Search results for "Gene Expression"

showing 10 items of 4085 documents

pap, reg I? andreg I? mRNAs are concomitantly up-regulated during human colorectal carcinogenesis

1999

We have established the phenotype of a colorectal tumor by partial sequencing of 2166 transcripts that were eventually arrayed on high-density filters. These filters were used for differential screening with mRNAs of colorectal cancer and normal adjacent mucosa to characterize genes whose expression is altered in colorectal carcinoma. Three genes encoding related proteins, PAP, reg Iα and reg Iβ, were over-expressed in cancer. Northern-blot analysis confirmed that their expression was very low in normal colonic epithelial cells, but elevated in 75% of tumors. Western blotting with specific antibodies to pap and reg Iα revealed in tumors a single band of the expected size (15–16 kDa), demons…

Cancer ResearchReporter genePathologymedicine.medical_specialtyCancerBiologymedicine.disease_causemedicine.diseaseMolecular biologyBlotOncologyGene expressionmedicineCarcinomaGene silencingImmunohistochemistryCarcinogenesisInternational Journal of Cancer
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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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MicroRNAs in colorectal cancer stem cells: new regulators of cancer stemness?

2012

Recently, the hypothesis that colorectal tumors originate from a subpopulation of cells called ‘cancer stem cells' (CSCs) or tumor-initiating cells, which exhibit stem-like features, has been confirmed experimentally in various human cancers. Several studies have confirmed the existence of colorectal CSCs (CRCSCs) and have demonstrated that this rare cell population can be isolated by the expression of specific cell surface biomarkers. MicroRNAs (miRNAs) are a class of small non-coding RNAs, which are crucial for post-transcriptional regulation of gene expression and participate in a wide variety of biological functions, including development, cell proliferation, differentiation, metabolism…

Cancer ResearchSettore MED/06 - Oncologia MedicaPopulationReviewBiologymedicine.disease_causeBioinformaticsCSCstemnessCancer stem cellmicroRNAmedicineeducationMolecular BiologyRegulation of gene expressioneducation.field_of_studyCRC; CSCs; microRNAs; stemnessmicroRNACancermedicine.diseaseEmbryonic stem cellmicroRNAsCRCCancer researchCSCsStem cellCarcinogenesisOncogenesis
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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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Abstract 3193: Development of a colon cancer model system reveals epithelial contribution to poor-prognosis gene signatures

2016

Abstract Background: Recent consensus on molecular classification categorizes colorectal cancer (CRC) into 4 robust subtypes: CMS1 (epithelial-MSI), CMS2 (epithelial-canonical), CMS3 (epithelial-metabolic) and CMS4 (mesenchymal)1. CMS4 is linked to poor cancer prognosis and characterized by mesenchymal and epithelial-to-mesenchymal transition (EMT) gene expression2,3. Recent attempts to deconvolute the transcriptome from CRC tumors have suggested that the mesenchymal gene expression results from a large stromal compartment and is not due to epithelial cells with EMT-like features4,5. This challenges the classic notion that tumor cells activate the EMT program to undergo trans-differentiatio…

Cancer ResearchStromal cellColorectal cancerMesenchymal stem cellCancerBiologymedicine.diseaseBioinformaticsPhenotypeTranscriptomeOncologyGene expressionmedicineCancer researchGeneCancer Research
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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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