Search results for "rase"

showing 10 items of 4343 documents

Abstract 1138: The protein disulfide isomerase inhibitor XCE853 inhibits in vitro, ex-vivo and in vivo growth of human tumors

2017

Abstract Protein disulfide isomerase (PDI) is a chaperone protein that regulates oxidative protein folding as well as cell viability. Increased PDI levels have been documented in a variety of human cancers associated with a poor overall survival, including ovarian, prostate, brain and lung cancers. Inhibition of PDI activity leads to apoptosis in cancer, suggesting that PDI is a promising druggable target. XCE853 is a synthetic small molecule displaying an excellent docking with the catalytic domain of the human PDI. XCE853 inhibits in vitro recombinant PDI enzymatic activity. In addition, the proliferation of a large panel of human tumor cells is blocked by XCE853 with IC50s in the nanomol…

Cancer ResearchChemistryCancerProtein aggregationmedicine.diseaseMolecular biologyIn vitroCytolysisOncologyApoptosisIn vivomedicineViability assayProtein disulfide-isomeraseCancer Research
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Ultraviolet light-induced DNA damage triggers apoptosis in nucleotide excision repair-deficient cells via Bcl-2 decline and caspase-3/-8 activation.

2001

Ultraviolet (UV) light is a potent mutagenic and genotoxic agent. Whereas DNA damage induced by UV light is known to be responsible for UV-induced genotoxicity, its role in triggering apoptosis is still unclear. We addressed this issue by comparing nucleotide excision repair (NER) deficient 27-1 and 43-3B Chinese hamster (CHO) cells with the corresponding wild-type and ERCC-1 complemented cells. It is shown that NER deficient cells are dramatically hypersensitive to UV-C induced apoptosis, indicating that DNA damage is the major stimulus for the apoptotic response. Apoptosis triggered by UV-C induced DNA damage is related to caspase- and proteosome-dependent degradation of Bcl-2 protein. Th…

Cancer ResearchDNA RepairDNA repairDNA damageUltraviolet RaysPoly ADP ribose polymeraseFas-Associated Death Domain ProteinApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsCaspase 8TransfectionFas ligandMembrane PotentialsCricetinaeGeneticsUltraviolet lightAnimalsRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingCaspase 8Caspase 3Fas receptorMolecular biologyCaspase InhibitorsCaspase 9MitochondriaEnzyme ActivationProto-Oncogene Proteins c-bcl-2CaspasesPoly(ADP-ribose) PolymerasesCarrier ProteinsNucleotide excision repairDNA DamageOncogene
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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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T Cells Expressing Receptor Recombination/Revision Machinery Are Detected in the Tumor Microenvironment and Expanded in Genomically Over-unstable Mod…

2021

AbstractTumors undergo dynamic immunoediting as part of a process that balances immunologic sensing of emerging neoantigens and evasion from immune responses. Tumor-infiltrating lymphocytes (TIL) comprise heterogeneous subsets of peripheral T cells characterized by diverse functional differentiation states and dependence on T-cell receptor (TCR) specificity gained through recombination events during their development. We hypothesized that within the tumor microenvironment (TME), an antigenic milieu and immunologic interface, tumor-infiltrating peripheral T cells could reexpress key elements of the TCR recombination machinery, namely, Rag1 and Rag2 recombinases and Tdt polymerase, as a poten…

Cancer ResearchDatasets as TopicT-Cell Antigen Receptor SpecificityCD8-Positive T-LymphocytesMice0302 clinical medicineTumor MicroenvironmentRecombinaseT-cell receptorBreastRNA-SeqT Cells T Cell Receptor Recombination/Revision Machinery Tumor MicroenvironmentCancerAged 80 and overMice KnockoutRecombination GeneticNuclear Proteinshemic and immune systemsMiddle AgedDNA-Binding Proteins030220 oncology & carcinogenesisFemaleSingle-Cell AnalysisMutL Protein Homolog 1AdultImmunologyReceptors Antigen T-CellT cellsBreast Neoplasmschemical and pharmacologic phenomenaSettore MED/08 - Anatomia PatologicaBiologyRecombination-activating gene03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemAntigenDNA NucleotidylexotransferaseRAG2AnimalsHumansSettore MED/05 - Patologia ClinicaAgedHomeodomain ProteinsTumor microenvironmentT-cell receptorDisease Models AnimalImmunoeditingCancer researchDNA Damage030215 immunology
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Detection of the DCC gene product in normal and malignant colorectal tissues and its relation to a codon 201 mutation.

1998

Protein expression of the putative tumour-suppressor gene DCC on chromosome 18q was evaluated in a panel of 16 matched colorectal cancer and normal colonic tissue samples together with DCC mRNA expression and allelic deletions (loss of heterozygosity, LOH). Determined by a polymerase chain reaction (PCR)-LOH assay, 12 of the 16 (75%) cases were informative with LOH occurring in 2 of the 12 cases. For DCC mRNA, transcripts could be detected in all analysed normal tissues (eight out of eight) by RT-PCR, whereas 6 of the 15 tumours were negative. DCC protein expression, investigated by immunohistochemistry using the monoclonal antibody 15041 A directed against the intracellular domain, was hom…

Cancer ResearchDeleted in Colorectal CancerDNA Mutational AnalysisLoss of HeterozygosityReceptors Cell SurfaceBiologymedicine.disease_causePolymerase Chain ReactionLoss of heterozygosityGene productmedicineHumansGenes Tumor SuppressorRNA MessengerRNA NeoplasmCodonGeneMessenger RNAMutationTumor Suppressor ProteinsfungiDCC ReceptorImmunohistochemistryNeoplasm ProteinsBlotting SouthernOncologyCancer researchImmunohistochemistryColorectal NeoplasmsCell Adhesion MoleculesImmunostainingResearch ArticleBritish Journal of Cancer
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A new assay for O6-alkylguanine-DNA-alkyltransferase to determine DNA repair capacities using lambda-phage DNA as substrate.

1990

One O6-methylguanine (O6-meG) was introduced into each BamHI site of lambda-phage DNA as a substrate for the determination of the DNA repair protein O6-alkylguanine-DNA-alkyltransferase. A new assay using as the detection group 32P-labeled phosphate introduced at the 3' position of the modified nucleoside by incorporation of 32P-labeled TTP in the 3'-neighboring position proved highly sensitive: 10(-16) mol of the DNA lesion was still easily detectable. This DNA, which has greater than 1000 bp represents a good model for cellular DNA and was used as a substrate to measure the individual repair capacities for O6-meG in human lymphocytes of 20 healthy male and female donors. There were great …

Cancer ResearchGuanineDNA RepairDNA repairMolecular Sequence DataBiologySubstrate Specificitychemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseDNA Repair ProteinEscherichia coliHumansLymphocyteschemistry.chemical_classificationBase SequenceSubstrate (chemistry)General MedicineMethyltransferasesLambda phagebiology.organism_classificationBacteriophage lambdaIn vitroKineticsEnzymeBiochemistrychemistryDNA ViralBamHIDNACarcinogenesis
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Acquired resistance of melanoma cells to the antineoplastic agent fotemustine is caused by reactivation of the DNA repair gene mgmt

2001

Acquired resistance to antineoplastic agents is a frequent obstacle in tumor therapy. Malignant melanoma cells are particularly well known for their unresponsiveness to chemotherapy; only about 30% of tumors exhibit a transient clinical response to treatment. In our study, we investigated the molecular mechanism of acquired resistance of melanoma cells (MeWo) to the chloroethylating drug fotemustine. Determination of O6-methylguanine-DNA methyltransferase (MGMT) activity showed that MeWo cells that acquired resistance to fotemustine upon repeated treatment with the drug display high MGMT activity, whereas the parental cell line had no detectable MGMT. The resistant cell lines exhibit cross-…

Cancer ResearchGuanineMethyltransferaseDNA RepairDNA repairmedicine.medical_treatmentGene ExpressionAntineoplastic AgentsDrug resistanceBiologyNitrosourea CompoundsO(6)-Methylguanine-DNA MethyltransferaseEnzyme ReactivatorsOrganophosphorus CompoundsTumor Cells CulturedmedicineHumansEnzyme InhibitorsPromoter Regions GeneticMelanomaneoplasmsChemotherapyMelanomaGene AmplificationDNA Methylationmedicine.diseaseVirologydigestive system diseasesEnzyme ActivationBlotting SouthernOncologyDrug Resistance NeoplasmDNA methylationAzacitidineCancer researchFotemustinemedicine.drugAlkyltransferaseInternational Journal of Cancer
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Activating mutations in human c-Ha-ras-1 protooncogene induced by stereoisomeric fjord-region benzo[c]chrysene diol-epoxides.

1995

The mutagenicity of fjord-region benzo[c]chrysene diol-epoxide (BcCDE) stereoisomers((+) anti-BcCDE, (-)anti-BcCDE, (+)syn-BcCDE, and (-)syn-BcCDE) was studied in a forward-mutation system. pEC plasmid containing the human c-Ha-ras-1 proto-oncogene was reacted in vitro with each optically active isomer separately and transfected into NIH/3T3 cells. Morphologically transformed foci were cloned, and DNA obtained from these foci was tested for the presence of Ha-ras-1 sequence by Southern blot analysis. A total of 50 transformed foci (11-14 for each diastereomer) were generated. To determine the nature of mutations responsible for activating the proto-oncogene, regions of the gene likely to co…

Cancer ResearchGuanineMolecular Sequence DataGene mutationBiologymedicine.disease_causePolymerase Chain ReactionProto-Oncogene MasChryseneschemistry.chemical_compoundMicemedicineAnimalsHumansPoint MutationTransversionMolecular BiologyGeneSouthern blotMutationBase SequenceMutagenicity TestsPoint mutationNucleic Acid HybridizationStereoisomerism3T3 CellsMolecular biologyGenes raschemistryGene Expression RegulationMutationOligonucleotide ProbesDNAMutagensMolecular carcinogenesis
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Moguntinones--new selective inhibitors for the treatment of human colorectal cancer.

2014

Abstract 3-Indolyl and 3-azaindolyl-4-aryl maleimide derivatives, called moguntinones (MOG), have been selected for their ability to inhibit protein kinases associated with angiogenesis and induce apoptosis. Here, we characterize their mode of action and their potential clinical value in human colorectal cancer in vitro and in vivo. MOG-19 and MOG-13 were characterized in vitro using kinase, viability, and apoptosis assays in different human colon cancer (HT-29, HCT-116, Caco-2, and SW480) and normal colon cell lines (CCD-18Co, FHC, and HCoEpiC) alone or in combination with topoisomerase I inhibitors. Intracellular signaling pathways were analyzed by Western blotting. To determine their pot…

Cancer ResearchIndolesColorectal cancerAngiogenesisApoptosisBiologyPharmacologyMetastasisMaleimidesMiceIn vivomedicineAnimalsHumansPI3K/AKT/mTOR pathwayKinaseTOR Serine-Threonine Kinasesmedicine.diseaseXenograft Model Antitumor AssaysOncologyApoptosisSignal transductionCaco-2 CellsTopoisomerase I InhibitorsColorectal NeoplasmsHT29 CellsProto-Oncogene Proteins c-aktSignal TransductionMolecular cancer therapeutics
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