Search results for "Prom"

showing 10 items of 2286 documents

The Compass-like Locus, Exclusive to the Ambulacrarians, Encodes a Chromatin Insulator Binding Protein in the Sea Urchin Embryo

2013

Chromatin insulators are eukaryotic genome elements that upon binding of specific proteins display barrier and/or enhancer-blocking activity. Although several insulators have been described throughout various metazoans, much less is known about proteins that mediate their functions. This article deals with the identification and functional characterization in Paracentrotus lividus of COMPASS-like (CMPl), a novel echinoderm insulator binding protein. Phylogenetic analysis shows that the CMPl factor, encoded by the alternative spliced Cmp/Cmpl transcript, is the founder of a novel ambulacrarian-specific family of Homeodomain proteins containing the Compass domain. Specific association of CMPl…

Cancer ResearchEmbryo Nonmammalianchromatin insulators genome evolution alternative splicing sea urchin embryolcsh:QH426-470RepressorSettore BIO/11 - Biologia MolecolareRegulatory Sequences Nucleic AcidHistonesGene clusterGeneticsAnimalsPromoter Regions GeneticEnhancerMolecular BiologyPhylogenyGenetics (clinical)Ecology Evolution Behavior and SystematicsGeneticsMessenger RNAbiologyBinding proteinGene Expression Regulation DevelopmentalFusion proteinChromatinNucleosomesChromatinlcsh:GeneticsEnhancer Elements GeneticNucleoproteinsHistoneSea UrchinsParacentrotusbiology.proteinInsulator ElementsCarrier ProteinsResearch ArticleProtein BindingPLoS Genetics
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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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Acquired resistance of melanoma cells to the antineoplastic agent fotemustine is caused by reactivation of the DNA repair gene mgmt

2001

Acquired resistance to antineoplastic agents is a frequent obstacle in tumor therapy. Malignant melanoma cells are particularly well known for their unresponsiveness to chemotherapy; only about 30% of tumors exhibit a transient clinical response to treatment. In our study, we investigated the molecular mechanism of acquired resistance of melanoma cells (MeWo) to the chloroethylating drug fotemustine. Determination of O6-methylguanine-DNA methyltransferase (MGMT) activity showed that MeWo cells that acquired resistance to fotemustine upon repeated treatment with the drug display high MGMT activity, whereas the parental cell line had no detectable MGMT. The resistant cell lines exhibit cross-…

Cancer ResearchGuanineMethyltransferaseDNA RepairDNA repairmedicine.medical_treatmentGene ExpressionAntineoplastic AgentsDrug resistanceBiologyNitrosourea CompoundsO(6)-Methylguanine-DNA MethyltransferaseEnzyme ReactivatorsOrganophosphorus CompoundsTumor Cells CulturedmedicineHumansEnzyme InhibitorsPromoter Regions GeneticMelanomaneoplasmsChemotherapyMelanomaGene AmplificationDNA Methylationmedicine.diseaseVirologydigestive system diseasesEnzyme ActivationBlotting SouthernOncologyDrug Resistance NeoplasmDNA methylationAzacitidineCancer researchFotemustinemedicine.drugAlkyltransferaseInternational Journal of Cancer
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Stochastic Loss of Silencing of the Imprinted Ndn/NDN Allele, in a Mouse Model and Humans with Prader-Willi Syndrome, Has Functional Consequences

2013

Genomic imprinting is a process that causes genes to be expressed from one allele only according to parental origin, the other allele being silent. Diseases can arise when the normally active alleles are not expressed. In this context, low level of expression of the normally silent alleles has been considered as genetic noise although such expression has never been further studied. Prader-Willi Syndrome (PWS) is a neurodevelopmental disease involving imprinted genes, including NDN, which are only expressed from the paternally inherited allele, with the maternally inherited allele silent. We present the first in-depth study of the low expression of a normally silent imprinted allele, in path…

Cancer ResearchHeterozygotelcsh:QH426-470Apnea[SDV]Life Sciences [q-bio]Nerve Tissue ProteinsBiologyEpigenesis Genetic03 medical and health sciencesGenomic ImprintingMice0302 clinical medicineGeneticsAnimalsHumansEpigeneticsAlleleImprinting (psychology)Promoter Regions GeneticMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and SystematicsAlleles030304 developmental biologyGeneticsMice Knockout0303 health sciencesBrainNuclear ProteinsPhenotypeAllelic exclusionDisease Models Animallcsh:GeneticsGene Expression RegulationDNA methylationGenomic imprintingPrader-Willi Syndrome030217 neurology & neurosurgeryResearch Article
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The BCL6 gene in B-cell lymphomas with 3q27 translocations is expressed mainly from the rearranged allele irrespective of the partner gene

2003

The BCL6 gene, which functions as a transcription repressor, is the target of multiple chromosomal translocations in non-Hodgkin's lymphomas (NHL). These translocations occur in the nontranslated region of the BCL6 gene, juxtaposing regulatory sequences of the diverse partner genes to the open reading frame of the BCL6 gene and thus are thought to deregulate BCL6 gene expression. The levels of expression of the BCL6 gene and protein have been demonstrated to predict the clinical outcome of diffuse large B-cell lymphomas. By contrast, the prognostic significance of BCL6 gene translocations is unclear. In this study we have sought an explanation for this apparent discrepancy. We examined tumo…

Cancer ResearchLymphoma B-CellBiologyTranslocation Geneticimmune system diseasesProto-Oncogene Proteinshemic and lymphatic diseasesGene expressionTumor Cells CulturedHumansRNA MessengerAllelePromoter Regions GeneticGeneAllelesGene RearrangementGeneticsRegulation of gene expressionPromoterHematologyGene rearrangementBCL6Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsOncologyRegulatory sequenceMutationProto-Oncogene Proteins c-bcl-6Cancer researchChromosomes Human Pair 3Transcription FactorsLeukemia
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Negative transcriptional control of ERBB2 gene by MBP-1 and HDAC1: diagnostic implications in breast cancer

2013

Abstract Background The human ERBB2 gene is frequently amplified in breast tumors, and its high expression is associated with poor prognosis. We previously reported a significant inverse correlation between Myc promoter-binding protein-1 (MBP-1) and ERBB2 expression in primary breast invasive ductal carcinoma (IDC). MBP-1 is a transcriptional repressor of the c-MYC gene that acts by binding to the P2 promoter; only one other direct target of MBP-1, the COX2 gene, has been identified so far. Methods To gain new insights into the functional relationship linking MBP-1 and ERBB2 in breast cancer, we have investigated the effects of MBP-1 expression on endogenous ERBB2 transcript and protein lev…

Cancer ResearchMBP-1/EnolaseReceptor ErbB-2Breast NeoplasmsHistone Deacetylase 1BiologyERBB geneBreast cancerTranscriptional regulationTranscription (biology)Histone DeacetylaseBreast CancermedicineTranscriptional regulationBiomarkers TumorTumor Cells CulturedGeneticsHumansMBP-1ERBB2Promoter Regions Geneticskin and connective tissue diseasesGeneReporter geneCarcinoma Ductal BreastCancerTransfectionGenes erbB-2medicine.diseaseImmunohistochemistryHDAC1Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticSettore BIO/18 - GeneticaOncologyCancer researchChromatin immunoprecipitationResearch ArticleBMC Cancer
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Chimeric amplicons containing the c-myc gene in HL60 cells

1998

The major amplicon present in HL60 cells is chimeric in nature being composed of 70 kb of DNA sequence derived from the MYC locus linked to 80 kb of novel DNA sequence derived from a non contiguous region located telomeric to the c-myc gene at 8q24 (Feo et al., 1996). Here we show by fluorescence in situ hybridization (FISH) that these coamplified sequences, MCR (Myc Coamplified Region), are derived from a locus located 3-4 Mb telomeric to the c-myc gene in the q24.2-24.3 region of chromosome 8. Genomic cloning and Southern blot analysis indicate the arrangement of chimeric amplicons are in tandem arrays. Analysis of the DNA sequences at the juncture of the MYC locus and the MCR suggest tha…

Cancer ResearchOncogene Proteins FusionInverted repeatMolecular Sequence DataGenes mycHL-60 CellsLocus (genetics)BiologyMolecular cloningDNA sequencingLeukemia Promyelocytic AcuteGene mappingGeneticsHumansCloning MolecularMolecular BiologyGeneIn Situ Hybridization FluorescenceSouthern blotChromosome AberrationsRecombination GeneticGeneticsBase SequenceChromosome FragilityGene AmplificationSequence Analysis DNAAmpliconMolecular biologyBlotting SouthernChromosomes Human Pair 8Oncogene
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DNA repair protein MGMT protects against N-methyl-N-nitrosourea-induced conversion of benign into malignant tumors

2003

Tumor formation is a multi-step process that can be divided into the stages of tumor initiation, promotion and progression. Previously, we showed that overexpression in skin of mice of the DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) protects against N-methyl-N-nitrosourea (MNU)-induced tumor initiation without affecting tumor promotion. This indicated that O(6)-methylguanine, which is specifically repaired by MGMT, is a major tumor-initiating lesion. Here we extended this transgenic approach to the study of tumor progression. Benign papillomas that arose on the skin of CkMGMT transgenic mice upon initiation with 7,12-dimethylbenz[a]anthracene (DMBA) and promotion by 1…

Cancer ResearchPathologymedicine.medical_specialtySkin NeoplasmsMethyltransferaseDNA RepairDNA repairDMBAMice TransgenicTumor initiationBiologymedicine.disease_causeMiceO(6)-Methylguanine-DNA MethyltransferaseDNA Repair ProteinmedicineAnimalsneoplasmsPapillomaMethylnitrosoureaGeneral MedicineTumor progressionCarcinogensCancer researchTumor promotionCarcinogenesisCarcinogenesis
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Progressive multifocal encephalopathy in a patient with non-Hodgkin follicular lymphoma

2020

Progressive multifocal leukoencephalopathy (PML) is a rare and often fatal demyelinating disease of the central nervous system caused by John Cunningham virus (JCV). We present a case report of patient with non-Hodgkin follicular lymphoma, who developed PML after hematopoietic stem cell transplantation and rituximab-bendamustine therapy. JCV DNA was proven both in peripheral blood and cerebrospinal fluid. Patient with 4 years history of follicular lymphoma presented with progressing weakness in the right arm and leg and postural instability. Magnetic resonance imaging scans showed bilateral hyperintense lesions in the cerebellum and centrum semiovale consistent with findings in PML. JCV DNA…

Cancer ResearchPathologymedicine.medical_specialtyvirusesmedicine.medical_treatmentEncephalopathyFollicular lymphomaHematopoietic stem cell transplantationImmunocompromised HostCerebrospinal fluidAntineoplastic Combined Chemotherapy ProtocolsCentrum semiovalemedicineDemyelinating diseaseHumansLymphoma Follicularmedicine.diagnostic_testbusiness.industryProgressive multifocal leukoencephalopathyHematopoietic Stem Cell TransplantationLeukoencephalopathy Progressive MultifocalDisease ManagementMagnetic resonance imagingMiddle Agedmedicine.diseaseMagnetic Resonance ImagingTreatment OutcomeOncologyPositron-Emission TomographyFemaleTomography X-Ray ComputedbusinessExperimental Oncology
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Transforming Growth Factor-β–Mediated Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Expression and Apoptosis in Hepatoma Cells Requires Fun…

2008

Abstract Transforming growth factor-β (TGF-β) has been shown to induce apoptotic cell death in normal and transformed hepatocytes. We recently identified tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as an important mediator of TGF-β–induced apoptosis in hepatoma cells. In this study, we have further explored the mechanism by which TGF-β up-regulates TRAIL expression. The 5′-flanking region of the TRAIL gene was isolated and characterized. Deletion mutants of the 5′-untranslated region of the TRAIL gene revealed a region comprising nucleotides −1950 to −1100 responsible for TRAIL induction following treatment with TGF-β. Within this region, we have identified an activator …

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularMolecular Sequence DataApoptosisSmad ProteinsSMADBiologyTNF-Related Apoptosis-Inducing LigandTransforming Growth Factor betaCell Line TumorHumansGene SilencingPromoter Regions GeneticMolecular BiologySmad4 ProteinBase SequenceActivator (genetics)Liver NeoplasmsDNA NeoplasmTranscription Factor AP-1OncologyCell cultureApoptosisMutationCancer researchTumor necrosis factor alphaProtein BindingSignal TransductionTransforming growth factorFOSBMolecular Cancer Research
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