Search results for "H1"

showing 10 items of 1219 documents

Activation of the PD-1 Pathway Contributes to Immune Escape in EGFR-Driven Lung Tumors

2013

Abstract The success in lung cancer therapy with programmed death (PD)-1 blockade suggests that immune escape mechanisms contribute to lung tumor pathogenesis. We identified a correlation between EGF receptor (EGFR) pathway activation and a signature of immunosuppression manifested by upregulation of PD-1, PD-L1, CTL antigen-4 (CTLA-4), and multiple tumor-promoting inflammatory cytokines. We observed decreased CTLs and increased markers of T-cell exhaustion in mouse models of EGFR-driven lung cancer. PD-1 antibody blockade improved the survival of mice with EGFR-driven adenocarcinomas by enhancing effector T-cell function and lowering the levels of tumor-promoting cytokines. Expression of m…

Lung NeoplasmsT-LymphocytesT cellProgrammed Cell Death 1 ReceptorMice TransgenicLymphocyte ActivationB7-H1 AntigenArticleCell LineProinflammatory cytokineMiceCarcinoma Non-Small-Cell LungTumor MicroenvironmentmedicineAnimalsHumansCytotoxic T cellEpidermal growth factor receptorLung cancerEGFR inhibitorsTumor microenvironmentbiologyOncogenesmedicine.diseaseErbB ReceptorsGene Expression Regulation NeoplasticMice Inbred C57BLmedicine.anatomical_structureOncologyTumor EscapeImmunologyCancer researchbiology.proteinCytokinesTumor EscapeSignal TransductionCancer Discovery
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Erythropoietin activates cell survival pathways in breast cancer stem-like cells to protect them from chemotherapy

2013

Abstract Recombinant erythropoietin (EPO) analogs [erythropoiesis-stimulating agents (ESA)] are clinically used to treat anemia in patients with cancer receiving chemotherapy. After clinical trials reporting increased adverse events and/or reduced survival in ESA-treated patients, concerns have been raised about the potential role of ESAs in promoting tumor progression, possibly through tumor cell stimulation. However, evidence is lacking on the ability of EPO to directly affect cancer stem–like cells, which are thought to be responsible for tumor progression and relapse. We found that breast cancer stem–like cells (BCSC) isolated from patient tumors express the EPO receptor and respond to …

MAPK/ERK pathwayOncologyCancer Researchmedicine.medical_treatmentFluorescent Antibody TechniqueApoptosisMice SCIDImmunoenzyme TechniquesMiceCell MovementMice Inbred NODhemic and lymphatic diseasesTumor Cells CulturedCulturedBlottingAnemiaFlow CytometryTumor CellsTRIALSOncologyDisease ProgressionNeoplastic Stem CellsFemaleWesternSignal Transductionmedicine.drugSTIMULATING AGENTSEXPRESSIONmedicine.medical_specialtyBlotting WesternAntineoplastic AgentsBreast NeoplasmsSCIDRECOMBINANT-HUMAN-ERYTHROPOIETIN STIMULATING AGENTS EXPRESSION MORTALITY TRIALS ANEMIA ALPHA ALDH1Breast cancerIn vivoInternal medicinemedicineAnimalsHumansBreast cancer Cancer stem cellsALDH1ErythropoietinProtein kinase BCell ProliferationSettore MED/04 - Patologia GeneraleChemotherapybusiness.industryMORTALITYCancerRECOMBINANT-HUMAN-ERYTHROPOIETINmedicine.diseaseALPHAErythropoietinTumor progressionInbred NODAnemia; Animals; Antineoplastic Agents; Apoptosis; Blotting Western; Breast Neoplasms; Cell Movement; Cell Proliferation; Disease Progression; Erythropoietin; Female; Flow Cytometry; Fluorescent Antibody Technique; Humans; Immunoenzyme Techniques; Mice; Mice Inbred NOD; Mice SCID; Neoplastic Stem Cells; Signal Transduction; Tumor Cells Cultured; Cancer Research; Oncologybusiness
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The shadow economy in Portugal: An analysis with the MIMIC approach

2007

The paper estimates the Portuguese Shadow Economy (SE) from 1977 to 2004 and tests the statistical relationships between the SE and other economic variables. In order to carry out the econometric analysis, a multiple indicators multiple causes (MIMIC) model with means and intercepts is applied. The main causes of the Portuguese SE are analyzed and economic policies to reduce it are suggested. An appraisal on the reliability of estimates and an alternative benchmark strategy for the MIMIC approach are proposed.

MIMC model; Portugal; Shadow economyPortugalMIMC modeljel:C39language.human_languagejel:H10jel:H26EconomyOrder (exchange)Carry (investment)shadow economy MIIMIC model PortugallanguageEconomicsjel:O17PortugueseShadow economyGeneral Economics Econometrics and FinanceShadow (psychology)Journal of Applied Economics
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A Typical Immune T/B Subset Profile Characterizes Bicuspid Aortic Valve: In an Old Status?

2018

Bicuspid valve disease is associated with the development of thoracic aortic aneurysm. The molecular mechanisms underlying this association still need to be clarified. Here, we evaluated the circulating levels of T and B lymphocyte subsets associated with the development of vascular diseases in patients with bicuspid aortic valve or tricuspid aortic valve with and without thoracic aortic aneurysm. We unveiled that the circulating levels of the MAIT, CD4+IL−17A+, and NKT T cell subsets were significantly reduced in bicuspid valve disease cases, when compared to tricuspid aortic valve cases in either the presence or the absence of thoracic aortic aneurysm. Among patients with tricuspid aortic…

Male0301 basic medicineAortic valveAgingT-LymphocytesLymphocyteHeart Valve Diseases030204 cardiovascular system & hematologyBiochemistryImmunoglobulin D0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseBicuspid aortic valve aneurysm B cellsb-cellsnotch1Invariant t-cells; aneurysm formation; angiotensin-ii; signaling pathway; genetic-variants; apoptotic cells; b-cells; mechanisms; mutations; notch1B-Lymphocytesmechanismsbiologylcsh:Cytologyhemic and immune systemsGeneral MedicineMiddle Agedmedicine.anatomical_structureAortic ValveCardiologycardiovascular systemFemaleResearch Articlesignaling pathwaymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesaneurysm formationInvariant t-cellsArticle SubjectBicuspid aortic valveT cellNaive B cellchemical and pharmacologic phenomenaThoracic aortic aneurysm03 medical and health sciencesBicuspid valveInternal medicinemedicineHumansSettore MED/05 - Patologia Clinicacardiovascular diseaseslcsh:QH573-671angiotensin-iigenetic-variantsB cellsbusiness.industrySettore MED/23 - Chirurgia Cardiacaapoptotic cellsCell Biologymutationsmedicine.disease030104 developmental biologybiology.proteinaneurysmbusinessA Typical Immune T/B Subset Profile Bicuspid Aortic Valve
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Deregulation of Notch1 pathway and circulating endothelial progenitor cell (EPC) number in patients with bicuspid aortic valve with and without ascen…

2018

AbstractBicuspid aortic valve (BAV) is frequently associated with the development of ascending aortic aneurysm, even if the underlying mechanisms remain to be clarified. Here, we investigated if a deregulation of Notch1 signaling pathway and endothelial progenitor cells (EPCs) number is associated with BAV disease and an early ascending aortic aneurysm (AAA) onset. For this purpose, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mean age: 69.1 ± 12.8 years) and AAA complicated or not, were included. Interestingly, patients with AAA showed a significant increase in circulating Notch1 levels and EPC number than subje…

Male0301 basic medicineAortic valveNotch1 signaling pathwatHeart Valve Diseases030204 cardiovascular system & hematologyAortic aneurysm0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseNotch Signaling Pathwaycirculating EPC populationsReceptor Notch1ReceptorAortaEndothelial Progenitor CellsAged 80 and overMultidisciplinaryQRMiddle AgedAortic Aneurysmmedicine.anatomical_structureAortic Valvecardiovascular systemCardiologyMedicineFemaleTricuspid ValveSignal TransductionAdultmedicine.medical_specialtyBicuspid aortic valveEndothelial Progenitor Cells (EPC)ScienceNotch signaling pathwayBicuspid Aortic Valve (BAV)Endothelial progenitor cellArticleBicuspid aortic valve; Notch1 signaling pathwat; ascending aortic aneurysm03 medical and health sciencesascending aortic aneurysmInternal medicinemedicineHumansIn patientcardiovascular diseasesProgenitor cellNotch 1 signaling pathwayAgedTricuspid Aortic Valve (TAV)Ascending Aorta Aneurysm (AAA)business.industrySettore MED/23 - Chirurgia Cardiacamedicine.disease030104 developmental biologybusiness
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Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma

2016

Obesity increases hepatocellular carcinoma (HCC) risks via unknown mediators. We report that hepatic unconventional prefoldin RPB5 interactor (URI) couples nutrient surpluses to inflammation and non-alcoholic steatohepatitis (NASH), a common cause of HCC. URI-induced DNA damage in hepatocytes triggers inflammation via T helper 17 (Th17) lymphocytes and interleukin 17A (IL-17A). This induces white adipose tissue neutrophil infiltration mediating insulin resistance (IR) and fatty acid release, stored in liver as triglycerides, causing NASH. NASH and subsequently HCC are prevented by pharmacological suppression of Th17 cell differentiation, IL-17A blocking antibodies, and genetic ablation of t…

Male0301 basic medicineCancer ResearchCarcinoma HepatocellularInflammationWhite adipose tissueDiet High-FatMice03 medical and health sciencesNon-alcoholic Fatty Liver DiseasemedicineAnimalsHumansUnconventional prefoldin RPB5 interactorbiologyInterleukin-17Liver NeoplasmsFatty liverIntracellular Signaling Peptides and ProteinsCell Biologymedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologyNeutrophil InfiltrationOncologyHepatocellular carcinomaImmunologybiology.proteinTh17 CellsInterleukin 17SteatosisSteatohepatitismedicine.symptomDNA DamageCancer Cell
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Dual disruption of aldehyde dehydrogenases 1 and 3 promotes functional changes in the glutathione redox system and enhances chemosensitivity in nonsm…

2020

AbstractAldehyde dehydrogenases (ALDHs) are multifunctional enzymes that oxidize diverse endogenous and exogenous aldehydes. We conducted a meta-analysis based on The Cancer Genome Atlas and Gene Expression Omnibus data and detected genetic alterations in ALDH1A1, ALDH1A3, or ALDH3A1, 86% of which were gene amplification or mRNA upregulation, in 31% of nonsmall cell lung cancers (NSCLCs). The expression of these isoenzymes impacted chemoresistance and shortened survival times in patients. We hypothesized that these enzymes provide an oxidative advantage for the persistence of NSCLC. To test this hypothesis, we used genetic and pharmacological approaches with DIMATE, an irreversible inhibito…

Male0301 basic medicineCancer ResearchLung NeoplasmsCell- och molekylärbiologiCellAldehyde dehydrogenaseKaplan-Meier EstimateMicechemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsCytotoxicityMiddle AgedAldehyde OxidoreductasesGlutathioneCancer metabolismUp-Regulation3. Good healthCancer therapeutic resistancemedicine.anatomical_structureAlkynes030220 oncology & carcinogenesisFemale[SDV.CAN]Life Sciences [q-bio]/CancerBiologyIsozymeAldehyde Dehydrogenase 1 FamilyArticle03 medical and health sciencesTargeted therapiesDownregulation and upregulationCell Line TumorGeneticsmedicineAnimalsHumansSulfhydryl CompoundsLung cancerMolecular BiologyAgedCancer och onkologiGene AmplificationRetinal DehydrogenaseGlutathioneAldehyde Dehydrogenasemedicine.diseaseXenograft Model Antitumor AssaysALDH1A1030104 developmental biologychemistryDrug Resistance NeoplasmCancer and Oncologybiology.proteinCancer researchCisplatinReactive Oxygen SpeciesCell and Molecular Biologynonsmall cell lung cancer
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Exome Analysis Reveals Genomic Markers Associated with Better Efficacy of Nivolumab in Lung Cancer Patients

2019

Abstract Purpose: Immune checkpoint inhibitors revolutionized the treatment of non-small cell lung cancer (NSCLC). However, only one-quarter of patients benefit from these new therapies. PD-L1 assessment and tumor mutational burden (TMB) are available tools to optimize use of checkpoint inhibitors but novel tools are needed. Exome sequencing could generate many variables but their role in identifying predictors of response is unknown. Experimental Design: We performed somatic and constitutional exome analyses for 77 patients with NSCLC treated with nivolumab. We studied: one-tumor-related characteristics: aneuploidy, CNA clonality, mutational signatures, TMB, mutations in WNT, AKT, MAPK, an…

Male0301 basic medicineCancer ResearchLung NeoplasmsDNA repairAntineoplastic AgentsPembrolizumabAntibodies Monoclonal HumanizedB7-H1 AntigenDisease-Free Survival03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineCarcinoma Non-Small-Cell LungExome SequencingBiomarkers TumorHumansMedicineCTLA-4 AntigenLung cancerExomeExome sequencingAgedRetrospective StudiesAged 80 and overbusiness.industryGenomicsMiddle Agedmedicine.diseaseIpilimumabNivolumabTreatment Outcome030104 developmental biologyOncology030220 oncology & carcinogenesisMutationMonoclonalCancer researchBiomarker (medicine)FemaleNivolumabbusinessClinical Cancer Research
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PD-1, PD-L1, and CD163 in pancreatic undifferentiated carcinoma with osteoclast-like giant cells: A expression patterns and clinical implications

2018

Undifferentiated carcinoma with osteoclast-like giant cells (UCOGC), a variant of pancreatic ductal adenocarcinoma (PDAC), has a striking genetic similarity to PDAC but a significantly improved overall survival. We hypothesize that this difference could be due to the immune response to the tumor, and as such, we investigated the expression of PD-1, PD-L1, and CD163 in a series of UCOGC. To this aim, 27 pancreatic UCOGCs (11 pure and 16 PDAC-associated), 5 extrapancreatic tumors with osteoclast-like giant cells and 10 pancreatic anaplastic carcinomas were immunostained using antibodies against PD-1, PD-L1, and CD163. In pancreatic UCOGCs, PD-L1 was expressed in neoplastic cells of 17 (63%) o…

Male0301 basic medicineIndianaProgrammed Cell Death 1 ReceptorOsteoclast; PDAC; Pancreatic Cancer; Tumor-Associated Macrophages; UCOGCOsteoclastsGiant CellsB7-H1 Antigen0302 clinical medicineTumor-Associated MacrophagesTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]LymphocytesAged 80 and overbiologyTumor-associated macrophagesCell DifferentiationMiddle AgedOsteoclast; Pancreatic cancer; PDAC; Tumor-associated macrophages; UCOGC; 2734ImmunohistochemistryEuropePhenotypemedicine.anatomical_structure030220 oncology & carcinogenesisOsteoclastFemaleAntibodyCarcinoma Pancreatic DuctalAdult2734Antigens Differentiation MyelomonocyticReceptors Cell SurfaceUCOGCPathology and Forensic MedicinePancreatic Cancer03 medical and health sciencesImmune systemAll institutes and research themes of the Radboud University Medical CenterAntigens CDOsteoclastPD-L1Pancreatic cancerBiomarkers TumormedicineHumansHistiocyteAgedNeoplasm StagingPDACHistiocytesPancreatic cancermedicine.diseasePancreatic Neoplasms030104 developmental biologyGiant cellCancer researchbiology.proteinCD163
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Small Bowel Carcinomas in Coeliac or Crohn’s Disease: Clinico-pathological, Molecular, and Prognostic Features. A Study From the Small Bowel Cancer I…

2017

Background and aims An increased risk of small bowel carcinoma [SBC] has been reported in coeliac disease [CD] and Crohn's disease [CrD]. We explored clinico-pathological, molecular, and prognostic features of CD-associated SBC [CD-SBC] and CrD-associated SBC [CrD-SBC] in comparison with sporadic SBC [spo-SBC]. Methods A total of 76 patients undergoing surgical resection for non-familial SBC [26 CD-SBC, 25 CrD-SBC, 25 spo-SBC] were retrospectively enrolled to investigate patients' survival and histological and molecular features including microsatellite instability [MSI] and KRAS/NRAS, BRAF, PIK3CA, TP53, HER2 gene alterations. Results CD-SBC showed a significantly better sex-, age-, and st…

Male0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologySurvivalReceptor ErbB-2Colorectal cancermedicine.disease_causeInflammatory bowel diseaseInflammatory bowel diseasetumour-infiltrating lymphocyteErbB-20302 clinical medicineCrohn DiseaseRetrospective StudieRisk Factors80 and overChildClass I Phosphatidylinositol 3-KinaseAged 80 and overColonic NeoplasmSettore MED/12 - GastroenterologiaCrohn's diseaseMLH1 methylationTumour-infiltrating lymphocytesGastroenterologyGeneral MedicineMiddle AgedPrognosisInflammatory bowel disease; Microsatellite instability; MLH1 promoter methylation; Survival; Tumour-infiltrating lymphocytes; Gastroenterology030220 oncology & carcinogenesisColonic NeoplasmsSurvival AnalysiKRASHumanReceptorAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyPrognosiClass I Phosphatidylinositol 3-KinasesSettore MED/08 - Anatomia PatologicaNOProto-Oncogene Proteins p21(ras)MLH1 promoter methylationYoung Adult03 medical and health sciencesInternal medicinemedicineCarcinomaHumansMLH1 methylation; inflammatory bowel disease; microsatellite instability; survival; tumour-infiltrating lymphocytesneoplasmsAgedRetrospective StudiesInflammatory bowel disease; Microsatellite instability; MLH1 promoter methylation; Survival; Tumour-infiltrating lymphocytes; Adult; Aged; Aged 80 and over; Celiac Disease; Child; Class I Phosphatidylinositol 3-Kinases; Colonic Neoplasms; Crohn Disease; Humans; Male; Microsatellite Instability; Middle Aged; Prognosis; Proto-Oncogene Proteins B-raf; Proto-Oncogene Proteins p21(ras); Receptor ErbB-2; Retrospective Studies; Risk Factors; Survival Analysis; Tumor Suppressor Protein p53; Young Adult; Gastroenterologybusiness.industryTumour-infiltrating lymphocyteRisk FactorCancerMicrosatellite instabilityinflammatory bowel disease; microsatellite instability; MLH1 promoter methylation; tumour-infiltrating lymphocytes; survivalmedicine.diseaseSurvival Analysiseye diseasesdigestive system diseasesCeliac Disease030104 developmental biologyMicrosatellite instabilityTumor Suppressor Protein p53businessJournal of Crohn's and Colitis
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