Search results for "protein p53"

showing 10 items of 201 documents

Toward the development of metal-based synthetic nucleases: DNA binding and oxidative DNA cleavage of a mixed copper(II) complex with N-(9H-purin-6-yl…

2009

Abstract The complex [Cu(N9-ABS)(phen) 2 ]·3.6H 2 O, H 2 N9-ABS  = N -(9 H -purin-6-yl)benzenesulfonamide and phen = 1,10-phenanthroline, has been synthesized and then characterized with the aid of X-ray diffraction, analytical, and spectroscopic techniques. The geometry of Cu(II) is distorted square pyramidal with the equatorial positions occupied by three N atoms from two phenantroline molecules and one N atom from the adenine ring of the sulfonamide ligand. The interaction of the complex with DNA was studied by means of viscosity measurements and fluorescence spectroscopy. The results pointed to a classic intercalation of the complex between the DNA base pairs. The complex was found to b…

Base pairStereochemistryIntercalation (chemistry)Antineoplastic AgentsApoptosisCleavage (embryo)BiochemistryJurkat cellsInorganic ChemistryJurkat Cellschemistry.chemical_compoundOrganometallic CompoundsHumansDNA CleavageCytotoxicitySulfonamidesChemistryDNASquare pyramidal molecular geometryProto-Oncogene Proteins c-bcl-2ApoptosisCaco-2 CellsTumor Suppressor Protein p53CopperDNAPhenanthrolinesJournal of Inorganic Biochemistry
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Relationship Between Thymidylate Synthase and p53 and Response to FEC Versus Taxane Adjuvant Chemotherapy for Breast Carcinoma

2011

Many drugs can be used for adjuvant therapy of breast cancer, including anthracyclines, cyclophosphamide, 5-fluorouracil (5-fU) and, recently, taxanes (TXT) have shown promising results. 5-FU blocks thymidylate synthase (TS) which cross-links p53 mRNA, inhibiting its synthesis. TS overexpression is one of the main mechanisms involved in 5-FU drug resistance. Enough p53 mutations can confer resistance to chemotherapy using anthracyclines and 5-FU, while are associated with improved responses to TXT. The aim of this study was to examine the TS and p53 levels in tumor samples and to compare the efficacy of FEC (5-FU, epirubicin, cyclophosphamide) and TXT chemotherapy in a group of patients wit…

Bridged-Ring CompoundsOncologymedicine.medical_specialtyCyclophosphamidemedicine.medical_treatmentBreast NeoplasmsThymidylate synthaseBreast cancerInternal medicineAntineoplastic Combined Chemotherapy ProtocolsBiomarkers TumormedicineAdjuvant therapyHumansPharmacology (medical)CyclophosphamideEpirubicinNeoplasm StagingPharmacologyChemotherapyTaxanebiologybusiness.industryThymidylate SynthasePrognosismedicine.diseaseImmunohistochemistryInfectious DiseasesOncologyChemotherapy AdjuvantFluorouracilbiology.proteinCancer researchFemaleTaxoidsFluorouracilTumor Suppressor Protein p53businessmedicine.drugEpirubicinJournal of Chemotherapy
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Tumorigenic conversion of endothelial cells.

2003

Tumors of endothelial origin develop rarely. Until now, only two angiosarcoma (AS)-derived endothelial cell lines have been be isolated, ISO-HAS and AS-M. Both AS-derived endothelial cell lines presented the typical endothelial characteristics, such as the expression of CD31 and von Willebrand factor, but differed from normal endothelial cells in a nuclear expression of p53, in a delayed angiogenic reaction, and a reduced expression of caveolin. In addition, differences in the expression of cytokines and cell adhesion molecules responsive to proinflammatory stimuli were observed. While AS-M showed an expression pattern similar to that of human umbilical vein endothelial cells (HUVEC), ISO-H…

CD31AdultLipopolysaccharidesTelomerasePathologymedicine.medical_specialtyClinical BiochemistryCaveolin 1Vascular Cell Adhesion Molecule-1BiologyCaveolinsPathology and Forensic Medicinevon Willebrand FactormedicineCell AdhesionHumansMolecular BiologyTelomeraseCells CulturedCell NucleusCell adhesion moleculeReverse Transcriptase Polymerase Chain ReactionGranulocyte-Macrophage Colony-Stimulating FactorTelomereIntercellular Adhesion Molecule-1Cell biologyVascular endothelial growth factor BEndothelial stem cellDNA-Binding ProteinsPlatelet Endothelial Cell Adhesion Molecule-1Vascular endothelial growth factor ACell Transformation NeoplasticVascular endothelial growth factor CCell cultureEndothelium VascularTumor Suppressor Protein p53Experimental and molecular pathology
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Nitric oxide enhances Th9 cell differentiation and airway inflammation

2014

International audience; Th9 cells protect hosts against helminthic infection but also mediate allergic disease. Here we show that nitric oxide (NO) promotes Th9 cell polarization of murine and human CD4(+) T cells. NO de-represses the tumour suppressor gene p53 via nitrosylation of Mdm2. NO also increases p53-mediated IL-2 production, STAT5 phosphorylation and IRF4 expression, all essential for Th9 polarization. NO also increases the expression of TGFβR and IL-4R, pivotal to Th9 polarization. OVA-sensitized mice treated with an NO donor developed more severe airway inflammation. Transferred Th9 cells induced airway inflammation, which was exacerbated by NO and blocked by anti-IL-9 antibody.…

CD4-Positive T-LymphocytesInterleukin 2[SDV]Life Sciences [q-bio]Cellular differentiationNitric Oxide Synthase Type IIGeneral Physics and AstronomyMice TransgenicInflammationCell SeparationNitric OxideArticleGeneral Biochemistry Genetics and Molecular BiologyNitric oxideMicechemistry.chemical_compoundEosinophiliaSTAT5 Transcription FactormedicineAnimalsHumansInterleukin 9Cells CulturedInflammationMice Inbred BALB CMultidisciplinarybiologyNitrosylationInterleukin-9Cell DifferentiationGeneral Chemistryrespiratory systemFlow Cytometry3. Good healthCell biologyMice Inbred C57BLchemistryInterferon Regulatory FactorsImmunologyLeukocytes Mononuclearbiology.proteinInterleukin-2Mdm2Tumor Suppressor Protein p53medicine.symptomAntibodymedicine.drugNature Communications
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Cooperation of Human Tumor-Reactive CD4+ and CD8+ T Cells after Redirection of Their Specificity by a High-Affinity p53A2.1-Specific TCR

2004

Abstract Efficient immune attack of malignant disease requires the concerted action of both CD8 + CTL and CD4 + Th cells. We used human leukocyte antigen (HLA)-A*0201 (A2.1) transgenic mice, in which the mouse CD8 molecule cannot efficiently interact with the α3 domain of A2.1, to generate a high-affinity, CD8-independent T cell receptor (TCR) specific for a commonly expressed, tumor-associated cytotoxic T lymphocyte (CTL) epitope derived from the human p53 tumor suppressor protein. Retroviral expression of this CD8-independent, p53-specific TCR into human T cells imparted the CD8 + T lymphocytes with broad tumor-specific CTL activity and turned CD4 + T cells into potent tumor-reactive, p53…

CD4-Positive T-LymphocytesT cellImmunologyReceptors Antigen T-CellMice TransgenicT-Cell Antigen Receptor SpecificityCD8-Positive T-LymphocytesBiologyMiceInterleukin 21Transduction GeneticTumor Cells CulturedmedicineAnimalsHumansImmunology and AllergyCytotoxic T cellCloning MolecularAntigen-presenting cellT-cell receptorFlow CytometryNatural killer T cellCell biologyCTL*Infectious Diseasesmedicine.anatomical_structureImmunologyTumor Suppressor Protein p53CD8T-Lymphocytes CytotoxicImmunity
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TP53 mutations and hepatocellular carcinoma: insights into the etiology and pathogenesis of liver cancer.

2007

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and the major risk factors include chronic infections with the hepatitis B (HBV) or C (HCV) virus, and exposure to dietary aflatoxin B(1) (AFB(1)) or alcohol consumption. Multiple genetic and epigenetic changes are involved in the molecular pathogenesis of HCC, for example, somatic mutations in the p53 tumor suppressor gene (TP53) and the activation of the WNT signal transduction pathway. AFB(1) frequently induces G:C to T:A transversions at the third base in codon 249 of TP53 and cooperates with HBV in causing p53 mutations in HCC. The detection of TP53 mutant DNA in plasma is a biomarker of both AFB(1) exposur…

Cancer ResearchAflatoxin B1Carcinoma HepatocellularTumor suppressor geneDNA damageDNA repairBiologymedicine.disease_causeHepatitis VirusesGeneticsmedicineHumansGenetic Predisposition to DiseaseEpigeneticsMolecular BiologyGeneHepatitis ChronicIncidenceLiver Neoplasmsmedicine.diseaseVirologydigestive system diseasesHBxMutagenesisHepatocellular carcinomaMutationCancer researchTumor Suppressor Protein p53CarcinogenesisOncogene
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MYCN sensitizes human neuroblastoma to apoptosis by HIPK2 activation through a DNA damage response.

2010

Abstract MYCN amplification occurs in approximately 20% of human neuroblastomas and is associated with early tumor progression and poor outcome, despite intensive multimodal treatment. However, MYCN overexpression also sensitizes neuroblastoma cells to apoptosis. Thus, uncovering the molecular mechanisms linking MYCN to apoptosis might contribute to designing more efficient therapies for MYCN-amplified tumors. Here we show that MYCN-dependent sensitization to apoptosis requires activation of p53 and its phosphorylation at serine 46. The p53S46 kinase HIPK2 accumulates on MYCN expression, and its depletion by RNA interference impairs p53S46 phosphorylation and apoptosis. Remarkably, MYCN ind…

Cancer ResearchApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein-Serine-Threonine KinaseAtaxia Telangiectasia Mutated ProteinNeuroblastomaCell Cycle ProteinSerinePhosphorylationNuclear ProteinOncogene Proteinseducation.field_of_studyN-Myc Proto-Oncogene ProteinAntibiotics AntineoplasticKinaseOncogene ProteinNuclear ProteinsDNA-Binding ProteinsOncologyPhosphorylationRNA InterferenceHumanDNA damageDNA-Binding ProteinPopulationBlotting WesternBiologyProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinBleomycinNeuroblastomaCell Line TumormedicineHumanseducationneoplasmsMolecular BiologyTumor Suppressor ProteinTumor Suppressor ProteinsApoptosimedicine.diseaseTumor progressionApoptosisMutationCancer researchTumor Suppressor Protein p53Carrier ProteinCarrier ProteinsDNA DamageMolecular cancer research : MCR
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Selective induction of apoptosis in multidrug resistant HL60R cells by the thiazolobenzoimidazole derivative 1-(2,6-difluorophenyl)-1H,3H-thiazolo [3…

1999

We investigated the antitumour effects of 1-(2,6-difluorophenyl)-1H,3H-thiazolo [3,4-a]benzimidazole (TBZ) a new anti-HIV-1 agent, on human promyelocytic HL60 leukaemia, both a parental and a multidrug resistant form (HL60R). HL60R overexpresses P-glycoprotein and, like HL60, lacks p53 protein expression. HL60 and HL60R show similar levels of Bcl-2 protein. In contrast to the conventional chemotherapeutic agents daunorubicin, etoposide and mitoxantrone, TBZ caused equal or even greater cytotoxicity in HL60R than in HL60, and this result was associated with a more marked induction of apoptosis in the drug resistant cells. The antitumour activity of TBZ occurred in the range of concentrations…

Cancer ResearchBenzimidazoleAnti-HIV AgentsDaunorubicinHL60ApoptosisHL-60 CellsDrug resistancePharmacologychemistry.chemical_compoundmedicineHumansATP Binding Cassette Transporter Subfamily B Member 1CytotoxicityP-glycoproteinbiologyFlow CytometryVirologyDrug Resistance MultipleMultiple drug resistanceThiazolesProto-Oncogene Proteins c-bcl-2OncologychemistryDrug Resistance NeoplasmApoptosisbiology.proteinBenzimidazolesDrug Screening Assays AntitumorTumor Suppressor Protein p53medicine.drugEuropean Journal of Cancer
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Hepatitis C Virus Core Protein Inhibits Tumor Suppressor Protein Promyelocytic Leukemia Function in Human Hepatoma Cells

2005

Abstract Tumor suppressor protein promyelocytic leukemia (PML) is implicated in apoptosis regulation and antiviral response. PML localizes predominantly to PML-nuclear bodies (PML-NB), nuclear macromolecular complexes regulating tumor suppressor protein p53 activity. Consistent with the function of PML in the cellular antiviral response, PML-NBs represent preferential targets in viral infections. In the case of hepatitis C virus (HCV) infection, important characteristics are nonresponsiveness to IFN therapy and development of hepatocellular carcinoma. However, the mechanisms which lead to the development of hepatocellular carcinoma are largely unknown. Here, we show that HCV core protein lo…

Cancer ResearchCarcinoma HepatocellularTumor suppressor genevirusesApoptosisPromyelocytic Leukemia ProteinBiologyTransfectionmedicine.disease_causePromyelocytic leukemia proteinCell Line TumorCoactivatormedicineHumansProtein IsoformsPhosphorylationCell NucleusTumor Suppressor ProteinsViral Core ProteinsLiver NeoplasmsNuclear Proteinsvirus diseasesAcetylationFas receptorHepatitis Cdigestive system diseasesNeoplasm ProteinsOncologyApoptosisAcetylationbiology.proteinCancer researchPhosphorylationTumor Suppressor Protein p53CarcinogenesisTranscription FactorsCancer Research
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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