Search results for "Phenotype"

showing 10 items of 1875 documents

Flow cytometric analysis of T cell/monocyte ratio in clinically isolated syndrome identifies patients at risk of rapid disease progression.

2015

Background: Multiple sclerosis is a chronic inflammatory central nervous system disease diagnosed by clinical presentation and characteristic magnetic resonance imaging findings. The role of cerebrospinal fluid (CSF) analysis has been emphasized in particular in the context of differential diagnosis in patients with a first episode suggestive of multiple sclerosis. Objective: We investigated here the potential additional value of analysis of CSF cellularity by fluorescence activated cell sorting (FACS) in the setting of a routine diagnostic work-up in our inpatient clinic. Methods: CSF cells from back-up samples from patients with suspected chronic inflammatory central nervous system disord…

0301 basic medicineCD4-Positive T-LymphocytesMalePathologyTime FactorsLipopolysaccharide ReceptorsCell SeparationCD8-Positive T-LymphocytesMonocytes0302 clinical medicineCerebrospinal fluidCerebrospinal FluidClinically isolated syndromemedicine.diagnostic_testMiddle AgedFlow CytometryPrognosisMagnetic Resonance Imagingmedicine.anatomical_structurePhenotypeNeurologyDisease ProgressionFemaleAdultmedicine.medical_specialtyMultiple SclerosisAdolescentT cellImmunophenotypingCentral nervous system disease03 medical and health sciencesYoung AdultPredictive Value of TestsmedicineHumansB cellAgedbusiness.industryMonocyteMultiple sclerosisOligoclonal BandsMagnetic resonance imagingmedicine.diseaseAntigens CD20030104 developmental biologyImmunologyNeurology (clinical)business030217 neurology & neurosurgeryBiomarkersDemyelinating DiseasesMultiple sclerosis (Houndmills, Basingstoke, England)
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Incomplete Timothy syndrome secondary to a mosaic mutation of the CACNA1C gene diagnosed using next-generation sequencing.

2016

Autosomal dominant genetic diseases can occur de novo and in the form of somatic mosaicism, which can give rise to a less severe phenotype, and make diagnosis more difficult given the sensitivity limits of the methods used. We report the case of female child with a history of surgery for syndactyly of the hands and feet, who was admitted at 6 years of age to a pediatric intensive care unit following cardiac arrest. The electrocardiogram (ECG) showed a long QT interval that on occasions reached 500 ms. Despite the absence of facial dysmorphism and the presence of normal psychomotor development, a diagnosis of Timothy syndrome was made given the association of syndactyly and the ECG features.…

0301 basic medicineCalcium Channels L-TypeLong QT syndromeDNA Mutational AnalysisTimothy syndrome030204 cardiovascular system & hematologyBioinformaticsDNA sequencing03 medical and health sciencessymbols.namesakeElectrocardiography0302 clinical medicineGeneticsmedicineMissense mutationHumansSyndactylyAutistic DisorderChildCodonGenetics (clinical)AllelesGenetic Association StudiesSanger sequencingbiologyMosaicismKCNE2High-Throughput Nucleotide Sequencingmedicine.diseaseLong QT Syndrome030104 developmental biologyPhenotypeAmino Acid SubstitutionMutation (genetic algorithm)Mutationsymbolsbiology.proteinFemaleSyndactylyAmerican journal of medical genetics. Part A
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AKT3 Expression in Mesenchymal Colorectal Cancer Cells Drives Growth and Is Associated with Epithelial-Mesenchymal Transition

2021

Simple Summary Colorectal cancer can be subdivided into four distinct subtypes that are characterised by different clinical features and responses to therapies currently used in the clinic to treat this disease. One of those subtypes, called CMS4, is associated with a worse prognosis and poor response to therapies compared to other subtypes. We therefore set out to explore what proteins are differentially expressed and used in CMS4 to find potential new targets for therapy. We found that protein AKT3 is highly expressed in CMS4, and that active AKT3 inhibits a protein that stalls growth of cancer cells (p27KIP1). We can target AKT3 with inhibitors which leads to strongly reduced growth of c…

0301 basic medicineCancer ResearchColorectal cancergrowthBiologylcsh:RC254-282AKT3Article03 medical and health sciences0302 clinical medicinemedicinemesenchymal CRCEpithelial–mesenchymal transitionAKT3CMSMesenchymal stem cellCell cyclemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPhenotypeGene expression profiling030104 developmental biologyOncology030220 oncology & carcinogenesisCancer cellCancer researchSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioCancers
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HMG-CoA reductase promotes protein prenylation and therefore is indispensible for T-cell survival.

2017

AbstractStatins are a well-established family of drugs that lower cholesterol levels via the competitive inhibition of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR). In addition, the pleiotropic anti-inflammatory effects of statins on T cells make them attractive as therapeutic drugs in T-cell-driven autoimmune disorders. Since statins do not exclusively target HMGCR and thus might have varying effects on different cell types, we generated a new mouse strain allowing for the tissue-specific deletion of HMGCR. Deletion of HMGCR expression in T cells led to a severe decrease in their numbers with the remaining cells displaying an activated phenotype, with an increased pro…

0301 basic medicineCancer ResearchGeranylgeranyl pyrophosphateCell SurvivalT cellT-LymphocytesImmunologyProtein PrenylationMevalonic AcidCell CountMevalonic acidLymphocyte ActivationT-Lymphocytes Regulatory03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinePolyisoprenyl PhosphatesmedicineAnimalsbiologyCell DeathIntegrasesCholesterolCell BiologyHydroxymethylglutaryl-CoA reductaseCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurePhenotypeBiochemistrychemistryHMG-CoA reductasebiology.proteinProtein prenylationlipids (amino acids peptides and proteins)Hydroxymethylglutaryl CoA ReductasesOriginal ArticleMevalonate pathway030217 neurology & neurosurgeryGene DeletionCell deathdisease
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Stem-cell derived hepatocyte-like cells for the assessment of drug-induced liver injury.

2019

Drug-induced liver injury is a major cause of drug discovery failure in clinical trials and a leading cause of liver disease. Current preclinical drug testing does not predict hepatotoxicity which highlights the importance of developing highly predictive cell-based models. The use of stem cell technology and differentiation into hepatocyte-like cells (HLCs) could provide a stable source of hepatocytes for multiple applications, including drug screening. HLCs derived from both embryonic and induced pluripotent stem cells have been used to accurately predict hepatotoxicity as well as to test individual-specific toxicity. Although there are still many limitations, mainly related to the lack of…

0301 basic medicineCancer ResearchPopulationCellInduced Pluripotent Stem CellsDrug Evaluation PreclinicalBiology03 medical and health sciencesLiver disease0302 clinical medicinemedicineAnimalsHumansInduced pluripotent stem celleducationMolecular BiologyEmbryonic Stem Cellseducation.field_of_studyDrug discoveryCell DifferentiationCell Biologymedicine.diseaseEmbryonic stem cell030104 developmental biologymedicine.anatomical_structurePhenotypeHepatocyteCancer researchHepatocytesStem cellChemical and Drug Induced Liver Injury030217 neurology & neurosurgeryDevelopmental BiologyDifferentiation; research in biological diversity
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Melanoma Lesions Independently Acquire T-cell Resistance during Metastatic Latency

2016

Abstract Melanoma often recurs after a latency period of several years, presenting a T cell–edited phenotype that reflects a role for CD8+ T cells in maintaining metastatic latency. Here, we report an investigation of a patient with multiple recurrent lesions, where poorly immunogenic melanoma phenotypes were found to evolve in the presence of autologous tumor antigen–specific CD8+ T cells. Melanoma cells from two of three late recurrent metastases, developing within a 6-year latency period, lacked HLA class I expression. CD8+ T cell–resistant, HLA class I–negative tumor cells became clinically apparent 1.5 and 6 years into stage IV disease. Genome profiling by SNP arrays revealed that HLA …

0301 basic medicineCancer ResearchT cellmedicine.medical_treatmentMedizinHuman leukocyte antigenCD8-Positive T-LymphocytesBiology03 medical and health sciencesAntigens NeoplasmmedicineHumansNeoplasm MetastasisMelanomaMelanomaCancerImmunosuppressionmedicine.diseasePhenotypeNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureOncologyLatency stageImmunologyCD8Cancer Research
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Cadmium-Associated Molecular Signatures in Cancer Cell Models

2021

Simple Summary The exposure of cancer cells to cadmium compounds may be associated with the acceleration of tumor progression. It is known that cadmium is a transcriptional regulator, and the study of differentially expressed genes has enabled the identification and classification of cadmium-associated molecular signatures as useful biomarkers that are potentially transferable to clinical research. This review recapitulates the studies that report the detection of such signatures in breast, gastric, colon, liver, lung, and nasopharyngeal tumor cell models, as specifically demonstrated by individual gene or whole genome expression profiling. Abstract The exposure of cancer cells to cadmium a…

0301 basic medicineCancer Researchcadmiumnasopharyngeal cancerReviewBiologygene signaturedifferential expressionliver cancer03 medical and health sciences0302 clinical medicinebreast cancerGene silencingSettore BIO/06 - Anatomia Comparata E CitologiaRC254-282Regulation of gene expressiongastric cancerNeoplasms. Tumors. Oncology. Including cancer and carcinogensGene signaturein vitro cell modelsPhenotypein vitro cell modelGene expression profilinglung cancer030104 developmental biologyOncologycolon cancerTumor progression030220 oncology & carcinogenesisCancer cellCancer researchReprogrammingCancers
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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Identification of clinical phenotypes and related survival in patients with large hccs

2021

Background. Hepatocellular carcinoma (HCC) factors, especially maximum tumor diameter (MTD), tumor multifocality, portal vein thrombosis (PVT), and serum alpha-fetoprotein (AFP), influence survival. Aim. To examine patterns of tumor factors in large HCC patients. Methods. A database of large HCC patients was examined. Results. A multiple Cox proportional hazard model on death identified low serum albumin levels and the presence of PVT and multifocality, with each having a hazard ratio ≥2.0. All combinations of these three parameters were examined in relation to survival. Using univariate Cox analysis, the combination of albumin &gt

0301 basic medicineCancer Researchmedicine.medical_specialtyPVTSettore MED/12 - GASTROENTEROLOGIASerum albuminlcsh:RC254-282GastroenterologyArticle03 medical and health sciences0302 clinical medicineInternal medicineMedicinePlateletHCCneoplasmsSurvival ratePVT.biologybusiness.industryProportional hazards modelAlbuminHazard ratioSettore MED/09 - MEDICINA INTERNAAlbuminMultifocalityHCC; large; phenotypes; PVT; multifocality; albuminlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasedigestive system diseasesPortal vein thrombosisAlbumin; HCC; Large; Multifocality; Phenotypes; PVTPhenotypesPhenotype030104 developmental biologyOncology030220 oncology & carcinogenesisHepatocellular carcinomabiology.proteinLargebusiness
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Diversity of Clinically Relevant Outcomes Resulting from Hypofractionated Radiation in Human Glioma Stem Cells Mirrors Distinct Patterns of Transcrip…

2020

Hypofractionated radiotherapy is the mainstay of the current treatment for glioblastoma. However, the efficacy of radiotherapy is hindered by the high degree of radioresistance associated with glioma stem cells comprising a heterogeneous compartment of cell lineages differing in their phenotypic characteristics, molecular signatures, and biological responses to external signals. Reconstruction of radiation responses in glioma stem cells is necessary for understanding the biological and molecular determinants of glioblastoma radioresistance. To date, there is a paucity of information on the longitudinal outcomes of hypofractionated radiation in glioma stem cells. This study addresses long-te…

0301 basic medicineCancer Researchmedicine.medical_treatmentCell150610Biologylcsh:RC254-282ArticleTranscriptome03 medical and health sciences0302 clinical medicineRadioresistanceGliomamedicineCell growthglioblastomamedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPhenotypeRadiation therapyradioresistance030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchglioma stem cellsStem cellhypofractionated radiationCancers
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