of VEGF and CXCR4 was found in 71.0 and 64.0% of tumors, respectively. The mean levels…

Microbiology (medical)gastric cancer; VEGF; CXCR4; angiogenesis; lymphangiogenesis; lymph node metastasesGeneral MedicineMolecular BiologyMicrobiologyCurrent Issues in Molecular Biology
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CXCR7 Reactivates ERK Signaling to Promote Resistance to EGFR Kinase Inhibitors in NSCLC

2019

Abstract Although EGFR mutant–selective tyrosine kinase inhibitors (TKI) are clinically effective, acquired resistance can occur by reactivating ERK. We show using in vitro models of acquired EGFR TKI resistance with a mesenchymal phenotype that CXCR7, an atypical G protein-coupled receptor, activates the MAPK–ERK pathway via β-arrestin. Depletion of CXCR7 inhibited the MAPK pathway, significantly attenuated EGFR TKI resistance, and resulted in mesenchymal-to-epithelial transition. CXCR7 overexpression was essential in reactivation of ERK1/2 for the generation of EGFR TKI–resistant persister cells. Many patients with non–small cell lung cancer (NSCLC) harboring an EGFR kinase domain mutatio…

0301 basic medicineMAPK/ERK pathwayCancer ResearchLung NeoplasmsDrug ResistanceDrug resistanceTransgenicMiceChemokine receptor0302 clinical medicineNeoplasmsCarcinoma Non-Small-Cell LungReceptorsMedicineNon-Small-Cell LungCXCRReceptorLungbeta-ArrestinsCancerEGFR inhibitorsTumorKinaseLung CancerErbB ReceptorsOncology5.1 Pharmaceuticals030220 oncology & carcinogenesisDevelopment of treatments and therapeutic interventionsTyrosine kinaseEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemOncology and CarcinogenesisMice TransgenicArticleCell LineExperimental03 medical and health sciencesClinical ResearchCell Line TumorAnimalsHumansOncology & CarcinogenesisProtein Kinase InhibitorsReceptors CXCRbusiness.industryCarcinomaNeoplasms Experimentalrespiratory tract diseases030104 developmental biologyProtein kinase domainDrug Resistance NeoplasmMutationCancer researchNeoplasmbusinessCancer Research
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Chemokine receptor CXCR4-prognostic factor for gastrointestinal tumors

2008

To review the implication of CXCR4 for gastrointestinal cancer, a "Pubmed" analysis was performed in order to evaluate the relevance of CXCR4 and its ligands for gastrointestinal cancers. Search terms applied were "cancer, malignoma, esophageal, gastric, colon, colorectal, hepatic, pancreatic, CXCR4, SDF-1alpha, and SDF-1beta". CXCR4 expression correlated with dissemination of diverse gastrointestinal malignomas. The CXCR4 ligand SDF-1alpha might act as "chemorepellent" while SDF-1beta might act as "chemorepellent" for CTLs, inducing tumor rejection. The paracrine expression of SDF-1alpha was furthermore closely associated with neoangiogenesis. CXCR4 and its ligands influence the disseminat…

Receptors CXCR4Prognostic factorGastrointestinal tumorsBiologyLigandsCXCR4Paracrine signallingChemokine receptorBiomarkers TumormedicineAnimalsHumansNeoplasm InvasivenessGastrointestinal cancerNeoplasm MetastasisGastrointestinal NeoplasmsGastroenterologyCancerGeneral Medicinemedicine.diseaseChemokine CXCL12EditorialTreatment OutcomeSearch termsImmunologyCancer researchWorld Journal of Gastroenterology
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Docosahexaenoic acid reduces suppressive and migratory functions of CD4CD25 regulatory T-cells

2009

Immunological tolerance is one of the fundamental aspects of the immune system. The CD4(+)CD25(+) regulatory T (Treg) cells have emerged as key players in the development of tolerance to self and foreign antigens. However, little is known about the endogenous factors and mechanisms controlling their suppressive capacity on immune response. In this study, we observed that docosahexaenoic acid (DHA), an n-3 polyunsaturated fatty acid, diminished, in a dose-dependent manner, the capacity of Treg cells to inhibit the CD4(+)CD25(-) effector T-cell proliferation. DHA not only reduced the migration of Treg cells toward chemokines but also downregulated the mRNA expression of CCR-4 and CXCR-4 in Tr…

MaleReceptors CXCR4Chemokineextracellular signal-regulated kinase 1/2Receptors CCR4Docosahexaenoic Acidschemical and pharmacologic phenomenaQD415-436T-Lymphocytes RegulatoryBiochemistryMicehistone desacetylase 7EndocrinologyImmune systemAntigenAntigens CDCell MovementTransforming Growth Factor betaAnimalsCTLA-4 AntigenRNA MessengerIL-2 receptorCells CulturedCell ProliferationDose-Response Relationship DrugbiologySmad7Reverse Transcriptase Polymerase Chain ReactionInterleukin-2 Receptor alpha SubunitFOXP3Forkhead Transcription Factorshemic and immune systemsCell BiologyTransforming growth factor betaInterleukin-10Cell biologyMice Inbred C57BLInterleukin 10Docosahexaenoic acidImmunologybiology.proteinResearch ArticleJournal of Lipid Research
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A 588-gene microarray analysis of the peripheral blood mononuclear cells of spondyloarthropathy patients

2002

OBJECTIVES: To identify genes which are more highly expressed in the peripheral blood mononuclear cells (PBMC) of patients with spondyloarthropathy (SpA), rheumatoid arthritis (RA) and psoriatic arthritis (PsA), in comparison to normal subjects. METHODS: A 588-gene microarray was used as a screening tool to select a panel of such genes from PBMC of these subjects and of normal subjects. Results were then validated by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The following genes were more highly expressed in arthritis patients than in normal subjects: macrophage differentiation marker MNDA (myeloid nuclear differentiation antigen), MRP8 and MRP14 (migratory inhibitor…

AdultGenetic MarkersMaleCCR1Receptors CXCR4AdolescentSpondyloarthropathyArthritisPeripheral blood mononuclear cellArthritis RheumatoidPsoriatic arthritisRheumatologymedicineHumansSpondylitis AnkylosingPharmacology (medical)AgedOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain Reactionbusiness.industryJanus kinase 3Arthritis PsoriaticSynovial MembraneMNDAInterleukinDNAMiddle Agedmedicine.diseaseAntigens DifferentiationChemokine CXCL12ImmunologyLeukocytes MononuclearFemalebusinessChemokines CXCRheumatology (Oxford, England)
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Functional effects of proinflammatory factors present in Sjögren's syndrome salivary microenvironment in an in vitro model of human salivary gland.

2017

AbstractPrimary Sjögren’s syndrome (pSS) is an autoimmune exocrinopathy in which the role that the immune response plays in reducing exocrine gland function, including the glandular microenvironment of cytokines, has not been fully understood. Epithelial cells from biopsies of human parotid gland (HPG) were used to establish a model of human salivary gland in vitro. In this model, the functional consequences of several proinflammatory soluble factors present in the pSS glandular microenvironment were assessed. Stimulation with isoproterenol and calcium produced a significant increase in the basal activity of amylase in the HPG cell supernatants. Under these conditions, the presence of TNF-α…

0301 basic medicinemedicine.medical_specialtyExocrine glandmedicine.medical_treatmentInterleukin-1betalcsh:MedicineSalivary GlandsArticleProinflammatory cytokine03 medical and health sciencesInterferon-gammaImmune systemstomatognathic systemTransforming Growth Factor betaInternal medicinemedicineHumansSecretionAmylaselcsh:ScienceCells CulturedCell ProliferationMultidisciplinarybiologySalivary glandChemistryTumor Necrosis Factor-alphalcsh:REpithelial CellsChemokine CXCL12Parotid gland030104 developmental biologyEndocrinologyCytokinemedicine.anatomical_structureSjogren's SyndromeImmunologyAmylasesbiology.proteinlcsh:QScientific reports
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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Mast Cells and Th17 Cells Contribute to the Lymphoma-Associated Pro-Inflammatory Microenvironment of Angioimmunoblastic T-Cell Lymphoma

2010

Reports focusing on the immunological microenvironment of peripheral T-cell lymphomas (PTCL) are rare. Here we studied the reciprocal contribution of regulatory (Treg) and interleukin-17-producing (Th17) T-cells to the composition of the lymphoma-associated microenvironment of angioimmunoblastic T-cell lymphoma (AITL) and PTCL not otherwise specified on tissue microarrays from 30 PTCLs not otherwise specified and 37 AITLs. We found that Th17 but not Treg cells were differently represented in the two lymphomas and correlated with the amount of mast cells (MCs) and granulocytes, which preferentially occurred in the cellular milieu of AITL cases. We observed that MCs directly synthesized inter…

Angioimmunoblastic T-cell lymphomaLymphomaInflammationBiologymedicine.disease_causeCXCR3Lymphoma T-CellCXCR5Pathology and Forensic MedicineAutoimmunityAnimals Chemokine CXCL13; immunology Cytokines; genetics/immu/nology Forkhead Transcription Factors; immunology Gene Expression Profiling Humans Immunoblastic Lymphadenopathy; immunology/pathology Inflammation; immunology Interleukin-17; immunology Interleukin-6; immunology Lymphoma; T-Cell; immunology/pathology Mast Cells; immunology Microarray Analysis Th17 Cells; immunology Tumor MicroenvironmentimmunologymedicineTumor MicroenvironmentAnimalsHumansMast CellsInflammationTumor microenvironmentInterleukin-6Gene Expression ProfilingInterleukin-17Forkhead Transcription FactorsMast cellmedicine.diseaseT-CellMicroarray AnalysisChemokine CXCL13humanitiesgenetics/immu/nologyLymphomamedicine.anatomical_structureImmunoblastic LymphadenopathyImmunologyCytokinesimmunology/pathologyTh17 CellsMast Cell microenvironment angioimmunoblasticmedicine.symptomRegular Articles
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A novel CXCR4 antagonist counteracts paradoxical generation of cisplatin-induced pro-metastatic niches in lung cancer.

2021

Platinum-based chemotherapy remains widely used in advanced non-small cell lung cancer (NSCLC) despite experimental evidence of its potential to induce long-term detrimental effects, including the promotion of pro-metastatic microenvironments. In this study, we investigated the interconnected pathways underlying the promotion of cisplatin-induced metastases. In tumor-free mice, cisplatin treatment resulted in an expansion in the bone marrow of CCR2+CXCR4+Ly6Chigh inflammatory monocytes (IMs) and an increase in lung levels of stromal SDF-1, the CXCR4 ligand. In experimental lung metastasis assays, cisplatin-induced IMs promoted the extravasation of tumor cells and the expansion of CD133+CXCR…

MaleReceptors CXCR4Stromal cellLung NeoplasmsSettore MED/08 - Anatomia PatologicaMonocytesMetastasisMiceCarcinoma Non-Small-Cell LungCell Line TumorDrug DiscoveryGeneticsMedicineSettore MED/05 - Patologia ClinicaAnimalsHumansDrug InteractionsAC133 AntigenNeoplasm MetastasisLung cancerMolecular BiologyPharmacologyCisplatinCXCR4 antagonistchemotherapy combination therapy inflammatory monocytes lung cancer stem cells metastasis peptide anti-CXCR4 SDF-1/CXCR4 axisbusiness.industrymedicine.diseasePrimary tumorXenograft Model Antitumor AssaysExtravasationChemokine CXCL12medicine.anatomical_structureRAW 264.7 CellsA549 CellsCancer researchNeoplastic Stem CellsMolecular MedicineBone marrowCisplatinbusinessPeptidesmedicine.drugMolecular therapy : the journal of the American Society of Gene Therapy
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Association of increased CCL5 and CXCL7 chemokine expression with neutrophil activation in severe stable COPD

2009

BACKGROUND: Increased numbers of activated neutrophils have been reported in the bronchial mucosa of patients with stable chronic obstructive pulmonary disease (COPD), particularly in severe disease. OBJECTIVES: To investigate the expression of neutrophilic chemokines and adhesion molecules in bronchial biopsies from patients with stable COPD of different severity (GOLD stages I-IV) compared with age-matched control subjects, smokers with normal lung function and never smokers. METHODS: The expression of CCL5, CXCL1, 5, 6, 7 and 8, CXCR1, CXCR2, CD11b and CD44 was measured in the bronchial mucosa using immunohistochemistry, confocal immunofluorescence, real-time quantitative polymerase chai…

MalePulmonary and Respiratory MedicineChemokinePathologymedicine.medical_specialtyCOPD neutrophils bronchial mucosa CCL5 CXCL7BronchiRespiratory MucosaGranulocyteNeutrophil ActivationCCL5Pulmonary Disease Chronic ObstructiveneutrophilsSubmucosaCOPDHumansMedicineCXC chemokine receptorsChemokine CCL5AgedCOPDbronchial mucosaCCL5biologySettore BIO/16 - Anatomia UmanaCD11 Antigensbusiness.industryCD44Epithelial CellsMiddle Agedrespiratory systemmedicine.diseaseRespiratory Function Testsrespiratory tract diseasesCXCL1Hyaluronan Receptorsmedicine.anatomical_structureAcute DiseaseImmunologyCXCL7biology.proteinFemaleLeukocyte ElastasebusinessCOPD; neutrophils; bronchial mucosa; CCL5; CXCL7Chemokines CXCCOPD CCL5CXCL7NEUTROPHILThorax
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