Search results for "Liver"

showing 10 items of 4961 documents

NUPR1, a new target in liver cancer: implication in controlling cell growth, migration, invasion and sorafenib resistance

2016

AbstractSorafenib, an oral multikinase inhibitor, is the only approved agent for the treatment of advanced hepatocellular carcinoma (HCC). However, its benefits are modest, and as its mechanisms of action remain elusive, a better understanding of its anticancer effects is needed. Based on our previous study results, we investigated here the implication of the nuclear protein 1 (NUPR1) in HCC and its role in sorafenib treatment. NUPR1 is a stress-inducible protein that is overexpressed in various malignancies, but its role in HCC is not yet fully understood. We found that NUPR1 expression was significantly higher in primary human HCC samples than in the normal liver. Knockdown of NUPR1 signi…

0301 basic medicineMaleCancer ResearchHepatocellular carcinomaCore Binding Factor Alpha 1 Subunit0302 clinical medicineCell MovementBasic Helix-Loop-Helix Transcription FactorsMolecular Targeted TherapyRNA Small InterferingRegulation of gene expressionAged 80 and overGene knockdownRELBLiver NeoplasmsMiddle AgedSorafenib3. Good healthNeoplasm ProteinsSorafenib.Gene Expression Regulation Neoplastic030220 oncology & carcinogenesisGene Knockdown TechniquesOriginal ArticleFemalemedicine.drugSorafenibNiacinamideCarcinoma HepatocellularRUNX2 GeneCell SurvivalIER3ImmunologyDown-RegulationBiology03 medical and health sciencesCellular and Molecular NeuroscienceYoung AdultmedicineGene silencingHumansNeoplasm InvasivenessGene SilencingneoplasmsAgedCell ProliferationCell growthGene Expression ProfilingPhenylurea CompoundsTranscription Factor RelBComputational BiologyMembrane ProteinsCell BiologyNuclear protein-1digestive system diseases030104 developmental biologyDrug Resistance NeoplasmCancer researchApoptosis Regulatory ProteinsTranscriptomeCell Death & Disease
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Safety and effectiveness of regorafenib in patients with metastatic colorectal cancer in routine clinical practice in the prospective, observational …

2019

Abstract Background Regorafenib prolonged overall survival (OS) versus placebo in patients with treatment-refractory metastatic colorectal cancer (mCRC) in phase III trials. We conducted an observational study of regorafenib for patients with mCRC in real-world clinical practice. Methods The international, prospective, CORRELATE study recruited patients with mCRC previously treated with approved therapies, for whom the decision to treat with regorafenib was made by the treating physician according to the local health authority approved label. The primary objective was safety, assessed by treatment-emergent adverse events (TEAEs; National Cancer Institute Common Terminology Criteria for Adve…

0301 basic medicineMaleCancer ResearchLung NeoplasmsColorectal cancerPyridinesGTP Phosphohydrolaseschemistry.chemical_compound0302 clinical medicineObservational studyProspective StudiesNeoplasm MetastasisFatiguePeritoneal NeoplasmsRegorafenibAged 80 and overLiver NeoplasmsCommon Terminology Criteria for Adverse EventsMiddle AgedProgression-Free SurvivalOncology030220 oncology & carcinogenesisHypertensionFemaleHand-Foot SyndromeColorectal NeoplasmsAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyBone NeoplasmsPlaceboProto-Oncogene Proteins p21(ras)03 medical and health sciencesYoung AdultRegorafenibInternal medicinemedicineHumansAdverse effectSurvival analysisAgedAdverse effectsbusiness.industryPhenylurea CompoundsCarcinomaCancerMembrane ProteinsSurvival analysismedicine.disease030104 developmental biologychemistryObservational studyLymph NodesbusinessAdverse effects; Observational study; Regorafenib; Survival analysisEuropean journal of cancer (Oxford, England : 1990)
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Maternal eNOS deficiency determines a fatty liver phenotype of the offspring in a sex dependent manner

2016

ABSTRACT Maternal environmental factors can impact on the phenotype of the offspring via the induction of epigenetic adaptive mechanisms. The advanced fetal programming hypothesis proposes that maternal genetic variants may influence the offspring's phenotype indirectly via epigenetic modification, despite the absence of a primary genetic defect. To test this hypothesis, heterozygous female eNOS knockout mice and wild type mice were bred with male wild type mice. We then assessed the impact of maternal eNOS deficiency on the liver phenotype of wild type offspring. Birth weight of male wild type offspring born to female heterozygous eNOS knockout mice was reduced compared to offspring of wil…

0301 basic medicineMaleCancer Researchmedicine.medical_specialtyHeterozygoteNitric Oxide Synthase Type IIIOffspringBiology03 medical and health sciencesGenomic ImprintingMiceSex FactorsEnosInternal medicineFetal programmingmedicineAnimalsEpigeneticsMolecular BiologyGeneFatty liverWild typeHeterozygote advantageDNA Methylationmedicine.diseasebiology.organism_classificationFatty LiverMice Inbred C57BL030104 developmental biologyEndocrinologyPhenotypeKnockout mouseeNOSCarbohydrate MetabolismFemaleEpigeneticsInstitut für ErnährungswissenschaftmetabolismResearch Paper
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Rare Pathogenic Variants Predispose to Hepatocellular Carcinoma in Nonalcoholic Fatty Liver Disease

2019

AbstractNonalcoholic fatty liver disease (NAFLD) is a rising cause of hepatocellular carcinoma (HCC). We examined whether inherited pathogenic variants in candidate genes (n = 181) were enriched in patients with NAFLD-HCC. To this end, we resequenced peripheral blood DNA of 142 NAFLD-HCC, 59 NAFLD with advanced fibrosis, and 50 controls, and considered 404 healthy individuals from 1000 G. Pathogenic variants were defined according to ClinVar, likely pathogenic as rare variants predicted to alter protein activity. In NAFLD-HCC patients, we detected an enrichment in pathogenic (p = 0.024), and likely pathogenic variants (p = 1.9*10−6), particularly in APOB (p = 0.047). APOB variants were asso…

0301 basic medicineMaleCandidate geneApolipoprotein Blcsh:MedicineGastroenterologyLiver diseasechemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseSequestosome-1 ProteinGenetic riskHCClcsh:ScienceMultidisciplinarybiologyLiver NeoplasmsMiddle Aged3. Good healthCholesterolHepatocellular carcinomaApolipoprotein B-100FemaleAged; Apolipoprotein B-100; Carcinoma Hepatocellular; Case-Control Studies; Cholesterol HDL; Female; Genetic Predisposition to Disease; Glial Cell Line-Derived Neurotrophic Factor Receptors; Humans; Liver Neoplasms; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Reproducibility of Results; Risk Factors; Sequestosome-1 Proteinmedicine.medical_specialtyCarcinoma HepatocellularGlial Cell Line-Derived Neurotrophic Factor ReceptorsHDLSettore BIO/18 - GENETICAdigestive systemArticle03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseGeneAgedCholesterolbusiness.industrylcsh:RCarcinomaCholesterol HDLnutritional and metabolic diseasesReproducibility of ResultsHepatocellularmedicine.diseasedigestive system diseases030104 developmental biologychemistryNASH HCCCase-Control Studiesbiology.proteinlcsh:Qgeneticbusiness030217 neurology & neurosurgery
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LXR agonist treatment of blastic plasmacytoid dendritic cell neoplasm restores cholesterol efflux and triggers apoptosis

2016

International audience; Blastic plasmacytoid dendritic cell (PDC) neoplasm (BPDCN) is an aggressive hematological malignancy with a poor prognosis that derives from PDCs. No consensus for optimal treatment modalities is available today and the full characterization of this leukemia is still emerging. We identified here a BPDCN-specific transcriptomic profile when compared with those of acute myeloid leukemia and T-acute lymphoblastic leukemia, as well as the transcriptomic signature of primary PDCs. This BPDCN gene signature identified a dysregulation of genes involved in cholesterol homeostasis, some of them being liver X receptor (LXR) target genes. LXR agonist treatment of primary BPDCN …

0301 basic medicineMaleCellProliferationApoptosisExpressionPlasmacytoid dendritic cellPrecursor T-Cell Lymphoblastic Leukemia-LymphomaBiochemistryMice0302 clinical medicinepolycyclic compoundsSTAT5 Transcription Factor[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyATP Binding Cassette Transporter Subfamily G Member 1Liver X ReceptorsInhibitionMyeloid NeoplasiabiologyMyeloid leukemiafood and beveragesMyeloid-Leukemia[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematologyInterleukin-3 Receptor3. Good healthLeukemiamedicine.anatomical_structureCholesterol030220 oncology & carcinogenesisFemalelipids (amino acids peptides and proteins)In-VivoATP Binding Cassette Transporter 1ImmunologyActivationAntineoplastic Agentsdigestive system03 medical and health sciencesCell Line TumormedicineAnimalsHumansLiver X receptorProtein kinase BCell ProliferationCell growthCell BiologyDendritic Cellsmedicine.diseaseXenograft Model Antitumor Assays030104 developmental biologyProstate-Cancer CellsABCA1biology.proteinCancer researchDensity-Lipoprotein ReceptorInterleukin-3Proto-Oncogene Proteins c-akt
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Genome-wide association study of non-alcoholic fatty liver and steatohepatitis in a histologically characterised cohort☆

2020

Background & Aims: Genetic factors associated with nonalcoholic fatty liver disease (NAFLD) remain incompletely understood. To date, most genome-wide association studies (GWASs) have adopted radiologically assessed hepatic triglyceride content as the reference phenotype and so cannot address steatohepatitis or fibrosis. We describe a GWAS encompassing the full spectrum of histologically characterised NAFLD. Methods: The GWAS involved 1,483 European NAFLD cases and 17,781 genetically matched controls. A replication cohort of 559 NAFLD cases and 945 controls was genotyped to confirm signals showing genome-wide or close to genome-wide significance. Results: Case-control analysis identified…

0301 basic medicineMaleCirrhosis17-Hydroxysteroid DehydrogenasesFibrosiVARIANTLOCIPROGRESSIONGenome-wide association studyDiseaseBioinformaticsDISEASECohort Studies0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsGWASINCREASED RISKCONFERS SUSCEPTIBILITYeducation.field_of_studyFatty liverNASHMiddle Aged3. Good healthNAFLD; NASH; Fibrosis; GWAS; PNPLA3; TM6SF2; GCKR; HSD17B13; SNPPhenotypeLiver030211 gastroenterology & hepatologyFemaleLife Sciences & BiomedicineGCKRAdultPopulationSNP610 Medicine & healthGastroenterology and HepatologyPolymorphism Single NucleotideTM6SF2HSD17B1303 medical and health sciencesNAFLDmedicineGastroenterologiHumansGenetic Predisposition to DiseaseeducationPNPLA3Adaptor Proteins Signal TransducingScience & TechnologyGastroenterology & HepatologyHepatologybusiness.industrynutritional and metabolic diseasesMembrane ProteinsLipasemedicine.diseaseFibrosisPOLYMORPHISMLEPTIN RECEPTOR GENE030104 developmental biology3121 General medicine internal medicine and other clinical medicineCase-Control StudiesHuman medicineSteatosisSteatohepatitisbusinessTM6SF2Genome-Wide Association StudyJournal of Hepatology
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Genetic Variation in HSD17B13 Reduces the Risk of Developing Cirrhosis and Hepatocellular Carcinoma in Alcohol Misusers.

2020

Background and aims Carriage of rs738409:G in patatin-like phospholipase domain containing 3 (PNPLA3) is associated with an increased risk for developing alcohol-related cirrhosis and hepatocellular carcinoma (HCC). Recently, rs72613567:TA in hydroxysteroid 17-beta dehydrogenase 13 (HSD17B13) was shown to be associated with a reduced risk for developing alcohol-related liver disease and to attenuate the risk associated with carriage of PNPLA3 rs738409:G. This study explores the risk associations between these two genetic variants and the development of alcohol-related cirrhosis and HCC. Approach and results Variants in HSD17B13 and PNPLA3 were genotyped in 6,171 participants, including 1,03…

0301 basic medicineMaleCirrhosis17-Hydroxysteroid DehydrogenasesVARIANTPROGRESSIONGastroenterologyCohort StudiesLiver disease0302 clinical medicineSNP RS738409G ALLELEDEPENDENCELiver Cirrhosis Alcoholic600 Technology610 Medicine & healthAged 80 and overeducation.field_of_studyFramingham Risk ScoreLiver NeoplasmsASSOCIATIONlipotoxicityMiddle AgedAlcoholism1101 Medical Biochemistry and Metabolomics1107 ImmunologyHepatocellular carcinomaadiponutrin030211 gastroenterology & hepatologyFemalecandidate genesLife Sciences & Biomedicinemedicine.medical_specialtyCarcinoma HepatocellularPopulation610 Medicine & healthLower riskRisk Assessment03 medical and health sciencesLIVER-DISEASEInternal medicinemedicinegenetic risk associationHumansAdiponutrineducationPNPLA3METAANALYSISAgedDISEASE-ASSOCIATED MORTALITYScience & TechnologyHepatologyGastroenterology & Hepatologybusiness.industryfibrosisGenetic Variation1103 Clinical SciencesOdds ratiomedicine.disease030104 developmental biologyhost geneticsbusinessgenetic susceptibility
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Prevalence and determinants of non-alcoholic fatty liver disease in lifelines: A large Dutch population cohort

2017

BACKGROUND & AIMS Non-alcoholic fatty liver disease is an increasing health issue that develops rather unnoticed with obesity, type 2 diabetes mellitus and metabolic syndrome. We investigated prevalence, determinants and associated metabolic abnormalities of non-alcoholic fatty liver disease in the largest population-based cohort to date. METHODS Biochemical characteristics, type 2 diabetes mellitus and metabolic syndrome were determined in the Lifelines Cohort Study (N = 167,729), a population-based cohort in the North of the Netherlands. Non-alcoholic fatty liver disease was defined as Fatty Liver Index (FLI)≥60. Exclusion criteria were age <18 years, immigrants, missing data to assess FL…

0301 basic medicineMaleCirrhosislcsh:MedicineGastroenterologyBiochemistryGLOMERULAR-FILTRATION-RATESTEATOHEPATITISWhite Blood Cells0302 clinical medicineEndocrinologyNon-alcoholic Fatty Liver DiseaseRisk FactorsAnimal CellsPrevalenceMedicine and Health SciencesDiabetes diagnosis and managementlcsh:ScienceNetherlandsMETABOLIC SYNDROME2. Zero hungerINSULIN-RESISTANCEMultidisciplinaryLiver DiseasesFatty liverMiddle AgedLipids3. Good healthType 2 DiabetesCholesterolHypertension030211 gastroenterology & hepatologyFemaleAnatomyCellular TypesResearch ArticleAdultmedicine.medical_specialtyHbA1cEndocrine DisordersImmune CellsImmunologyUNITED-STATESGastroenterology and Hepatology03 medical and health sciencesInsulin resistanceInternal medicineDiabetes mellitusmedicineDiabetes MellitusHumansHemoglobinHEPATIC STEATOSISHepatitisBlood Cellsbusiness.industryCholesterol HDLlcsh:RType 2 Diabetes MellitusBiology and Life SciencesProteinsRenal SystemCell Biologymedicine.diseaseDiagnostic medicineFatty LiverSERUM CREATININE VALUESRENAL-DISEASE030104 developmental biologyEndocrinologyCross-Sectional StudiesDiabetes Mellitus Type 2ATHEROSCLEROSISHyperglycemiaMetabolic DisordersRISK-FACTORSlcsh:QSteatohepatitisMetabolic syndromebusiness
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Mouse tissue distribution and persistence of the food-born fusariotoxins Enniatin B and Beauvericin

2016

The fusariotoxins Enniatin B (Enn B) and Beauvericin (Bea) have recently aroused interest as food contaminants and as potential anticancer drugs. However, limited data are available about their toxic profile. Aim of this study was to investigate their pharmacological behavior in vivo and their persistence in mice. Therefore, liquid chromatography tandem mass spectrometry (LC-MS/MS) was used to analyze the distribution of Enn B and Bea in selected tissue samples and biological fluids originating from mice treated intraperitoneally with these cyclohexadepsipeptides. Overall, no toxicological signs during life time or pathological changes were observed. Moreover, both fusariotoxins were found …

0301 basic medicineMaleColonBiological AvailabilityAntineoplastic AgentsUrinePharmacologyToxicologyTandem mass spectrometryArticlePersistence (computer science)03 medical and health scienceschemistry.chemical_compoundMice0404 agricultural biotechnologyLiquid chromatography–mass spectrometryIn vivoTandem Mass SpectrometryDepsipeptidesAnimalsTissue DistributionDepsipeptide04 agricultural and veterinary sciencesGeneral MedicineMetabolism040401 food scienceBeauvericinT-2 Toxin030104 developmental biologychemistryLiverChromatography Liquid
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Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses

2016

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0301 basic medicineMaleEpidemiologyPhysiologychemistry.chemical_compoundinsufficient sleep0302 clinical medicineHigh-density lipoproteinFinlandSleep restrictionGENERAL-POPULATIONINSULIN-RESISTANCEeducation.field_of_studyMultidisciplinarytulehdusCARDIOVASCULAR RISKGLUCOSE-METABOLISMta3142Chronic inflammationMiddle AgedSleep in non-human animals3. Good healthSleep deprivationCholesterolMetabolomeFemalemedicine.symptomAdultmedicine.medical_specialtyACUTE-PHASE RESPONSELIVER-X-RECEPTORSPopulationBiologyta3111Articlesleep restriction03 medical and health sciencesInsulin resistanceMetabolic DiseasesInternal medicinemedicineMetabolomeHumansCORONARY-HEART-DISEASEeducationLiver X receptorDyslipidaemiasAgedCASSETTE TRANSPORTER G1Gene Expression Profilingta1182ta3121medicine.diseaseSleep deprivation030104 developmental biologyEndocrinologychemistryinflammationcholesterol metabolismSleep Deprivation3111 BiomedicineGene expressionHIGH-DENSITY-LIPOPROTEIN030217 neurology & neurosurgeryBlood Chemical AnalysisScientific Reports
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