Search results for "oncogene"

showing 10 items of 1005 documents

Molecular mechanisms involved in the hormonal prevention of aging in the rat.

2008

Previous data from our group have provided support for the role of GH, melatonin and estrogens in the prevention of aging of several physiological parameters from bone, liver metabolism, vascular activity, the central nervous system (CNS), the immune system and the skin. In the present work data on the molecular mechanisms involved are presented. A total of 140 male and female rats have been submitted to different treatments over 10 weeks, between 22 and 24 months of age. Males have been treated with GH and melatonin. Females were divided in two groups: intact and castrated at 12 months of age. The first group was treated with GH and melatonin and the second with the two latter compounds an…

Central Nervous SystemMalemedicine.medical_specialtyAgingmedicine.drug_classEndocrinology Diabetes and MetabolismOvariectomyClinical BiochemistryMitochondria LiverBiologymedicine.disease_causeNitric OxideBiochemistryMelatoninchemistry.chemical_compoundEndocrinologyCytosolInternal medicineSkin Physiological PhenomenamedicineAnimalsRats WistarMolecular BiologyMelatoninchemistry.chemical_classificationEstradiolGlutathione peroxidaseDentate gyrusNeurogenesisCytochromes cEstrogensCell BiologyGlutathioneIsoflavonesRatsEndocrinologychemistryLiverProto-Oncogene Proteins c-bcl-2EstrogenApoptosisGrowth HormoneMolecular MedicineFemaleOxidative stressmedicine.drugThe Journal of steroid biochemistry and molecular biology
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Induction of identified mesodermal cells by CNS midline progenitors in Drosophila.

1997

ABSTRACT The Drosophila ventral midline cells generate a discrete set of CNS lineages, required for proper patterning of the ventral ectoderm. Here we provide the first evidence that the CNS midline cells also exert inductive effects on the mesoderm. Mesodermal progenitors adjacent to the midline progenitor cells give rise to ventral somatic mucles and a pair of unique cells that come to lie dorsomedially on top of the ventral nerve cord, the so-called DM cells. Cell ablation as well as cell transplantation experiments indicate that formation of the DM cells is induced by midline progenitors in the early embryo. These results are corroborated by genetic analyses. Mutant single minded embryo…

Central Nervous SystemMesodermanimal structuresSomatic cellCellEctodermNerve Tissue ProteinsBiologyMesodermCell MovementProto-Oncogene ProteinsmedicineMorphogenesisAnimalsDrosophila ProteinsProgenitor cellEye ProteinsMolecular BiologyEmbryonic InductionEpidermal Growth FactorCell growthGene Expression Regulation DevelopmentalMembrane ProteinsEmbryoAnatomyCell biologyDNA-Binding Proteinsmedicine.anatomical_structureDrosophila melanogasterVentral nerve cordembryonic structuresDevelopmental BiologySignal TransductionTranscription FactorsDevelopment (Cambridge, England)
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Exacerbated experimental autoimmune encephalomyelitis in mast-cell-deficient KitW-sh/W-sh mice

2011

Mast cell (MC)-deficient c-Kit mutant Kit(W/W-v) mice are protected against experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, suggesting a detrimental role for MCs in this disease. To further investigate the role of MCs in EAE, we took advantage of a recently characterized model of MC deficiency, Kit(W-sh/W-sh). Surprisingly, we observed that myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE was exacerbated in Kit(W-sh/W-sh) compared with Kit(+/+) mice. Kit(W-sh/W-sh) mice showed more inflammatory foci in the central nervous system (CNS) and increased T-cell response against myelin. To understand whether the discrepant results obtaine…

Central Nervous SystemT-LymphocytesEncephalomyelitisexperimental autoimmune encephalomyelitismast cellsInbred C57BLSeverity of Illness IndeximmunologyMiceMyelinPeptide Fragmentimmune system diseasesMast CellEncephalomyelitisMyelin SheathbiologyExperimental autoimmune encephalomyelitisMast cellProto-Oncogene Proteins c-kitPhenotypemedicine.anatomical_structuremastcell-deficient miceBone Marrow Cellgenetics/immunology/pathology/prevention /&/ controlc-kit mutationsc-kit mutations; experimental autoimmune encephalomyelitis; granulocytes; mast cellsEncephalomyelitis Autoimmune ExperimentalCentral nervous systemBone Marrow CellsPathology and Forensic MedicineMyelin oligodendrocyte glycoproteinExperimentalAnimals Antibody Formation Bone Marrow Cells; pathology Central Nervous System; pathology Encephalomyelitis; Autoimmune; Experimental; genetics/immunology/pathology/prevention /&/ control Glycoproteins; immunology Granulocytes; pathology Immunization Mast Cells; pathology Mice Mice; Inbred C57BL Mutation Myelin Sheath; immunology Myelin-Oligodendrocyte Glycoprotein Peptide Fragments; immunology Phenotype Proto-Oncogene Proteins c-kit; deficiency/genetics/metabolism Severity of Illness Index T-Lymphocytes; pathologyAntigendeficiency/genetics/metabolismmedicineAnimalsMolecular BiologyGlycoproteinsAnimalMultiple sclerosismast-cell-deficient Kit W-sh/W-sh mice.Experimental autoimmune encephalomyelitis; mast-cell-deficient Kit W-sh/W-sh mice.GranulocytegranulocytesCell Biologymedicine.diseaseEncephalomyelitiExperimental autoimmune encephalomyelitiPeptide FragmentsMice Inbred C57BLT-LymphocyteAntibody FormationMutationImmunologybiology.proteinexperimental autoimmune encephalomyelitis; mastcell-deficient mice; mast cellspathologyImmunizationMyelin-Oligodendrocyte GlycoproteinGlycoproteinAutoimmuneLaboratory Investigation
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Successive specification ofDrosophilaneuroblasts NB 6-4 and NB 7-3 depends on interaction of the segment polarity geneswingless,gooseberryandnaked cu…

2001

The Drosophila central nervous system derives from neural precursor cells, the neuroblasts (NBs), which are born from the neuroectoderm by the process of delamination. Each NB has a unique identity, which is revealed by the production of a characteristic cell lineage and a specific set of molecular markers it expresses. These NBs delaminate at different but reproducible time points during neurogenesis (S1-S5) and it has been shown for early delaminating NBs (S1/S2) that their identities depend on positional information conferred by segment polarity genes and dorsoventral patterning genes. We have studied mechanisms leading to the fate specification of a set of late delaminating neuroblasts,…

Central Nervous SystemTime FactorsCellular differentiationWnt1 ProteinBiologyCell fate determinationNeuroblastProto-Oncogene ProteinsAnimalsDrosophila ProteinsHedgehog ProteinsMolecular BiologyBody PatterningHomeodomain ProteinsNeuronsGeneticsNeuroectodermStem CellsNeurogenesisNuclear ProteinsCell DifferentiationengrailedCell biologyDNA-Binding ProteinsNaked cuticleDrosophila melanogasterSegment polarity geneembryonic structuresTrans-ActivatorsInsect ProteinsTranscription FactorsDevelopmental BiologyDevelopment
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Anandamide-induced apoptosis in Chang liver cells involves ceramide and JNK/AP-1 pathway

2006

In the present study we demonstrate that anandamide, the most important endogenous cannabinoid, markedly induced apoptosis in Chang liver cells, an immortalized non-tumor cell line derived from normal liver tissue, while it induced only modest effects in a number of hepatoma cell lines. The apoptotic effect was reduced by methyl-beta-cyclodextrin, a membrane cholesterol depletor, suggesting an interaction between anandamide and the membrane microdomains named lipid rafts. Anandamide effects were mediated by the production of ceramide, as demonstrated by experiments performed with the sphingomyelinase inhibitor, desipramine, or with the sphingomyelinase activator, melittin. This conclusion w…

CeramideProgrammed cell deathFas Ligand ProteinCell SurvivalPolyunsaturated AlkamidesLiver cytologyp38 mitogen-activated protein kinasesBlotting WesternApoptosisArachidonic AcidsBiologyCeramidesCell LineMembrane Potentialschemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsGeneticsHumansEnzyme InhibitorsMembrane GlycoproteinsBcl-2-Like Protein 11Dose-Response Relationship DrugDesipramineJNK Mitogen-Activated Protein KinasesMembrane ProteinsFree Radical ScavengersGeneral MedicineAnandamideEndocannabinoid systemAcetylcysteineCell biologyEnzyme ActivationTranscription Factor AP-1cannabinoids apoptosis tumor cells JNK/AP1LiverchemistryApoptosisCaspasesMitochondrial MembranesTumor Necrosis FactorsApoptosis Regulatory ProteinsSphingomyelinEndocannabinoidsSignal TransductionInternational Journal of Molecular Medicine
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Generation of a DNA microarray for determination of E6 natural variants of human papillomavirus type 16.

2003

Infection with high-risk types of human papillomavirus (HPV) is necessary for the development of cervical cancer. However, the majority of the HPV infections are efficiently cleared by the immune system and only a minority persist and induce the development of malignant lesions. Several studies provided evidence that intratype genetic variations are implicated in determining the clinical outcome of HPV infections. In this study, we describe a DNA chip based on arrayed primer extension (APEX) for the analysis of the natural variants of HPV16, the most frequently detected type in cervical cancer world-wide. We show that HPV16 E6 variants are detected efficiently by APEX. In addition, APEX is …

Cervical cancerGeneticsMicroarrayvirus diseasesGenetic VariationOncogene Proteins ViralBiologymedicine.diseaseGenomefemale genital diseases and pregnancy complicationsDNA sequencingPrimer extensionVirusRepressor ProteinsVirologyGenetic variationDNA ViralmedicineHumansFemaleDNA microarrayOligonucleotide Array Sequence AnalysisJournal of virological methods
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Liquid Biopsy in Cancer Patients: The Hand Lens to Investigate Tumor Evolution

2017

In recent years the treatment of cancer patients has profoundly changed due to a better comprehension of the biological processes underlying tumor development and progression. Several tumors are defined as “oncogene addicted” and this discovery has led the way to the development of target therapies that are able to specifically kill cancer cells sparing normal cells from toxicity. Nowadays treatment decision is strictly dependent on the molecular characterization of the tumor; thus the path of cancer patients’ survival is tissue dependent but this may have several limitations. Indeed a single tissue biopsy represents only a snapshot limited in time and space but we are learning that tumor e…

Change over timePathologymedicine.medical_specialtyOncogenebusiness.industryCancer cellMedicineTreatment decision makingTarget therapyLiquid biopsybusinessBioinformaticsTissue biopsy
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Genome-wide association analysis in primary sclerosing cholangitis identifies two non-HLA susceptibility loci

2011

Primary sclerosing cholangitis (PSC) is a chronic bile duct disease affecting 2.4-7.5% of individuals with inflammatory bowel disease. We performed a genome-wide association analysis of 2,466,182 SNPs in 715 individuals with PSC and 2,962 controls, followed by replication in 1,025 PSC cases and 2,174 controls. We detected non-HLA associations at rs3197999 in MST1 and rs6720394 near BCL2L11 (combined P = 1.1 x 10(-16) and P = 4.1 x 10(-8), respectively).

Cholangitis SclerosingPATHOGENESISSingle-nucleotide polymorphismGenome-wide association studyHuman leukocyte antigenBiologyInflammatory bowel diseasePolymorphism Single Nucleotidedigestive systemArticlePrimary sclerosing cholangitisPathogenesisCohort StudiesHLA AntigensProto-Oncogene ProteinsGeneticsmedicineHumansGenetic Predisposition to DiseaseBOWEL-DISEASEGenetic associationBcl-2-Like Protein 11Bile ductHepatocyte Growth FactorGene Expression Profilingdigestive oral and skin physiologyMembrane Proteinsmedicine.diseasedigestive system diseasesmedicine.anatomical_structureGenetic LociImmunologyApoptosis Regulatory ProteinsGenome-Wide Association Study
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TFIIH Operates through an Expanded Proximal Promoter To Fine-Tune c-myc Expression

2004

A continuous stream of activating and repressing signals is processed by the transcription complex paused at the promoter of the c-myc proto-oncogene. The general transcription factor IIH (TFIIH) is held at promoters prior to promoter escape and so is well situated to channel the input of activators and repressors to modulate c-myc expression. We have compared cells expressing only a mutated p89 (xeroderma pigmentosum complementation group B [XPB]), the largest TFIIH subunit, with the same cells functionally complemented with the wild-type protein (XPB/wt-p89). Here, we show structural, compositional, and functional differences in transcription complexes between XPB and XPB/wt-89 cells at t…

Chromatin ImmunoprecipitationDNA ComplementaryCell SurvivalUltraviolet RaysBlotting WesternGreen Fluorescent ProteinsGene ExpressionRepressorCellular homeostasisBiologyTransfectionModels BiologicalProto-Oncogene MasProto-Oncogene Proteins c-mycTranscription Factors TFIIRibonucleasesPotassium PermanganateTranscription (biology)HumansRNA MessengerPromoter Regions GeneticMolecular BiologyModels GeneticGeneral transcription factorCell CycleGenetic Complementation TestDNA HelicasesPromoterCell BiologyFibroblastsFlow CytometryMolecular biologyDNA-Binding ProteinsKineticsTranscription Factor TFIIHMicroscopy FluorescenceMutationTranscription preinitiation complexTranscription factor II HTranscription Factor TFIIHPlasmidsMolecular and Cellular Biology
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Antitumor effects of the novel NF-κB inhibitor dehydroxymethyl-epoxyquinomicin on human hepatic cancer cells: analysis of synergy with cisplatin and …

2006

We tested the novel NF-kappaB inhibitor dehydroxymethylepoxyquinomicin (DHMEQ) in the hepatic cancer (HCC) HepG2, HA22T/VGH and HuH-6 cells. The sensitivity to the cell growth inhibitory and apoptotic effects of the agent increased along with the levels of constitutively activated NF-kappaB, which were low in HepG2 and higher in HA22T/VGH and HuH-6. In HA22T/VGH, DHMEQ exhibited synergy with cisplatin. In the same cells, DHMEQ exerted dose-dependent decreases in the nuclear levels of activated NF-kappaB and attenuated NF-kappaB activation by cisplatin. It down-regulated Bcl-XL mRNA in a dose-dependent manner and up-regulated that of Bcl-XS. It also decreased interleukin 6 (IL-6), NAIP and, …

CisplatinCancer Researchmedicine.medical_specialtyOncogeneCell growthmedicine.medical_treatmentBiologyXIAPEndocrinologyCytokineOncologyApoptosisInternal medicineCancer cellmedicineCancer researchAutocrine signallingmedicine.drugInternational Journal of Oncology
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