Search results for "Tumor cell"

showing 10 items of 694 documents

Apoptotic induction in transformed follicular lymphoma cells by Bcl-2 downregulation.

1998

The roles of Bcl-2 protein and the protein ratio of Bcl-2/Bax in regulating cell growth in various lymphoma cell lines were examined. A dose-dependent decrease in Bcl-2 protein expression was observed in the different lymphomas incubated with lipid-incorporated bcl-2 antisense oligonucleotides (L-bcl-2). Growth inhibition was observed in a transformed follicular lymphoma (FL) cell line, which has the t(14;18) translocation and Bcl-2 protein overexpression. One of the mechanisms by which L-bcl-2 growth inhibition is mediated in these transformed FL cells might be through apoptotic induction, because the treated cells had an increased apoptotic index and showed the typical DNA fragmentation. …

Cancer ResearchFollicular lymphomaDown-RegulationApoptosisBiologychemistry.chemical_compoundDownregulation and upregulationProto-Oncogene ProteinsmedicineTumor Cells CulturedHumansLymphoma Follicularbcl-2-Associated X ProteinDrug CarriersCell growthHematologyOligonucleotides Antisensemedicine.diseaseLymphomaGene Expression Regulation NeoplasticCell Transformation NeoplasticOncologychemistryProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureLiposomesCancer researchDNA fragmentationGrowth inhibitionCell DivisionLeukemialymphoma
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The AC133 epitope, but not the CD133 protein, is lost upon cancer stem cell differentiation.

2010

Abstract Colon cancer stem cells (CSC) can be identified with AC133, an antibody that detects an epitope on CD133. However, recent evidence suggests that expression of CD133 is not restricted to CSCs, but is also expressed on differentiated tumor cells. Intriguingly, we observed that detection of the AC133 epitope on the cell surface decreased upon differentiation of CSC in a manner that correlated with loss of clonogenicity. However, this event did not coincide with a change in CD133 promoter activity, mRNA, splice variant, protein expression, or even cell surface expression of CD133. In contrast, we noted that with CSC differentiation, a change occured in CD133 glycosylation. Thus, AC133 …

Cancer ResearchGlycosylationGlycosylationCellular differentiationCellAC 133 EpitopeDown-RegulationMice SCIDEpitopechemistry.chemical_compoundEpitopesMiceCancer stem cellAntigens CDMice Inbred NODProminin-1medicineTumor Cells CulturedAnimalsHumansProtein IsoformsAC133 AntigenRNA MessengerPromoter Regions GeneticneoplasmsGlycoproteinsbiologyCell DifferentiationMolecular biologycarbohydrates (lipids)Gene Expression Regulation Neoplasticmedicine.anatomical_structureOncologychemistryembryonic structuresColonic Neoplasmsbiology.proteinNeoplastic Stem CellsAntibodyStem cellPeptidesCancer research
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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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Influence of glutathione levels and heat-shock on the steady-state levels of oxidative DNA base modifications in mammalian cells

1999

The effects of thiols, ascorbic acid and thermal stress on the basal (steady-state) levels of oxidative DNA base modifications were studied. In various types of untreated cultured mammalian cells, the levels of total glutathione were found to be inversely correlated with the levels of DNA base modifications sensitive to the repair endonuclease Fpg protein, which include 8-hydroxyguanine (8-oxoG). A depletion of glutathione by treatment with buthionine sulphoximine increased the steady-state level in AS52 Chinese hamster cells by approximately 50%. However, additional thiols in the culture medium did not reduce the level of Fpg-sensitive base modifications: 0-10 mM N-acetylcysteine had no ef…

Cancer ResearchHot TemperatureDNA damageGlutathione reductaseOxidative phosphorylationmedicine.disease_causeCell LineMicechemistry.chemical_compoundHsp27CricetinaeTumor Cells CulturedmedicineAnimalsHumansEnzyme InhibitorsButhionine SulfoximineN-Glycosyl HydrolasesHeat-Shock ProteinsbiologyChemistryGeneral MedicineGlutathioneAscorbic acidGlutathioneOxidative StressDNA-Formamidopyrimidine GlycosylaseBiochemistrybiology.proteinOxidative stressDNA DamageHeLa CellsCysteineCarcinogenesis
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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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A novel tumour associated leucine zipper protein targeting to sites of gene transcription and splicing

2002

We describe here the definition and characterization of antigen CT-8/HOM-TES-85 encoded by a previously unknown gene and identified by serological expression screening using antibodies from a seminoma patient. Intriguingly, the leucine zipper region of CT-8/HOM-TES-85 shows an atypical amphipathy with clusters of hydrophobic residues that is exclusively shared by the N-myc proto-oncogene. CT-8/HOM-TES-85 gene is tightly silenced in normal tissues except for testis. However, it is frequently activated in human neoplasms of different types including lung cancer, ovarian cancer, melanoma and glioma. Endogenous as well as heterogeneously expressed CT-8/HOM-TES-85 targets predominantly to the nu…

Cancer ResearchLeucine zipperDNA ComplementaryTranscription GeneticGreen Fluorescent ProteinsImmunoblottingBiologymedicine.disease_causeModels BiologicalProto-Oncogene MasAntigens NeoplasmTranscription (biology)Protein targetingTumor Cells CulturedGeneticsmedicineHumansTissue DistributionAntigensMolecular BiologyGeneLeucine ZippersATF3GenomeReverse Transcriptase Polymerase Chain ReactionAlternative splicingfood and beveragesBlotting NorthernPhenotypeProtein Structure TertiaryDNA-Binding ProteinsAlternative SplicingLuminescent ProteinsPhenotypeMicroscopy FluorescenceModels ChemicalRNA splicingCancer researchOncogene
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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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Cytolytic T cell reactivity against melanoma-associated differentiation antigens in peripheral blood of melanoma patients and healthy individuals

1996

Antigenic peptides derived from several differentiation antigens of the melanocyte lineage were recently identified in human melanomas as targets for HLA-A2.1-restricted cytotoxic T lymphocytes (CTLs). To examine their potential role in tumour-directed immune responses in vivo, we determined CTL reactivity against seven antigenic peptides derived from the Melan A/MART-1, tyrosinase and gp100/Pmel17 antigens in the peripheral blood of 10 HLA-A2+ healthy controls and 26 HLA-A2+ melanoma patients. The influenza matrix peptide (GILGFVFTL) presented by HLA-A2.1 was used as a control peptide. CTL reactivity was assessed in a mixed lymphocyte 'peptide' culture assay. Reactivity against Melan A/MAR…

Cancer ResearchLymphocyte10050 Institute of Pharmacology and Toxicology610 Medicine & healthDermatologyPeripheral blood mononuclear cell2708 DermatologyMART-1 AntigenImmune systemMelanocyte differentiationAntigenAntigens NeoplasmTumor Cells CulturedmedicineHumansCytotoxic T cell1306 Cancer ResearchAmino Acid SequenceMelanomaneoplasmsMembrane GlycoproteinsMonophenol Monooxygenasebusiness.industryMelanomaProteinsmedicine.diseaseAntigens DifferentiationNeoplasm ProteinsCTL*medicine.anatomical_structureOncologyImmunology570 Life sciences; biology2730 OncologybusinessT-Lymphocytes Cytotoxicgp100 Melanoma AntigenMelanoma Research
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Cellular immune response to human renal-cell carcinomas: Definition of a common antigen recognized by HLA-A2-restricted cytotoxic T-Lymphocyte (CTL) …

1994

Cytotoxic T lymphocyte (CTL) clones directed against autologous renal-cell carcinoma (RCC) cell lines were generated by mixed lymphocyte/tumor-cell culture (MLTC) using peripheral blood lymphocytes (PBL). A CD8+, CD4- CTL clone MZ1257-CTL 5/30 with high cytolytic activity for the autologous tumor cell line MZ1257-RCC was established. No lysis of the autologous EBV-transformed B lymphocytes (EBV-B) or K562 cells was observed. A panel of HLA-A2-matched allogeneic RCC lines was recognized by CTL 5/30. Further specificity analysis showed a cross-reactivity with HLA-A2-matched allogeneic tumor cells of various origins, especially melanoma. CTL 5/30 was also cross-reactive with several HLA-A2-pos…

Cancer ResearchLymphocyteCross ReactionsBiologyKidneyImmune systemAntigenAntigens NeoplasmHLA-A2 AntigenTumor Cells CulturedmedicineHumansCytotoxic T cellCarcinoma Renal CellMelanomaImmunity CellularHistocompatibility Antigens Class IAntibodies MonoclonalT lymphocyteAntigens DifferentiationAutologous tumor cellKidney NeoplasmsCTL*medicine.anatomical_structureOncologyImmunologyLymphocyte Culture Test MixedClone (B-cell biology)T-Lymphocytes CytotoxicInternational Journal of Cancer
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The BCL6 gene in B-cell lymphomas with 3q27 translocations is expressed mainly from the rearranged allele irrespective of the partner gene

2003

The BCL6 gene, which functions as a transcription repressor, is the target of multiple chromosomal translocations in non-Hodgkin's lymphomas (NHL). These translocations occur in the nontranslated region of the BCL6 gene, juxtaposing regulatory sequences of the diverse partner genes to the open reading frame of the BCL6 gene and thus are thought to deregulate BCL6 gene expression. The levels of expression of the BCL6 gene and protein have been demonstrated to predict the clinical outcome of diffuse large B-cell lymphomas. By contrast, the prognostic significance of BCL6 gene translocations is unclear. In this study we have sought an explanation for this apparent discrepancy. We examined tumo…

Cancer ResearchLymphoma B-CellBiologyTranslocation Geneticimmune system diseasesProto-Oncogene Proteinshemic and lymphatic diseasesGene expressionTumor Cells CulturedHumansRNA MessengerAllelePromoter Regions GeneticGeneAllelesGene RearrangementGeneticsRegulation of gene expressionPromoterHematologyGene rearrangementBCL6Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsOncologyRegulatory sequenceMutationProto-Oncogene Proteins c-bcl-6Cancer researchChromosomes Human Pair 3Transcription FactorsLeukemia
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