Search results for "Red"

showing 10 items of 23890 documents

Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase inhibition

2017

Advanced lung cancer has poor survival with few therapies. EGFR tyrosine kinase inhibitors (TKIs) have high response rates in patients with activating EGFR mutations, but acquired resistance is inevitable. Acquisition of the EGFR T790M mutation causes over 50% of resistance; MET amplification is also common. Preclinical data suggest synergy between MET and EGFR inhibitors. We hypothesized that EGFR-MET dimerization determines response to MET inhibition, depending on EGFR mutation status, independently of MET copy number. We tested this hypothesis by generating isogenic cell lines from NCI-H1975 cells, which co-express L858R and T790M EGFR mutations, namely H1975L858R/T790M (EGFR TKI resista…

0301 basic medicineLung NeoplasmsKinase InhibitorsCancer Treatmentlcsh:MedicinePhysical ChemistryBiochemistryFluorophotometryT790MSpectrum Analysis Techniques0302 clinical medicineFluorescence Resonance Energy TransferMedicine and Health SciencesPhosphorylationEnzyme Inhibitorslcsh:ScienceExtracellular Signal-Regulated MAP KinasesEGFR inhibitorsStainingMice Inbred BALB CMultidisciplinaryFluorescent in Situ HybridizationPhysicsCell StainingProto-Oncogene Proteins c-metPrecipitation TechniquesErbB ReceptorsChemistryOncologySpectrophotometry030220 oncology & carcinogenesisPhysical SciencesErlotinibDimerizationProtein BindingResearch Articlemedicine.drugChemical physicsMice NudeMolecular Probe TechniquesAdenocarcinoma of LungAdenocarcinomaBiologyResearch and Analysis Methods03 medical and health sciencesGefitinibGrowth factor receptorCell Line TumormedicineAnimalsHumansImmunoprecipitationMolecular Biology TechniquesLung cancerProtein Kinase InhibitorsMolecular BiologyCell ProliferationCell growthlcsh:RReproducibility of ResultsBiology and Life SciencesDimers (Chemical physics)medicine.diseaseMolecular biologyIsogenic human disease modelsProbe Hybridizationrespiratory tract diseasesHEK293 Cells030104 developmental biologyChemical PropertiesSpecimen Preparation and TreatmentFocal Adhesion Protein-Tyrosine KinasesMutationEnzymologylcsh:QProtein MultimerizationProto-Oncogene Proteins c-aktCytogenetic TechniquesPLOS ONE
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Stinging nettle (Urtica dioica L.) as a functional food additive in egg pasta: Enrichment and bioaccessibility of Lutein and β-carotene

2018

Abstract The use of stinging nettles as an ingredient in egg pasta has been evaluated with respect to food enrichment with carotenoids. Bioaccessibility of lutein and β-carotene has been estimated by dynamic simulation of the digestion process, with particular attention to duodenum and colon stages. Higher bioaccessibility for the two carotenoids occurs between 2 and 24 h of colonic fermentation and it is around 35% for lutein and 10% for β-carotene. However, the results reveal that the food matrix has a significant role in carotenoid release during the digestion process. In general, nettle enriched pasta has a lower carotenoid bioaccessibility than dietary supplement at duodenum and after …

0301 basic medicineLuteinCarotenoid-enriched foodmedicine.medical_treatmentDietary supplementLutein β-Carotene Stinging nettle Carotenoid-enriched food Bioaccessibility HPLC-UV/Vis-APCI-MS/MSMedicine (miscellaneous)Bioaccessibilityβ-CaroteneStinging nettle01 natural sciencesNOHPLC-UV/Vis-APCI-MS/MS03 medical and health sciencesIngredientchemistry.chemical_compoundFunctional foodmedicineTX341-641Food scienceUrtica dioicaCarotenoidchemistry.chemical_classification030109 nutrition & dieteticsNutrition and DieteticsNutrition. Foods and food supplyLutein010401 analytical chemistryCarotenefood and beverages0104 chemical scienceschemistryDigestionFood ScienceJournal of Functional Foods
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Plasma phospholipid transfer protein (PLTP) modulates adaptive immune functions through alternation of T helper cell polarization

2016

International audience; Objective: Plasma phospholipid transfer protein (PLTP) is a key determinant of lipoprotein metabolism, and both animal and human studies converge to indicate that PLTP promotes atherogenesis and its thromboembolic complications. Moreover, it has recently been reported that PLTP modulates inflammation and immune responses. Although earlier studies from our group demonstrated that PLTP can modify macrophage activation, the implication of PLTP in the modulation of T-cell-mediated immune responses has never been investigated and was therefore addressed in the present study. Approach and results: In the present study, we demonstrated that PLTP deficiency in mice has a pro…

0301 basic medicineLymphocyteIpid Transfer ProteinAdaptive ImmunityCardiovascular-DiseaseT-Lymphocytes RegulatoryLipoprotein MetabolismLeukocyte CountPhospholipid transfer proteinPolarizationImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyHypersensitivity DelayedPhospholipid Transfer ProteinsCell PolarityCell DifferentiationT-Lymphocytes Helper-InducerT helper cellFlow CytometryAcquired immune systemCell biologyInfectious Diseasesmedicine.anatomical_structureEndothelial-CellsCytokines[SDV.IMM]Life Sciences [q-bio]/ImmunologyLymphocytemedicine.symptomResearch ArticleDensity-Lipoprotein[SDV.IMM] Life Sciences [q-bio]/ImmunologyHuman Atherosclerotic PlaquesT cellCirculating Interleukin-18ImmunologyT CellAntigen-Presenting CellsInflammationAcute Myocardial-InfarctionGATA3 Transcription FactorBiology03 medical and health sciencesImmune systemmedicineAnimalsAntigen-presenting cellDeficient MiceAlpha-TocopherolMice Inbred C57BL030104 developmental biologyImmunologyVitamin-ET-Box Domain ProteinsBiomarkersSpleen
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Homeobox NKX2-3 promotes marginal-zone lymphomagenesis by activating B-cell receptor signalling and shaping lymphocyte dynamics

2016

NKX2 homeobox family proteins have a role in cancer development. Here we show that NKX2-3 is overexpressed in tumour cells from a subset of patients with marginal-zone lymphomas, but not with other B-cell malignancies. While Nkx2-3-deficient mice exhibit the absence of marginal-zone B cells, transgenic mice with expression of NKX2-3 in B cells show marginal-zone expansion that leads to the development of tumours, faithfully recapitulating the principal clinical and biological features of human marginal-zone lymphomas. NKX2-3 induces B-cell receptor signalling by phosphorylating Lyn/Syk kinases, which in turn activate multiple integrins (LFA-1, VLA-4), adhesion molecules (ICAM-1, MadCAM-1) a…

0301 basic medicineLymphoid TissueScienceB-cell receptorReceptors Antigen B-CellGeneral Physics and AstronomySykKaplan-Meier EstimateBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyNKX2-303 medical and health sciencesChemokine receptorstomatognathic systemLYNhemic and lymphatic diseasesmedicineAnimalsHumansSyk KinaseLymphocytesPhosphorylationB cellHomeodomain ProteinsMice KnockoutCàncer -- Aspectes molecularsMultidisciplinaryCell adhesion moleculeKinaseGene Expression ProfilingQLymphoma B-Cell Marginal ZoneGeneral Chemistryrespiratory system3. Good healthMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureembryonic structurescardiovascular systemCancer researchCell Adhesion MoleculesProteïnesSignal TransductionTranscription FactorsNature Communications
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Molecular similarities and differences from human pulmonary fibrosis and corresponding mouse model: MALDI imaging mass spectrometry in comparative me…

2017

Animal models can reproduce some model-specific aspects of human diseases, but some animal models translate poorly or fail to translate to the corresponding human disease. Here, we develop a strategy to systematically compare human and mouse tissues, and conduct a proof-of-concept experiment to identify molecular similarities and differences using patients with idiopathic pulmonary fibrosis and a bleomycin-induced fibrosis mouse model. Our novel approach employs high-throughput tissue microarrays (TMAs) of humans and mice, high-resolution matrix-assisted laser desorption/ionization-Fourier transform-ion cyclotron resonance-mass spectrometry imaging (MALDI-FT-ICR-MSI) to spatially resolve ma…

0301 basic medicineMALDI imagingPulmonary FibrosisSecondary MetabolismComputational biologyBiologyBioinformaticsProof of Concept StudyPathology and Forensic MedicineBleomycinMice03 medical and health sciencesIdiopathic pulmonary fibrosisMetabolomicsSpecies SpecificityFibrosisAdministration InhalationSpectroscopy Fourier Transform InfraredPulmonary fibrosismedicineAnimalsCluster AnalysisHumansMetabolomicsLungPhysiology ComparativeMolecular BiologyAntibiotics AntineoplasticTissue microarrayCell BiologyCyclotronsmedicine.diseaseImmunohistochemistryDisease Models AnimalMatrix-assisted laser desorption/ionization030104 developmental biologyTissue Array AnalysisSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationImmunohistochemistryLaboratory Investigation
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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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Ellagitannin-rich cloudberry inhibits hepatocyte growth factorinduced cell migration and phosphatidylinositol 3-kinase/AKT activation in colon carcin…

2016

// Anne-Maria Pajari 1, 2 , Essi Paivarinta 1 , Lassi Paavolainen 3 , Elina Vaara 1 , Tuuli Koivumaki 4 , Ritu Garg 5 , Anu Heiman-Lindh 1 , Marja Mutanen 1 , Varpu Marjomaki 3 , Anne J. Ridley 2, 5 1 Department of Food and Environmental Sciences, Division of Nutrition, University of Helsinki, Helsinki, Finland 2 University College London, Ludwig Institute for Cancer Research, London, UK 3 Department of Biological and Environmental Science / Nanoscience Center, University of Jyvaskyla, Jyvaskyla, Finland 4 Department of Food and Environmental Sciences, Division of Food Chemistry, University of Helsinki, Helsinki, Finland 5 Randall Division of Cell & Molecular Biophysics, King’s College Lond…

0301 basic medicineMAPK/ERK pathwaycell migrationColorectal cancerCellMetastasisMicePhosphatidylinositol 3-Kinases0302 clinical medicineCell MovementHepatocyte Growth FactorHydrolyzable Tanninsmedicine.anatomical_structureOncology030220 oncology & carcinogenesisColonic NeoplasmsHepatocyte growth factormedicine.drugResearch PapersolumigraatioAntineoplastic Agentscolorectal cancerMet receptorAdenocarcinoma03 medical and health sciencesCell Line TumorellagitanninsmedicineJournal ArticleAnimalsHumansCell migrationProtein kinase Bbusiness.industryPlant Extractsta1182Cancerta3122medicine.diseaseMice Mutant StrainsMin mouseEnzyme ActivationMice Inbred C57BL030104 developmental biologyCancer cellImmunologyCancer researchbusinessRubusProto-Oncogene Proteins c-akt
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NEGR1 and FGFR2 cooperatively regulate cortical development and core behaviours related to autism disorders in mice.

2018

See Contreras and Hippenmeyer (doi:10.1093/brain/awy218) for a scientific commentary on this article. Autism spectrum disorders (ASDs) are complex conditions with diverse aetiologies. Szczurkowska et al. demonstrate that two ASD-related molecules – FGFR2 and Negr1 – physically interact to act on the same downstream pathway, and regulate cortical development and ASD-relevant behaviours in mice. Identifying common mechanisms in ASDs may reveal targets for pharmacological intervention.

0301 basic medicineMAPK/ERK pathwaygenetic structuresAutism Spectrum DisorderFGFR2 signalingFibroblast growth factorReceptor tyrosine kinaseMiceautism; development; cell adhesion; in utero electroporation; FGFR2 signaling0302 clinical medicineCell MovementCerebral CortexMice KnockoutbiologyBehavior AnimalKinaseCell adhesion moleculeCell biologyProtein TransportSignal Transductionmusculoskeletal diseasesMAP Kinase Signaling SystemCell Adhesion Molecules NeuronalDendritic SpinesNeurogenesisautismDown-Regulationbehavioral disciplines and activities03 medical and health sciencesmental disordersmedicineAnimalsHumansAutistic DisorderReceptor Fibroblast Growth Factor Type 2developmentProtein kinase BFibroblast growth factor receptor 2Cell Membranecell adhesionOriginal Articlesin utero electroporationmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologyHEK293 Cellsbiology.proteinAutismNeurology (clinical)030217 neurology & neurosurgeryBrain : a journal of neurology
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ESCRT Requirements for Murine Leukemia Virus Release

2016

The Murine Leukemia Virus (MLV) is a gammaretrovirus that hijack host components of the endosomal sorting complex required for transport (ESCRT) for budding. To determine the minimal requirements for ESCRT factors in MLV viral and viral-like particles (VLP) release, an siRNA knockdown screen of ESCRT(-associated) proteins was performed in MLV-producing human cells. We found that MLV VLPs and virions primarily engage the ESCRT-I factor Tsg101 and marginally the ESCRT-associated adaptors Nedd4-1 and Alix to enter the ESCRT pathway. Conversely, the inactivation of ESCRT-II had no impact on VLP and virion egress. By analyzing the effects of individual ESCRT-III knockdowns, VLP and virion releas…

0301 basic medicineMLV; VLPs; retroviral budding; viral late domain; ESCRT; MVB pathway; CHMP1AEndosomevirusesGenetic Vectorslcsh:QR1-502CHMP1AGene ExpressionGene Products gagMLVmacromolecular substanceslcsh:MicrobiologyArticleESCRTCell LineESCRTMice03 medical and health sciencesviral late domainMVB pathwayVirologyGene OrderMurine leukemia virusAnimalsHumansVLPsTSG101Viral sheddingVirus Releaseretroviral buddingGammaretrovirusBuddingEndosomal Sorting Complexes Required for Transportbiologybiochemical phenomena metabolism and nutritionbiology.organism_classificationVirologyVirus ReleaseLeukemia Virus Murine030104 developmental biologyInfectious DiseasesGene Knockdown TechniquesRetroviridae InfectionsViruses
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