Search results for "INHIBITOR"

showing 10 items of 3742 documents

Wheat amylase-trypsin inhibitors exacerbate intestinal and airway allergic immune responses in humanized mice.

2017

Background Amylase-trypsin inhibitors (ATIs) in wheat and related cereals are potent activators of myeloid innate immune cells via engagement of TLR4. Furthermore, ATIs have been shown to serve as adjuvants in experimental intestinal inflammatory diseases. Objective The aim of this study was to analyze whether ATIs are also modifiers of allergic inflammation. Methods Therefore, CD4 + T cells from donors sensitized to grass or birch pollen were stimulated with autologous allergen-pulsed dendritic cells in the presence or absence of ATIs or the control storage protein zein from corn. To analyze allergen-induced gut and lung inflammation, immunodeficient mice were engrafted with PBMCs from the…

0301 basic medicineCD4-Positive T-LymphocytesMaleAllergyTHP-1 Cellsmedicine.medical_treatmentImmunologyInflammationOmalizumabImmunoglobulin EAllergic inflammation03 medical and health sciencesMice0302 clinical medicineImmune systemImmunology and AllergyMedicineAnimalsHumansTriticumPlant ProteinsMice KnockoutInnate immune systembiologybusiness.industryfood and beveragesmedicine.diseaseAsthmaImmunity Innate030104 developmental biologyCytokineImmunologyAmylasesbiology.protein030211 gastroenterology & hepatologyFemalemedicine.symptombusinessTrypsin Inhibitorsmedicine.drugThe Journal of allergy and clinical immunology
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The iNOS Activity During an Immune Response Controls the CNS Pathology in Experimental Autoimmune Encephalomyelitis

2019

Inducible nitric oxide synthase (iNOS) plays a critical role in the regulation of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Previous studies have shown that iNOS plays pathogenic as well as regulatory roles in MS and EAE. However, how does iNOS alters the pathophysiology of the central nervous system (CNS) in neuronal autoimmunity is not clearly understood. In the present work, we show that treatment of mice with L-NAME, an iNOS inhibitor, during the antigen-priming phase primarily alters brain pathology, while in the subsequent effector phase of the immune response, the spinal cord is involved. Inhibition of iNOS during the priming phase of the immune res…

0301 basic medicineCD4-Positive T-LymphocytesPathologyexperimental autoimmune encephalomyelitisNitric Oxide Synthase Type IIApoptosismedicine.disease_causeAutoimmunityMice0302 clinical medicineImmunology and AllergyEnzyme InhibitorsOriginal ResearchMice KnockoutbiologyExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationNitric oxide synthaseOligodendrogliamedicine.anatomical_structureNG-Nitroarginine Methyl EsterIntegrin alpha Mlcsh:Immunologic diseases. Allergymedicine.medical_specialtyEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisLymphoid TissueCentral nervous systemImmunology03 medical and health sciencesInterferon-gammaImmune systemmedicineAnimalsHumansNOS2−/− neuroinflammationNeuroinflammationbusiness.industryMultiple sclerosisinducible nitric oxide synthaseDendritic Cellsmedicine.diseasecentral nervous systemMice Inbred C57BL030104 developmental biologybiology.proteinbusinesslcsh:RC581-607030215 immunologyGranulocytesFrontiers in Immunology
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Macrophage Migration Inhibitory Factor Induces Inflammation and Predicts Spinal Progression in Ankylosing Spondylitis

2017

Objectives: To understand the role of macrophage migration inhibitory factor (MIF) in the pathogenesis of Ankylosing Spondylitis (AS). Methods: AS patients satisfying the modified New York criteria were recruited for the study. Healthy volunteers, rheumatoid arthritis and osteoarthritis patients were included as controls. Based on the annual rate of increase in mSASSS scores, AS patients were classified as progressors or non-progressors. MIF levels were quantitated by ELISA in the serum and synovial fluid. Predictors of AS progression were studied by logistic regression analysis. Immunohistochemistry of ileal tissue was performed to identify MIF producing cells. Flow cytometry was used to r…

0301 basic medicineCD74animal diseasesImmunologychemical and pharmacologic phenomenaInflammationPathogenesis03 medical and health sciences0302 clinical medicineRheumatologyotorhinolaryngologic diseasesmedicineImmunology and AllergySynovial fluid030203 arthritis & rheumatologyAnkylosing spondylitisbusiness.industryrespiratory systemmedicine.diseasebiological factors3. Good health030104 developmental biologyRheumatoid arthritisImmunologyMacrophage migration inhibitory factorTumor necrosis factor alphamedicine.symptombusinessArthritis & Rheumatology
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The receptor protein tyrosine phosphatase PTPRJ negatively modulates the CD98hc oncoprotein in lung cancer cells.

2018

PTPRJ, a receptor protein tyrosine phosphatase strongly downregulated in human cancer, displays tumor suppressor activity by negatively modulating several proteins involved in proliferating signals. Here, through a proteomic-based approach, we identified a list of potential PTPRJ-interacting proteins and among them we focused on CD98hc, a type II glycosylated integral membrane protein encoded by SLC3A2, corresponding to the heavy chain of a heterodimeric transmembrane amino-acid transporter, including LAT1. CD98hc is widely overexpressed in several types of cancers and contributes to the process of tumorigenesis by interfering with cell proliferation, adhesion, and migration. We first valid…

0301 basic medicineCD98hcChemistryCell growthCellPTPRJProtein tyrosine phosphatasemedicine.disease_causeProtein tyrosine phosphatase03 medical and health scienceschemistry.chemical_compound030104 developmental biologymedicine.anatomical_structureProteasomal degradationOncologyMG132Cancer cellCancer researchmedicineProteasome inhibitorGene silencingLung cancerCarcinogenesismedicine.drugResearch Paper
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ER+ Breast Cancers Resistant to Prolonged Neoadjuvant Letrozole Exhibit an E2F4 Transcriptional Program Sensitive to CDK4/6 Inhibitors

2018

AbstractPurpose: This study aimed to identify biomarkers of resistance to endocrine therapy in estrogen receptor–positive (ER+) breast cancers treated with prolonged neoadjuvant letrozole.Experimental Design: We performed targeted DNA and RNA sequencing in 68 ER+ breast cancers from patients treated with preoperative letrozole (median, 7 months).Results: Twenty-four tumors (35%) exhibited a PEPI score ≥4 and/or recurred after a median of 58 months and were considered endocrine resistant. Integration of the 47 most upregulated genes (log FC > 1, FDR < 0.03) in letrozole-resistant tumors with transcription-binding data showed significant overlap with 20 E2F4-regulated genes (P =…

0301 basic medicineCancer ResearchBreast NeoplasmsE2F4 Transcription FactorArticle03 medical and health sciences0302 clinical medicineText miningDownregulation and upregulationCell Line TumorBiomarkers TumormedicineHumansEndocrine systemProtein Kinase InhibitorsE2F4GeneAgedCell ProliferationAged 80 and overAromatase Inhibitorsbusiness.industryGene Expression ProfilingLetrozoleEndocrine therapyComputational BiologyMiddle AgedEMTREE drug terms: aromatase inhibitorcyclin dependent kinase 4cyclin dependent kinase 6cyclin dependent kinase inhibitorfulvestrantletrozolepaclitaxelpalbociclibtranscription factor E2F4estrogen receptorletrozoleprotein kinase inhibitortranscription factor E2F4transcriptometumor marker030104 developmental biologyReceptors EstrogenOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisLetrozoleMutationRetreatmentCancer researchFemaleTranscriptomebusinessmedicine.drug
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Oleocanthal exerts antitumor effects on human liver and colon cancer cells through ROS generation

2017

The beneficial health properties of the Mediterranean diet are well recognized. The principle source of fat in Mediterranean diet is extra-virgin olive oil (EVOO). Oleocanthal (OC) is a naturally occurring minor phenolic compound isolated from EVOO, which has shown a potent anti-inflammatory activity, by means of its ability to inhibit the cyclooxygenase (COX) enzymes COX-1 and COX-2. A large body of evidence indicates that phenols exhibit anticancer activities. The aim of the present study was to evaluate the potential anticancer effects of OC in hepatocellular carcinoma (HCC) and colorectal carcinoma (CRC) models. A panel of human HCC (HepG2, Huh7, Hep3B and PLC/PRF/5) and CRC (HT29, SW48…

0301 basic medicineCancer ResearchCarcinoma HepatocellularHepatocellular carcinomaOleocanthalExtra-virgin olive oilCellApoptosisCyclopentane Monoterpenes03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePhenolsOleocanthalmedicineHumansCyclooxygenase InhibitorsViability assayOlive OilCaspaseCell ProliferationAldehydesbiologyCell growthLiver NeoplasmsApoptosiHep G2 CellsCell cycledigestive system diseasesColorectal carcinoma030104 developmental biologymedicine.anatomical_structureOncologychemistryApoptosisCell culture030220 oncology & carcinogenesisImmunologybiology.proteinCancer researchReactive oxygen specieColorectal NeoplasmsReactive Oxygen SpeciesDNA DamageInternational Journal of Oncology
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Targeting chemoresistant colorectal cancer via systemic administration of a BMP7 variant

2020

Abstract Despite intense research and clinical efforts, patients affected by advanced colorectal cancer (CRC) have still a poor prognosis. The discovery of colorectal (CR) cancer stem cell (CSC) as the cell compartment responsible for tumor initiation and propagation may provide new opportunities for the development of new therapeutic strategies. Given the reduced sensitivity of CR-CSCs to chemotherapy and the ability of bone morphogenetic proteins (BMP) to promote colonic stem cell differentiation, we aimed to investigate whether an enhanced variant of BMP7 (BMP7v) could sensitize to chemotherapy-resistant CRC cells and tumors. Thirty-five primary human cultures enriched in CR-CSCs, includ…

0301 basic medicineCancer ResearchColorectal cancerBone Morphogenetic Protein 7Cellular differentiationCellAntineoplastic AgentsTumor initiationBiologyArticleMice03 medical and health sciences0302 clinical medicineSettore MED/04 - PATOLOGIA GENERALECancer stem cellCell Line TumorGeneticsmedicineAnimalsHumansbmp7Molecular BiologyPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsCancer stem cellsMesenchymal stem cellWnt signaling pathwayCell Differentiationmedicine.diseasecolorectal cancer bmp7Colorectal cancerXenograft Model Antitumor Assays030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisMutationNeoplastic Stem CellsCancer researchColorectal NeoplasmsOncogene
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Targeting prohibitins with chemical ligands inhibits KRAS-mediated lung tumours.

2017

KRAS is one of the most frequently mutated oncogenes in human non-small cell lung cancers (NSCLCs). RAS proteins trigger multiple effector signalling pathways including the highly conserved RAF-MAPK pathway. CRAF, a direct RAS effector protein, is required for KRAS-mediated tumourigenesis. Thus, the molecular mechanisms driving the activation of CRAF are intensively studied. Prohibitin 1 (PHB1) is an evolutionarily conserved adaptor protein and interaction of CRAF with PHB1 at the plasma membrane is essential for CRAF activation. Here, we demonstrate that PHB1 is highly expressed in NSCLC patients and correlates with poor survival. Targeting of PHB1 with two chemical ligands (rocaglamide an…

0301 basic medicineCancer ResearchEGF Family of ProteinsLung NeoplasmsBiologyLigandsProto-Oncogene Proteins p21(ras)03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineGrowth factor receptorRocaglamideEpidermal growth factorCarcinoma Non-Small-Cell LungCell Line TumorProhibitinsGeneticsAnimalsHumansMolecular Targeted TherapyProhibitinMolecular BiologyBenzofuransCell ProliferationRas InhibitorMice KnockoutTNF Receptor-Associated Factor 3EffectorXenograft Model Antitumor Assaysrespiratory tract diseasesCell biologyProto-Oncogene Proteins p21(ras)Gene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologychemistry030220 oncology & carcinogenesisras Proteinsraf KinasesSignal transductionSignal TransductionOncogene
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PHD3 Controls Lung Cancer Metastasis and Resistance to EGFR Inhibitors through TGFα.

2018

Abstract Lung cancer is the leading cause of cancer-related death worldwide, in large part due to its high propensity to metastasize and to develop therapy resistance. Adaptive responses to hypoxia and epithelial–mesenchymal transition (EMT) are linked to tumor metastasis and drug resistance, but little is known about how oxygen sensing and EMT intersect to control these hallmarks of cancer. Here, we show that the oxygen sensor PHD3 links hypoxic signaling and EMT regulation in the lung tumor microenvironment. PHD3 was repressed by signals that induce EMT and acted as a negative regulator of EMT, metastasis, and therapeutic resistance. PHD3 depletion in tumors, which can be caused by the EM…

0301 basic medicineCancer ResearchEpithelial-Mesenchymal TransitionLung NeoplasmsMice NudeAntineoplastic AgentsSMADDrug resistanceMetastasisHypoxia-Inducible Factor-Proline DioxygenasesMitochondrial Proteins03 medical and health sciencesErlotinib HydrochlorideMice0302 clinical medicineDownregulation and upregulationCell Line TumorTumor MicroenvironmentMedicineAnimalsHumansNeoplasm MetastasisLung cancerProtein Kinase InhibitorsEGFR inhibitorsbusiness.industryIntracellular Signaling Peptides and ProteinsCancerTransforming Growth Factor alphamedicine.diseaseHCT116 CellsXenograft Model Antitumor AssaysCell HypoxiaErbB Receptors030104 developmental biologyOncologyA549 CellsDrug Resistance Neoplasm030220 oncology & carcinogenesisembryonic structuresCancer researchFemaleErlotinibbusinessApoptosis Regulatory Proteinsmedicine.drugCancer research
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Tumour mutational burden as a biomarker for immunotherapy: Current data and emerging concepts

2020

International audience; Treatment with immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) or its ligand (PD-L1) can generate durable responses in various cancer types, but only in a subset of patients. The use of predictive biomarkers for response to PD-1/PD-L1 inhibitors is critical for patient selection. Expression of PD-L1 has demonstrated utility in patient selection. Tumour mutational burden (TMB) is an emerging biomarker for response to PD-1/PD-L1 inhibitors. The evaluation of this biomarker is based on the hypothesis that a high number of mutations in somatic exonic regions will lead to an increase in neoantigen production, which could then be recognised by…

0301 basic medicineCancer ResearchImmune checkpoint inhibitorsmedicine.medical_treatment[SDV]Life Sciences [q-bio]DNA Mutational AnalysisProgrammed Cell Death 1 ReceptorTumour mutational burdenBioinformaticsArticleB7-H1 Antigen03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineImmune systemNeoplasmsBiomarkers TumorHumansMedicineIn patientGenetic TestingPredictive biomarkerbusiness.industryPatient SelectionCancerBiomarkerImmunotherapymedicine.disease3. Good healthBiomarker (cell)[SDV] Life Sciences [q-bio]030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationImmunotherapybusinessCD8
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