Search results for "HERA"

showing 10 items of 14928 documents

Pharmacokinetics of a sustained release formulation of PDGFβ-receptor directed carrier proteins to target the fibrotic liver

2018

Liver fibrogenesis is associated with excessive production of extracellular matrix by myofibroblasts that often leads to cirrhosis and consequently liver dysfunction and death. Novel protein-based antifibrotic drugs show high specificity and efficacy, but their use in the treatment of fibrosis causes a high burden for patients, since repetitive and long-term parenteral administration is required as most proteins and peptides are rapidly cleared from the circulation. Therefore, we developed biodegradable polymeric microspheres for the sustained release of proteinaceous drugs. We encapsulated the drug carrier pPB-HSA, which specifically binds to the PDGF beta R that is highly upregulated on a…

0301 basic medicineLiver CirrhosisMaleCirrhosisPolymersLiver fibrosisPharmaceutical Science02 engineering and technologyPharmacologyMULTIBLOCK-COPOLYMERReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesPharmacokineticsFibrosisIn vivomedicinein vitro in vivo correlationAnimalsControlled releaseFIBROSISBiodegradable polymeric microspheresDRUG-DELIVERYSerum AlbuminIN-VIVOMice KnockoutPOLYMERIC MICROSPHERESDrug CarriersINTERFERON-GAMMAChemistryProtein deliveryAlbuminPDGF beta-receptor targeted drug carrier021001 nanoscience & nanotechnologymedicine.diseaseControlled releaseIMPLANTSMicrospheresANTIFIBROTIC THERAPIESMice Inbred C57BLMICE030104 developmental biologyDelayed-Action PreparationsDrug delivery0210 nano-technologyDrug carrierGROWTH-FACTOR RECEPTOR
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A randomized, placebo-controlled trial of cenicriviroc for treatment of nonalcoholic steatohepatitis with fibrosis

2018

The aim of this study was to evaluate cenicriviroc (CVC), a dual antagonist of C-C chemokine receptor types 2 and 5, for treatment of nonalcoholic steatohepatitis (NASH) with liver fibrosis. A randomized, double-blind, multinational phase 2b study enrolled subjects with NASH, a nonalcoholic fatty liver disease activity score [NAS] ≥4, and liver fibrosis (stages 1-3, NASH Clinical Research Network) at 81 clinical sites. Subjects (N = 289) were randomly assigned CVC 150 mg or placebo. Primary outcome was ≥2-point improvement in NAS and no worsening of fibrosis at year 1. Key secondary outcomes were: resolution of steatohepatitis and no worsening of fibrosis; improvement in fibrosis by ≥1 stag…

0301 basic medicineLiver CirrhosisMalePlacebo-controlled studyMedical Biochemistry and MetabolomicsGastroenterologyOral and gastrointestinallaw.inventionHepatitisNASH NAFLD CVC nonalcoholic fatty liver inflammationSteatohepatitis/Metabolic Liver Disease0302 clinical medicineRandomized controlled trialFibrosislawNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseeducation.field_of_studyCVCLiver DiseaseNASHImidazolesMiddle AgedTreatment OutcomeTolerabilityLiverSulfoxides6.1 PharmaceuticalsCCR5 Receptor Antagonists030211 gastroenterology & hepatologyOriginal ArticleFemalePatient SafetyAdultmedicine.medical_specialtyPopulationChronic Liver Disease and CirrhosisClinical Trials and Supportive ActivitiesClinical SciencesImmunologyPlacebo03 medical and health sciencesDouble-Blind MethodClinical ResearchInternal medicineNAFLDmedicinenonalcoholic fatty liverHumanseducationAgedHepatologyGastroenterology & Hepatologybusiness.industryEvaluation of treatments and therapeutic interventionsOriginal Articlesmedicine.diseaseequipment and suppliesSurgeryCVC; NAFLD; NASH; inflammation; nonalcoholic fatty liver030104 developmental biologyinflammationHuman medicineSteatohepatitisbusinessDigestive DiseasesBiomarkers
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Elafibranor, an Agonist of the Peroxisome Proliferator-Activated Receptor-alpha and -delta, Induces Resolution of Nonalcoholic Steatohepatitis Withou…

2016

International audience; BACKGROUND & AIMS: Elafibranor is an agonist of the peroxisome proliferator-activated receptor-α and peroxisome proliferator-activated receptor-δ. Elafibranor improves insulin sensitivity, glucose homeostasis, and lipid metabolism and reduces inflammation. We assessed the safety and efficacy of elafibranor in an international, randomized, double-blind placebo-controlled trial of patients with nonalcoholic steatohepatitis (NASH).METHODS: Patients with NASH without cirrhosis were randomly assigned to groups given elafibranor 80 mg (n = 93), elafibranor 120 mg (n = 91), or placebo (n = 92) each day for 52 weeks at sites in Europe and the United States. Clinical and …

0301 basic medicineLiver CirrhosisMaleTime FactorsIntention to Treat Analysi[SDV]Life Sciences [q-bio]BiopsyPLACEBO-CONTROLLED TRIALTHERAPYGastroenterologySeverity of Illness IndexChalcone0302 clinical medicineChalconesNon-alcoholic Fatty Liver DiseaseGastrointestinal AgentNonalcoholic fatty liver diseasePropionateMedicine and Health SciencesOdds RatioMedicineGlucose homeostasisVITAMIN-Eeducation.field_of_studyGastrointestinal agentFatty liverRemission InductionGastroenterologyMiddle Aged3. Good healthIntention to Treat AnalysisPPARDEuropeTreatment OutcomeLiverACIDPIOGLITAZONE030211 gastroenterology & hepatologyFemalePPARAHumanSignal TransductionAdultCLINICAL-OUTCOMESmedicine.medical_specialtyLogistic ModelTime FactorLiver CirrhosiPopulationfatty liver; NAFLD; PPARA; PPARD; Adult; Biomarkers; Biopsy; Chalcones; Double-Blind Method; Europe; Female; Gastrointestinal Agents; Humans; Intention to Treat Analysis; Liver; Liver Cirrhosis; Logistic Models; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Odds Ratio; PPAR alpha; PPAR gamma; Propionates; Remission Induction; Severity of Illness Index; Signal Transduction; Time Factors; Treatment Outcome; United States; GastroenterologyPlacebo03 medical and health sciencesDouble-Blind MethodGastrointestinal AgentsInternal medicineNAFLDHumansPPAR alphaeducationFATTY LIVER-DISEASEfatty liverHepatologybusiness.industryBiomarkerAMERICAN ASSOCIATIONOdds ratiomedicine.diseaseConfidence intervalUnited StatesPPAR gammaRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]030104 developmental biologyEndocrinologyLogistic ModelsHuman medicinePropionatesbusinessBiomarkers
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In Vivo siRNA Delivery to Immunosuppressive Liver Macrophages by alpha-Mannosyl-Functionalized Cationic Nanohydrogel Particles

2020

Macrophages are the front soldiers of the innate immune system and are vital for immune defense, tumor surveillance, and tissue homeostasis. In chronic diseases, including cancer and liver fibrosis, macrophages can be forced into an immunosuppressive and profibrotic M2 phenotype. M2-type macrophages overexpress the mannose receptor CD206. Targeting these cells via CD206 and macrophage repolarization towards an immune stimulating and antifibrotic M1 phenotype through RNA interference represents an appealing therapeutic approach. We designed nanohydrogel particles equipped with mannose residues on the surface (ManNP) that delivered siRNA more efficiently to M2 polarized macrophages compared t…

0301 basic medicineLiver CirrhosissiRNA deliveryTHP-1 Cellsmedicine.medical_treatmentmannose targetingMice0302 clinical medicineDrug Delivery SystemsFibrosisMacrophageM2 macrophagesRNA Small Interferinglcsh:QH301-705.5Tissue homeostasisMice Inbred BALB CChemistryHydrogelsGeneral MedicineHep G2 CellsLiver030220 oncology & carcinogenesisFemaleimmunotherapyMannose receptorMannose ReceptorReceptors Cell Surfacegene knock-downArticlenanohydrogels03 medical and health sciencesImmune systemIn vivomedicineImmune ToleranceAnimalsHumanscancerLectins C-TypeInnate immune systemMacrophagesfibrosisImmunotherapyMacrophage Activationmedicine.disease030104 developmental biologyMannose-Binding LectinsRAW 264.7 Cellslcsh:Biology (General)Cancer researchNanoparticlesMannose
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The potential of neurotrophic tyrosine kinase (NTRK) inhibitors for treating lung cancer

2016

Abstract: Introduction: Molecular alterations in neurotrophic tyrosine kinase (NTRK) genes have been identified in several solid tumors including lung cancer. Pre-clinical and clinical evidence suggested their potential role as oncogenic drivers and predictive biomarkers for targeted inhibition, leading to the clinical development of a new class of compounds blocking the NTRK molecular pathway, which are currently undner early clinical investigation. Area covered: This review describes the biology of the NTRK pathway and its molecular alterations in lung cancer. It focuses on the pre-clinical and clinical development of emerging NTRK inhibitors, which have shown very promising activity in e…

0301 basic medicineLung NeoplasmsNTRKinhibitorsNTRK1/2/3Settore MED/06 - Oncologia Medicamedicine.medical_treatmentReceptor Protein-Tyrosine KinasesEntrectinibPharmacologyTargeted therapy03 medical and health sciences0302 clinical medicineMedicineAnimalsHumansPharmacology (medical)In patientNTRKinhibitorLung cancerProtein Kinase InhibitorsTrkA/B/CPharmacologyNTRK1/2/3; TrkA/B/C; NTRKinhibitors; targeted therapy; lung cancerbiologybusiness.industryPharmacology. TherapyReceptor Protein-Tyrosine KinasesGeneral Medicinemedicine.diseasetargeted therapySettore CHIM/08 - Chimica Farmaceuticalung cancer030104 developmental biology030220 oncology & carcinogenesisbiology.proteinCancer researchbusinessEarly phaseTyrosine kinaseNeurotrophin
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Targeting BRAF and RAS in Colorectal Cancer

2021

Simple Summary In colorectal cancer, mutations of the KRAS and BRAF genes are quite common and can contribute to the activation of cell signaling pathways that lead to cell proliferation and differentiation. These processes promote cancer growth, and in some cases, they may cause cells to develop resistance to certain types of treatment, notably EGFR inhibitors. We summarize recent knowledge regarding the effects of KRAS and BRAF mutations in the setting of colorectal cancer and discuss the new therapies under development. Abstract Colorectal cancer (CRC) is still one of the most frequent forms of cancer in the world in terms of incidence. Around 40% of CRC patients carry a mutation of the …

0301 basic medicineMAPK/ERK pathwayCancer ResearchColorectal cancerAngiogenesismedicine.medical_treatmentcolorectal cancerReviewmedicine.disease_causeBRAFTargeted therapy03 medical and health sciences0302 clinical medicineKRASmedicineneoplasmsRC254-282EGFR inhibitorsMutationbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensCancertargeted therapymedicine.diseasedigestive system diseases030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchKRASbusinessCancers
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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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Autocrine CCL5 Effect Mediates Trastuzumab Resistance by ERK Pathway Activation in HER2-Positive Breast Cancer.

2020

Abstract HER2-positive breast cancer is currently managed with chemotherapy in combination with specific anti-HER2 therapies, including trastuzumab. However, a high percentage of patients with HER2-positive tumors do not respond to trastuzumab (primary resistance) or either recur (acquired resistance), mostly due to molecular alterations in the tumor that are either unknown or undetermined in clinical practice. Those alterations may cause the tumor to be refractory to treatment with trastuzumab, promoting tumor proliferation and metastasis. Using continued exposure of a HER2-positive cell line to trastuzumab, we generated a model of acquired resistance characterized by increased expression …

0301 basic medicineMAPK/ERK pathwayCancer ResearchMAP Kinase Signaling SystemReceptor ErbB-2medicine.medical_treatmentMice NudeApoptosisBreast NeoplasmsCCL5Metastasis03 medical and health sciencesMice0302 clinical medicineBreast cancerAntineoplastic Agents ImmunologicalTrastuzumabmedicineBiomarkers TumorTumor Cells CulturedGene silencingAnimalsHumansskin and connective tissue diseasesAutocrine signallingneoplasmsChemokine CCL5Neoadjuvant therapyCell Proliferationbusiness.industryGene Expression ProfilingTrastuzumabmedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticAutocrine Communication030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer researchFemalebusinessmedicine.drugMolecular cancer therapeutics
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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Uncovering the Signaling Pathway behind Extracellular Guanine-Induced Activation of NO System: New Perspectives in Memory-Related Disorders

2018

Mounting evidence suggests that the guanine-based purines stand out as key player in cell metabolism and in several models of neurodegenerative disorders, such as Parkinson's and Alzheimer's diseases. Guanosine (GUO) and guanine (GUA) are extracellular signaling molecules derived from the breakdown of the correspondent nucleotide, GTP, and their intracellular and extracellular levels are regulated by the fine-tuned activity of two major enzymes, purine nucleoside phosphorylase (PNP) and guanine deaminase (GDA). Noteworthy, GUO and GUA, seem to play opposite roles in the modulation of cognitive functions, such as learning and memory. Indeed GUO, despite exerting neuroprotective, anti-apoptot…

0301 basic medicineMAPK/ERK pathwayCell signalingGuanineGuanosine03 medical and health scienceschemistry.chemical_compoundGuanine deaminase0302 clinical medicineCGMP; ERK; Guanine; L-NAME; Nitric oxide; SH-SY5Y cell line; Pharmacology; Pharmacology (medical)L-NAMEnitric oxideExtracellularguaninePharmacology (medical)Original ResearchPharmacologyChemistrylcsh:RM1-950Cell biologycGMPERKlcsh:Therapeutics. Pharmacology030104 developmental biologySignal transductionSH-SY5Y cell line030217 neurology & neurosurgeryIntracellularFrontiers in Pharmacology
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