Search results for "blas"

showing 10 items of 2217 documents

Glioblastoma cells induce differential glutamatergic gene expressions in human tumor-associated microglia/macrophages and monocyte-derived macrophages

2015

Glioblastoma cells produce and release high amounts of glutamate into the extracellular milieu and subsequently can trigger seizure in patients. Tumor-associated microglia/macrophages (TAMs), consisting of both parenchymal microglia and monocytes-derived macrophages (MDMs) recruited from the blood, are known to populate up to 1/3 of the glioblastoma tumor environment and exhibit an alternative, tumor-promoting and supporting phenotype. However, it is unknown how TAMs respond to the excess extracellular glutamate in the glioblastoma microenvironment. We investigated the expressions of genes related to glutamate transport and metabolism in human TAMs freshly isolated from glioblastoma resecti…

Cancer ResearchAntigens Differentiation MyelomonocyticGlutamic AcidglutamateAMPA receptorSLC7A11Antigens CDTumor Cells CulturedExtracellularmedicineHumansReceptors AMPAGRIA2PharmacologyCD11b AntigenbiologyMicrogliaBrain NeoplasmsMacrophagesmonocyte-derived macrophagesCalcium-Binding ProteinsMicrofilament Proteinsglioblastomatumor-associated microglia/macrophagesGlutamate receptorSLC1A2Coculture TechniquesDNA-Binding ProteinsGlutaminemedicine.anatomical_structureGene Expression RegulationOncologyAstrocytesImmunologybiology.proteinCancer researchLeukocyte Common AntigensMolecular MedicineMicrogliaResearch PaperCancer Biology & Therapy
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MYCN sensitizes human neuroblastoma to apoptosis by HIPK2 activation through a DNA damage response.

2010

Abstract MYCN amplification occurs in approximately 20% of human neuroblastomas and is associated with early tumor progression and poor outcome, despite intensive multimodal treatment. However, MYCN overexpression also sensitizes neuroblastoma cells to apoptosis. Thus, uncovering the molecular mechanisms linking MYCN to apoptosis might contribute to designing more efficient therapies for MYCN-amplified tumors. Here we show that MYCN-dependent sensitization to apoptosis requires activation of p53 and its phosphorylation at serine 46. The p53S46 kinase HIPK2 accumulates on MYCN expression, and its depletion by RNA interference impairs p53S46 phosphorylation and apoptosis. Remarkably, MYCN ind…

Cancer ResearchApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein-Serine-Threonine KinaseAtaxia Telangiectasia Mutated ProteinNeuroblastomaCell Cycle ProteinSerinePhosphorylationNuclear ProteinOncogene Proteinseducation.field_of_studyN-Myc Proto-Oncogene ProteinAntibiotics AntineoplasticKinaseOncogene ProteinNuclear ProteinsDNA-Binding ProteinsOncologyPhosphorylationRNA InterferenceHumanDNA damageDNA-Binding ProteinPopulationBlotting WesternBiologyProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinBleomycinNeuroblastomaCell Line TumormedicineHumanseducationneoplasmsMolecular BiologyTumor Suppressor ProteinTumor Suppressor ProteinsApoptosimedicine.diseaseTumor progressionApoptosisMutationCancer researchTumor Suppressor Protein p53Carrier ProteinCarrier ProteinsDNA DamageMolecular cancer research : MCR
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Role of glutathione in the induction of apoptosis and c-fos and c-jun mRNAs by oxidative stress in tumor cells.

2003

We have used two tumor cell clones (B9 and G2), derived from the methylcholanthrene-induced murine fibrosarcoma GR9 and normal BALB/c3T3 fibroblasts, to study the ability of t-BOOH derived reactive oxygen radicals to induce oxidative stress, apoptosis and c-fos and c-jun mRNA transcription. These clones differ in terms of their major histocompatibility complex (MHC) (H-2) class I genes expression, their tumor induction and metastatic potential and their reduced glutathione (GSH) levels. Incubation of both cell clones in the presence of t-BOOH results in the increase of 8-oxo-2'-deoxyguanosine (8-oxo-dG) and malondialdehyde and the decrease of GSH. The xenobiotic also induces the transcripti…

Cancer ResearchBALB 3T3 CellsTranscription GeneticProto-Oncogene Proteins c-junFibrosarcomaCellApoptosisBiologymedicine.disease_causeAntioxidantsSuperoxide dismutasechemistry.chemical_compoundMicetert-ButylhydroperoxideCell CloneMalondialdehydemedicineTumor Cells CulturedAnimalsRNA MessengerDNA Primerschemistry.chemical_classificationReactive oxygen speciesReverse Transcriptase Polymerase Chain Reactionc-junHistocompatibility Antigens Class IDeoxyguanosineGlutathioneFibroblastsMolecular biologyGlutathioneOxidative Stressmedicine.anatomical_structureOncologychemistryGene Expression RegulationApoptosis8-Hydroxy-2'-Deoxyguanosinebiology.proteinReactive Oxygen SpeciesProto-Oncogene Proteins c-fosOxidative stressCancer letters
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Morphological transformation and DNA adduct formation by dibenz[a,h]anthracene and its metabolites in C3H10T1/2CL8 cells.

1994

The major routes of metabolic activation of dibenz[a,h]-anthracene (DBA) have been studied in transformable C3H10T1/2CL8 (C3H10T1/2) mouse embryo fibroblasts in culture. The morphological transforming activities of three potential intermediates formed by metabolism of DBA by C3H10T1/2 cells, trans-3,4-dihydroxy-3,4-dihydro-DBA-(DBA-3,4-diol), trans-dihydroxy-3,4-dihydro-DBA-anti-1,2-oxide (DBA-3,4-diol-1,2-oxide) and DBA-5,6-oxide were determined. DBA-3,4-diol-1,2-oxide was a strong morphological transforming agent giving a mean of 73% dishes with Type II or III foci and 1.63 Type II and III foci per dish at 0.5 microgram/ml. DBA-3,4-diol produced a mean of 42% dishes with Type II or III fo…

Cancer ResearchBiologychemistry.chemical_compoundDNA AdductsMiceStructure-Activity Relationshippolycyclic compoundsmedicineBenz(a)AnthracenesDeoxyguanosineDibenz(ah)anthraceneAnimalsFibroblastCarcinogenBiotransformationMice Inbred C3HGeneral MedicineMetabolismFibroblastsIn vitromedicine.anatomical_structureCell Transformation NeoplasticchemistryBiochemistryCell cultureIsotope LabelingOxidation-ReductionPhosphorus RadioisotopesDNACarcinogenesis
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Differences in the mechanisms of growth control in contact-inhibited and serum-deprived human fibroblasts

1997

In the present work we studied mechanisms of growth control in contact-inhibited and serum-deprived human diploid fibroblasts. The observation that the effects on [3H]thymidine incorporation and reduction of retinoblastoma gene product-phosphorylation were additive when contact-inhibition and serum-deprivation were combined led us to the conclusion that the underlying mechanisms might be different. Both contact-inhibition and serum-deprivation led to a strong decrease of cdk4-kinase-activity and cdk2-phosphorylation at Thr 160, while the total amounts of cdk4 and cdk2 remained constant. In contact-inhibited cells, we revealed a strong protein accumulation of the cdk2-inhibitor p27 and a sli…

Cancer ResearchCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinCulture Media Serum-FreeS PhaseCyclin D1CyclinsProto-Oncogene ProteinsCDC2-CDC28 KinasesGeneticsmedicineHumansCyclin D1Cyclin D3PhosphorylationCyclin D3FibroblastMolecular BiologyCyclin-Dependent Kinase Inhibitor p16CyclinbiologyCell growthTumor Suppressor ProteinsCyclin-Dependent Kinase 2Cyclin-dependent kinase 2G1 PhaseCyclin-Dependent Kinase 4FibroblastsDiploidyCyclin-Dependent KinasesCulture MediaCell biologymedicine.anatomical_structureCell culturebiology.proteinbiological phenomena cell phenomena and immunitySignal transductionMicrotubule-Associated ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p27Oncogene
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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P11.09 Pan-RTK inhibition of sLRIG1 mediates AXL downregulation in Glioblastoma

2019

Abstract INTRODUCTION Aberrant regulation of receptor tyrosine kinase (RTK) activity is characteristic of Glioblastoma (GBM). However, RTK-based targeted therapies have been largely unsuccessful in GBM patients, partially due to the complexity and redundance of RTK signaling. LRIG1 (Leucine-rich Repeats and ImmunoGlobulindomains protein 1) is known as an endogenous inhibitor of epidermal growth factor receptor (EGFR) during health and disease, however its mechanism of action is poorly understood. We previously showed that the soluble form of LRIG1 potently inhibits of GBM growth in vivo, irrespective of EGFR expression level and status, suggesting the involvement of other RTKs. Here, we aim…

Cancer ResearchCell growthChemistrymedicine.diseasePoster PresentationsOncologyDownregulation and upregulationmedicineCancer researchNeurology (clinical)Cellular MorphologyTransluminal attenuation gradientSignal transductionGlioblastoma
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Expression of type I interferon receptor and its relation with other prognostic factors in human neuroblastoma.

1998

Expression of type I interferon receptor (IFN-R) has been found in several normal tissues and in malignant neoplasms, mainly those with epithelial differentiation. In order to analyze the immunohistochemical expression of type I IFN-R we studied 79 cases of neuroblastoma. Results of expression of type I IFN-R were statistically correlated with histopathology, stage, bcl-2 and PCNA expression, N-myc amplification and apoptosis. We found expression of type I IFN-R in 54/79 cases showing statistical correlation with bcl-2 expression (P=0.017) and favourable histopathology (P=0.015). The overexpression found in ganglion cells suggests that IFN-R could be involved in the pathway of neuroblastoma…

Cancer ResearchCellular differentiationmedicine.medical_treatmentGenes mycAlpha interferonApoptosisReceptor Interferon alpha-betaBiologyImmunoenzyme TechniquesNeuroblastomaProliferating Cell Nuclear AntigenNeuroblastomaGene expressionBiomarkers TumormedicineHumansChildInterferon alfaNeoplasm StagingReceptors InterferonOncogeneGene AmplificationInfantMembrane ProteinsCell DifferentiationGeneral MedicinePrognosismedicine.diseaseNeoplasm ProteinsCytokineProto-Oncogene Proteins c-bcl-2OncologySpainChild PreschoolCancer researchImmunohistochemistrymedicine.drugOncology Reports
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A sphingosine kinase inhibitor combined with temozolomide induces glioblastoma cell death through accumulation of dihydrosphingosine and dihydroceram…

2014

AbstractGlioblastomas (GBMs) are very aggressive tumors with low chemosensitivity. The DNA-alkylating agent temozolomide (TMZ) is currently the most efficient chemotoxic drug for GBM therapy; however, many patients develop resistance to TMZ. Combining TMZ with another agent could present an improved treatment option if it could overcome TMZ resistance and avoid side effects. Sphingosine kinase inhibitors (SKIs) have emerged as anticancer agents. Sphingosine kinases are often overexpressed in tumors where their activity of phosphorylating sphingosine (Sph) contributes to tumor growth and migration. They control the levels of the pro-apoptotic ceramide (Cer) and Sph and of the pro-survival sp…

Cancer ResearchCeramideProgrammed cell deathImmunologySphingosine kinaseAntineoplastic AgentsApoptosisBiologyCeramidesCellular and Molecular Neurosciencechemistry.chemical_compoundSphingosineCell Line TumorAutophagyTemozolomideHumansEnzyme InhibitorsCytotoxicitySphingosineCell DeathKinaseBrain NeoplasmsAutophagyCell BiologyEndoplasmic Reticulum StressCell biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)chemistryApoptosisDrug Resistance NeoplasmCancer researchDrug Therapy CombinationOriginal ArticleGlioblastomaCell deathdisease
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A phase III study of futibatinib (TAS-120) versus gemcitabine-cisplatin (gem-cis) chemotherapy as first-line (1L) treatment for patients (pts) with a…

2020

TPS600 Background: Pts with adv CCA have poor survival outcomes, and chemotherapy offers limited survival benefit (5-year survival rates, 5–10%; median overall survival [OS], 8–12 months). FGFR2 gene rearrangements are known to be early drivers of oncogenesis in ~15% of pts with intrahepatic (i) CCA. Futibatinib, an oral, highly selective, irreversible FGFR1-4 inhibitor has shown antitumor activity against a broad spectrum of FGFR-deregulated tumors in preclinical studies. In a previous study, futibatinib demonstrated clinical activity and tolerability in heavily pretreated pts with adv CCA harboring FGFR2 gene rearrangements. This phase 3 trial (FOENIX-CCA3) is designed to evaluate futiba…

Cancer ResearchChemotherapyFibroblast growth factor receptor 2business.industrymedicine.medical_treatmentFirst lineGemcitabine/cisplatinstomatognathic diseases03 medical and health sciences0302 clinical medicineSurvival benefitOncology030220 oncology & carcinogenesisOverall survivalmedicineCancer researchbusinessGene030215 immunologyJournal of Clinical Oncology
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