Search results for "expression profiling"

showing 10 items of 658 documents

Induction of cancer cell stemness by depletion of macrohistone H2A1 in hepatocellular carcinoma.

2017

Hepatocellular carcinomas (HCC) contain a subpopulation of cancer stem cells (CSCs), which exhibit stem cell–like features and are responsible for tumor relapse, metastasis, and chemoresistance. The development of effective treatments for HCC will depend on a molecular-level understanding of the specific pathways driving CSC emergence and stemness. MacroH2A1 is a variant of the histone H2A and an epigenetic regulator of stem-cell function, where it promotes differentiation and, conversely, acts as a barrier to somatic-cell reprogramming. Here, we focused on the role played by the histone variant macroH2A1 as a potential epigenetic factor promoting CSC differentiation. In human HCC section…

0301 basic medicineCarcinoma HepatocellularBiologyMetastasisHistones03 medical and health sciencesCancer stem cellHistone H2AmedicineHumansEpigeneticsPhosphorylationCell ProliferationHepatologyCell growthGene Expression ProfilingLiver NeoplasmsTranscription Factor RelAHep G2 Cellsmedicine.disease030104 developmental biologyHistoneCancer cellCancer researchbiology.proteinNeoplastic Stem CellsReprogrammingHepatology (Baltimore, Md.)
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JNK ‐dependent gene regulatory circuitry governs mesenchymal fate

2015

The epithelial to mesenchymal transition (EMT) is a biological process in which cells lose cell-cell contacts and become motile. EMT is used during development, for example, in triggering neural crest migration, and in cancer metastasis. Despite progress, the dynamics of JNK signaling, its role in genomewide transcriptional reprogramming, and involved downstream effectors during EMT remain largely unknown. Here, we show that JNK is not required for initiation, but progression of phenotypic changes associated with EMT. Such dependency resulted from JNK-driven transcriptional reprogramming of critical EMT genes and involved changes in their chromatin state. Furthermore, we identified eight no…

MAP Kinase Kinase 4MAP Kinase Signaling SystemCellular differentiationGene regulatory networkBiologyTime-Lapse ImagingGeneral Biochemistry Genetics and Molecular BiologyCell LineMesodermTranscriptometranscription factorsmetastasisHumansGene Regulatory NetworksEpithelial–mesenchymal transitionMolecular BiologyTranscription factorJNK signalingGeneticsRegulation of gene expressionGeneral Immunology and MicrobiologyGene Expression ProfilingGeneral NeuroscienceCell CycleEMTCell DifferentiationArticles3. Good healthChromatinCell biologyembryonic structuresgene regulationReprogrammingThe EMBO Journal
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Integrative genomic and proteomic analyses identify targets for Lkb1 deficient metastatic lung tumors

2010

SummaryIn mice, Lkb1 deletion and activation of KrasG12D results in lung tumors with a high penetrance of lymph node and distant metastases. We analyzed these primary and metastatic de novo lung cancers with integrated genomic and proteomic profiles, and have identified gene and phosphoprotein signatures associated with Lkb1 loss and progression to invasive and metastatic lung tumors. These studies revealed that SRC is activated in Lkb1-deficient primary and metastatic lung tumors, and that the combined inhibition of SRC, PI3K, and MEK1/2 resulted in synergistic tumor regression. These studies demonstrate that integrated genomic and proteomic analyses can be used to identify signaling pathw…

ProteomicsCancer ResearchLung NeoplasmsMAP Kinase Kinase 2MAP Kinase Kinase 1CELLCYCLEAMP-Activated Protein Kinasesmedicine.disease_causeMice0302 clinical medicineAMP-Activated Protein Kinase KinasesCell MovementCarcinoma Non-Small-Cell LungEnzyme InhibitorsNeoplasm MetastasisPhosphorylationLymph nodePhosphoinositide-3 Kinase Inhibitors0303 health sciencesTOR Serine-Threonine KinasesIntracellular Signaling Peptides and ProteinsGenomicsCell cycleProtein-Tyrosine KinasesPenetrance3. Good healthUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structuresrc-Family KinasesOncologySIGNALING030220 oncology & carcinogenesisDrug Therapy CombinationFemaleRNA InterferenceKRASSignal TransductionMice NudeBiologyProtein Serine-Threonine KinasesArticleProto-Oncogene Proteins p21(ras)03 medical and health sciencesCell Line TumorProto-Oncogene ProteinsmedicineCell AdhesionAnimalsHumansEpithelial–mesenchymal transitionProtein Kinase Inhibitors030304 developmental biologyFocal AdhesionsGene Expression ProfilingCell BiologyXenograft Model Antitumor AssaysMice Mutant StrainsGene expression profilingFocal Adhesion Protein-Tyrosine KinasesCancer cellCell TransdifferentiationCancer researchras ProteinsCarcinogenesis
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Cre-mediated cell ablation contests mast cell contribution in models of antibody- and T cell-mediated autoimmunity.

2011

SummaryImmunological functions of mast cells remain poorly understood. Studies in Kit mutant mice suggest key roles for mast cells in certain antibody- and T cell-mediated autoimmune diseases. However, Kit mutations affect multiple cell types of both immune and nonimmune origin. Here, we show that targeted insertion of Cre-recombinase into the mast cell carboxypeptidase A3 locus deleted mast cells in connective and mucosal tissues by a genotoxic Trp53-dependent mechanism. Cre-mediated mast cell eradication (Cre-Master) mice had, with the exception of a lack of mast cells and reduced basophils, a normal immune system. Cre-Master mice were refractory to IgE-mediated anaphylaxis, and this defe…

Cell typeEncephalomyelitis Autoimmune ExperimentalCarboxypeptidases AT cellT-LymphocytesImmunologyAutoimmunityImmunoglobulin E03 medical and health sciencesMice0302 clinical medicineImmune systemTh2 CellsmedicineImmunology and AllergyAnimalsGenetic Predisposition to DiseaseMast CellsIntestinal MucosaInterleukin 5Anaphylaxis030304 developmental biologyAutoantibodiesMice Knockout0303 health sciencesStem Cell FactorbiologyIntegrasesGene Expression ProfilingImmunoglobulin EMast cellArthritis Experimental3. Good healthInterleukin 33Mice Inbred C57BLDisease Models Animalmedicine.anatomical_structureInfectious DiseasesImmunologyGene Targetingbiology.proteinAntibodyTumor Suppressor Protein p53030215 immunologyImmunity
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Lasting downregulation of the lipid peroxidation enzymes in the prefrontal cortex of mice susceptible to stress-induced anhedonia

2015

International audience; Antioxidant enzymes and lipid peroxidation in the brain are involved in neuropsychiatric pathologies, including depression. 14- or 28-day chronic stress model induced a depressive syndrome defined by lowered reward sensitivity in C57BL/6J mice and changed gene expression of peroxidation enzymes as shown in microarray assays. We studied how susceptibility or resilience to anhedonia is related to lipid peroxidation in the prefrontal cortex (PFC). With 14-day stress, a comparison of the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) and accumulation of malondialdehyde (MDA) revealed a decrease of the first two measures in suscepti…

Malemedicine.medical_specialtyImipramineAnhedoniaLipid peroxidationDown-RegulationMotor ActivityMicroarrayHippocampusImipraminePrefrontal cortexGene Expression Regulation EnzymologicSuperoxide dismutaseLipid peroxidationFood PreferencesMiceBehavioral Neurosciencechemistry.chemical_compoundNeurochemicalMalondialdehydeInternal medicinemedicineAnimalsChronic stresschemistry.chemical_classificationGlutathione PeroxidasebiologySuperoxide Dismutasebusiness.industryGene Expression ProfilingGlutathione peroxidaseAnhedoniaResilience PsychologicalCatalaseMalondialdehydeAggressionEndocrinologychemistrybiology.protein[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]medicine.symptombusinessChronic stress depression modelStress Psychologicalmedicine.drug
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Congenital undifferentiated sarcoma associated to BCOR-CCNB3 gene fusion

2017

Small round cell sarcomas are aggressive bone and soft tissue tumors that predominantly affect children and young adults. A new group of sarcomas with a recurrent BCOR-CCNB3 gene fusion has been recently identified in previously unclassifiable small round cell sarcomas. BCOR-CCNB3 sarcomas share clinical and pathologic similarities with Ewing sarcoma, but show a stronger male predilection and less aggressiveness, as well as distinct gene expression profiling and pangenomic SNP array analyses. We report the unusual case of a congenital BCOR-CCNB3 retroperitoneal sarcoma in a female born at 34th gestational week, which was diagnosed in necropsy after 21hours of life. Immunohistochemical analy…

Adult0301 basic medicinePathologymedicine.medical_specialtyOncogene Proteins FusionTumor suppressor geneCD99Soft Tissue NeoplasmsCyclin BBiologyPathology and Forensic MedicineDiagnosis DifferentialFusion gene03 medical and health sciences0302 clinical medicineProto-Oncogene ProteinsBiomarkers TumormedicineHumansSMARCB1SarcomaCell Biologymedicine.diseaseRepressor ProteinsGene expression profiling030104 developmental biology030220 oncology & carcinogenesisCancer researchImmunohistochemistryFemaleSarcomaGene FusionSNP arrayPathology - Research and Practice
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Identifying Early Warning Signals for the Sudden Transition from Mild to Severe Tobacco Etch Disease by Dynamical Network Biomarkers

2019

This article belongs to the Special Issue The Complexity of the Potyviral Interaction Network.

0106 biological sciences0301 basic medicineComplex systemsSystems biologyPotyvirusDiseaseBiologytobacco etch virusSeverity of Illness Index01 natural sciencesArticlePlant VirusesTranscriptomeViral Proteins03 medical and health sciencesPlant-virus interactionpotyvirusGene Expression Regulation PlantVirologyProtein Interaction MappingTobaccoGene Regulatory NetworksProtein Interaction Mapscomplex systemsGenePlant DiseasesGeneticsTransition (genetics)Tobacco etch virusGene Expression Profilingsystems biologyDNBBiotic stressresponse to infectionbiology.organism_classificationplant-virus interactionTobacco etch virusphase transitionsprotein-protein interaction networks030104 developmental biologyInfectious DiseasesPhase transitionsHost-Pathogen InteractionsMutationBiomarker (medicine)BiomarkersSignal Transduction010606 plant biology & botanyViruses
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Predictive and Prognostic Molecular Factors in Diffuse Large B-Cell Lymphomas.

2021

Diffuse large B-cell lymphoma (DLBCL) is the commonest form of lymphoid malignancy, with a prevalence of about 40% worldwide. Its classification encompasses a common form, also termed as “not otherwise specified” (NOS), and a series of variants, which are rare and at least in part related to viral agents. Over the last two decades, DLBCL-NOS, which accounts for more than 80% of the neoplasms included in the DLBCL chapter, has been the object of an increasing number of molecular studies which have led to the identification of prognostic/predictive factors that are increasingly entering daily practice. In this review, the main achievements obtained by gene expression profiling (with respect t…

0301 basic medicineOncologymedicine.medical_specialtydiagnosisdiffuse large B-cell lymphomaReviewSettore MED/08 - Anatomia Patologica03 medical and health sciences0302 clinical medicineInternal medicineDaily practicemedicineTumor MicroenvironmentHumanslcsh:QH301-705.5B celltherapybusiness.industryGene Expression ProfilingNot Otherwise SpecifiedHigh-Throughput Nucleotide SequencingGeneral Medicinemedicine.diseaseMicroarray AnalysisPrognosisLymphomaGene expression profilingdiagnosi030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)Lymphoid malignancyclassification030220 oncology & carcinogenesisnext-generation sequencingLymphoma Large B-Cell DiffusebusinessDiffuse large B-cell lymphomaprognosiCells
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Comparison of RNA-seq and microarray-based models for clinical endpoint prediction

2015

Background Gene expression profiling is being widely applied in cancer research to identify biomarkers for clinical endpoint prediction. Since RNA-seq provides a powerful tool for transcriptome-based applications beyond the limitations of microarrays, we sought to systematically evaluate the performance of RNA-seq-based and microarray-based classifiers in this MAQC-III/SEQC study for clinical endpoint prediction using neuroblastoma as a model. Results We generate gene expression profiles from 498 primary neuroblastomas using both RNA-seq and 44 k microarrays. Characterization of the neuroblastoma transcriptome by RNA-seq reveals that more than 48,000 genes and 200,000 transcripts are being …

AdultMaleMicroarrayAdolescentEndpoint DeterminationNEUROBLASTOMA PATIENTSgenetic processesRNA-SeqBiologyBioinformaticsRISK STRATIFICATIONTranscriptomeNeuroblastomaYoung AdultREPRODUCIBILITYClinical endpointTumor Cells CulturedBREAST-CANCERHumansnatural sciencesTRANSCRIPTOMEChildGENE-EXPRESSIONOligonucleotide Array Sequence AnalysisSettore BIO/11 - BIOLOGIA MOLECOLAREEXPRESSION-BASED CLASSIFICATIONModels GeneticSequence Analysis RNAGene Expression ProfilingResearchSIGNATUREInfant NewbornBiology and Life SciencesInfantHuman genetics3. Good healthPROSTATE-CANCERGene expression profilingDIFFERENTIATIONChild PreschoolEndpoint DeterminationFemaleDNA microarray
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The p53 Tumor Suppressor Network Is a Key Responder to Microenvironmental Components of Chronic Inflammatory Stress

2005

Abstract Activation of the p53 network plays a central role in the inflammatory stress response associated with ulcerative colitis and may modulate cancer risk in patients afflicted with this chronic disease. Here, we describe the gene expression profiles associated with four microenvironmental components of the inflammatory response (NO•, H2O2, DNA replication arrest, and hypoxia) that result in p53 stabilization and activation. Isogenic HCT116 and HCT116 TP53−/− colon cancer cells were exposed to the NO• donor Sper/NO, H2O2, hypoxia, or hydroxyurea, and their mRNA was analyzed using oligonucleotide microarrays. Overall, 1,396 genes changed in a p53-dependent manner (P < 0.001), wit…

Cancer ResearchTumor suppressor geneColorectal cancerInflammationBiologymedicine.disease_causeArticleGene expressionmedicineHumansNitric Oxide DonorsInflammationReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleHydrogen PeroxideCell cycleHypoxia (medical)Flow CytometryHCT116 Cellsmedicine.diseaseCell HypoxiaGene expression profilingOxidative StressOncologyImmunologyNitrogen OxidesSpermineTumor Suppressor Protein p53medicine.symptomOxidative stressCancer Research
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