Search results for "Cell Differentiation"

showing 10 items of 907 documents

Use of HT-29, a cultured human colon cancer cell line, to study the effect of fermented milks on colon cancer cell growth and differentiation.

1995

International audience; Epidemiological and in vivo and in vitro experimental studies have suggested that fermented milks may interfere with the emergence and/or the development of colon cancer. The results, however, remain inconclusive. This prompted us to develop a new approach based on the use of HT-29, a cultured human colon cancer cell line, to study at the cellular level the effect of fermented milks on colon cancer cell growth and differentiation characteristics. Undifferentiated HT-29 cells have been grown in the continuous presence of milks fermented by one of the following bacterial populations: Lactobacillus helveticus, Bifidobacterium, L.acidophilus or a mix of Streptococcus the…

Cancer ResearchColorectal cancerCellular differentiationDipeptidyl Peptidase 4Bacterial growthSensitivity and SpecificityMicrobiology03 medical and health sciences0302 clinical medicine[ CHIM.ORGA ] Chemical Sciences/Organic chemistrymedicineFermented milk productsTumor Cells CulturedAnimalsHumans030304 developmental biologyBifidobacterium0303 health sciencesbiologyCell growth[CHIM.ORGA]Chemical Sciences/Organic chemistryStreptococcusfood and beveragesCell DifferentiationGeneral Medicinemedicine.diseasebiology.organism_classificationMilk Proteins[CHIM.ORGA] Chemical Sciences/Organic chemistryLactobacillusMilkCell culture030220 oncology & carcinogenesisCancer cellColonic NeoplasmsFermentationBifidobacteriumCell Division
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Cancer stem cell definitions and terminology:the devil is in the details

2012

The cancer stem cell (CSC) concept has important therapeutic implications, but its investigation has been hampered both by a lack of consistency in the terms used for these cells and by how they are defined. Evidence of their heterogeneous origins, frequencies and their genomic, as well as their phenotypic and functional, properties has added to the confusion and has fuelled new ideas and controversies. Participants in The Year 2011 Working Conference on CSCs met to review these issues and to propose a conceptual and practical framework for CSC terminology. More precise reporting of the parameters that are used to identify CSCs and to attribute responses to them is also recommended as key t…

Cancer ResearchGeneral MathematicsACUTE MYELOID-LEUKEMIAPERIPHERAL-BLOODBiologyAnimals; Cell Differentiation; Cell Transformation Neoplastic; Clonal Evolution; Humans; Neoplastic Stem Cells; Terminology as Topic; Oncology; Cancer ResearchBioinformaticsCell TransformationSomatic evolution in cancerTumor Initiating CellsTerminologyClonal EvolutionIN-VITRO PROPAGATIONPHENOTYPIC HETEROGENEITYREPOPULATING CELLSConsistency (negotiation)Cancer stem cellCancer stem cells (CSC)Settore MED/04 - PATOLOGIA GENERALETerminology as TopicmedicineAnimalsHumansIn patientACUTE LYMPHOBLASTIC-LEUKEMIAGENE-EXPRESSIONConfusionSettore MED/04 - Patologia GeneraleMELANOMA-CELLSCognitive scienceNeoplasticAnimalApplied MathematicsSTEM/PROGENITOR CELLSCell DifferentiationTUMOR-INITIATING CELLSPeripheral bloodCell Transformation Neoplasticcancer stem cells differentiation tumor definitionsOncologyNeoplastic Stem CellsNeoplastic Stem Cellmedicine.symptomHuman
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The AC133 epitope, but not the CD133 protein, is lost upon cancer stem cell differentiation.

2010

Abstract Colon cancer stem cells (CSC) can be identified with AC133, an antibody that detects an epitope on CD133. However, recent evidence suggests that expression of CD133 is not restricted to CSCs, but is also expressed on differentiated tumor cells. Intriguingly, we observed that detection of the AC133 epitope on the cell surface decreased upon differentiation of CSC in a manner that correlated with loss of clonogenicity. However, this event did not coincide with a change in CD133 promoter activity, mRNA, splice variant, protein expression, or even cell surface expression of CD133. In contrast, we noted that with CSC differentiation, a change occured in CD133 glycosylation. Thus, AC133 …

Cancer ResearchGlycosylationGlycosylationCellular differentiationCellAC 133 EpitopeDown-RegulationMice SCIDEpitopechemistry.chemical_compoundEpitopesMiceCancer stem cellAntigens CDMice Inbred NODProminin-1medicineTumor Cells CulturedAnimalsHumansProtein IsoformsAC133 AntigenRNA MessengerPromoter Regions GeneticneoplasmsGlycoproteinsbiologyCell DifferentiationMolecular biologycarbohydrates (lipids)Gene Expression Regulation Neoplasticmedicine.anatomical_structureOncologychemistryembryonic structuresColonic Neoplasmsbiology.proteinNeoplastic Stem CellsAntibodyStem cellPeptidesCancer research
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Prognostic significance of interferon regulating factor 4 (IRF4) in node-negative breast cancer.

2014

620 Background: The transcription factor IRF4 (interferon regulating factor 4) regulates immunoglobulin class switch recombination as well as plasma cell differentiation. We examined the prognostic significance of IRF4 mRNA expression in node-negative breast cancer. Methods: Microarray based gene-expression data for IRF4 (204562_at) were analysed in four previously published cohorts (Mainz, Rotterdam, Transbig, Yu) of node-negative breast cancer patients not treated with adjuvant therapy (n=824). A meta-analysis of previously published cohorts was performed using a random effects model. Prognostic significance of IRF4 on metastasis-free survival (MFS) was examined in the whole cohort and in…

Cancer ResearchMicroarraybusiness.industrymedicine.diseaseBreast cancerOncologyInterferonPlasma cell differentiationImmunologyCancer researchmedicineAdjuvant therapyAurora Kinase Askin and connective tissue diseasesbusinessTranscription factorIRF4medicine.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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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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MLL-Rearranged Leukemia Is Dependent on Aberrant H3K79 Methylation by DOT1L

2011

SummaryThe histone 3 lysine 79 (H3K79) methyltransferase Dot1l has been implicated in the development of leukemias bearing translocations of the Mixed Lineage Leukemia (MLL) gene. We identified the MLL-fusion targets in an MLL-AF9 leukemia model, and conducted epigenetic profiling for H3K79me2, H3K4me3, H3K27me3, and H3K36me3 in hematopoietic progenitor and leukemia stem cells (LSCs). We found abnormal profiles only for H3K79me2 on MLL-AF9 fusion target loci in LSCs. Inactivation of Dot1l led to downregulation of direct MLL-AF9 targets and an MLL translocation-associated gene expression signature, whereas global gene expression remained largely unaffected. Suppression of MLL translocation-a…

Cancer ResearchOncogene Proteins FusionCellular differentiationApoptosisBiologyMethylationArticleHistonesMice03 medical and health sciences0302 clinical medicinehemic and lymphatic diseasesmedicineAnimalsHumansEpigeneticsMyeloid Ecotropic Viral Integration Site 1 ProteinneoplasmsMyeloid Progenitor Cells030304 developmental biologyGene RearrangementHomeodomain Proteins0303 health sciencesLysineMyelodysplastic syndromesCell CycleCell DifferentiationCell BiologyHistone-Lysine N-MethyltransferaseMethyltransferasesMethylationDOT1Lmedicine.diseaseMolecular biologyHematopoiesisNeoplasm Proteins3. Good healthLeukemiaCell Transformation NeoplasticOncologyGenetic Loci030220 oncology & carcinogenesisHistone methyltransferaseCancer researchH3K4me3Protein Processing Post-TranslationalMyeloid-Lymphoid Leukemia ProteinCancer Cell
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Mechanisms of tumor invasion: evidence from in vivo observations.

1985

The major mechanisms of tumor invasion in vivo are discussed in the present review. A special emphasis is placed on tumor dedifferentiation which has proved to be of paramount importance for the invasion process. Based on in vivo observations obtained from various human and animal tumors a concept for the mechanism of tumor invasion is proposed which mainly comprises the following basic events: the first and essential step in tumor invasion is the tumor dedifferentiation and dissociation at the invasion front. This apparently temporary and reversible process mobilizes the tumor cells out of the main tumor bulk and enables them to invade the host tissue by active locomotion. This mechanism i…

Cancer ResearchPathologymedicine.medical_specialtyCell divisionColonCellular differentiationBiologyHost tissueBasement MembraneExtracellular matrixIn vivoCell MovementmedicineAnimalsEdemaHumansNeoplasm InvasivenessProcess (anatomy)Cells CulturedDimethylhydrazinesCell DifferentiationMuscle SmoothCell biology12-DimethylhydrazineExtracellular MatrixNeoplasm ProteinsRatsOxygenInterstitial edemaIntercellular JunctionsOncologyColonic NeoplasmsAtrophyIntracellularCell DivisionPeptide HydrolasesCancer metastasis reviews
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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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