Search results for "script"

showing 10 items of 5143 documents

Whole-epigenome analysis in multiple myeloma reveals DNA hypermethylation of B cell-specific enhancers

2015

Abstract Analyzing the DNA methylome of multiple myeloma (MM), a plasma cell neoplasm, by whole-genome bisulfite sequencing and high-density arrays, we observed regional DNA hypermethylation embedded in extensive global hypomethylation. In contrast to the widely reported DNA hypermethylation of promoter-associated CpG islands (CGIs) in cancer, hypermethylated sites in MM as compared to normal plasma cells were located outside CpG islands and were unexpectedly associated with intronic enhancer regions active in normal B cells. Both RNA-seq and in vitro reporter assays indicated that enhancer hypermethylation is globally associated with downregulation of its host genes. ChIP-seq and DNAseI-se…

Cancer ResearchCellular differentiationCèl·lules BADNBisulfite sequencingImmunologyPlasma CellsDown-RegulationBiologyBiochemistryEpigenesis GeneticEpigènesiCell Line TumorGeneticsMielomatosiHumansEpigeneticsEnhancerPromoter Regions GeneticGeneMolecular BiologyGenetics (clinical)EpigenomicsB cellsGenome HumanResearchCell DifferentiationMethylationDNACell BiologyHematologyDNA NeoplasmPlasma cell neoplasmDNA MethylationMolecular biologyMyeloproliferative disordersGene Expression Regulation NeoplasticEnhancer Elements GeneticOncologyCpG siteDNA methylationNeoplastic Stem CellsCpG IslandsMultiple MyelomaEpigenesisTranscription FactorsGenome Research
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Dual regulation of SPI1/PU.1 transcription factor by heat shock factor 1 (HSF1) during macrophage differentiation of monocytes

2014

International audience; : In addition to their cytoprotective role in stressful conditions, heat shock proteins (HSPs) are involved in specific differentiation pathways, e.g. we have identified a role for HSP90 in macrophage differentiation of human peripheral blood monocytes exposed to Macrophage Colony-Stimulating Factor (M-CSF). Here, we show that deletion of the main transcription factor involved in heat shock gene regulation, heat shock factor 1 (HSF1), affects M-CSF-driven differentiation of mouse bone marrow cells. HSF1 transiently accumulates in the nucleus of human monocytes undergoing macrophage differentiation, including M-CSF-treated peripheral blood monocytes and phorbol ester-…

Cancer ResearchCellular differentiation[SDV]Life Sciences [q-bio][SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Mice0302 clinical medicineHeat Shock Transcription FactorsHSF1[SDV.BDD]Life Sciences [q-bio]/Development BiologyCells CulturedComputingMilieux_MISCELLANEOUSRegulation of gene expression0303 health sciencesMice Inbred BALB C[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematology[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]3. Good healthDNA-Binding ProteinsOncology030220 oncology & carcinogenesismonocytesProteasome Endopeptidase ComplexAntigens Differentiation MyelomonocyticReceptors Cell Surface[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesAntigens CDHeat shock proteinProto-Oncogene Proteinstranscription factorsAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyTranscription factor030304 developmental biologySPI1Macrophagesheat-shock proteinsfungi[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMolecular biologyHsp70Heat shock factorMice Inbred C57BLcell differentiationGene Expression RegulationTrans-Activators[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Functional impact and evolution of a novel human polymorphic inversion that disrupts a gene and creates a fusion transcript

2015

Despite many years of study into inversions, very little is known about their functional consequences, especially in humans. A common hypothesis is that the selective value of inversions stems in part from their effects on nearby genes, although evidence of this in natural populations is almost nonexistent. Here we present a global analysis of a new 415-kb polymorphic inversion that is among the longest ones found in humans and is the first with clear position effects. This inversion is located in chromosome 19 and has been generated by non-homologous end joining between blocks of transposable elements with low identity. PCR genotyping in 541 individuals from eight different human populatio…

Cancer ResearchDNA End-Joining Repairlcsh:QH426-470GenotypeChromosome inversionPopulationChromosome BreakpointsBiologyChromosome breakpointsGenoma humàPolymorphism Single NucleotideEvolution MolecularChromosome Breakpoints03 medical and health sciences0302 clinical medicinePolymorphism Single nucleotideChromosome 19DNA end-joining repairGeneticsTranscription factorsHumansAlleleeducationMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologyChromosomal inversionGeneticsGene expression regulation0303 health scienceseducation.field_of_studyGenètica de poblacionsHaplotypelcsh:GeneticsDNA transposable elementsGenetics PopulationGene Expression RegulationFusion transcriptChromosome InversionDNA Transposable ElementsChromosomes Human Pair 19030217 neurology & neurosurgeryResearch ArticleTranscription Factors
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Phosphorylation of the DNA repair protein APE/REF-1 by CKII affects redox regulation of AP-1

1999

The DNA repair protein apurinic endonuclease (APE/Ref-1) exerts several physiological functions such as cleavage of apurinic/apyrimidinic sites and redox regulation of the transcription factor AP-1, whose activation is part of the cellular response to DNA damaging treatments. Here we demonstrate that APE/Ref-1 is phosphorylated by casein kinase II (CKII). This was shown for both the recombinant APE/Ref-1 protein (Km=0.55 mM) and for APE/Ref-1 expressed in COS cells. Phosphorylation of APE/Ref-1 did not alter the repair activity of the enzyme, whereas it stimulated its redox capability towards AP-1, thus promoting DNA binding activity of AP-1. Inhibition of CKII mediated phosphorylation of A…

Cancer ResearchDNA RepairProto-Oncogene Proteins c-junDNA repairDNA damageCarbon-Oxygen LyasesCHO CellsProtein Serine-Threonine KinasesBiologyTransfectionSubstrate SpecificityCricetinaeDNA Repair ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsAnimalsHumansAP sitePhosphorylationCasein Kinase IIProtein kinase AMolecular BiologyMethyl MethanesulfonateCyclic AMP-Dependent Protein KinasesMolecular biologyDNA-(apurinic or apyrimidinic site) lyaseTranscription Factor AP-1COS CellsPhosphorylationCasein kinase 2Oxidation-ReductionDNA DamageHeLa CellsMutagensOncogene
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Expression of DNA repair proteins hMSH2, hMSH6, hMLH1,O6-methylguanine-DNA methyltransferase and N-methylpurine-DNA glycosylase in melanoma cells wit…

1999

Malignant melanoma is well known for its primary unresponsiveness to chemotherapy. The mechanisms conferring this intrinsic resistance are unclear. In this study, we investigated the role of genes involved in DNA repair in a panel of human melanoma cell variants exhibiting low and high levels of resistance to 4 commonly used drugs in melanoma treatment, i.e., vindesine, etoposide, fotemustine and cisplatin. We show that in melanoma cells exhibiting resistance to cisplatin, etoposide and vindesine, the nuclear content of each of the DNA mismatch repair (MMR) proteins hMLH1, hMSH2 and hMSH6 was reduced by 30–70%. A decreased expression level of up to 80% of mRNAs encoding hMLH1 and hMSH2 was …

Cancer ResearchDNA RepairTranscription GeneticVindesineDNA repairAntineoplastic AgentsBiologyNitrosourea CompoundsDNA GlycosylasesO(6)-Methylguanine-DNA MethyltransferaseOrganophosphorus CompoundsProto-Oncogene ProteinsmedicineHumansRNA MessengerPromoter Regions GeneticMelanomaN-Glycosyl HydrolasesneoplasmsEtoposideAdaptor Proteins Signal TransducingEtoposideCisplatinMelanomaNuclear Proteinsmedicine.diseaseMolecular biologyDrug Resistance Multipledigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinOncologyDNA glycosylaseFotemustineVindesineDNA mismatch repairCisplatinCarrier ProteinsMutL Protein Homolog 1medicine.drugInternational Journal of Cancer
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Spontaneous mutagenesis in Csb(m/m)Ogg1⁻(/)⁻ mice is attenuated by dietary resveratrol.

2010

Oxidative DNA modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are generated endogenously in apparently all living cells. The defect of the repair of 8-oxoG in Csb m/m Ogg1 ―/― mice results in elevated basal levels of these lesions and increased frequencies of spontaneous mutations, which initiate tumorigenesis in the liver if cell proliferation is stimulated. Here, we describe that the phytoalexin resveratrol, applied either for 7 days per gavage (100 mg/kg body wt) or for 3―9 months in the diet (0.04% ad libitum), reduces the endogenous oxidative DNA base damage in the livers of the Csb m/m Ogg1 ―/― mice by 20―30% (P < 0.01). A small but consistent effect is also observed in the wi…

Cancer ResearchDNA damageSOD1SOD2Gene ExpressionMice TransgenicBiologyResveratrolSuperoxide dismutasechemistry.chemical_compoundMiceStilbenesAnimalschemistry.chemical_classificationReverse Transcriptase Polymerase Chain ReactionGlutathione peroxidaseMutagenesisAntimutagenic AgentsGeneral MedicineMolecular biologyDietOxidative StressCell killingchemistryBiochemistryLiverMutagenesisResveratrolbiology.proteinDNA DamageCarcinogenesis
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STAT5 and STAT5 Inhibitors in Hematological Malignancies

2019

The JAK-STAT pathway is an important physiologic regulator of different cellular functions including proliferation, apoptosis, differentiation, and immunological responses. Out of six different STAT proteins, STAT5 plays its main role in hematopoiesis and constitutive STAT5 activation seems to be a key event in the pathogenesis of several hematological malignancies. This has led many researchers to develop compounds capable of inhibiting STAT5 activation or interfering with its functions. Several anti-STAT5 molecules have shown potent STAT5 inhibitory activity in vitro. However, compared to the large amount of clinical studies with JAK inhibitors that are currently widely used in the clini…

Cancer ResearchFLT3-ITDAntineoplastic Agents03 medical and health sciences0302 clinical medicineMyeloproliferative DisordersCancer stem cellSettore BIO/13 - Biologia Applicatahemic and lymphatic diseasesSTAT5 Transcription FactormedicineAnimalsHumansBCR-ABLSTAT5030304 developmental biologyPharmacology0303 health sciencesSTAT transcription factorbiologybusiness.industryfood and beveragesCancerHematopoietic stem cellMyeloid leukemiamedicine.diseaseSTAT5 inhibitorleukemia.Leukemiamedicine.anatomical_structureHematologic Neoplasms030220 oncology & carcinogenesisJak2V617Fbiology.proteinCancer researchSettore BIO/14 - FarmacologiaMolecular MedicinebusinessTyrosine kinase
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The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistan…

2013

The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules. Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells. Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells. Moreover, it showed a…

Cancer ResearchFusion Proteins bcr-ablApoptosisPiperazinesSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundhemic and lymphatic diseasesSTAT5 Transcription FactorCytotoxic T cellPharmacology (medical)Cyclin D1STAT5biologyDrug SynergismCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiaOncologyProto-Oncogene Proteins c-bcl-2BenzamidesImatinib MesylateGrowth inhibitionmedicine.drugbcl-X ProteinDown-RegulationAntineoplastic AgentsBone Marrow CellsResting Phase Cell CycleColony-Forming Units AssayBenzophenonesNecrosisCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansneoplasmsBenzofuransPharmacologyG1 PhaseImatinibBCR-ABL chronic myeloid leukemia imatinib resistance STAT5 tyrosine kinase inhibitorsmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGenes bcl-1Genes bcl-2PyrimidineschemistryApoptosisDrug Resistance NeoplasmSettore BIO/14 - FarmacologiaCancer researchbiology.proteinK562 CellsK562 cells
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Transcriptomic responses generated by hepatocarcinogens in a battery of liver-based in vitro models

2013

As the conventional approach to assess the potential of a chemical to cause cancer in humans still includes the 2-year rodent carcinogenicity bioassay, development of alternative methodologies is needed. In the present study, the transcriptomics responses following exposure to genotoxic (GTX) and non-genotoxic (NGTX) hepatocarcinogens and non-carcinogens (NC) in five liver-based in vitro models, namely conventional and epigenetically stabilized cultures of primary rat hepatocytes, the human hepatoma-derived cell lines HepaRG and HepG2 and human embryonic stem cell-derived hepatocyte-like cells, are examined. For full characterization of the systems, several bioinformatics approaches are emp…

Cancer ResearchGene Expressiongene expression profilingComputational biologyBiologyPharmacologyTranscriptomeRats Sprague-Dawley03 medical and health sciences0302 clinical medicineCell Line TumorBioassayAnimalsHumansGeneCarcinogenEmbryonic Stem Cells030304 developmental biology0303 health sciencesGene Expression ProfilingLiver Neoplasmspathwaysbased analysis liver-based in vitro modelGeneral MedicineHep G2 CellsEmbryonic stem cellIn vitro3. Good healthRatsgenotoxic carcinogens non-genotoxic carcinogensGene expression profilingLiverCell culture030220 oncology & carcinogenesisCarcinogensHepatocytesTumor Suppressor Protein p53TranscriptomeMutagens
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Efficacy of BET Bromodomain Inhibition in Kras-Mutant Non–Small Cell Lung Cancer

2013

Abstract Purpose: Amplification of MYC is one of the most common genetic alterations in lung cancer, contributing to a myriad of phenotypes associated with growth, invasion, and drug resistance. Murine genetics has established both the centrality of somatic alterations of Kras in lung cancer, as well as the dependency of mutant Kras tumors on MYC function. Unfortunately, drug-like small-molecule inhibitors of KRAS and MYC have yet to be realized. The recent discovery, in hematologic malignancies, that bromodomain and extra-terminal (BET) bromodomain inhibition impairs MYC expression and MYC transcriptional function established the rationale of targeting KRAS-driven non–small cell lung cance…

Cancer ResearchLKB1Lung NeoplasmsMutantApoptosisMYCAMP-Activated Protein KinasesProtein Serine-Threonine KinasesBiologyNSCLCmedicine.disease_causeArticleProto-Oncogene Proteins c-mycProto-Oncogene Proteins p21(ras)MiceRNA interferenceCarcinoma Non-Small-Cell LungCell Line TumorKRASmedicineAnimalsRNA Small InterferingLung cancerneoplasmsCell ProliferationMice KnockoutGene knockdownCell growthNuclear ProteinsCancerAzepinesTriazolesBETmedicine.diseaseMolecular biologydigestive system diseasesrespiratory tract diseasesBromodomainOncologyCancer researchRNA InterferenceKRASSignal TransductionTranscription FactorsClinical Cancer Research
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