Search results for "model [interaction]"

showing 10 items of 1495 documents

A 13 mer LNA-i-miR-221 Inhibitor Restores Drug Sensitivity in Melphalan-Refractory Multiple Myeloma Cells.

2016

Abstract Purpose: The onset of drug resistance is a major cause of treatment failure in multiple myeloma. Although increasing evidence is defining the role of miRNAs in mediating drug resistance, their potential activity as drug-sensitizing agents has not yet been investigated in multiple myeloma. Experimental Design: Here we studied the potential utility of miR-221/222 inhibition in sensitizing refractory multiple myeloma cells to melphalan. Results: miR-221/222 expression inversely correlated with melphalan sensitivity of multiple myeloma cells. Inhibition of miR-221/222 overcame melphalan resistance and triggered apoptosis of multiple myeloma cells in vitro, in the presence or absence of…

0301 basic medicineMelphalanCancer ResearchStromal cellApoptosisDrug resistancePharmacologyArticle03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinemyeloma microRNA mir-221 melphalanimmune system diseasesIn vivohemic and lymphatic diseasesCell Line TumorProto-Oncogene ProteinsmedicineAnimalsHumansMelphalanMultiple myelomaNOD miceCell Proliferationbusiness.industryCancermedicine.diseaseXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyOncologychemistryDrug Resistance Neoplasm030220 oncology & carcinogenesisGrowth inhibitionMultidrug Resistance-Associated ProteinsbusinessApoptosis Regulatory ProteinsMultiple Myelomamedicine.drugClinical cancer research : an official journal of the American Association for Cancer Research
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Apoptotic Activity of MeCP2 Is Enhanced by C-Terminal Truncating Mutations.

2016

Methyl-CpG binding protein 2 (MeCP2) is a widely abundant, multifunctional protein most highly expressed in post-mitotic neurons. Mutations causing Rett syndrome and related neurodevelopmental disorders have been identified along the entire MECP2 locus, but symptoms vary depending on mutation type and location. C-terminal mutations are prevalent, but little is known about the function of the MeCP2 C-terminus. We employ the genetic efficiency of Drosophila to provide evidence that expression of p.Arg294* (more commonly identified as R294X), a human MECP2 E2 mutant allele causing truncation of the C-terminal domains, promotes apoptosis of identified neurons in vivo. We confirm this novel find…

0301 basic medicineMethyl-CpG-Binding Protein 2lcsh:MedicineApoptosisBiochemistryPhosphoserine0302 clinical medicineAnimal CellsDrosophila ProteinsPost-Translational ModificationPhosphorylationlcsh:ScienceNeuronsMotor NeuronsGeneticsMultidisciplinaryCell DeathbiologyDrosophila MelanogasterAnimal ModelsInsectsFOXG1Cell ProcessesCaspasesPhosphorylationDrosophilaBiological CulturesCellular TypesDrosophila melanogasterResearch ArticleGene isoformcongenital hereditary and neonatal diseases and abnormalitiesArthropodaProtein domainMouse ModelsMotor ActivityResearch and Analysis MethodsTransfectionModels BiologicalMECP203 medical and health sciencesModel OrganismsProtein Domainsmental disordersAnimalsHumansMolecular Biology TechniquesImmunohistochemistry TechniquesMolecular BiologyTranscription factorBinding proteinlcsh:ROrganismsBiology and Life SciencesProteinsCell BiologyCell Culturesbiology.organism_classificationInvertebratesHistochemistry and Cytochemistry TechniquesHEK293 Cells030104 developmental biologyCellular NeuroscienceMutationImmunologic TechniquesMutant Proteinslcsh:Q030217 neurology & neurosurgeryNeuroscienceTranscription FactorsPLoS ONE
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The mitochondria-targeted antioxidant MitoQ modulates oxidative stress, inflammation and leukocyte-endothelium interactions in leukocytes isolated fr…

2016

It is not known if the mitochondria-targeted antioxidants such as mitoquinone (MitoQ) can modulate oxidative stress and leukocyte-endothelium interactions in T2D patients. We aimed to evaluate the beneficial effect of MitoQ on oxidative stress parameters and leukocyte-endothelium interactions in leukocytes of T2D patients. The study population consisted of 98 T2D patients and 71 control subjects. We assessed metabolic and anthropometric parameters, mitochondrial reactive oxygen species (ROS) production, glutathione peroxidase 1 (GPX-1), NFκB-p65, TNFα and leukocyte-endothelium interactions. Diabetic patients exhibited higher weight, BMI, waist circumference, SBP, DBP, glucose, insulin, HOMA…

0301 basic medicineMitochondrial ROSMaleGPX1Antioxidantendocrine system diseasesUbiquinonemedicine.medical_treatmentBMI body mass indexClinical BiochemistryLDL low density lipoprotein cholesterolAnti-Inflammatory AgentsTPP triphenylphosphonium030204 cardiovascular system & hematologyPharmacologymedicine.disease_causeBiochemistryMitoQAntioxidantschemistry.chemical_compound0302 clinical medicineGlutathione Peroxidase GPX1IR insulin resistanceLeukocyteslcsh:QH301-705.5chemistry.chemical_classificationlcsh:R5-920AnthropometryChemistryGlutathione peroxidaseType 2 diabetesMiddle AgedFemalemedicine.symptomlcsh:Medicine (General)Research PaperPMN polymorphonuclear leukocyteshs-CRP high-sensitive C-reactive proteinHOMA-IR homeostasis model assessment of insulin resistanceInflammationT2D type 2 diabetes03 medical and health sciencesOrganophosphorus CompoundsmedicineDBP diastolic blood pressure HbA1c glycated hemoglobinHUVEC human umbilical vein endothelial cellsHumansEndotheliumAgedInflammationReactive oxygen speciesMitoQGlutathione PeroxidaseTumor Necrosis Factor-alphaSBP systolic blood pressureOrganic ChemistryTranscription Factor RelAnutritional and metabolic diseasesHDL high density lipoprotein cholesterolOxidative Stress030104 developmental biologylcsh:Biology (General)Diabetes Mellitus Type 2ImmunologyReactive Oxygen SpeciesOxidative stressRedox Biology
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Insulin Resistance in PCOS Patients Enhances Oxidative Stress and Leukocyte Adhesion: Role of Myeloperoxidase

2016

Cardiovascular diseases and oxidative stress are related to polycystic ovary syndrome (PCOS) and insulin resistance (IR). We have evaluated the relationship between myeloperoxidase (MPO) and leukocyte activation in PCOS patients according to homeostatic model assessment of IR (HOMA-IR), and have explored a possible correlation between these factors and endocrine and inflammatory parameters. This was a prospective controlled study conducted in an academic medical center. The study population consisted of 101 PCOS subjects and 105 control subjects. We divided PCOS subjects into PCOS non-IR (HOMA-IR2.5). Metabolic and anthropometric parameters, total and mitochondrial reactive oxygen species (…

0301 basic medicineMitochondrial ROSendocrine system diseasesmedicine.medical_treatment030204 cardiovascular system & hematologyPathology and Laboratory Medicinemedicine.disease_causeBiochemistryWhite Blood CellsFluorescence MicroscopyEndocrinology0302 clinical medicineAnimal CellsMedicine and Health SciencesLeukocytesInsulinImmune ResponseEnergy-Producing OrganellesMicroscopyMultidisciplinaryQRLight MicroscopyPolycystic ovaryMitochondriaOncologyMyeloperoxidaseHomeostatic model assessmentCytokinesMedicineFemaleCellular TypesCellular Structures and OrganellesInflammation MediatorsResearch ArticlePolycystic Ovary SyndromeAdultmedicine.medical_specialtyAdhesion MoleculesImmune CellsScienceImmunologyBioenergeticsBiologyResearch and Analysis MethodsProinflammatory cytokineYoung Adult03 medical and health sciencesSigns and SymptomsInsulin resistanceDiagnostic MedicineInternal medicineCell AdhesionmedicineHumansPeroxidaseInflammationDiabetic EndocrinologyBlood CellsInsulinBiology and Life SciencesCancers and Neoplasmsnutritional and metabolic diseasesCell BiologyMolecular Developmentmedicine.diseaseHormonesOxidative Stress030104 developmental biologyEndocrinologybiology.proteinInsulin ResistanceReactive Oxygen SpeciesGynecological TumorsOxidative stressDevelopmental Biology
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Oncogenic Deregulation of EZH2 as an Opportunity for Targeted Therapy in Lung Cancer.

2016

Abstract As a master regulator of chromatin function, the lysine methyltransferase EZH2 orchestrates transcriptional silencing of developmental gene networks. Overexpression of EZH2 is commonly observed in human epithelial cancers, such as non–small cell lung carcinoma (NSCLC), yet definitive demonstration of malignant transformation by deregulated EZH2 remains elusive. Here, we demonstrate the causal role of EZH2 overexpression in NSCLC with new genetically engineered mouse models of lung adenocarcinoma. Deregulated EZH2 silences normal developmental pathways, leading to epigenetic transformation independent of canonical growth factor pathway activation. As such, tumors feature a transcrip…

0301 basic medicineModels MolecularLung Neoplasmsmedicine.medical_treatmentMolecular ConformationGene ExpressionAntineoplastic Agentsmacromolecular substancesBiologymedicine.disease_causeArticleMalignant transformationTargeted therapy03 medical and health sciencesMiceStructure-Activity RelationshipCell Line TumormedicineAnimalsHumansEnhancer of Zeste Homolog 2 ProteinMolecular Targeted TherapyLung cancerPromoter Regions GeneticGene Expression ProfilingEZH2Cancermedicine.diseaseMagnetic Resonance ImagingXenograft Model Antitumor AssaysChromatinrespiratory tract diseasesGene Expression Regulation NeoplasticDisease Models Animal030104 developmental biologyCell Transformation NeoplasticEnhancer Elements GeneticOncologyDrug DesignCancer researchAdenocarcinomaKRASEpigenetic therapyCancer discovery
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Evolving Notch polyQ tracts reveal possible solenoid interference elements.

2016

ABSTRACTPolyglutamine (polyQ) tracts in regulatory proteins are extremely polymorphic. As functional elements under selection for length, triplet repeats are prone to DNA replication slippage and indel mutations. Many polyQ tracts are also embedded within intrinsically disordered domains, which are less constrained, fast evolving, and difficult to characterize. To identify structural principles underlying polyQ tracts in disordered regulatory domains, here I analyze deep evolution of metazoan Notch polyQ tracts, which can generate alleles causing developmental and neurogenic defects. I show that Notch features polyQ tract turnover that is restricted to a discrete number of conserved “polyQ …

0301 basic medicineModels MolecularProtein Structure ComparisonProtein FoldingHuntingtinlcsh:MedicineCarboxamideAnkyrin Repeat DomainBiochemistryProtein Structure SecondaryDatabase and Informatics Methods0302 clinical medicineProtein structureMacromolecular Structure AnalysisDrosophila Proteinslcsh:ScienceGeneticsHuntingtin ProteinMultidisciplinaryReceptors NotchChemistryDrosophila MelanogasterAnimal ModelsCell biologyInsectsExperimental Organism SystemsProtein foldingDrosophilaSequence AnalysisResearch ArticleMultiple Alignment CalculationProtein StructureArthropodamedicine.drug_classBioinformaticsProtein domainSequence alignmentBiologyIntrinsically disordered proteinsResearch and Analysis MethodsTerminal loopEvolution Molecular03 medical and health sciencesModel OrganismsProtein DomainsSequence Motif AnalysisComputational TechniquesmedicineHuntingtin ProteinAnimalsIndelMolecular BiologyRepetitive Sequences Nucleic AcidModels GeneticSequence Homology Amino Acidlcsh:RDNA replicationOrganismsBiology and Life SciencesProteinsHydrogen BondingInvertebratesSplit-Decomposition MethodIntrinsically Disordered Proteins030104 developmental biologyAnkyrin repeatlcsh:QPeptidesSequence Alignment030217 neurology & neurosurgeryPLoS ONE
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Antibody-mediated blockade of JMJD6 interaction with collagen I exerts antifibrotic and antimetastatic activities

2017

JMJD6 is known to localize in the nucleus, exerting histone arginine demethylase and lysyl hydroxylase activities. A novel localization of JMJD6 in the extracellular matrix, resulting from its secretion as a soluble protein, was unveiled by a new anti-JMJD6 mAb called P4E11, which was developed to identify new targets in the stroma. Recombinant JMJD6 binds with collagen type I (Coll-I), and distinct JMJD6 peptides interfere with collagen fibrillogenesis, collagen-fibronectin interaction, and adhesion of human tumor cells to the collagen substrate. P4E11 and collagen binding to JMJD6 are mutually exclusive because the amino acid sequences of JMJD6 necessary for the interaction with Coll-I ar…

0301 basic medicineMonoclonal antibodyXenograft Model Antitumor AssayArginineLysyl hydroxylaseEnzyme-Linked Immunosorbent AssayReceptors Cell SurfacePlasma protein bindingBiochemistryCollagen Type IExtracellular matrix03 medical and health sciencesMiceFibrosisPeptide LibraryCell Line TumormedicineGeneticsAnimalsHumansOsteonectinCell NucleuMolecular BiologyCell NucleusMice KnockoutMice Inbred BALB CbiologyChemistryJmjC familyAnimalAntibodies MonoclonalFibrillogenesisExtracellular matrixmedicine.diseaseXenograft Model Antitumor AssaysImmunohistochemistryCell biologyIn vivo treatment030104 developmental biologybiology.proteinOsteonectinSignal transductionExtracellular matrix; In vivo treatment; JmjC family; Monoclonal antibody; Peptide library; Animals; Antibodies Monoclonal; Cell Line Tumor; Cell Nucleus; Collagen Type I; Enzyme-Linked Immunosorbent Assay; Extracellular Matrix; Humans; Immunohistochemistry; Mice; Mice Inbred BALB C; Mice Knockout; Osteonectin; Peptide Library; Protein Binding; Receptors Cell Surface; Signal Transduction; Xenograft Model Antitumor Assays; Biotechnology; Biochemistry; Molecular Biology; GeneticsHumanProtein BindingSignal TransductionBiotechnology
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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TEM8/ANTXR1-Specific CAR T Cells as a Targeted Therapy for Triple-Negative Breast Cancer.

2018

Abstract Triple-negative breast cancer (TNBC) is an aggressive disease lacking targeted therapy. In this study, we developed a CAR T cell–based immunotherapeutic strategy to target TEM8, a marker initially defined on endothelial cells in colon tumors that was discovered recently to be upregulated in TNBC. CAR T cells were developed that upon specific recognition of TEM8 secreted immunostimulatory cytokines and killed tumor endothelial cells as well as TEM8-positive TNBC cells. Notably, the TEM8 CAR T cells targeted breast cancer stem–like cells, offsetting the formation of mammospheres relative to nontransduced T cells. Adoptive transfer of TEM8 CAR T cells induced regression of established…

0301 basic medicineOncologyCancer ResearchAdoptive cell transfermedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentT-LymphocytesCell- and Tissue-Based TherapyReceptors Antigen T-CellApoptosisReceptors Cell SurfaceTriple Negative Breast NeoplasmsTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerAntigenInternal medicineBiomarkers TumorTumor Cells CulturedMedicineAnimalsHumansTriple-negative breast cancerCell Proliferationbusiness.industryMicrofilament ProteinsCancerImmunotherapyTriple Negative Breast Neoplasmsmedicine.diseasePrognosisXenograft Model Antitumor AssaysNeoplasm ProteinsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisCase-Control StudiesFemaleImmunotherapybusinessFollow-Up StudiesCancer research
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Patient-derived solitary fibrous tumour xenografts predict high sensitivity to doxorubicin/dacarbazine combination confirmed in the clinic and highli…

2017

Abstract Background Preclinical models that mimic pathological and molecular features of solitary fibrous tumour (SFT) represent an important tool to select effective regimes and novel compounds to be tested in the clinic. This study was aimed at developing two preclinical models of SFT, assessing their predictive value in the clinic and selecting potential novel effective treatments. Material and methods Two dedifferentiated-SFT (D-SFT) models obtained from patients' biopsies were grown in immunodeficient mice. The antitumour activity on these models of doxorubicin, dacarbazine (DTIC), ifosfamide (monotherapy or combination), trabectedin and eribulin was tested. Twelve SFT patients were tr…

0301 basic medicineOncologyMaleCancer Researchmedicine.medical_treatmentSolitary fibrous tumourSoft Tissue NeoplasmsDioxoleMice SCIDPharmacologyAnthracyclineMetastasichemistry.chemical_compound0302 clinical medicineSolitary Fibrous TumorRetrospective StudieTetrahydroisoquinolinesAntineoplastic Combined Chemotherapy ProtocolsTetrahydroisoquinolineMeningeal NeoplasmsMeningeal NeoplasmPleural NeoplasmTrabectedinIfosfamideKidney NeoplasmSarcomaKetonesMiddle AgedMice modelKetoneKidney NeoplasmsDacarbazineSurvival RateOncologyResponse Evaluation Criteria in Solid TumorsSolitary Fibrous Tumors030220 oncology & carcinogenesisFemalemedicine.drugEribulinHumanAdultmedicine.medical_specialtyXenograft Model Antitumor AssayAnthracyclinePleural NeoplasmsDacarbazineBlotting WesternResponse Evaluation Criteria in Solid TumorDioxolesDisease-Free Survival03 medical and health sciencesInternal medicinemedicineAnimalsHumansChemotherapyFuranDoxorubicinRetroperitoneal NeoplasmsEribulinIfosfamideSoft Tissue NeoplasmCerebellar NeoplasmsFuransResponse Evaluation Criteria in Solid TumorsRetrospective StudiesAgedChemotherapyAntineoplastic Combined Chemotherapy ProtocolRetroperitoneal Neoplasmbusiness.industryAnimalXenograftCerebellar NeoplasmXenograft Model Antitumor AssaysTreatment030104 developmental biologychemistryDoxorubicinbusinessTrabectedin
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