Search results for " Regulation"

showing 10 items of 3187 documents

Human FOXP3 and cancer.

2010

FOXP3 is a transcription factor necessary and sufficient for induction of the immunosuppressive functions in regulatory T lymphocytes. Its expression was first considered as specific of this cell type, but FOXP3 can also be transiently expressed in T-cell antigen receptor-activated human nonregulatory T cells. Recent data indicate that FOXP3 is also expressed by some nonlymphoid cells, in which it can repress various oncogenes that are restored following FOXP3 deletion or mutation. This review summarizes major advances in (1) the understanding of Foxp3 functions in human regulatory T cells, (2) the prognostic significance of Foxp3-expressing T cells in human malignancies and (3) the signifi…

Cancer ResearchRegulatory T cellchemical and pharmacologic phenomenaBiologyT-Lymphocytes RegulatoryEpigenesis GeneticInterleukin 21AntigenNeoplasmsGeneticsmedicineCytotoxic T cellHumansGenes Tumor SuppressorIL-2 receptorMolecular BiologyZAP70FOXP3hemic and immune systemsForkhead Transcription FactorsNatural killer T cellPrognosismedicine.anatomical_structureGene Expression RegulationImmunologyCancer researchDNA DamageOncogene
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Regulon-Specific Control of Transcription Elongation across the Yeast Genome

2009

Transcription elongation by RNA polymerase II was often considered an invariant non-regulated process. However, genome-wide studies have shown that transcriptional pausing during elongation is a frequent phenomenon in tightly-regulated metazoan genes. Using a combination of ChIP-on-chip and genomic run-on approaches, we found that the proportion of transcriptionally active RNA polymerase II (active versus total) present throughout the yeast genome is characteristic of some functional gene classes, like those related to ribosomes and mitochondria. This proportion also responds to regulatory stimuli mediated by protein kinase A and, in relation to cytosolic ribosomal-protein genes, it is medi…

Cancer ResearchSaccharomyces cerevisiae Proteinslcsh:QH426-470Transcription GeneticComputational Biology/Transcriptional RegulationRNA polymerase IISaccharomyces cerevisiaeRegulonGenètica molecularSaccharomycesTranscripció genèticaTranscription (biology)GeneticsTranscriptional regulationMolecular BiologyRNA polymerase II holoenzymeGeneGenetics (clinical)Ecology Evolution Behavior and SystematicsGeneticsbiologyGenetics and Genomics/Functional GenomicsMolecular Biology/Transcription ElongationHigh Mobility Group ProteinsGenetics and Genomics/Gene ExpressionElongation factorDNA-Binding Proteinslcsh:GeneticsTAF4biology.proteinRNARNA Polymerase IITranscription factor II DGenome FungalTranscriptional Elongation FactorsBiochemistry/Transcription and TranslationResearch Article
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HIF-1 is involved in the negative regulation of AURKA expression in breast cancer cell lines under hypoxic conditions

2013

Numerous microarray-based gene expression studies performed on several types of solid tumors revealed significant changes in key genes involved in progression and regulation of the cell cycle, including AURKA that is known to be overexpressed in many types of human malignancies. Tumor hypoxia is associated with poor prognosis in several cancer types, including breast cancer (BC). Since hypoxia is a condition that influences the expression of many genes involved in tumorigenesis, proliferation, and cell cycle regulation, we performed a microarray-based gene expression analysis in order to identify differentially expressed genes in BC cell lines exposed to hypoxia. This analysis showed that h…

Cancer ResearchSettore MED/06 - Oncologia MedicaDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeAURKA Breast cancer Cell cycle HIF-1a HypoxiaCell Line TumorGene expressionTranscriptional regulationmedicineHumansPromoter Regions GeneticAurora Kinase ARegulation of gene expressionGene knockdownTumor hypoxiaCell cycleHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMolecular biologyCell HypoxiaGene Expression Regulation NeoplasticOncologyGene Knockdown TechniquesCancer researchFemalemedicine.symptomCarcinogenesisBreast Cancer Research and Treatment
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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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Molecular principles of cancer invasion and metastasis (Review)

2009

The main threat and the reason for most cancer deaths are not the primary neoplasias, but secondary tumors, the metastases. Drastic phenotypic and biochemical changes occur during the metamorphosis of a normal tissue cell into an invasive cancer cell. These alterations concern various areas such as growth factor signaling, cell-cell adhesion, gene expression, motility or cell shape. Cancer cells of epithelial origin can even shed their typical qualities and characteristics and adopt a mesenchymal-like phenotype. This is often referred to as an epithelial-mesenchymal transition. Various oncogenes, tumor suppressor genes and metastasis suppressor genes are known to affect the invasiveness and…

Cancer ResearchStromal cellBiologyModels BiologicalMetastasisCell MovementCancer stem cellNeoplasmsCell AdhesionmedicineHumansGenes Tumor SuppressorNeoplasm InvasivenessNeoplasm MetastasisCell ShapeCell ProliferationCancerSuicide geneAcquired immune systemmedicine.diseaseGene Expression Regulation NeoplasticMetastasis Suppressor GeneCell Transformation NeoplasticOncologyImmunologyCancer cellCancer researchCytokinesSignal TransductionInternational Journal of Oncology
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Interleukin-6 and the soluble interleukin-6 receptor induce stem cell factor and Flt-3L expression in vivo and in vitro.

2001

Abstract Objective We recently established transgenic animals expressing either interleukin-6 (IL-6) or the soluble IL-6 receptor (sIL-6R) alone, or both components, IL-6 and the sIL-6R, in the liver. This animal model demonstrated that the expression of IL-6 in combination with its sIL-6R led to extramedullary expansion of hematopoietic progenitor cells in the spleen and liver. Materials and Methods We studied other relevant hematopoietic cytokines involved in the IL-6/sIL-6R–induced stimulation of hematopoiesis. Results Using immunohistochemistry, we showed that cell-associated stem cell factor (SCF) and Flt-3L expression were upregulated in liver and spleen only in double transgenic mice…

Cancer ResearchStromal cellCD34Fluorescent Antibody TechniqueStem cell factorMice TransgenicMiceDownregulation and upregulationIn vivoGeneticsAnimalsHumansRNA MessengerReceptorInterleukin 6Molecular BiologyImmunosorbent TechniquesStem Cell FactorbiologyInterleukin-6Membrane ProteinsCell BiologyHematology3T3 CellsFibroblastsBlotting NorthernHematopoietic Stem CellsMolecular biologyImmunohistochemistryReceptors Interleukin-6HaematopoiesisGene Expression RegulationLiverSolubilityHematopoiesis Extramedullarybiology.proteinSpleenExperimental hematology
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Regulation of CD1d expression by murine tumor cells: escape from immunosurveillance or alternate target molecules?

2002

alpha beta+ TCR T cells recognize peptide fragments displayed by MHC-class I or -class II molecules. Recently, additional mechanisms of antigen recognition by T cells have been identified, including CD1-mediated presentation of nonpeptide antigens. Only a limited number of CD1 antigens is retained in the mouse, i.e., the group II CD1 antigens, which are split into CD1D1 and CD1d2. Several T cell subsets have been shown to interact with murine CD1 antigens, including NK cells or "natural T cells" with the invariant V alpha 14 J alpha 281 TCR chain. Even if TAP defects may prevent classical endogenous antigen presentation in tumor cell lines, antigen presentation via CD1 is still functional. …

Cancer ResearchT cellAntigen presentationCD1chemical and pharmacologic phenomenaBiologyNatural killer cellAntigens CD1Immunoenzyme TechniquesInterferon-gammaMiceNK-92Monitoring ImmunologicmedicineCytotoxic T cellAnimalsRNA MessengerAntigen-presenting cellCells CulturedDNA PrimersMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionAntibodies MonoclonalGranulocyte-Macrophage Colony-Stimulating Factorhemic and immune systemsNeoplasms ExperimentalCytotoxicity Tests ImmunologicFlow CytometryCell biologyGene Expression Regulation NeoplasticKiller Cells NaturalMice Inbred C57BLmedicine.anatomical_structureOncologyCD1DImmunologybiology.proteinCytokinesAntigens CD1dInternational journal of cancer
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Blockade of PD-L1 (B7-H1) augments human tumor-specific T cell responsesin vitro

2006

Human tumors frequently escape immune destruction, despite the presence of cytotoxic T cells (CTL) recognizing tumor-associated antigens (TAA). We have previously shown that programmed death ligand-1 (PD-L1), a recently identified ligand of the B7 superfamily, is expressed on murine tumors and can inhibit antitumor immune responses. To evaluate the clinical relevance of our animal model findings, we examined human tumors and tumor-specific T cells. We found PD-L1 to be constitutively expressed on human renal cell carcinoma (RCC) cell lines and upregulated on human melanoma cell lines upon exposure to interferon-gamma. Similarly, we found binding of anti-PD-L1 monoclonal antibody (mAb) on fr…

Cancer ResearchT cellAntineoplastic AgentsB7-H1 AntigenInterleukin 21Immune systemAntigenAntigens CDTumor Cells CulturedmedicineHumansCytotoxic T cellCTLA-4 AntigenIL-2 receptorAntigen-presenting cellCarcinoma Renal CellMelanomabusiness.industryAntibodies MonoclonalFlow CytometryAntigens DifferentiationImmunohistochemistryKidney NeoplasmsUp-RegulationGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyImmunologyB7-1 AntigenCancer researchbusinessB7-H1 AntigenT-Lymphocytes CytotoxicInternational Journal of Cancer
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Toll-like receptors: Expression and involvement in Multiple Myeloma

2010

Multiple Myeloma (MM) cells express and respond to a broad range of TLRs. Accumulating evidences suggest that TLRs act as double-edged sword in MM biology. Indeed, TLR9 or TLR3 ligands could enhance immunity against MM cells or directly induce cell apoptosis, whereas various TLR agonists could induce MM survival, proliferation, and immune escape. This review is focused on the heterogeneous expression and function of TLRs in MM and on the potential implication of TLR ligands of infectious or endogenous origin in MM emergence, resistance, or progression.

Cancer ResearchTLR9ApoptosisEndogenyHematologyBiologyLigandsmedicine.diseaseToll-Like Receptor 3Cell biologyGene Expression Regulation NeoplasticImmune systemOncologyApoptosisImmunityToll-Like Receptor 9TLR3medicineAnimalsHumansTumor EscapeMultiple MyelomaReceptorMultiple myelomaLeukemia Research
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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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