Search results for "Neoplastic"

showing 10 items of 2901 documents

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
researchProduct

The expression of HSP60 and HSP10 in large bowel carcinomas with lymph node metastase

2005

Abstract Background The involvement of Heat Shock Proteins (HSP) in cancer development and progression is a widely debated topic. The objective of the present study was to evaluate the presence and expression of HSP60 and HSP10 in a series of large bowel carcinomas and locoregional lymph nodes with and without metastases. Methods 82 Astler and Coller's stage C2 colorectal cancers, of which 48 well-differentiated and 34 poorly-differentiated, were selected along with 661 lymph nodes, including 372 with metastases and 289 with reactive hyperplasia only, from the same tumours. Primitive tumours and both metastatic and reactive lymph nodes were studied; specifically, three different compartment…

Cancer ResearchPathologymedicine.medical_specialtyTime FactorsColonColorectal cancerBlotting Westernlcsh:RC254-282Surgical oncologyIntestinal NeoplasmsBiomarkers TumorChaperonin 10GeneticsmedicineCarcinomaHumansIntestine LargeNeoplasm MetastasisStage (cooking)Lymph nodeInflammationAnalysis of VarianceHyperplasiabusiness.industryCarcinomaCell DifferentiationChaperonin 60Hyperplasialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseImmunohistochemistryGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyLymphatic MetastasisDisease ProgressionImmunohistochemistryhspLymph NodesLymphbusinessResearch ArticleBMC Cancer
researchProduct

Aurora-A Transcriptional Silencing and Vincristine Treatment Show a Synergistic Effect in Human Tumor Cells

2008

Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G 2 /M cell cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide-, and paclitaxel-induced apoptosis.Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of hu…

Cancer ResearchPathologymedicine.medical_specialtyTranscription GeneticApoptosismacromolecular substancesProtein Serine-Threonine KinasesBiologyTransfectionPLK1Aurora KinasesRNA interferenceCell Line TumormedicineHumansGene silencingGene SilencingRNA Small InterferingMitotic catastropheCentrosomeCisplatinCarcinomaCell CycleDrug SynergismAuroraA/stk15centrosome amplificationAneuploidy CINGeneral MedicineCell cycleAneuploidyAntineoplastic Agents PhytogenicGene Expression Regulation NeoplasticSettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)OncologyVincristineCentrosomeColonic Neoplasmsembryonic structuresCancer cellCancer researchbiological phenomena cell phenomena and immunityHeLa Cellsmedicine.drugOncology Research Featuring Preclinical and Clinical Cancer Therapeutics
researchProduct

Progressive multifocal encephalopathy in a patient with non-Hodgkin follicular lymphoma

2020

Progressive multifocal leukoencephalopathy (PML) is a rare and often fatal demyelinating disease of the central nervous system caused by John Cunningham virus (JCV). We present a case report of patient with non-Hodgkin follicular lymphoma, who developed PML after hematopoietic stem cell transplantation and rituximab-bendamustine therapy. JCV DNA was proven both in peripheral blood and cerebrospinal fluid. Patient with 4 years history of follicular lymphoma presented with progressing weakness in the right arm and leg and postural instability. Magnetic resonance imaging scans showed bilateral hyperintense lesions in the cerebellum and centrum semiovale consistent with findings in PML. JCV DNA…

Cancer ResearchPathologymedicine.medical_specialtyvirusesmedicine.medical_treatmentEncephalopathyFollicular lymphomaHematopoietic stem cell transplantationImmunocompromised HostCerebrospinal fluidAntineoplastic Combined Chemotherapy ProtocolsCentrum semiovalemedicineDemyelinating diseaseHumansLymphoma Follicularmedicine.diagnostic_testbusiness.industryProgressive multifocal leukoencephalopathyHematopoietic Stem Cell TransplantationLeukoencephalopathy Progressive MultifocalDisease ManagementMagnetic resonance imagingMiddle Agedmedicine.diseaseMagnetic Resonance ImagingTreatment OutcomeOncologyPositron-Emission TomographyFemaleTomography X-Ray ComputedbusinessExperimental Oncology
researchProduct

Underuse of long-term routine hospital follow-up care in patients with a history of breast cancer?

2011

Abstract Background After primary treatment for breast cancer, patients are recommended to use hospital follow-up care routinely. Long-term data on the utilization of this follow-up care are relatively rare. Methods Information regarding the utilization of routine hospital follow-up care was retrieved from hospital documents of 662 patients treated for breast cancer. Utilization of hospital follow-up care was defined as the use of follow-up care according to the guidelines in that period of time. Determinants of hospital follow up care were evaluated with multivariate analysis by generalized estimating equations (GEE). Results The median follow-up time was 9.0 (0.3-18.1) years. At fifth and…

Cancer ResearchPediatricsMultivariate analysisAftercareComorbidityGUIDELINESGeelaw.inventionCohort StudiesRandomized controlled triallawNetherlandsAged 80 and overSURVIVORSmedicine.diagnostic_testBreast neoplasmFollow-upNeoplasms Second PrimaryMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensCombined Modality TherapyUtilizationOncologyPractice Guidelines as TopicRECURRENCESHormonal therapyFemaleGuideline AdherenceHEALTHResearch ArticleCohort studyMammographyAdultmedicine.medical_specialtyOutpatient Clinics HospitalAntineoplastic Agents HormonalMatched-Pair AnalysisBreast Neoplasmslcsh:RC254-282Breast cancerGeneticsmedicineHumansMammographyMETAANALYSISAgedbusiness.industryPatient Acceptance of Health Caremedicine.diseaseComorbidityTRENDSRANDOMIZED-TRIALHealth Care SurveysPhysical therapyPatient ComplianceUPDATESURVEILLANCE MAMMOGRAPHYbusinessFollow-Up Studies
researchProduct

Early deaths in acute lymphoblastic leukemia (ALL): results of the Italian Pediatric Cooperative Group for Therapy of Acute Leukemia (AIL-AIEOP).

1984

In this retrospective multicentric study, we report on early deaths (ie, those that occurred during the first month of treatment) in a total of 943 newly diagnosed ALL pediatric patients registered from 1976 to 1981 at 21 centers of the AIL-AIEOP. Objectives of this study were as follows: (1) to verify the incidence and the cause of early death in a wide population of children with ALL and (2) to elucidate factors associated with early death and therefore to identify “high-risk” groups of patients. Out of the 943 ALL patients, 39 (4.1%) early deaths were registered. Main causes were infection, 20 patients (51.3%); hemorrhage, 11 patients (28.3%); uric acid nephropathy, 2 patients (5.1%); ca…

Cancer ResearchPediatricsmedicine.medical_specialtyAdolescentHeart DiseasesLymphoblastic LeukemiaPopulationEarly deathHemorrhageInfectionsMediastinal NeoplasmsNephropathyAntineoplastic Combined Chemotherapy ProtocolsmedicineHumanseducationChildRetrospective Studieseducation.field_of_studyAcute leukemiabusiness.industryIncidence (epidemiology)Age FactorsMediastinumInfantmedicine.diseasePrognosisLeukemia Lymphoidmedicine.anatomical_structureOncologyChild PreschoolPediatrics Perinatology and Child HealthSyndrome of inappropriate antidiuretic hormone secretionKidney DiseasesbusinessMedical and pediatric oncology
researchProduct

Diorganotin(IV) and triorganotin(IV) complexes of meso-tetra(4-sulfonatophenyl) porphine induce apoptosis in A375 human melanoma cells

2006

The cytotoxic effect of several diorganotin(IV) and triorganotin(IV)-meso-tetra(4-sulfonatophenyl)porphine derivatives was tested and only the (Bu(2)Sn)(2)TPPS and the (Bu(3)Sn)(4)TPPS showed cytotoxicity on A375 human melanoma cells. To examine the pathway of (Bu(2)Sn)(2)TPPS or (Bu(3)Sn)(4)TPPS induced A375 cell death, DNA fragmentation analysis, Annexin V binding and PI uptake as well as caspases activation analysis by Western blot were carried out. A375 cells treated exhibited several typical characteristics of apoptosis. Both the (Bu(2)Sn)(2)TPPS and the (Bu(3)Sn)(4)TPPS compounds activate caspase-8 and caspase-9 leading to caspase-3 activation. Thus, we propose that these two porphiri…

Cancer ResearchPorphyrinsCytotoxicityMelamoma cellAntineoplastic AgentsApoptosisDNA FragmentationWestern blotAnnexinCell Line TumorOrganotin CompoundsPimedicineHumansCytotoxic T cellCytotoxicityMelanomaCaspasebiologymedicine.diagnostic_testTriorganotin(IV)ApoptosiFlow CytometryMolecular biologyMicroscopy FluorescenceOncologyApoptosisCaspasesbiology.proteinDNA fragmentationDiorganotin(IV)
researchProduct

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
researchProduct

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
researchProduct

Histone deacetylase inhibition by valproic acid down-regulates c-FLIP/CASH and sensitizes hepatoma cells towards CD95-and TRAIL receptor-mediated apo…

2005

Hepatocellular carcinoma (HCC) is highly resistant to chemotherapy, leading to a poor prognosis of advanced disease. Inhibitors of histone deacetylase (HDACi) induce re-differentiation in tumor cells and thereby re-establish sensitivity towards apoptotic stimuli. HDACi are entering the clinical stage of tumor treatment, and several substances are currently being tested in clinical trials to prove their efficacy in the treatment of leukemias and solid tumors. In this study, we investigated the impact of the HDACi valproic acid (VA) on TRAIL- and CD95-mediated apoptosis in hepatoma cells, as well as its sensitizing effect on a chemotherapeutic agent. Treatment of HepG2 cells with VA increased…

Cancer ResearchProgrammed cell deathCarcinoma Hepatocellularmedicine.medical_treatmentCellCASP8 and FADD-Like Apoptosis Regulating ProteinDown-RegulationCaspase 3ApoptosisBiologyReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansfas ReceptorEpirubicinChemotherapyMembrane GlycoproteinsCaspase 3Tumor Necrosis Factor-alphaValproic AcidLiver NeoplasmsIntracellular Signaling Peptides and ProteinsGeneral MedicineCell cycleFas receptorHistone Deacetylase Inhibitorsmedicine.anatomical_structureOncologyApoptosisDrug Resistance NeoplasmCaspasesCancer researchHistone deacetylaseApoptosis Regulatory Proteins
researchProduct