Search results for "Cell Differentiation"

showing 10 items of 907 documents

Interclonal heterogeneity in a human epithelioid-sarcoma cell line (Gru-1)

1994

Three clonal sub-populations, GRU-IA, GRU-IB, and GRU-IC, isolated from the human epithelioid sarcoma cell line GRU-I, were characterized morphologically, cytogenetically and with regard to proliferation kinetics. Immunocytochemically, major differences became evident in the expression of cytokeratin 18 and neurofilament proteins, which are indicative for epithelial and neural differentiation respectively. Vimentin, a mesenchymal differentiation marker, however, could be detected in all tumor cells of each sub-population. Laminin, a major compound of basement membranes, formed abundant intercellular network-like patterns in GRU-IB and GRU-IC, whereas GRU-IA was characterized by a diffuse in…

Cancer ResearchPathologymedicine.medical_specialtyEpithelioid sarcomaMice NudeVimentinBiologyGenetic HeterogeneityMiceCytokeratinNeurofilament ProteinsLamininTumor Cells CulturedmedicineAnimalsHumansVimentinSecretionMembrane GlycoproteinsMucin-1MucinsCell DifferentiationSarcomaDNA NeoplasmAneuploidyFlow Cytometrymedicine.diseaseMolecular biologyClone CellsGene Expression Regulation NeoplasticOncologyCell culturebiology.proteinKeratinsNeural differentiationLamininCell DivisionIntracellularInternational Journal of Cancer
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Mesenchymal stromal-cell transplants induce oligodendrocyte progenitor migration and remyelination in a chronic demyelination model.

2013

Demyelinating disorders such as leukodystrophies and multiple sclerosis are neurodegenerative diseases characterized by the progressive loss of myelin that may lead toward a chronic demyelination of the brain’s white matter, impairing normal axonal conduction velocity and ultimately causing neurodegeneration. Current treatments modifying the pathological mechanisms are capable of ameliorating the disease; however, frequently, these therapies are not sufficient to repress the progressive demyelination into a chronic condition and permanent loss of function. To this end, we analyzed the effect that bone marrow-derived mesenchymal stromal cell (BM-MSC) grafts exert in a chronically demyelinate…

Cancer ResearchPathologymedicine.medical_specialtyNeurogenesisImmunologyNeural ConductionBiologyMesenchymal Stem Cell TransplantationModels Biologicaltrophic releaseCuprizoneMiceCellular and Molecular NeuroscienceMyelinNerve FibersCell MovementmedicineSubependymal zoneAnimalsNerve Growth FactorsStem Cell NicheProgenitor cellRemyelinationMyelin Sheathdemyelinating mouse modelMultiple sclerosisMesenchymal stem cellCell DifferentiationMesenchymal Stem CellsCell Biologymedicine.diseaseAxonsOligodendrocyteTransplantationDisease Models AnimalOligodendrogliaremyelinationmedicine.anatomical_structureChronic DiseaseDentate GyrusImmunologyoligodendrocyte activationOriginal Articlemesenchymal stromal cellsGenèticaDemyelinating Diseases
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PDGFRβ and FGFR2 mediate endothelial cell differentiation capability of triple negative breast carcinoma cells

2014

Triple negative breast cancer (TNBC) is a very aggressive subgroup of breast carcinoma, still lacking specific markers for an effective targeted therapy and with a poorer prognosis compared to other breast cancer subtypes. In this study we investigated the possibility that TNBC cells contribute to the establishment of tumor vascular network by the process known as vasculogenic mimicry, through endothelial cell differentiation. Vascular-like functional properties of breast cancer cell lines were investigated in vitro by tube formation assay and in vivo by confocal microscopy, immunofluorescence or immunohistochemistry on frozen tumor sections. TNBCs express endothelial markers and acquire th…

Cancer ResearchPathologymedicine.medical_specialtyPDGFRmedicine.medical_treatmentTriple Negative Breast NeoplasmsMice SCIDBiologyEndothelial cell differentiationTargeted therapyReceptor Platelet-Derived Growth Factor betachemistry.chemical_compoundBreast cancerCell Line TumorGeneticsmedicineAnimalsHumansVasculogenic mimicryBreastRNA Small InterferingReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesTriple-negative breast cancerResearch ArticlesNeovascularization PathologicFGFREndothelial CellsCell DifferentiationGeneral MedicineTriple Negative Breast Neoplasmsmedicine.diseaseImmunohistochemistryVascular endothelial growth factorOncologychemistryVasculogenic mimicryCancer researchMolecular MedicineTNBC; Vasculogenic mimicry; PDGFR; FGFRTriple-Negative Breast CarcinomaFemaleRNA InterferenceTNBC
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The expression of HSP60 and HSP10 in large bowel carcinomas with lymph node metastase

2005

Abstract Background The involvement of Heat Shock Proteins (HSP) in cancer development and progression is a widely debated topic. The objective of the present study was to evaluate the presence and expression of HSP60 and HSP10 in a series of large bowel carcinomas and locoregional lymph nodes with and without metastases. Methods 82 Astler and Coller's stage C2 colorectal cancers, of which 48 well-differentiated and 34 poorly-differentiated, were selected along with 661 lymph nodes, including 372 with metastases and 289 with reactive hyperplasia only, from the same tumours. Primitive tumours and both metastatic and reactive lymph nodes were studied; specifically, three different compartment…

Cancer ResearchPathologymedicine.medical_specialtyTime FactorsColonColorectal cancerBlotting Westernlcsh:RC254-282Surgical oncologyIntestinal NeoplasmsBiomarkers TumorChaperonin 10GeneticsmedicineCarcinomaHumansIntestine LargeNeoplasm MetastasisStage (cooking)Lymph nodeInflammationAnalysis of VarianceHyperplasiabusiness.industryCarcinomaCell DifferentiationChaperonin 60Hyperplasialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseImmunohistochemistryGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyLymphatic MetastasisDisease ProgressionImmunohistochemistryhspLymph NodesLymphbusinessResearch ArticleBMC Cancer
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The effect of 3-aminobenzamide, inhibitor of poly(ADP-ribose) polymerase, on human osteosarcoma cells

2003

This study demonstrates that in human osteosarcoma cells treatment with 3-aminobenzamide (3-AB), a potent inhibitor of poly(ADP-ribose) polymerase (PARP), induces morphological and biochemical features of differentiation, the duration of which depends on whether or not the normal RB gene is expressed. In Saos-2 cells expressing a non-functional Rb protein, 3-AB treatment induced the formation of transient, short dendritic-like protrusions. In RB-transfected-Saos-2 cells (a clone previously generated in our laboratory that shows stable expression of wild-type Rb protein), 3-AB induced marked and prolonged changes with the formation of long dendritic-like protrusions and the appearance of ste…

Cancer ResearchProgrammed cell deathCell typeTime FactorsTranscription GeneticCell SurvivalPoly ADP ribose polymeraseCellular differentiationBlotting WesternApoptosisDNA FragmentationPoly(ADP-ribose) Polymerase InhibitorsBiologyTransfectionPolymerase Chain ReactionRetinoblastoma Proteinchemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsHumansMicroscopy Phase-ContrastRNA MessengerEnzyme Inhibitorsbcl-2-Associated X ProteinOsteosarcomaLamin Type BCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationDendritesCell cycleAlkaline PhosphataseFlow CytometryMolecular biologyChromatinHyaluronan ReceptorsProto-Oncogene Proteins c-bcl-2OncologychemistryApoptosis3-AminobenzamideCaspasesBenzamides3-aminobenzamide osteosarcoma cells PARP activityAlkaline phosphataseInternational Journal of Oncology
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Targeting apoptosis proteins in hematological malignancies

2010

The apoptotic machinery plays a key role in hematopoietic cell homeostasis. Terminally differentiated cells are eliminated, at least in part, by apoptosis, whereas part of the apoptotic machinery, including one or several caspases, is required to go through very specific steps of the differentiation pathways. A number of hematological diseases involve a deregulation of this machinery, which in most cases is a decrease in cell sensitivity to pro-apoptotic signals through over-expression of anti-apoptotic molecules. In some situations however, e.g. in the erythroid lineage of low grade myelodysplastic syndromes, cell sensitivity to apoptosis is increased in a death receptor-dependent manner a…

Cancer ResearchProgrammed cell deathFas Ligand ProteinMyeloidCellular differentiationAmino Acid MotifsAntineoplastic AgentsApoptosisLigandsInhibitor of apoptosisTNF-Related Apoptosis-Inducing LigandCell Line TumormedicineHumansReceptorCaspasebiologyIntrinsic apoptosisCell DifferentiationCell biologyGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyApoptosisHematologic Neoplasmsbiology.proteinDrug Screening Assays AntitumorApoptosis Regulatory ProteinsSignal TransductionCancer Letters
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Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

2008

Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required. We observed that galangin, a non-toxic, naturally occurring flavonoid was effective as anti-proliferative, and apoptotic agent in Bcr-Abl expressing K562 and KCL22 cells and in imatinib mesylate resistant K562-R and KCL22-R cells. Galangin induced an arrest of cells in G0–G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells. Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activi…

Cancer ResearchSettore MED/17 - Malattie InfettiveSettore MED/06 - Oncologia MedicaApoptosisPharmacologyResting Phase Cell CyclePiperazineschemistry.chemical_compoundCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansCytotoxic T cellChrysinneoplasmsFlavonoidsLeukemiaG1 PhaseApoptosiCell DifferentiationImatinibmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGalanginLeukemiaPyrimidinesImatinib mesylateOncologychemistryDrug Resistance NeoplasmImatinibBenzamidesSettore BIO/14 - FarmacologiaImatinib MesylateK562 CellsFisetinBcr-AblK562 cellsmedicine.drugCancer Letters
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Paraoxonase-2 alters hematopoietic stem cell differentiation through redox signalling

2017

Cancer ResearchSignallingHematopoietic stem cell differentiationChemistryGeneticsParaoxonase-2Cell BiologyHematologyMolecular BiologyRedoxCell biologyExperimental Hematology
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Bovine seminal ribonuclease is cytotoxic for both malignant and normal telomerase-positive cells

2005

Bovine seminal-ribonuclease (BS-RNase) is a member of the 'ribonucleases with special biological actions' family since it possesses specific anti-tumour, anti-spermatogenic and embryotoxic activities and exerts an immunosuppressive effect on T lymphocytes. In previous studies it was demonstrated that BS-RNase induced apoptosis in proliferating, malignant and normal cells and that telomerase activity loss also caused apoptotic death in neoplastic cells. Since an obvious relationship between cell proliferation and telomerase activity exists, the aim of this work was to study if the pro-apoptotic cytotoxic action exerted by BS-RNase on proliferating malignant cells (HT29) and proliferating nor…

Cancer ResearchTelomeraseTime FactorsT-LymphocytesCellular differentiationCytotoxicityBlotting WesternDown-RegulationTetrazolium SaltsAntineoplastic AgentsApoptosisEnzyme-Linked Immunosorbent AssayBiologyHT29 CellsCell Line TumorEndoribonucleasesAnimalsHumansCytotoxic T cellTelomerase reverse transcriptaseLymphocytesRNA MessengerTelomeraseBovine seminal-ribonuclease; Cytotoxicity; HTR; Nucleolar localization; TelomeraseCell ProliferationReverse Transcriptase Polymerase Chain ReactionCell growthCell DifferentiationCell cycleNucleolar localizationMolecular biologyThiazolesBovine seminal-ribonucleaseMicroscopy FluorescenceOncologyCell cultureLeukocytes MononuclearMicroscopy Electron ScanningRNACattleHTRCell NucleolusImmunosuppressive Agents
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Bmi1 and Cell of Origin Determinants of Brain Tumor Phenotype

2007

Glioblastomas frequently express oncogenic EGFR and loss of the Ink4a/Arf locus. Bmi1, a positive regulator of stem cell self renewal, may be critical to drive brain tumor growth. In this issue of Cancer Cell, Bruggeman and colleagues suggest that brain tumors with these molecular alterations can be initiated in both neural precursor and differentiated cell compartments in the absence of Bmi1; however, tumorigenicity is reduced, and tumors contain fewer precursor cells. Surprisingly, tumors appear less malignant when initiated in precursor cells. Bmi1-deficient tumors also had fewer neuronal lineage cells, suggesting a role for Bmi1 in determination of cell lineage and tumor phenotype.

Cancer ResearchTime FactorsCell of originCellular differentiationBrain tumormacromolecular substancesBiologyMiceProto-Oncogene ProteinsPrecursor cellmedicineAnimalsHumansCyclin-Dependent Kinase Inhibitor p16Cell ProliferationNeoplasm StagingMice KnockoutNeuronsPolycomb Repressive Complex 1Brain NeoplasmsCell growthStem CellsNuclear ProteinsCell DifferentiationNeoplasms ExperimentalCell Biologymedicine.diseaseStem Cell Self-RenewalErbB ReceptorsGene Expression Regulation NeoplasticRepressor ProteinsCell Transformation NeoplasticPhenotypeOncologyBMI1AstrocytesMutationCancer cellCancer researchGlioblastomaSignal TransductionCancer Cell
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