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showing 10 items of 15058 documents

Neurochemical Phenotype of Reelin Immunoreactive Cells in the Piriform Cortex Layer II

2016

Reelin, a glycoprotein expressed by Cajal-Retzius neurons throughout the marginal layer of developing neocortex, has been extensively shown to play an important role during brain development, guiding neuronal migration and detachment from radial glia. During the adult life, however, many studies have associated Reelin expression to enhanced neuronal plasticity. Although its mechanism of action in the adult brain remains mostly unknown, Reelin is expressed mainly by a subset of mature interneurons. Here, we confirm the described phenotype of this subpopulation in the adult neocortex. We show that these mature interneurons, although being in close proximity, lack polysialylated neural cell ad…

0301 basic medicineLow-density lipoprotein receptor-related protein 8PSA-NCAMlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neurosciencepiriform cortex0302 clinical medicineADULT-RATSYNAPTIC PLASTICITYCEREBRAL-CORTEXPiriform cortexmedicineMESSENGER-RNA EXPRESSIONPSA-NCAM EXPRESSIONReelinCajal-Retzius cellslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryOriginal ResearchNeocortexbiology3112 NeurosciencesNONHUMAN-PRIMATESReelinDAB1DoublecortinDOUBLECORTIN-EXPRESSING CELLS030104 developmental biologymedicine.anatomical_structureSTRUCTURAL PLASTICITYnervous systemDCXbiology.proteinNeural cell adhesion moleculeNeuNNeuroscienceHIPPOCAMPAL CONNECTIONS030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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Amphiregulin contained in NSCLC-exosomes induces osteoclast differentiation through the activation of EGFR pathway

2017

AbstractNon-small cell lung cancer (NSCLC) remains the leading cause of cancer-related deaths worldwide. The majority of patients are diagnosed in advanced disease stage. Bone metastasis is the most frequent complication in NSCLC resulting in osteolytic lesions. The perfect balance between bone-resorbing osteoclasts and bone-forming osteoblasts activity is lost in bone metastasis, inducing osteoclastogenesis. In NSCLC, the epidermal growth factor receptor (EGFR) pathway is constitutively activated. EGFR binds Amphiregulin (AREG) that is overexpressed in several cancers such as colon, breast and lung. Its levels in plasma of NSCLC patients correlate with poor prognosis and AREG was recently …

0301 basic medicineLung NeoplasmsCellular differentiationAmphiregulin exosomes NSCLC EGFROsteoclastsExosomes NSCLC AmphiregulinNSCLCExosomesMice0302 clinical medicineSettore BIO/13 - Biologia ApplicataCarcinoma Non-Small-Cell LungMedicineEpidermal growth factor receptorRNA Small InterferingMultidisciplinarybiologyQProteolytic enzymesRBone metastasisCell Differentiation3. Good healthErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureRANKL030220 oncology & carcinogenesisMedicineEngineering sciences. TechnologySciencePrimary Cell CultureBone NeoplasmsAmphiregulinArticle03 medical and health sciencesAmphiregulinOsteoclastCell Line TumorAnimalsHumansbusiness.industryRANK LigandBiological Transportmedicine.diseaseMicrovesiclesCoculture Techniquesrespiratory tract diseases030104 developmental biologyRAW 264.7 CellsImmunologybiology.proteinCancer researchbusiness
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A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer's Disease, Glioblastoma and Lung cancer.

2017

Epidemiological studies indicate that patients suffering from Alzheimer’s disease have a lower risk of developing lung cancer, and suggest a higher risk of developing glioblastoma. Here we explore the molecular scenarios that might underlie direct and inverse co-morbidities between these diseases. Transcriptomic meta-analyses reveal significant numbers of genes with inverse patterns of expression in Alzheimer’s disease and lung cancer, and with similar patterns of expression in Alzheimer’s disease and glioblastoma. These observations support the existence of molecular substrates that could at least partially account for these direct and inverse co-morbidity relationships. A functional analy…

0301 basic medicineLung NeoplasmsMolecular biology[SDV]Life Sciences [q-bio]Gene ExpressionDiseaseCàncer--Fisiologia patològicaComorbidityTranscriptomeMedicineDinàmica molecularMultidisciplinaryQLung Cancer:Enginyeria biomèdica [Àrees temàtiques de la UPC]R3. Good healthAlzheimer's disease (AD)MedicineDisease SusceptibilityAlzheimer's diseaseSignal transductionSignal TransductionCentral Nervous System (CNS)ScienceModels BiologicalArticle03 medical and health sciencesImmune systemcáncerAlzheimer DiseaseDementia[CHIM]Chemical SciencesHumansLung cancerbusiness.industryGenetic Variationmedicine.diseaseComorbidityCNS cancerAlzheimer Malaltia d'030104 developmental biologyGliobastomas (GBM)ImmunologyCancer researchDementiabusinessGlioblastomaReactive Oxygen SpeciesNon-small-cell lung cancerBiomarkers
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Comprehensive Analysis of SWI/SNF Inactivation in Lung Adenocarcinoma Cell Models

2020

Simple Summary: Mammalian SWI/SNF complexes regulate gene expression by reorganizing the way DNA is packaged into chromatin. SWI/SNF subunits are recurrently altered in tumors at multiple levels, including DNA mutations as well as alteration of the levels of RNA and protein. Cancer cell lines are often used to study SWI/SNF function, but their patterns of SWI/SNF alterations can be complex. Here, we present a comprehensive characterization of DNA mutations and RNA and protein expression of SWI/SNF members in 38 lung adenocarcinoma (LUAD) cell lines. We show that over 85% of our cell lines harbored at least one alteration in one SWI/SNF subunit. In addition, over 75% of our cell lines lacked…

0301 basic medicineLung adenocarcinomaCancer ResearchcellsCellgenetic processesmacromolecular substancesBiologylcsh:RC254-282Articlelaw.inventionTranscriptome03 medical and health sciences0302 clinical medicinelawmedicineEpigeneticsMulti-omicsSWI/SNF complexepigeneticsCancermulti-omicslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaselung adenocarcinomaSWI/SNFcell models3. Good healthCell biologyChromatinenzymes and coenzymes (carbohydrates)lung cancer030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCell modelSuppressorEpigeneticsbiological phenomena cell phenomena and immunityLung cancerSWI/SNF complex
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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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Interactions between immune challenges and cancer cells proliferation: timing does matter!

2015

Using first a theoretical framework, we show that repeated short immune challenges could impact the accumulation of cancerous cells through continuous perturbation of immune system efficiency. We discuss for a new indirect role for infectious disease in cancer progression.

0301 basic medicineMALADIEHealth Toxicology and Mutagenesismedicine.medical_treatmentMedicine (miscellaneous)[SDV.CAN]Life Sciences [q-bio]/CancerBiologyinfectious diseases[ SDV.CAN ] Life Sciences [q-bio]/Cancer03 medical and health sciences0302 clinical medicineImmune systemINFECTIONEpidemiology of cancermedicinecancer[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyOriginal Research ArticleEcology Evolution Behavior and SystematicsIMMUNITEMODELE MATHEMATIQUEimmunosenescenceimmunosuppressionCancerImmunosuppressionImmunosenescencePREVENTION SANITAIREbiochemical phenomena metabolism and nutritionmedicine.diseaseCANCER3. Good health030104 developmental biologyCancer incidence13. Climate action030220 oncology & carcinogenesisImmunologyCancer cell[SDV.IMM]Life Sciences [q-bio]/ImmunologyCancer riskAGENT PATHOGENE
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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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Pharmacological basis of the anxiolytic and antidepressant properties of Silexan®, an essential oil from the flowers of lavender.

2021

Silexan®, a proprietary essential oil manufactured by steam distillation from Lavandula angustifolia flowers showed pronounced anxiolytic effects in patients with subthreshold anxiety disorders and was also efficacious in patients with Generalized Anxiety disorder (GAD). Moreover, evidences for antidepressant-like properties of Silexan® have been observed in anxious patients suffering from comorbid depressive symptoms and in patients with mixed anxiety-depression disorder (ICD-10 F41.2). In accordance with the clinical data Silexan® is active in several behavioral models in rodents at rather low concentrations indicating potent anxiolytic and antidepressive properties. As possible mechanism…

0301 basic medicineMAPK/ERK pathwayGeneralized anxiety disordermedicine.drug_classPregabalinFlowersPharmacologyAnxietyCREBAnxiolytic03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineOils VolatileAnimalsHumansPlant OilsbiologyVoltage-dependent calcium channelChemistryDepressionCell Biologymedicine.diseaseCalcium Channel BlockersAntidepressive Agents030104 developmental biologyLavandulaMechanism of actionAnti-Anxiety Agentsbiology.proteinAntidepressantCalcium Channelsmedicine.symptom030217 neurology & neurosurgerymedicine.drugNeurochemistry international
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ERK3/MAPK6 controls IL-8 production and chemotaxis

2020

ERK3 is a ubiquitously expressed member of the atypical mitogen activated protein kinases (MAPKs) and the physiological significance of its short half-life remains unclear. By employing gastrointestinal 3D organoids, we detect that ERK3 protein levels steadily decrease during epithelial differentiation. ERK3 is not required for 3D growth of human gastric epithelium. However, ERK3 is stabilized and activated in tumorigenic cells, but deteriorates over time in primary cells in response to lipopolysaccharide (LPS). ERK3 is necessary for production of several cellular factors including interleukin-8 (IL-8), in both, normal and tumorigenic cells. Particularly, ERK3 is critical for AP-1 signaling…

0301 basic medicineMAPK/ERK pathwayMouseQH301-705.5ScienceERK3General Biochemistry Genetics and Molecular BiologyCell Line03 medical and health sciencesMice0302 clinical medicineOrganoidmetastasisAnimalsHumansInterleukin 8Biology (General)chemotaxisMitogen-Activated Protein Kinase 6Gene knockdownGeneral Immunology and MicrobiologyIL-8ChemistryKinaseGeneral NeuroscienceQInterleukin-8RChemotaxisGeneral MedicineCell BiologyMAPKgastrointestinal organoidsIn vitroCell biologysecretomeChemotaxis Leukocyte030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisMedicineHeterograftsSignal transductionsignal transductionResearch ArticleHumaneLife
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