Search results for "Tumor cell"

showing 10 items of 694 documents

Genomic Abnormalities Acquired in the Blastic Transformation of Splenic Marginal Zone B-cell Lymphoma

2003

Among 20 cases of typical splenic marginal zone lymphoma (SMZL), two cases had blastic transformation. The genetic mechanisms underlying the morphologic transformation were investigated by comparing genetic changes in initial and blastic phases. A complex karyotype including trisomy of 3q and genomic gain of 17q22-q24 was seen in both cases at diagnosis. However, the extra copy of 3q was lost during the transformation process in both tumors. Additionally, the Karpas 1718 cell line, which was derived from a patient with transformed SMZL and carried a trisomy of 3q, also evidenced the spontaneous loss of the extra 3q during the culturing process. Other acquired abnormalities observed exclusiv…

Cancer ResearchPathologymedicine.medical_specialtyLymphoma B-CellTrisomyChromosomal translocationBiologyComplex KaryotypeTumor Cells CulturedmedicineChromosomes HumanHumansSplenic marginal zone lymphomaChromosome AberrationsLymphoma Non-HodgkinSplenic NeoplasmsHematologymedicine.diseaseTransformation (genetics)OncologyKaryotypingDisease ProgressionB-Cell Non-Hodgkin LymphomaChromosomes Human Pair 3Chromosome DeletionAbnormalityBlast CrisisTrisomyChromosomes Human Pair 17Comparative genomic hybridizationLeukemia & Lymphoma
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De novo expression of intercellular adhesion molecule 1 (ICAM-1, CD54) in pancreas cancer.

1993

We examined the expression of intercellular--adhesion molecule-I (ICAM-I, CD54) in 6 surgically removed pancreatic tumors and 8 pancreatic tumor cell lines. Immunohistochemistry revealed a varying percentage of ICAM-I-positive pancreas tumor cells, while normal pancreatic tissue (except for slight reactivity of endothelial cells) was not stained. The presence of the ICAM-I molecule on the cell surface and the expression of ICAM-I mRNA were investigated for 8 different pancreatic tumor cell lines. Three of these (Capan-I, Capan-2, QGP-I) expressed ICAM-I constitutively. In 4 of the ICAM-I-negative pancreas cancer cell lines, it was possible to induce a remarkable expression of ICAM-I by incu…

Cancer ResearchPathologymedicine.medical_specialtyPancreatic diseaseCellMolecular Sequence DataBiologyProinflammatory cytokineImmunoenzyme TechniquesPancreatic tumorAntigens CDmedicineTumor Cells CulturedHumansRNA MessengerRNA NeoplasmBase SequenceCell adhesion moleculeCancermedicine.diseaseIntercellular Adhesion Molecule-1Molecular biologyPancreatic Neoplasmsmedicine.anatomical_structureOncologyCell culturePancreasCell Adhesion MoleculesInternational journal of cancer
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Neural and mesenchymal differentiations in Ewing's sarcoma cell lines. Morphological, immunophenotypic, molecular biological and cytogenetic evidence

1995

Three established Ewing's sarcoma (ES) cell lines (TC106, 6647, A4573), grown both in vitro and as xenograft tumors, were analyzed. In all 3 lines and tumors, the ES characteristic reciprocal translocation (11;22), as well as the presence of the ES-associated p30/32M1C2 antigen, were documented. However, these cell lines showed discrepancies in their neural and mesenchymal differentiation. The TC106 line was characterized by expression of the neuroendocrine marker secretogranin II (SgII) which was detectable by Northern blot and by radioimmunological detection (RIA) in the culture medium of secretoneurin, a proteolytic product of SgII. In contrast, TC106 cells were immunohistochemically and…

Cancer ResearchPathologymedicine.medical_specialtyRadioimmunoassayMice NudeSarcoma EwingBiologyNeuroendocrine differentiationImmunophenotypingMiceNeuroblastomaTumor Cells CulturedmedicineAnimalsHumansNeuroectodermal Tumors Primitive PeripheralNorthern blotMice Inbred BALB CSecretoneurinNeuropeptidesMesenchymal stem cellEwing's sarcomaChromogranin ABlotting Northernmedicine.diseaseImmunohistochemistryChromosome BandingOncologySecretogranin IICell cultureKaryotypingbiology.proteinCancer researchSarcomaInternational Journal of Cancer
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A new cell line (8701-BC) from primary ductal infiltrating carcinoma of human breast

1989

A cell line, designated 8701-BC, was established in culture from tissue fragments of primary ductal infiltrating carcinoma of human breast. The cell cultures after the sixth passage were devoid of contaminating fibroblasts as judged by the positive staining of all cells with the specific epithelial cell markers carcinoembryonic antigen (CEA), tissue polypeptide antigen (TPA) and cytokeratin 8. The epithelial nature of these cells was confirmed by ultrastructural analyses which demonstrated the retention of specific structural properties characteristic of the original tumour. The cells possessed an abnormal karyotype with 55-60 chromosomes per cell with numerous rearrangements. They do not e…

Cancer ResearchPathologymedicine.medical_specialtyStromal cellbiologyTissue Polypeptide AntigenCellBreast NeoplasmsMolecular biologyEpitheliumCell LineCarcinoma Intraductal Noninfiltratingmedicine.anatomical_structureCarcinoembryonic antigenOncologyCell cultureKaryotypingTumor Cells Culturedmedicinebiology.proteinKeratin 8HumansNeoplastic cellResearch ArticleBritish Journal of Cancer
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Development of resistance towards artesunate in MDA-MB-231 human breast cancer cells.

2011

Breast cancer is the most common cancer and the second leading cause of cancer death in industrialized countries. Systemic treatment of breast cancer is effective at the beginning of therapy. However, after a variable period of time, progression occurs due to therapy resistance. Artesunate, clinically used as anti-malarial agent, has recently revealed remarkable anti-tumor activity offering a role as novel candidate for cancer chemotherapy. We analyzed the anti-tumor effects of artesunate in metastasizing breast carcinoma in vitro and in vivo. Unlike as expected, artesunate induced resistance in highly metastatic human breast cancer cells MDA-MB-231. Likewise acquired resistance led to abol…

Cancer ResearchPhytochemistryPhytopharmacologyCancer TreatmentArtesunateApoptosisElectrophoretic Mobility Shift AssayDrug resistanceNude MiceMetastasischemistry.chemical_compoundMiceMolecular Cell BiologyDrug DiscoveryBreast TumorsBasic Cancer ResearchMedicinebcl-2-Associated X ProteinMultidisciplinaryQRNF-kappa BArtemisininsChemistryOncologyMedicineFemaleMatrix Metalloproteinase 1Breast carcinomamedicine.drugResearch Article570Drugs and DevicesDrug Research and DevelopmentCell SurvivalScienceMice Nude570 Life SciencesBreast NeoplasmsTumor Cell Line610 Medical Sciences MedicineBreast cancerComplementary and Alternative MedicineCell Line TumorAnimalsHumansDoxorubicinBiologyNeoplasm Drug Resistancebusiness.industryCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseaseXenograft Model Antitumor AssaysTranscription Factor AP-1chemistryTumor progressionArtesunateDrug Resistance NeoplasmCancer cellImmunologyEthnopharmacologyCancer researchbusinessPloS one
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Lactate-induced inhibition of tumor cell proliferation.

1988

Abstract Culture medium that was recovered from tumor cell or fibroblast cultures during the plateau phase, and that was replenished by addition of glucose, glutamine, and serum and readjustment of pH had a distinct growth-inhibiting effect on monolayer cell cultures. The effect, which was not specific for a given cell strain, may be partially responsible for the "density inhibition" commonly observed in malignant cells grown in monolayer cultures. By modifying fresh growth media, it was shown that the growth inhibition observed can be partly attributed to the accumulation of lactate in the culture medium of plateau phase cells. This substance reduced the plating efficiency and the number o…

Cancer ResearchPlating efficiencyPlateau (mathematics)law.inventionchemistry.chemical_compoundMiceIn vivolawMonolayerTumor Cells CulturedMedicineAnimalsHumansRadiology Nuclear Medicine and imagingLactic AcidAmino AcidsRadiationbusiness.industryPetri dishCell biologyCulture MediaGlutamineOncologychemistryCell cultureImmunologyLactatesGrowth inhibitionbusinessCell DivisionInternational journal of radiation oncology, biology, physics
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Mcl-1 is an anti-apoptotic factor for human hepatocellular carcinoma

2005

Defects in apoptosis signaling in hepatocytes contribute to tumorigenesis in hepatocellular carcinoma (HCC). In addition, treatment with chemotherapeutic drugs is often ineffective in HCC patients due to the apoptosis resistance of cancer cells. Anti-apoptotic members of the Bcl-2 family, including myeloid cell leukemia-1 (Mcl-1), which regulate intrinsic apoptosis induction at the mito-chondrial level, are often overexpressed in human cancer, and are implicated with disease grade and prognosis. Yet, little is known about the role of Mcl-1 in HCC. In this study, we analyzed the relevance of Mcl-1 expression for the apop-tosis resistance of human HCC. Mcl-1 protein expression was considerabl…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularApoptosisBiologyPhosphatidylinositol 3-KinasesEpidermal growth factorhemic and lymphatic diseasesTumor Cells CulturedmedicineHumansneoplasmsProtein kinase BPI3K/AKT/mTOR pathwayAkt/PKB signaling pathwayGene Expression ProfilingLiver NeoplasmsIntrinsic apoptosisPrognosisdigestive system diseasesNeoplasm ProteinsProto-Oncogene Proteins c-bcl-2OncologyImmunologyCancer cellCancer researchMyeloid Cell Leukemia Sequence 1 ProteinHepatocyte growth factorProto-Oncogene Proteins c-aktmedicine.drugInternational Journal of Oncology
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Effective infection, apoptotic cell killing and gene transfer of human hepatoma cells but not primary hepatocytes by parvovirus H1 and derived vector…

2001

Autonomous parvoviruses preferentially replicate in and kill in vitro–transformed cells and reduce the incidence of spontaneous and implanted tumors in animals. Because of these natural oncotropic and oncolytic properties, parvoviruses deserve to be considered as potential antitumor vectors. Here, we assessed whether parvovirus H1 is able to kill human hepatoma cells by induction of apoptosis but spares primary human liver cells, and whether the former cells can efficiently be transduced by H1 virus–based vectors. Cell death, infectivity, and transgene transduction were investigated in Hep3B, HepG2, and Huh7 cells and in primary human hepatocytes with natural and recombinant H1 virus. All h…

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularParvovirus H-1Cell SurvivalvirusesGenetic VectorsApoptosisVirus ReplicationVirusCell LineParvoviridae InfectionsParvovirusTransduction (genetics)Transduction GeneticTumor Cells CulturedHumansMolecular BiologybiologyParvovirusLiver NeoplasmsGene Transfer Techniquesbiology.organism_classificationVirologyMolecular biologydigestive system diseasesOncolytic virusCell killingApoptosisDNA ViralHepatocytesMolecular MedicineCancer gene therapy
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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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Artesunate induces oxidative DNA damage, sustained DNA double-strand breaks, and the ATM/ATR damage response in cancer cells.

2011

Abstract Artesunate, the active agent from Artemisia annua L. used in the traditional Chinese medicine, is being applied as a first-line drug for malaria treatment, and trials are ongoing that include this drug in cancer therapy. Despite increasing interest in its therapeutic application, the mode of cell killing provoked by artesunate in human cells is unknown. Here, we show that artesunate is a powerful inducer of oxidative DNA damage, giving rise to formamidopyrimidine DNA glycosylase–sensitive sites and the formation of 8-oxoguanine and 1,N6-ethenoadenine. Oxidative DNA damage was induced in LN-229 human glioblastoma cells dose dependently and was paralleled by cell death executed by ap…

Cancer ResearchProgrammed cell deathDNA RepairRAD51Drug Evaluation PreclinicalArtesunateApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine KinasesModels Biologicalchemistry.chemical_compoundNeoplasmsTumor Cells CulturedHumansDNA Breaks Double-StrandedTumor Suppressor ProteinsMolecular biologyAntineoplastic Agents PhytogenicArtemisininsUp-RegulationNon-homologous end joiningDNA-Binding ProteinsOxidative StressCell killingOncologychemistryArtesunateApoptosisCancer cellHomologous recombinationDNA DamageMolecular cancer therapeutics
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