Search results for "Gene expression"

showing 10 items of 4085 documents

Exon-level expression analyses identify MYCN and NTRK1 as major determinants of alternative exon usage and robustly predict primary neuroblastoma out…

2012

BACKGROUND: Using mRNA expression-derived signatures as predictors of individual patient outcome has been a goal ever since the introduction of microarrays. Here, we addressed whether analyses of tumour mRNA at the exon level can improve on the predictive power and classification accuracy of gene-based expression profiles using neuroblastoma as a model. METHODS: In a patient cohort comprising 113 primary neuroblastoma specimens expression profiling using exon-level analyses was performed to define predictive signatures using various machine-learning techniques. Alternative transcript use was calculated from relative exon expression. Validation of alternative transcripts was achieved using q…

Cancer ResearchMedizinComputational biologyBiologyexon arraysBioinformaticsN-Myc Proto-Oncogene ProteinExonNeuroblastomaRisk FactorsNeuroblastomaCell Line TumorGene expressionmedicineHumansRNA MessengerReceptor trkAGeneSurvival analysisOncogene ProteinsN-Myc Proto-Oncogene ProteinGene Expression ProfilingInfantNuclear ProteinsGenetics and GenomicspredictionExonsalternative transcript usemedicine.diseasePrognosisSurvival AnalysisGene expression profilingOncologyChild PreschoolPAMDNA microarray
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Deletion of the PER3 Gene on Chromosome 1p36 in Recurrent ER-Positive Breast Cancer

2010

El pdf del artículo es la versión de autor.-- et al.

Cancer ResearchMicroarrayGene DosageGene ExpressionEstrogen receptorBreast NeoplasmsGene dosageMiceBreast cancerOriginal ReportsAnimalsHumansMedicineGenetic Predisposition to DiseaseCopy-number variationskin and connective tissue diseasesSequence Deletionbusiness.industryCancerPeriod Circadian ProteinsPrognosismedicine.diseaseSurvival AnalysisDisease Models AnimalReceptors EstrogenOncologyChromosomes Human Pair 1Cancer researchFemaleBreast diseaseNeoplasm Recurrence LocalbusinessTamoxifenmedicine.drugJournal of Clinical Oncology
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A role for the transcription intermediary factor 2 in zebrafish myelopoiesis.

2007

Objective TIF2 is fused with MOZ in the inv(8)(p11q13) acute myeloid leukemia. TIF2, member of the p160 family, is a histone acetyl transferase (HAT). Deletion of p160 genes were performed in mice. Some observations suggest that p160 family members may perform overlapping functions in mice. Therefore, we decided to choose the zebrafish model to study TIF2. The aim of this study was to characterize the role of this HAT during embryonic development. Material and Methods We use antisense, morpholino-modified oligomers to transiently knockdown tif2 gene, thus determining whether TIF2 plays a role in zebrafish early development. Results We show that tif2 is involved in embryogenesis and in primi…

Cancer ResearchMorpholinesEmbryonic DevelopmentIn situ hybridizationBiologyAngioblastSensitivity and SpecificityNuclear Receptor Coactivator 2Structure-Activity RelationshipNotochordGeneticsmedicineAnimalsRNA MessengerMolecular BiologyZebrafishZebrafishGeneticsMyelopoiesisGene knockdownMembrane GlycoproteinsEmbryogenesisMicrofilament ProteinsGene Expression Regulation DevelopmentalCell DifferentiationCell BiologyHematologyOligonucleotides Antisensebiology.organism_classificationCell biologymedicine.anatomical_structurePhenotypeFLI1Models AnimalRNAMyelopoiesisExperimental hematology
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SOCS2 controls proliferation and stemness of hematopoietic cells under stress conditions and its deregulation marks unfavorable acute leukemias

2015

Abstract Hematopoietic stem cells (HSC) promptly adapt hematopoiesis to stress conditions, such as infection and cancer, replenishing bone marrow–derived circulating populations, while preserving the stem cell reservoir. SOCS2, a feedback inhibitor of JAK–STAT pathways, is expressed in most primitive HSC and is upregulated in response to STAT5-inducing cytokines. We demonstrate that Socs2 deficiency unleashes HSC proliferation in vitro, sustaining STAT5 phosphorylation in response to IL3, thrombopoietin, and GM-CSF. In vivo, SOCS2 deficiency leads to unrestricted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC function along serial bone marro…

Cancer ResearchMyeloidSuppressor of Cytokine Signaling ProteinsMice TransgenicNeoplasm ProteinMiceBone MarrowSuppressor of Cytokine Signaling ProteinmedicineAnimalsHumansMEF2 Transcription FactorThrombopoietinSTAT5Cell ProliferationRegulation of gene expressionABLLeukemiabiologyMEF2 Transcription FactorsAnimalMedicine (all)Animals; Bone Marrow; Cell Differentiation; Cell Proliferation; Fluorouracil; Gene Expression Regulation Neoplastic; Hematopoietic Stem Cells; Humans; Leukemia; MEF2 Transcription Factors; Mice; Mice Transgenic; Neoplasm Proteins; Neoplastic Stem Cells; Suppressor of Cytokine Signaling Proteins; Cancer Research; Oncology; Medicine (all)breakpoint cluster regionCell DifferentiationHematopoietic Stem CellHematopoietic Stem CellsNeoplasm ProteinsGene Expression Regulation NeoplasticHaematopoiesismedicine.anatomical_structureOncologyImmunologybiology.proteinCancer researchNeoplastic Stem CellsFluorouracilNeoplastic Stem CellStem cellHuman
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Newly-Discovered Neural Features Expand the Pathobiological Knowledge of Blastic Plasmacytoid Dendritic Cell Neoplasm

2021

Simple Summary For the first time, neuronal features are described in blastic plasmacytoid dendritic cell neoplasm (BPDCN) by a complex array of molecular techniques, including microRNA and gene expression profiling, RNA and Chromatin immunoprecipitation sequencing, and immunohistochemistry. The discovery of unexpected neural features in BPDCN may change our vision of this disease, leading to the designing of a new BPDCN cell model and to re-thinking the relations occurring between BPDCN and nervous system. The observed findings contribute to explaining the extreme tumor aggressiveness and also to propose novel therapeutic targets. In view of this, the identification, in this work of new po…

Cancer ResearchNeurogenesisNeoplasms. Tumors. Oncology. Including cancer and carcinogensMicroRNA Expression ProfilesequencingBiologySettore MED/08 - Anatomia PatologicaBPDCN MiRNA Network Neurogenesis SequencingBPDCNArticleChromatinGene expression profilingBPDCN; MiRNA; Network; Neurogenesis; SequencingneurogenesisOncologyDownregulation and upregulationmicroRNAnetworkCancer researchImmunohistochemistrySettore MED/05 - Patologia ClinicaNeurogenesiRC254-282ProgenitormiRNACancers
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Notch inhibition restores TRAIL-mediated apoptosis via AP1-dependent upregulation of DR4 and DR5 TRAIL receptors in MDA-MB-231 breast cancer cells.

2013

Notch is a family of transmembrane receptors whose activation through proteolytic cleavage by γ-secretase targets genes which participate in cell development, differentiation and tumorigenesis. Notch signaling is constitutively activated in various cancers, including breast cancer and its upregulation is usually related with poor clinical outcomes. Therefore, targeting Notch signaling with γ-secretase inhibitors (GSIs) is considered a promising strategy for cancer treatment. We report that the γ-secretase inhibitor-I (GSI-I) sensitizes human breast cancer cells to apoptosis mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). The antiproliferative GSI-I/TRAIL synergi…

Cancer ResearchNotch signaling pathwayApoptosisBreast NeoplasmsBiologymedicine.disease_causeTNF-Related Apoptosis-Inducing LigandDownregulation and upregulationGenes junSettore BIO/10 - BiochimicaSurvivinmedicineHumansTranscription factorReceptors NotchCell DifferentiationCell biologyGene Expression Regulation NeoplasticReceptors TNF-Related Apoptosis-Inducing LigandOncologyApoptosisCancer cellMCF-7 CellsFemalenotch signaling γ-secretase inhibitor-I/TRAIL combined treatment apoptosis breast cancer cells AP-1Signal transductionAmyloid Precursor Protein SecretasesCarcinogenesisSignal TransductionInternational journal of oncology
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Oligodendroglioma cells synthesize the differentiation-specific linker histone H1˚ and release it into the extracellular environment through shed ves…

2013

Chromatin remodelling can be involved in some of the epigenetic modifications found in tumor cells. One of the mechanisms at the basis of chromatin dynamics is likely to be synthesis and incorporation of replacement histone variants, such as the H1° linker histone. Regulation of the expression of this protein can thus be critical in tumorigenesis. In developing brain, H1° expression is mainly regulated at the post-transcriptional level and RNA-binding proteins (RBPs) are involved. In the past, attention mainly focused on the whole brain or isolated neurons and little information is available on H1° expression in other brain cells. Even less is known relating to tumor glial cells. In this st…

Cancer ResearchOligodendrogliomaGene Expressionmedicine.disease_causeHistonessheddingHistone H1Settore BIO/10 - BiochimicaGene expressionmedicineAnimalsRNA MessengerEpigeneticsRats WistarSettore BIO/06 - Anatomia Comparata E CitologiaTransport Vesicleshistone variantsCells CulturedCell NucleusMessenger RNAbiologyBrain NeoplasmsastrocytesBrainRNA-Binding ProteinsArticlesH1° histoneCell cycleChromatin Assembly and DisassemblyRatsChromatinCell biologyCell Transformation Neoplasticoligodendroglioma cellsHistoneOncologyoligodendroglioma cells astrocytes post-transcriptional regulation histone variants H1˚ histone RNA-binding proteins extracellular vesicles sheddingbiology.proteinextracellular vesiclesCarcinogenesispost-transcriptional regulation
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Clinical use of RNA sequencing and oncobox analytics to predict personalized targeted therapeutic efficacy.

2020

e13676 Background: Analysis of mutation profiles in cancer patients does not provide clinical benefits in 80-90% of cases in the US (Marquart et al., 2018). Gene expression analysis potentially complements standard detection of clinically relevant mutations. Methods: 239 adult late-stage cancer patients. RNA gene expression sequencing completed on solid tumor samples using FFPE blocks. Patient mRNA profiles were analyzed using Oncobox bioinformatics, prioritizing target drugs according to their personalized predicted efficacy. Summary reports were provided to oncologists and resulting treatment selection and outcomes were assessed. Results: As of February 2020, feedback was received from p…

Cancer ResearchOncologybusiness.industryAnalyticsGene expressionMutation (genetic algorithm)medicineCancerRNAComputational biologymedicine.diseasebusinessJournal of Clinical Oncology
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Role of the Ha-ras gene in the malignant transformation of rat liver oval cells.

1997

We have shown that the oval cell line OCICDE 22 can be transformed by the highly carcinogenic fiord-region diol epoxides of benzo[c]phenanthrene. Mutational activation of the ras proto-oncogene family has been proposed to be a critical event in the formation of tumors induced by polycyclic aromatic hydrocarbons. Therefore, we investigated whether in the earlier transformed OCICDE 22 cells any point mutations were detected in the ras proto-oncogene. The results indicate that the malignant transformation of OCICDE 22 cells by the 4 stereoisomeric benzo[c]phenan-threne diol epoxides in vitro is independent of activation of the Ha-ras proto-oncogene. In addition, Northern and Western blot analy…

Cancer ResearchPathologymedicine.medical_specialtyCellular differentiationBiologymedicine.disease_causeTransfectionProto-Oncogene MasMalignant transformationCell LineRats Sprague-DawleyLiver Neoplasms ExperimentalmedicineAnimalsHumansCell LineageCarcinogenOncogeneCarcinomaCell DifferentiationEpithelial CellsTransfectionPhenanthrenesMolecular biologyIn vitroRatsGene Expression Regulation NeoplasticCell Transformation NeoplasticGenes rasOncologyLiverUrinary Bladder NeoplasmsCell cultureCarcinogensNeoplastic Stem CellsBile DuctsCarcinogenesisNeoplasm TransplantationInternational journal of cancer
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Breast cancer cell lines contain functional cancer stem cells with metastatic capacity and a distinct molecular signature.

2009

Abstract Tumors may be initiated and maintained by a cellular subcomponent that displays stem cell properties. We have used the expression of aldehyde dehydrogenase as assessed by the ALDEFLUOR assay to isolate and characterize cancer stem cell (CSC) populations in 33 cell lines derived from normal and malignant mammary tissue. Twenty-three of the 33 cell lines contained an ALDEFLUOR-positive population that displayed stem cell properties in vitro and in NOD/SCID xenografts. Gene expression profiling identified a 413-gene CSC profile that included genes known to play a role in stem cell function, as well as genes such as CXCR1/IL-8RA not previously known to play such a role. Recombinant int…

Cancer ResearchPathologymedicine.medical_specialtyCellular differentiation[SDV.CAN]Life Sciences [q-bio]/CancerBreast Neoplasms[SDV.BC]Life Sciences [q-bio]/Cellular BiologyMice SCIDBiologyStem cell markerArticleCell LineReceptors Interleukin-8AMetastasisMice03 medical and health sciences0302 clinical medicineMice Inbred NODCancer stem cellCell Line TumorBiomarkers TumormedicineAnimalsHomeostasisHumansBreastRNA MessengerRNA NeoplasmNeoplasm MetastasisOligonucleotide Array Sequence Analysis030304 developmental biologySettore MED/04 - Patologia Generale0303 health sciencesReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingStem CellsCancerAldehyde DehydrogenaseFlow Cytometrymedicine.disease3. Good healthOncologyCell culture030220 oncology & carcinogenesisCancer researchFemaleStem cellImmortalised cell lineAldefluor breast cancer cell
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