Search results for "uci"

showing 10 items of 5317 documents

Quality, comparability and methods of analysis of data on childhood cancer in Europe (1978-1997): report from the Automated Childhood Cancer Informat…

2006

International audience; In collaboration with 62 population-based cancer registries contributing to the Automated Childhood Cancer Information System (ACCIS), we built a database to study incidence and survival of children and adolescents with cancer in Europe. We describe the methods and evaluate the quality and internal comparability of the database, by geographical region, period of registration, type of registry and other characteristics. Data on 88,465 childhood and 15,369 adolescent tumours registered during 1978-1997 were available. Geographical differences in incidence are caused partly by differences in definition of eligible cases. The observed increase in incidence rates cannot b…

Cancer ResearchPediatricsDatabases FactualMESH: RegistriesMESH : Child Preschool[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineMESH : ChildNeoplasmsMESH: ChildEpidemiologyMedicineMESH: NeoplasmsRegistries030212 general & internal medicineMESH: IncidenceChildeducation.field_of_studyIncidenceIncidence (epidemiology)ComparabilityMESH: Infant NewbornQuality - methods - childhood cancer - EuropeMESH : InfantMESH : AdultMESH: InfantMESH : Incidence3. Good healthEuropeMESH: Reproducibility of ResultsOncologyChild Preschool030220 oncology & carcinogenesisMESH: Survival AnalysisAdultmedicine.medical_specialtyAdolescentPopulationMESH : EuropeMEDLINE[SDV.CAN]Life Sciences [q-bio]/CancerMESH : Databases FactualMESH : Infant Newborn03 medical and health sciencesEnvironmental healthMESH : AdolescentHumanseducationSurvival analysisMESH: AdolescentMESH: Humansbusiness.industryMESH : Reproducibility of ResultsMESH: Child PreschoolMESH : HumansInfant NewbornInfantReproducibility of ResultsCancerMESH: Adultmedicine.diseaseSurvival AnalysisMESH: Databases FactualMESH : NeoplasmsData qualityMESH: EuropeMESH : Survival AnalysisbusinessMESH : Registries
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Prognostic and predictive factors in patients treated with ramucirumab (RAM) with advanced hepatocellular carcinoma (aHCC) and elevated alpha-fetopro…

2021

4146 Background: Elevated AFP in patients with aHCC is a poor prognostic factor with distinct molecular features, including high vascular endothelial growth factor (VEGF) signalling and increased angiogenesis. RAM, a human IgG1 monoclonal antibody, VEGF receptor 2 (VEGFR2) inhibitor, demonstrated improved survival vs placebo among patients with elevated AFP in the REACH-2 trial and is accepted as a standard of care for management of aHCC. We analyzed prognostic factors in patients with AFP ≥400 ng/mL and predictors of clinical benefit to RAM in an individual participant data (IPD) meta-analysis of the REACH and REACH-2 Phase III trials. Methods: Patients with aHCC, Child-Pugh A, ECOG perfo…

Cancer ResearchPrognostic factorPhase iii trialsElevated alpha-fetoproteinbiologybusiness.industryVEGF receptorsmedicine.diseaseRamucirumabVascular endothelial growth factorchemistry.chemical_compoundOncologychemistryHepatocellular carcinomaCancer researchbiology.proteinmedicineIn patientbusinessJournal of Clinical Oncology
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Transforming Growth Factor-β–Mediated Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Expression and Apoptosis in Hepatoma Cells Requires Fun…

2008

Abstract Transforming growth factor-β (TGF-β) has been shown to induce apoptotic cell death in normal and transformed hepatocytes. We recently identified tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as an important mediator of TGF-β–induced apoptosis in hepatoma cells. In this study, we have further explored the mechanism by which TGF-β up-regulates TRAIL expression. The 5′-flanking region of the TRAIL gene was isolated and characterized. Deletion mutants of the 5′-untranslated region of the TRAIL gene revealed a region comprising nucleotides −1950 to −1100 responsible for TRAIL induction following treatment with TGF-β. Within this region, we have identified an activator …

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularMolecular Sequence DataApoptosisSmad ProteinsSMADBiologyTNF-Related Apoptosis-Inducing LigandTransforming Growth Factor betaCell Line TumorHumansGene SilencingPromoter Regions GeneticMolecular BiologySmad4 ProteinBase SequenceActivator (genetics)Liver NeoplasmsDNA NeoplasmTranscription Factor AP-1OncologyCell cultureApoptosisMutationCancer researchTumor necrosis factor alphaProtein BindingSignal TransductionTransforming growth factorFOSBMolecular Cancer Research
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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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IFN-alpha-induced apoptosis in hepatocellular carcinoma involves promyelocytic leukemia protein and TRAIL independently of p53.

2009

Abstract IFNs are pleiotropic cytokines that have been shown to be important regulators of cell growth. IFN-α has recently been recognized to harbor therapeutic potential in prevention and treatment of hepatocellular carcinoma (HCC). However, HCC cells respond differentially to IFN treatment, the mechanism of which is largely unknown. To address this issue, we analyzed the effect of IFN-α on different liver tumor cell lines. We found that growth inhibiting effects of IFN-α in hepatoma cells require PML-NB induction and, moreover, tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) expression on the mRNA and protein level. RNAi silencing of PML down-regulates TRAIL expression in …

Cancer ResearchProgrammed cell deathCarcinoma HepatocellularTumor suppressor genemedicine.medical_treatmentApoptosisPromyelocytic Leukemia ProteinTNF-Related Apoptosis-Inducing LigandPromyelocytic leukemia proteinMiceCell Line TumormedicineGene silencingAnimalsHumansRNA MessengerbiologyCell growthTumor Suppressor ProteinsLiver NeoplasmsInterferon-alphaNuclear ProteinsCytokineOncologyApoptosisbiology.proteinCancer researchTumor necrosis factor alphaRNA InterferenceTumor Suppressor Protein p53Transcription FactorsCancer research
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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
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Targeting apoptosis proteins in hematological malignancies

2010

The apoptotic machinery plays a key role in hematopoietic cell homeostasis. Terminally differentiated cells are eliminated, at least in part, by apoptosis, whereas part of the apoptotic machinery, including one or several caspases, is required to go through very specific steps of the differentiation pathways. A number of hematological diseases involve a deregulation of this machinery, which in most cases is a decrease in cell sensitivity to pro-apoptotic signals through over-expression of anti-apoptotic molecules. In some situations however, e.g. in the erythroid lineage of low grade myelodysplastic syndromes, cell sensitivity to apoptosis is increased in a death receptor-dependent manner a…

Cancer ResearchProgrammed cell deathFas Ligand ProteinMyeloidCellular differentiationAmino Acid MotifsAntineoplastic AgentsApoptosisLigandsInhibitor of apoptosisTNF-Related Apoptosis-Inducing LigandCell Line TumormedicineHumansReceptorCaspasebiologyIntrinsic apoptosisCell DifferentiationCell biologyGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2OncologyApoptosisHematologic Neoplasmsbiology.proteinDrug Screening Assays AntitumorApoptosis Regulatory ProteinsSignal TransductionCancer Letters
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Estrogen receptor α regulates non-canonical autophagy that provides stress resistance to neuroblastoma and breast cancer cells and involves BAG3 func…

2015

AbstractBreast cancer is a heterogeneous disease and approximately 70% of newly diagnosed breast cancers are estrogen receptor (ER) positive. Out of the two ER types, α and β, ERα is the only ER that is detectable by immunohistochemistry in breast cancer biopsies and is the predominant subtype expressed in breast tumor tissue. ER-positive tumors are currently treated with anti-hormone therapy to inhibit ER signaling. It is well known that breast cancer cells can develop endocrine resistance and resistance to anti-hormone therapy and this can be facilitated via the autophagy pathway, but so far the description of a detailed autophagy expression profile of ER-positive cancer cells is missing.…

Cancer ResearchProgrammed cell deathImmunologyEstrogen receptorBreast NeoplasmsBiologyBAG3Cellular and Molecular NeuroscienceNeuroblastomaBreast cancermedicineAutophagyEstrogen Receptor betaHumansPrecision MedicineEstrogen receptor betaPI3K/AKT/mTOR pathwayAdaptor Proteins Signal TransducingEstrogen Replacement TherapyEstrogen Receptor alphaCell Biologymedicine.disease3. Good healthCell biologyGene Expression Regulation NeoplasticCancer cellMCF-7 CellsOriginal ArticleFemaleApoptosis Regulatory ProteinsEstrogen receptor alphaSignal TransductionCell Death & Disease
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Oligodendroglioma cells shed microvesicles which contain TRAIL as well as molecular chaperones and induce cell death in astrocytes.

2011

Microvesicles (MVs) shed from G26/24 oligodendroglioma cells were previously reported to cause a reproducible, dose-dependent, inhibitory effect on neurite outgrowth, and eventually neuronal apoptosis, when added to primary cultures of rat cortical neurons. These effects were reduced but not abolished by functional monoclonal antibodies against Fas-L. In order to investigate whether MVs contain other factors able to induce cell death, we tested them for TRAIL and found clear evidence of its presence in the vesicles. This finding suggests the possibility that Fas-L and TRAIL cooperate in inducing brain cell death. Aimed at understanding the route through which the vesicles deliver their mess…

Cancer ResearchProgrammed cell deathNeuritemedicine.drug_classOligodendrogliomaCellCell CommunicationBiologyMonoclonal antibodyTNF-Related Apoptosis-Inducing LigandCell-Derived MicroparticlesmedicineAnimalsHSP70 Heat-Shock ProteinsRats WistarCells CulturedCell DeathVesicleHSC70 Heat-Shock ProteinsCell cycleMicrovesiclesRatsCell biologymedicine.anatomical_structureOncologyApoptosisAstrocytesCulture Media Conditionedmicrovesicles oligodendroglioma astrocytes TRAIL Hsp70Molecular Chaperones
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HIF-1 is involved in the negative regulation of AURKA expression in breast cancer cell lines under hypoxic conditions

2013

Numerous microarray-based gene expression studies performed on several types of solid tumors revealed significant changes in key genes involved in progression and regulation of the cell cycle, including AURKA that is known to be overexpressed in many types of human malignancies. Tumor hypoxia is associated with poor prognosis in several cancer types, including breast cancer (BC). Since hypoxia is a condition that influences the expression of many genes involved in tumorigenesis, proliferation, and cell cycle regulation, we performed a microarray-based gene expression analysis in order to identify differentially expressed genes in BC cell lines exposed to hypoxia. This analysis showed that h…

Cancer ResearchSettore MED/06 - Oncologia MedicaDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeAURKA Breast cancer Cell cycle HIF-1a HypoxiaCell Line TumorGene expressionTranscriptional regulationmedicineHumansPromoter Regions GeneticAurora Kinase ARegulation of gene expressionGene knockdownTumor hypoxiaCell cycleHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMolecular biologyCell HypoxiaGene Expression Regulation NeoplasticOncologyGene Knockdown TechniquesCancer researchFemalemedicine.symptomCarcinogenesisBreast Cancer Research and Treatment
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