Search results for "P53"

showing 10 items of 303 documents

Targeting p53, hdm2, and CD19: vaccination and immunologic strategies.

2000

Peptides presented by class I major histocompatibility complex (MHC) molecules and derived from normal self-proteins that are expressed at elevated levels by cells from a variety of human (Hu) malignancies provide, in theory, potential target antigens for a broad-spectrum, cytotoxic T lymphocyte (CTL)-based immunotherapy of cancer and hematologic malignancies. However, as such tumor- and leukemia-associated self-proteins are also expressed at low levels in some types of normal tissues, such as thymus, spleen and lymphohemopoietic cells, these self-MHC-self-peptide complexes may also represent thymic and/or peripheral tolerogens, thereby preventing immune responses. This is particularly true…

Antigen presentationAntigens CD19chemical and pharmacologic phenomenaMice TransgenicMajor histocompatibility complexEpitopeMiceImmune systemAntigenNeoplasmsProto-Oncogene ProteinsCytotoxic T cellAnimalsHumansAvidityTransplantationAntigen PresentationbiologyHistocompatibility Antigens Class IVaccinationNuclear ProteinsProto-Oncogene Proteins c-mdm2HematologyCTL*Immunologybiology.proteinTumor Suppressor Protein p53T-Lymphocytes CytotoxicBone marrow transplantation
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TP53 codon 72 polymorphism and cervical cancer

2009

Background Cervical cancer is caused primarily by human papillomaviruses (HPV). The polymorphism rs1042522 at codon 72 of the TP53 tumour-suppressor gene has been investigated as a genetic cofactor. More than 80 studies were done between 1998 and 2006, after it was initially reported that women who are homozygous for the arginine allele had a risk for cervical cancer seven times higher than women who were heterozygous for the allele. However, results have been inconsistent. Here we analyse pooled data from 49 studies to determine whether there is an association between TP53 codon 72 polymorphism and cervical cancer.Methods Individual data on 7946 cases and 7888 controls from 49 different st…

ArginineMESH : Polymorphism GeneticMESH: Genes p53MESH : AgedPhysiologyUterine Cervical NeoplasmsMESH: Papillomavirus Infections[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineGenotypeMESH : FemaleCervical cancerGeneticsMESH: AgedMESH : Papillomavirus Infections0303 health sciencesMESH: Middle AgedHPV infectionMESH: Genetic Predisposition to DiseaseMiddle AgedMESH : AdultWILD-TYPE P53Hardy–Weinberg principle3. Good healthMESH: Uterine Cervical NeoplasmsOncologyMESH: Young Adult030220 oncology & carcinogenesisMeta-analysisFemaleAdultAdolescentMESH : Uterine Cervical NeoplasmsMESH : Young Adult[SDV.CAN]Life Sciences [q-bio]/CancerMESH : Genes p5303 medical and health sciencesYoung AdultSQUAMOUS INTRAEPITHELIAL LESIONSMESH : AdolescentINDIAN WOMENMESH: Polymorphism GeneticmedicineHumansGenetic Predisposition to DiseaseMESH : Middle AgedAllele030304 developmental biologyAgedMESH: AdolescentMESH: HumansPolymorphism GeneticHUMAN-PAPILLOMAVIRUS TYPE-16business.industryP53 ARG72PRO POLYMORPHISMHEALTHY WOMENPapillomavirus InfectionsMESH : HumansMESH: AdultOdds ratiomedicine.diseaseGenes p53GENOTYPESHARDY-WEINBERG EQUILIBRIUMRISK-FACTORSMESH : Genetic Predisposition to DiseasebusinessMESH: FemaleHPV INFECTIONLancet Oncology
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Enhancement of cytotoxicity of artemisinins toward cancer cells by ferrous iron

2004

Abstract Iron(II) heme-mediated activation of the peroxide bond of artemisinins is thought to generate the radical oxygen species responsible for their antimalarial activity. We analyzed the role of ferrous iron in the cytotoxicity of artemisinins toward tumor cells. Iron(II)–glycine sulfate (Ferrosanol) and transferrin increased the cytotoxicity of free artesunate, artesunate microencapsulated in maltosyl-β-cyclodextrin, and artemisinin toward CCRF-CEM leukemia and U373 astrocytoma cells 1.5- to 10.3-fold compared with that of artemisinins applied without iron. Growth inhibition by artesunate and ferrous iron correlated with induction of apoptosis. Cell cycle perturbations by artesunate an…

ArtemisininsIronPopulationTransferrin receptorBiochemistryFerrousInhibitory Concentration 50chemistry.chemical_compoundAntigens CDCell Line TumorNeoplasmsPhysiology (medical)Receptors TransferrinHumansFerrous CompoundsRNA MessengereducationCell Proliferationchemistry.chemical_classificationeducation.field_of_studybiologyMolecular biologyArtemisininsAntigens Differentiation B-LymphocyteGene Expression RegulationBiochemistrychemistryTransferrinArtesunateCancer cellbiology.proteinTumor Suppressor Protein p53CeruloplasminFree Radical Biology and Medicine
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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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PathVisio Analysis: An Application Targeting the miRNA Network Associated with the p53 Signaling Pathway in Osteosarcoma

2021

MicroRNAs (miRNAs) are small single-stranded, non-coding RNA molecules involved in the pathogenesis and progression of cancer, including osteosarcoma. We aimed to clarify the pathways involving miRNAs using new bioinformatics tools. We applied WikiPathways and PathVisio, two open-source platforms, to analyze miRNAs in osteosarcoma using miRTar and ONCO.IO as integration tools. We found 1298 records of osteosarcoma papers associated with the word "miRNA". In osteosarcoma patients with good response to chemotherapy, miR-92a, miR- 99b, miR-193a-5p, and miR-422a expression is increased, while miR-132 is decreased. All identified miRNAs seem to be centered on the TP53 network. This is the first …

Bioinformatics Bone tumor Cancer CarcinogenesisMiRNA Oncology Osteosarcoma p53P53 Signaling PathwaymicroRNACancer researchmedicineOsteosarcomaGeneral MedicineBiologymedicine.disease
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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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