Search results for "BLAST"

showing 10 items of 2136 documents

Influence of nitric oxide on the generation and repair of oxidative DNA damage in mammalian cells

2002

We have analysed the effects of endogenously and exogenously generated nitric oxide (NO) in cultured mammalian fibroblasts on: (i) the steady-state (background) levels of oxidative DNA base modifications; (ii) the susceptibility of the cells to the induction of additional DNA damage and micronuclei by H(2)O(2); and (iii) the repair kinetics of various types of DNA modifications. Steady-state levels of oxidative DNA base modifications, measured by means of an alkaline elution assay in combination with the repair endonuclease Fpg protein, were similar in NO-overproducing B6 mouse fibroblasts stably transfected with an inducible NO synthase (iNOS) and in control cells. Increased oxidative dama…

Cancer ResearchDNA RepairDNA damageDNA repairNitric Oxide Synthase Type IIMutagenAlkenesBiologyNitric OxideTransfectionmedicine.disease_causeMicechemistry.chemical_compoundmedicineAnimalsNitric Oxide DonorsDose-Response Relationship DrugHydrogen PeroxideGeneral MedicineTransfectionFibroblastsCell biologyBiochemistrychemistryNitric Oxide SynthaseDNAGenotoxicityPeroxynitriteOxidative stressDNA DamageCarcinogenesis
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The DNA damage-induced decrease of Bcl-2 is secondary to the activation of apoptotic effector caspases.

2003

Apoptosis induced by DNA-damaging agents or radiation mainly proceeds through death receptor-independent caspase activation. The release of mitochondrial apoptogenic proteins, such as cytochrome c, into the cytoplasm leading to Apaf1-dependent activation of caspase-9 is a key event in this pathway. The permeability of the mitochondrial outer membrane is regulated by the various pro- and antiapoptotic Bcl-2 family proteins, and it is thought that DNA damage triggers apoptosis through the downregulation of antiapoptotic Bcl-2. Using murine embryonic fibroblasts (MEF) deficient and proficient in Apaf1, we show that DNA-damaging agents and radiation lead to a decline in Bcl-2 protein only in wt…

Cancer ResearchDNA damageCell TransplantationUltraviolet RaysTransplantation HeterologousApoptosisMice SCIDAdenocarcinomamedicine.disease_causeAdenoviridaeAmino Acid Chloromethyl KetonesMiceDownregulation and upregulationGeneticsmedicineTumor Cells CulturedAnimalsHumansAPAF1Enzyme InhibitorsMolecular BiologyCaspaseEtoposidebiologyDose-Response Relationship DrugCytochrome cProteinsDose-Response Relationship RadiationFibroblastsMolecular biologyCaspase InhibitorsCell biologyEnzyme ActivationPancreatic NeoplasmsApoptotic Protease-Activating Factor 1Proto-Oncogene Proteins c-bcl-2ApoptosisCytoplasmCaspasesbiology.proteinDactinomycinCarcinogenesisGene DeletionDNA DamageOncogene
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Coordinate mutation and transformation of mouse fibroblasts: induction by nitroquinoline oxide and modulation by caffeine

1981

Mutation and malignant transformation were followed in the same cells. Mouse fibroblasts (C3H 10T 1/2) were mutated and transformed by 4-nitroquinoline-1-oxide with similar, approximately linear dose-responses. The presence of caffeine immediately after exposure to 4-nitroquinoline-1-oxide potently inhibited mutation and transformation at high but not at low doses of 4-nitroquinoline-1-oxide. Whilst the coordinate induction of mutation and transformation could be explained by both a common target (DNA) or a common reactive species hitting several targets, the identical modulation by a DNA repair inhibitor of both end points suggests fundamental similarities in the nature of the lesions lead…

Cancer ResearchDNA repairDrug ResistanceBiologyMalignant transformationMicechemistry.chemical_compoundCaffeinemedicineAnimalsA-DNAOuabainFibroblastCells CulturedMice Inbred C3HNitroquinolinesDrug SynergismGeneral MedicineMolecular biology4-Nitroquinoline-1-oxideTransformation (genetics)Cell Transformation Neoplasticmedicine.anatomical_structurechemistryMutationMutation (genetic algorithm)Cancer researchCaffeineDNACarcinogenesis
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Characterization of bep1 and bep4 antigens involved in cell interactions during Paracentrotus lividus development

1992

Abstract We have identified and partially characterised two antigens, extracted with 3% butanol, from Paracentrotus lividus embryos dissociated at the blastula stage, and encoded by the cDNA clones previously described as bep1 and bep4 (bep-butanol extracted proteins). The cDNA fragments containing the specific central portions of bep1 and bep4 were expressed as MS2 polymerase fusion proteins in Escherichia coli. These two fusion proteins, called 1C1 (bep1) and 4A1 (bep4), were injected subcutaneously into rabbits and the corresponding polyclonal antibodies generated. Western blot analysis of proteins, extracted with 3% butanol, from sea urchin embryos at the blastula stage (b.e.p.), establ…

Cancer ResearchEmbryo Nonmammaliananimal structuresRecombinant Fusion ProteinsEmbryonic DevelopmentFluorescent Antibody TechniqueParacentrotus lividusCell–cell interactionWestern blotComplementary DNAbiology.animalmedicineAnimalsMolecular BiologySea urchinCell Aggregationbiologymedicine.diagnostic_testMembrane ProteinsCell Biologybiology.organism_classificationBlastulaMolecular biologyFusion proteinPolyclonal antibodiesSea Urchinsembryonic structuresbiology.proteinDevelopmental BiologyDifferentiation
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Cancer stem cell definitions and terminology:the devil is in the details

2012

The cancer stem cell (CSC) concept has important therapeutic implications, but its investigation has been hampered both by a lack of consistency in the terms used for these cells and by how they are defined. Evidence of their heterogeneous origins, frequencies and their genomic, as well as their phenotypic and functional, properties has added to the confusion and has fuelled new ideas and controversies. Participants in The Year 2011 Working Conference on CSCs met to review these issues and to propose a conceptual and practical framework for CSC terminology. More precise reporting of the parameters that are used to identify CSCs and to attribute responses to them is also recommended as key t…

Cancer ResearchGeneral MathematicsACUTE MYELOID-LEUKEMIAPERIPHERAL-BLOODBiologyAnimals; Cell Differentiation; Cell Transformation Neoplastic; Clonal Evolution; Humans; Neoplastic Stem Cells; Terminology as Topic; Oncology; Cancer ResearchBioinformaticsCell TransformationSomatic evolution in cancerTumor Initiating CellsTerminologyClonal EvolutionIN-VITRO PROPAGATIONPHENOTYPIC HETEROGENEITYREPOPULATING CELLSConsistency (negotiation)Cancer stem cellCancer stem cells (CSC)Settore MED/04 - PATOLOGIA GENERALETerminology as TopicmedicineAnimalsHumansIn patientACUTE LYMPHOBLASTIC-LEUKEMIAGENE-EXPRESSIONConfusionSettore MED/04 - Patologia GeneraleMELANOMA-CELLSCognitive scienceNeoplasticAnimalApplied MathematicsSTEM/PROGENITOR CELLSCell DifferentiationTUMOR-INITIATING CELLSPeripheral bloodCell Transformation Neoplasticcancer stem cells differentiation tumor definitionsOncologyNeoplastic Stem CellsNeoplastic Stem Cellmedicine.symptomHuman
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Aberrations of Genomic Imprinting in Glioblastoma Formation

2021

In human glioblastoma (GBM), the presence of a small population of cells with stem cell characteristics, the glioma stem cells (GSCs), has been described. These cells have GBM potential and are responsible for the origin of the tumors. However, whether GSCs originate from normal neural stem cells (NSCs) as a consequence of genetic and epigenetic changes and/or dedifferentiation from somatic cells remains to be investigated. Genomic imprinting is an epigenetic marking process that causes genes to be expressed depending on their parental origin. The dysregulation of the imprinting pattern or the loss of genomic imprinting (LOI) have been described in different tumors including GBM, being one …

Cancer ResearchGenomic imprintingSomatic cellSubventricular zonePopulationReviewBiologylcsh:RC254-282MethylationGliomamedicineEpigeneticsImprinting (psychology)educationneural stem cellsNeural stem cellseducation.field_of_studyglioblastomasubventricular zonelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseNeural stem cellgenomic imprintingnervous system diseasesOncologyCancer researchmethylationStem cellGenomic imprintingGlioblastoma
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Allelic loss but absence of mutations in the polyspecific transporter geneBWR1Aon 11p15.5 in hepatoblastoma

2004

Chromosomal region 11p15.5 shows frequent maternal allelic loss in embryonal tumors, including rhabdomyosarcoma (RMS), Wilms' tumor (WT) and hepatoblastoma (HB), consistent with the presence of at least one tumor suppressor gene in this region, which should be paternally imprinted, i.e., expressed from the maternal allele only. The BWR1A gene encodes a polyspecific transmembrane transporter and is located on 11p15.5. It is highly expressed in liver, paternally imprinted and was found to be mutated in an RMS cell line, making it a plausible tumor suppressor gene for HB. We therefore screened 62 HBs, 3 HB cell lines and 1 pediatric hepatocellular carcinoma for BWR1A mutations using single-str…

Cancer ResearchHepatoblastomaTumor suppressor geneBiologymedicine.diseaseMolecular biologyLoss of heterozygosityExonOncologyGene expressionChromosomal regionmedicineRhabdomyosarcomaGeneInternational Journal of Cancer
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Immune Therapy of Lympho-Hemopoietic Malignancies.

2017

Cancer ResearchImmunoconjugatesbusiness.industryAntibodies MonoclonalHematologyPrecursor Cell Lymphoblastic Leukemia-LymphomaImmune therapy03 medical and health sciencesHaematopoiesis0302 clinical medicineTreatment OutcomeOncologyLeukemia Myeloid030220 oncology & carcinogenesisHematologic NeoplasmsImmunologyAcute DiseaseMedicineHumans030212 general & internal medicineImmunotherapybusinessOncology research and treatment
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Chemokine stromal cell-derived factor-1alpha modulates VLA-4 integrin-dependent adhesion to fibronectin and VCAM-1 on bone marrow hematopoietic proge…

2001

Stromal cell-derived factor-1alpha (SDF-1alpha) is a potent chemoattractant for hematopoietic progenitor cells (HPC), suggesting that it could play an important role during their migration within or to the bone marrow (BM). The integrin VLA-4 mediates HPC adhesion to BM stroma by interacting with CS-1/fibronectin and VCAM-1. It is required during hematopoiesis and homing of HPC to the BM. As HPC migration in response to SDF-1alpha might require dynamic regulation of integrin function, we investigated if SDF-1alpha could modulate VLA-4 function on BM CD34(hi) cells.CD34(hi) BM cells and hematopoietic cell lines were tested for the effect of SDF-1alpha on VLA-4-dependent adhesion to CS-1/fibr…

Cancer ResearchIntegrinsReceptors CXCR4Stromal cellIntegrinCD34Receptors Lymphocyte HomingVascular Cell Adhesion Molecule-1Bone Marrow CellsIntegrin alpha4beta1Hematopoietic Cell Growth FactorsCell LineColony-Forming Units Assaychemistry.chemical_compoundMiceLeukemia Megakaryoblastic AcutePrecursor B-Cell Lymphoblastic Leukemia-LymphomaGeneticsCell AdhesionTumor Cells CulturedAnimalsHumansVCAM-1Cell adhesionMolecular BiologybiologyChemotaxisVLA-4Antibodies MonoclonalCell BiologyHematologyHematopoietic Stem CellsChemokine CXCL12Peptide FragmentsRecombinant ProteinsCell biologyFibronectinsFibronectinchemistryLiverbiology.proteinStromal CellsChemokines CXCHoming (hematopoietic)Signal TransductionExperimental hematology
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Antitumor effect of B16 melanoma cells genetically modified with the angiogenesis inhibitor rnasin.

2001

The growth of new blood vessels is an essential condition for the development of tumors with a diameter greater than 1-2 mm and also for their metastatic dissemination. RNasin, the placental ribonuclease inhibitor, is known to have antiangiogenic activity through the inhibition of angiogenin and basic fibroblast growth factor. Nevertheless, the administration of the recombinant form of a protein poses several limitations; as a result, we have studied the antitumor effect of RNasin in a murine gene therapy model. RNasin cDNA was subcloned into the pcDNA3 expression vector, and the resulting recombinant plasmid was used to transfect the B16 murine melanoma cell line. An RNasin inverted constr…

Cancer ResearchLung NeoplasmsAngiogeninTranscription GeneticGenetic enhancementCellBasic fibroblast growth factorGenetic VectorsMelanoma ExperimentalGene ExpressionAngiogenesis InhibitorsTransfectionNeovascularizationImmunoenzyme Techniqueschemistry.chemical_compoundMiceRibonucleasesmedicineTumor Cells CulturedAnimalsHumansRNA MessengerEnzyme InhibitorsMolecular BiologyDNA PrimersNeovascularization PathologicReverse Transcriptase Polymerase Chain ReactionMelanomaGenetic Therapymedicine.diseaseAngiogenesis inhibitormedicine.anatomical_structurechemistryCell cultureCancer researchMolecular Medicinemedicine.symptomPlacental HormonesCell DivisionCancer gene therapy
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