Search results for "Cell Division"

showing 10 items of 457 documents

Immunohistochemical evaluation of growth fractions in human breast cancers using monoclonal antibody Ki-67.

1991

We performed immunohistochemical analyses of 568 breast/cancer specimens using Ki-67, a monoclonal antibody specific for a nuclear antigen present in proliferating cells. The specimens were divided into three groups (I-III) according to the proportion of Ki-positive cells detected. These findings were compared with features of tumor extension as well as with certain prognostic variables. There was no detectable correlation between Ki-67 reactivity and either tumor size or node involvement. In contrast, a statistically significant correlation was found between Ki-67 reactivity and tumor grading, in that G-I tumors had small growth fractions, while a high proportion of G-III tumors exhibited …

Cancer ResearchPrognostic variablePathologymedicine.medical_specialtymedicine.drug_classMammary glandBreast NeoplasmsMonoclonal antibodyBreast cancerAntigenmedicineBiomarkers TumorHumansbiologyCancerAntibodies Monoclonalmedicine.diseasePrognosismedicine.anatomical_structureOncologyKi-67biology.proteinImmunohistochemistryFemaleCell DivisionFollow-Up StudiesBreast cancer research and treatment
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In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.

2003

In BCR-ABL-positive cells, the transcription factor STAT-5 is constitutively activated by tyrosine phosphorylation. STAT-5 activation results in upregulation of bcl-X(L) and increased resistance to induction of apoptosis. Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells. Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts. In contrast to JAK-2 and PI-3-kinase inhibition, exposure of K562 cells to imatinib mesylate resulted in obvious suppression of proliferation. R…

Cancer ResearchProgrammed cell deathBlotting WesternFusion Proteins bcr-ablDown-RegulationAntineoplastic AgentsApoptosisBiologyPiperazineschemistry.chemical_compoundDownregulation and upregulationhemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineIn Situ Nick-End LabelingSTAT5 Transcription FactorHumansEnzyme InhibitorsPhosphorylationCell growthCytarabineImatinibTyrosine phosphorylationDrug SynergismHematologyDNAU937 CellsProtein-Tyrosine KinasesMilk ProteinsPrecipitin TestsDNA-Binding ProteinsImatinib mesylatePyrimidinesOncologychemistryApoptosisCaspasesBenzamidesCancer researchImatinib MesylateTrans-ActivatorsTyrosinePoly(ADP-ribose) PolymerasesK562 CellsCell Divisionmedicine.drugK562 cellsSignal TransductionLeukemia
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Effects of interferon gamma on the proliferation and modulation of cell-surface structures of human ovarian carcinoma cell lines.

1993

Platinum-containing regimens are very effective in the primary treatment of ovarian cancer. However, upon subsequent treatment most tumors develop multidrug resistance. The clinical application of biological response modifiers like interferon gamma (IFN gamma) in advanced ovarian cancer is therefore of increasing interest. Permanent ovarian cancer cell lines are suitable for investigating the mode of action and the potential clinical effectiveness of such response modifiers. IFN gamma is known to modulate many cellular functions. In this study it was compared for its antiproliferative and antigen-modulatory activity on the expression of tumor-associated (CA-125, HMFG, CEA) and major histoco…

Cancer ResearchReceptor expressionCellInterferon-gammaAntigenEpidermal growth factorAntigens NeoplasmHLA AntigensMHC class ImedicineTumor Cells CulturedHumansAntigens Tumor-Associated CarbohydrateOvarian NeoplasmsMHC class IIbiologyCell growthCell MembraneGeneral Medicinemedicine.diseaseRecombinant ProteinsErbB ReceptorsGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyImmunologyAntigens Surfacebiology.proteinCancer researchFemaleOvarian cancerCell DivisionJournal of cancer research and clinical oncology
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Influence of interferon-alpha on cytokine expression by the bone marrow microenvironment--impact on treatment of myeloproliferative disorders.

1996

Myeloproliferative disorders (MPD) are characterized by several common clinical and biological features, although at the molecular level, each disease entity exhibits distinct abnormalities. IFN-alpha exerts beneficial therapeutic effects in chronic myelogenous leukemia, polycythemia vera and essential thrombocythemia, resulting in control of hematopoietic hyperplasia and, in a minority of patients, in induction of cytogenetic remission. The mechanism of action of IFN-alpha in MPD is poorly defined. Recently published in vitro findings suggest that IFN-alpha interacts with the regulation of hematopoiesis by multiple ways. Its antiproliferative activity is well known for more than a decade, …

Cancer ResearchStromal cellAlpha interferonBiologyPolycythemia veraMyeloproliferative DisordersBone Marrowhemic and lymphatic diseasesmedicineCell AdhesionHumansImmunologic FactorsProgenitor cellMyeloproliferative DisordersEssential thrombocythemiaInterferon-alphaHematologymedicine.diseaseHematopoietic Stem Cellsmedicine.anatomical_structureOncologyAdipose TissueGene Expression RegulationConnective TissueImmunologyCytokinesBone marrowCell DivisionChronic myelogenous leukemiaLeukemialymphoma
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Dendritic cells as mediators of tumor-induced tolerance in metastatic melanoma.

1997

Escape from immune surveillance is critical for tumor progression in metastatic melanoma. We assessed the function of melanoma-derived dendritic cells (DCs) in patients presenting simultaneously with responding (rM) or progressing (pM) melanoma metastases. These rare coincidences allowed us to compare syngeneically the function of tumor DCs. CD83+ DCs were purified freshly from large responding (rDCs) or progressing (pDCs) metastases following chemo-immunotherapy. rDCs were 5 times more potent inducers of allogeneic T-cell proliferation than the pDCs that were used as control. Phenotypic analysis showed a marked depression of CD86 expression on pDCs. Culture supernatants from pM showed prod…

Cancer ResearchT-LymphocytesImmune toleranceImmune systemAntigens CDAntigens NeoplasmAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansAntigen-presenting cellMelanomaCD86Membrane Glycoproteinsbusiness.industryMelanomaInterferon-alphahemic and immune systemsDendritic cellDendritic Cellsmedicine.diseaseInterleukin-10Neoplasm ProteinsTolerance inductionOncologyTumor progressionImmunologyCytokinesInterleukin-2Tumor EscapeB7-2 AntigenCisplatinbusinessCell DivisionInternational journal of cancer
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Involvement of protein kinase Cdelta in contact-dependent inhibition of growth in human and murine fibroblasts.

2001

There is evidence that protein kinase C delta (PKCdelta) is a tumor suppressor, although its physiological role has not been elucidated so far. Since important anti-proliferative signals are mediated by cell-cell contacts we studied whether PKCdelta is involved in contact-dependent inhibition of growth in human (FH109) and murine (NIH3T3) fibroblasts. Cell-cell contacts were imitated by the addition of glutardialdehyde-fixed cells to sparsely seeded fibroblasts. Downregulation of the PKC isoforms alpha, delta, epsilon, and mu after prolonged treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.1 microM) resulted in a significant release from contact-inhibition in FH109 cells. Bryosta…

Cancer ResearchTime FactorsBryostatin 1ImmunoprecipitationActive Transport Cell NucleusDown-RegulationBiologychemistry.chemical_compoundFixativesLactonesMiceDownregulation and upregulationGeneticsmedicineAnimalsHumansProtein IsoformsBenzopyransEnzyme InhibitorsFibroblastProtein kinase AMolecular BiologyProtein kinase CProtein Kinase CChemotaxisCell CycleAcetophenones3T3 CellsFibroblastsBryostatinsMolecular biologyBlotIsoenzymesProtein Kinase C-deltamedicine.anatomical_structurechemistryGlutaralTetradecanoylphorbol AcetateMacrolidesMitogensRottlerinCell DivisionProtein BindingOncogene
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Cell volume homeostatically controls the rDNA repeat copy number and rRNA synthesis rate in yeast

2021

[Abstract] The adjustment of transcription and translation rates to the changing needs of cells is of utmost importance for their fitness and survival. We have previously shown that the global transcription rate for RNA polymerase II in budding yeast Saccharomyces cerevisiae is regulated in relation to cell volume. Total mRNA concentration is constant with cell volume since global RNApol II-dependent nascent transcription rate (nTR) also keeps constant but mRNA stability increases with cell size. In this paper, we focus on the case of rRNA and RNA polymerase I. Contrarily to that found for RNA pol II, we detected that RNA polymerase I nTR increases proportionally to genome copies and cell s…

Cancer ResearchTranscription GeneticCellGene ExpressionRNA polymerase IIYeast and Fungal ModelsProtein SynthesisQH426-470HaploidyBiochemistryPolymerasesSirtuin 2Transcription (biology)RNA Polymerase IHomeostasisCell Cycle and Cell DivisionGenetics (clinical)Silent Information Regulator Proteins Saccharomyces cerevisiaebiologyTranscriptional ControlEukaryotaChemical SynthesisGenomicsCell biologyNucleic acidsmedicine.anatomical_structureExperimental Organism SystemsRibosomal RNARNA polymeraseCell ProcessesRNA Polymerase IIResearch ArticleCell biologyCellular structures and organellesSaccharomyces cerevisiae ProteinsBiosynthetic TechniquesSaccharomyces cerevisiaeSaccharomyces cerevisiaeResearch and Analysis MethodsDNA RibosomalSaccharomycesModel OrganismsCyclinsDNA-binding proteinsmedicineRNA polymerase IGeneticsGene RegulationNon-coding RNAMolecular BiologyEcology Evolution Behavior and SystematicsCell SizeMessenger RNACèl·lules eucariotesOrganismsFungiRNABiology and Life SciencesProteinsGenes rRNARibosomal RNAModels Theoreticalbiology.organism_classificationYeastGenòmicabiology.proteinAnimal StudiesRNARibosomes
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The aryl hydrocarbon receptor (AhR) in the regulation of cell–cell contact and tumor growth

2010

The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor, which is activated by a large group of environmental pollutants including polycyclic aromatic hydrocarbons, dioxins and planar polychlorinated biphenyls. Ligand binding leads to dimerization of the AhR with aryl hydrocarbon receptor nuclear translocator and transcriptional activation of several xenobiotic phase I and phase II metabolizing enzymes, such as cytochrome P4501A1 and glutathione- S -transferase, respectively. Since phase I enzymes convert inert carcinogens to active genotoxins, the AhR plays a key role in tumor initiation. Besides this classical route, the AhR mediates tumor promotion and recent evide…

Cancer Researchmedicine.medical_specialtyAryl hydrocarbon receptor nuclear translocatorReviewsTumor initiationCell Communicationmedicine.disease_causeInternal medicineNeoplasmsmedicineCell AdhesionHomeostasisHumansTranscription factorbiologyCell CycleCell MembraneContact inhibitionMembrane ProteinsEpithelial CellsGeneral MedicineAryl hydrocarbon receptorEndocrinologyReceptors Aryl HydrocarbonTumor progressionbiology.proteinCancer researchTumor promotionCarcinogenesisCell DivisionSignal Transduction
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Fetal calf serum and retinoic acid affect proliferation and terminal differentiation of a rat rhabdomyosarcoma cell line (BA-HAN-1C)

1989

We report on the establishment of a model for differentiation induction in sarcomas, using the clonal rhabdomyosarcoma cell line BA-HAN-1C. This rhabdomyosarcoma cell line is composed of morphologically undifferentiated mononuclear stem cells, some of which spontaneously fuse to form terminally differentiated multinuclear myotube-like giant cells. The deprivation of fetal calf serum (FCS) or the exposure to retinoic acid, respectively, resulted in a significant inhibition of proliferation (P less than 0.001) and a marked increase in cellular differentiation as shown by a significant increase in the number of myotube-like giant cells (P less than 0.001) and in the creatine kinase activity (P…

Cancer Researchmedicine.medical_specialtyCell divisionCellular differentiationRetinoic acidTretinoinBiologyCell Linechemistry.chemical_compoundTretinoinInternal medicineRhabdomyosarcomaTumor Cells CulturedmedicineAnimalsCell DifferentiationFetal BloodMolecular biologyRatsP19 cellEndocrinologyOncologychemistryGiant cellCell cultureCattleStem cellCell DivisionResearch Articlemedicine.drugBritish Journal of Cancer
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TCDD-dependent downregulation of gamma-catenin in rat liver epithelial cells (WB-F344).

2002

TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) is the most potent tumor promoter ever tested in rodents. Although it is known that most of the effects of TCDD are mediated by binding to the aryl hydrocarbon receptor (AHR), the mechanisms leading to tumor promotion still remain to be elucidated. Loss of contact-inhibition is a characteristic hallmark in tumorigenesis. In WB-F344 cells, TCDD induces a release from contact-inhibition manifested by a 2- to 3-fold increase in DNA-synthesis and the emergence of foci when TCDD (1 nM) is given to confluent cells. We focussed our interest on potential cell membrane proteins mediating contact-inhibition in WB-F344 cells, namely E-cadherin, alpha,- beta,-…

Cancer Researchmedicine.medical_specialtyPolychlorinated DibenzodioxinsTime FactorsOctoxynolBlotting WesternDetergentsDown-RegulationDownregulation and upregulationInternal medicinemedicineAnimalsFluorescent Antibody Technique IndirectCells Culturedbeta CateninConfluencybiologyReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsContact inhibitionEpithelial CellsDNAAryl hydrocarbon receptorActin cytoskeletonBlotting NorthernCadherinsCell biologyRatsCytoskeletal ProteinsEndocrinologyPhenotypeOncologyDesmoplakinsLiverMicroscopy FluorescenceCateninMutationbiology.proteinProteasome inhibitorCarcinogensTrans-ActivatorsTumor promotionEnvironmental Pollutantsgamma CateninCell Divisionalpha Cateninmedicine.drugInternational journal of cancer
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