Search results for "rase"

showing 10 items of 4343 documents

Carbonic anhydrase IX expression and tumor oxygenation status do not correlate at the microregional level in locally advanced cancers of the uterine …

2005

Abstract Purpose: Carbonic anhydrase IX (CA IX) can be induced by hypoxia in vitro and shows an immunohistochemical expression pattern that is predominantly found in perinecrotic tumor areas and correlates with exogenous markers of hypoxia, such as pimonidazole. CA IX might therefore serve as an endogenous marker of tumor hypoxia, although comparisons of CA IX immunostaining with direct oxygenation measurements using pO2 microsensors have thus far yielded contradictory results. Experimental Design: Because tumor heterogeneity may be among the factors responsible for the discrepancy between the two methods, CA IX expression in tissue samples originating from oxygen microelectrode tracks of l…

Cancer ResearchPathologymedicine.medical_specialtyUterine Cervical NeoplasmsBiologyIn vivoAntigens NeoplasmBiopsymedicinePimonidazoleHumansCarbonic Anhydrase IXCarbonic AnhydrasesNeoplasm StagingTumor hypoxiamedicine.diagnostic_testHypoxia (medical)Tumor OxygenationMiddle AgedImmunohistochemistryOxygenOncologyCancer researchImmunohistochemistryFemalemedicine.symptomImmunostainingClinical cancer research : an official journal of the American Association for Cancer Research
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Differential diagnosis of histogenetically distinct human epithelial renal tumours with a monoclonal antibody against gamma-glutamyltransferase.

1991

The localization of membrane-bound gamma-glutamyltransferase with monoclonal antibody (mAb) 138H11 proved to be of value for differential diagnosis of renal cancer, since it correlated with the histogenetic profile of human epithelial renal tumors. Immunoreactive gamma-glutamyltransferase was located in the proximal tubule in all normal human kidneys (15/15) examined thus far by both ultrastructural and immunohistochemical techniques. From 68 epithelial renal cancers tested 31/31 clear-cell carcinomas and 15/16 chromophilic carcinomas expressed the target epitope of mAb 138H11. In contrast, 0/11 oncytomas, 0/9 chromophobic carcinomas, and 0/1 Duct-Bellini carcinoma were immunoreactive. Thes…

Cancer ResearchPathologymedicine.medical_specialtymedicine.drug_classImmunologyHistogenesisBiologyurologic and male genital diseasesMonoclonal antibodyKidneyEpitopeEpitheliumDiagnosis DifferentialImmunoenzyme TechniquesFetusCarcinomamedicineImmunology and AllergyHumansMicroscopy ImmunoelectronKidneyCancerAntibodies Monoclonalgamma-GlutamyltransferaseClinical Enzyme Testsmedicine.diseaseKidney Neoplasmsmedicine.anatomical_structureOncologyImmunohistochemistryDifferential diagnosisCancer immunology, immunotherapy : CII
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Claudin-18 splice variant 2 is a pan-cancer target suitable for therapeutic antibody development

2008

Abstract Purpose: Antibody-based cancer therapies have emerged as the most promising therapeutics in oncology. The purpose of this study was to discover novel targets for therapeutic antibodies in solid cancer. Experimental Design: We combined data mining and wet-bench experiments to identify strictly gastrocyte lineage–specific cell surface molecules and to validate them as therapeutic antibody targets. Results: We identified isoform 2 of the tight junction molecule claudin-18 (CLDN18.2) as a highly selective cell lineage marker. Its expression in normal tissues is strictly confined to differentiated epithelial cells of the gastric mucosa, but it is absent from the gastric stem cell zone. …

Cancer ResearchPathologymedicine.medical_specialtymicemedicine.drug_classMolecular Sequence DataGene ExpressionBiologyMonoclonal antibodyMalignant transformationAntigenmedicineProtein IsoformsAnimalsHumansNeoplasms Glandular and EpithelialMembrane Proteins/geneticsAntibodies Monoclonal/immunologyProtein Isoforms/immunologyBase SequenceReverse Transcriptase Polymerase Chain ReactionNeoplasms Glandular and Epithelial/drug therapyAntibodies MonoclonalImmunotherapy ActiveMembrane ProteinsCancermedicine.diseaseFlow CytometryImmunohistochemistryImmunotherapy Active/methodsOncologyCancer cellClaudinsbiology.proteinCancer researchImmunohistochemistryAntibodyStem cell
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Studies on the importance of microsomal epoxide hydrolase in the detoxification of arene oxides using the heterologous expression of the enzyme in ma…

1994

In order to investigate the role of the microsomal epoxide hydrolase (mEH) in the detoxification of arene oxides in the presence of a high endogenous glutathione S-transferase (GST) activity-a situation found in several organs--we expressed the rat mEH cDNA in BHK21 Syrian hamster cells. These cells have high GST activities but contain an extremely low endogenous mEH enzyme activity. We obtained several cell clones which expressed the mEH heterologously, as determined by immunoblotting. The cell clone BHK21-mEH/Mz1 had the highest level of mEH protein. Immunofluorescence showed that the level of expression was almost homogeneous throughout the cell population. Total protein isolated from th…

Cancer ResearchPopulationCell Linechemistry.chemical_compoundCricetinaeMicrosomesAnimalsBenzopyrenesCloning MolecularEpoxide hydrolaseeducationGlutathione TransferaseEpoxide Hydrolaseseducation.field_of_studybiologyGeneral MedicineGlutathioneMolecular biologyEnzyme assayRecombinant ProteinsRatsGlutathione S-transferasechemistryBiochemistryMicroscopy FluorescenceCell cultureMicrosomal epoxide hydrolaseInactivation Metabolicbiology.proteinMicrosomeCarcinogenesis
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In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.

2003

In BCR-ABL-positive cells, the transcription factor STAT-5 is constitutively activated by tyrosine phosphorylation. STAT-5 activation results in upregulation of bcl-X(L) and increased resistance to induction of apoptosis. Here, we investigated the effects of imatinib mesylate and cytosine arabinoside (Ara-C) on STAT-5 tyrosine-phosphorylation, cellular proliferation and induction of apoptosis in cell lines and primary hematopoietic cells. Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts. In contrast to JAK-2 and PI-3-kinase inhibition, exposure of K562 cells to imatinib mesylate resulted in obvious suppression of proliferation. R…

Cancer ResearchProgrammed cell deathBlotting WesternFusion Proteins bcr-ablDown-RegulationAntineoplastic AgentsApoptosisBiologyPiperazineschemistry.chemical_compoundDownregulation and upregulationhemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineIn Situ Nick-End LabelingSTAT5 Transcription FactorHumansEnzyme InhibitorsPhosphorylationCell growthCytarabineImatinibTyrosine phosphorylationDrug SynergismHematologyDNAU937 CellsProtein-Tyrosine KinasesMilk ProteinsPrecipitin TestsDNA-Binding ProteinsImatinib mesylatePyrimidinesOncologychemistryApoptosisCaspasesBenzamidesCancer researchImatinib MesylateTrans-ActivatorsTyrosinePoly(ADP-ribose) PolymerasesK562 CellsCell Divisionmedicine.drugK562 cellsSignal TransductionLeukemia
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Hsp72 controls bortezomib-induced HepG2 cell death via interaction with pro-apoptotic factors.

2007

The proteasome inhibitor bortezomib is an efficacious inducer of apoptosis in the hepatoma HepG2 cell line. This study shows that bortezomib increased in these cells the level of the survival factor Hsp72 in a time- and dose-dependent manner. In a first phase of treatment, Hsp72 rapidly increased so that at 24 h of incubation with 50 nM bortezomib its level was approximately five-fold higher than the control. In this phase Hsp72 seemed to play a role in preventing HepG2 cell death, since it interacted with and sequestered the pro-apoptotic factors p53, AIF, Bax and Apaf-1. During a second day of treatment, although the nuclear levels of Hsp72, p53 and AIF increased, the interaction of Hsp72…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTime FactorsCellBlotting WesternApoptosisHSP72 Heat-Shock ProteinsAmino Acid Chloromethyl KetonesBortezomibCell Line TumormedicineHumansImmunoprecipitationProtease Inhibitorscardiovascular diseasesCaspasebcl-2-Associated X ProteinOncogenebiologyBortezomibReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsApoptosis Inducing Factorproteasome inhibitor hepatocarcinoma apoptosisGeneral MedicineCell cycleBoronic Acidsmedicine.anatomical_structureApoptotic Protease-Activating Factor 1OncologyApoptosisPyrazinesProteasome inhibitorCancer researchbiology.proteinTumor Suppressor Protein p53Apoptosis Regulatory Proteinsmedicine.drugProtein Binding
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Histone deacetylase inhibitors induce in human hepatoma HepG2 cells acetylation of p53 and histones in correlation with apoptotic effects

2007

This report shows that histone deacetylase inhibitors (HDACIs) induced apoptosis in human hepatoma HepG2 cells in a dose- and time-dependent manner. Trichostatin A (TSA), ITF2357 and suberoylanilide hydroxamic acid (SAHA), which were very effective agents, caused apoptotic effects after a lag phase of 12-16 h. In order to elucidate the mechanism of HDACIs action in HepG2 cells we have studied the effects of TSA, ITF2357 and SAHA on acetylation of p53 and histones H2A, H2B, H3 and H4. It was observed that HDACIs rapidly induced acetylation of these proteins, being the effects clearly visible already at 30 min of treatment at the same doses which caused apoptosis. Analysis of the immunocomple…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.drug_classAntineoplastic AgentsApoptosisBiologyHydroxamic AcidsHistonesCell Line TumorSettore BIO/10 - BiochimicamedicineHumansBenzothiazolesEnzyme InhibitorsRNA Small InterferingHistone AcetyltransferasesVorinostatHistone deacetylase inhibitors acetylation p53 histones apoptosis hepatoma cells.Liver NeoplasmsHistone deacetylase inhibitorAcetylationProto-Oncogene Proteins c-mdm2Molecular biologyHistone Deacetylase InhibitorsTrichostatin AHistoneOncologyPCAFAcetylationbiology.proteinHistone deacetylaseTumor Suppressor Protein p53DNA DamageToluenemedicine.drugInternational Journal of Oncology
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Sodium phenylbutyrate induces apoptosis in human retinoblastoma Y79 cells: The effect of combined treatment with the topoisomerase I-inhibitor topote…

2001

Our results demonstrate that sodium phenylbutyrate, a compound with a low degree of toxicity, exerted a cytotoxic effect on human retinoblastoma Y79 cells in a time- and dose-dependent manner. Treatment of Y79 cells for 72 h with phenylbutyrate reduced cell viability by 63% at 2 mM and 90% at 4 mM. Cell death caused by phenylbutyrate exhibited the typical features of apoptosis, as shown by light and fluorescent microscopy. Western blot analysis demonstrated that exposure of Y79 cells to phenylbutyrate decreased the level of the antiapoptotic factor Bcl-2 and induced the activation of caspase-3, a key enzyme in the execution phase of apoptosis. Moreover, treatment with phenylbutyrate markedl…

Cancer ResearchProgrammed cell deathCell SurvivalBlotting WesternApoptosisPhenylbutyrateHistonesSettore BIO/10 - BiochimicamedicineTumor Cells CulturedHumansretinoblastoma apoptosis sodium phenylbutirateViability assayEnzyme InhibitorsbiologyCaspase 3TopoisomeraseRetinoblastomaSodium phenylbutyrateAcetylationDrug SynergismCell cyclePhenylbutyrateseye diseasesEnzyme ActivationOncologyProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCancer researchTopotecanDrug Therapy CombinationTopoisomerase I InhibitorsTumor Suppressor Protein p53Topotecanmedicine.drug
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The effect of 3-aminobenzamide, inhibitor of poly(ADP-ribose) polymerase, on human osteosarcoma cells

2003

This study demonstrates that in human osteosarcoma cells treatment with 3-aminobenzamide (3-AB), a potent inhibitor of poly(ADP-ribose) polymerase (PARP), induces morphological and biochemical features of differentiation, the duration of which depends on whether or not the normal RB gene is expressed. In Saos-2 cells expressing a non-functional Rb protein, 3-AB treatment induced the formation of transient, short dendritic-like protrusions. In RB-transfected-Saos-2 cells (a clone previously generated in our laboratory that shows stable expression of wild-type Rb protein), 3-AB induced marked and prolonged changes with the formation of long dendritic-like protrusions and the appearance of ste…

Cancer ResearchProgrammed cell deathCell typeTime FactorsTranscription GeneticCell SurvivalPoly ADP ribose polymeraseCellular differentiationBlotting WesternApoptosisDNA FragmentationPoly(ADP-ribose) Polymerase InhibitorsBiologyTransfectionPolymerase Chain ReactionRetinoblastoma Proteinchemistry.chemical_compoundCell Line TumorProto-Oncogene ProteinsHumansMicroscopy Phase-ContrastRNA MessengerEnzyme Inhibitorsbcl-2-Associated X ProteinOsteosarcomaLamin Type BCaspase 3Reverse Transcriptase Polymerase Chain ReactionCell DifferentiationDendritesCell cycleAlkaline PhosphataseFlow CytometryMolecular biologyChromatinHyaluronan ReceptorsProto-Oncogene Proteins c-bcl-2OncologychemistryApoptosis3-AminobenzamideCaspasesBenzamides3-aminobenzamide osteosarcoma cells PARP activityAlkaline phosphataseInternational Journal of Oncology
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Apoptosis and the liver

2000

Regulation of the homeostatic balance between cell proliferation and programmed cell death, apoptosis, is essential for development and maintenance of multicellular organisms. Apoptosis is a genetically and evolutionarily highly conserved process. Analysis of the molecular mechanisms of apoptosis has led to a better understanding of many human diseases. Notably in cancer, but also in infectious or autoimmune disease, a deficiency in apoptosis is one of the key events in pathophysiology. On the other hand, overefficient apoptosis, as observed in fulminant liver failure, may be equally harmful for the organism indicating that a tight regulation of the apoptotic machinery is essential for surv…

Cancer ResearchProgrammed cell deathCeramideHepatitis Viral HumanDNA damageCellGenes mycApoptosisBiologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundmedicineHumansfas ReceptorLiver DiseasesLiver NeoplasmsIntrinsic apoptosisGenes p53Genes bcl-2Liver TransplantationCell biologymedicine.anatomical_structureLiverchemistryUVB-induced apoptosisApoptosisImmunologyPoly(ADP-ribose) PolymerasesSignal transductionReceptors Transforming Growth Factor betaSeminars in Cancer Biology
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