Search results for " glioblastoma"

showing 10 items of 24 documents

RNA-sequencing and bioinformatic analysis to pre-assess sensitivity to targeted therapeutics in recurrent glioblastoma.

2019

e13533 Background: This study developed molecular guided tools for individualized selection of chemotherapeutics for recurrent glioblastoma (rGB). A consortium involving clinical neurooncologists, molecular biologists and bioinformaticians identified gene expression patterns in rGB and quantitatively analyzed pathways involved in response to FDA approved oncodrugs. Methods: From2016 to 2018 biopsies from GB were collected using a multisampling approach. Biopsy material was used to isolate glioma stem-like cells and examined by RNA-sequencing. RNA-seq results were subjected to differential expression (DE) analysis and Oncobox analysis – a bioinformatic tool for quantitative pathway activati…

Cancer Researchbusiness.industryRecurrent glioblastomaRNAComputational biology03 medical and health sciences0302 clinical medicineOncology030220 oncology & carcinogenesisMedicineSensitivity (control systems)businessSelection (genetic algorithm)030215 immunologyJournal of Clinical Oncology
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Design, synthesis and biological evaluation of new anticancer drugs: FGFR inhibitors

2021

Fibroblast growth factor receptors (FGFRs) constitute a family of tyrosine kinases receptors (RTKs) that exert pivotal physiological functions in human embryonic and adult tissues. Hyperactivated FGFR signaling drives tumorigenesis in multiple cancer types, including lung and brain cancers. Great effort has been laid on the development of new compounds that specifically target the FGFR axis. However, cancer cell- based and microenvironmental resistance mechanisms against FGFR inhibitors often arise and are currently poorly understood. Furthermore, FGFR-targeted therapy often presents different side effects, e due to the broad biological spectrum of the FGFR signaling axis as well as to its …

DesignhypoxiabrainglioblastomatransitionAnticancer drugs FGFR Drug design Ubiquitin Brain tumor Glioblastoma Lung cancer NSCLC SCLC Copper complexes Hypoxia activated drugs Metal drugsSettore BIO/11 - Biologia MolecolareSettore CHIM/08 - Chimica Farmaceuticalungmetal complexeFGFR1Settore CHIM/03 - Chimica Generale E InorganicacopperSettore BIO/10 - BiochimicaFGFR4Settore BIO/14 - Farmacologiacancersynthesi
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A BMP7 Variant Inhibits Tumor Angiogenesis In Vitro and In Vivo through Direct Modulation of Endothelial Cell Biology

2015

Bone morphogenetic proteins (BMPs), members of the TGF-β superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Using an in vitro co-culture endothelial cord formation assay, we investigated the role of a BMP7 variant (BMP7v) in VEGF, bFGF, and tumor-driven angiogenesis. BMP7v treatment led to disruption of neo-endothelial cord formation and regression of existing VEGF and bFGF cords in vitro. Using a series of tumor cell models capable of driving angiogenesis in vitro, BMP7v treatment completely blocked cord formation. Pre-treatment of endothelial cells with BMP7v significantly reduced their cord forming ability, indicating …

Genetics and Molecular Biology (all)MaleVascular Endothelial Growth Factor AFibroblast Growth FactorAngiogenesisBone Morphogenetic Protein 7Nudelcsh:MedicineSmad ProteinsFibroblast growth factorBiochemistryNeovascularizationMiceCell Movementlcsh:ScienceBMP7 Angiogenesis TumorTumorMultidisciplinaryCell DeathNeovascularization PathologicMedicine (all)Cell migrationCell biologyEndothelial stem cellSettore MED/26 - NEUROLOGIAVascular endothelial growth factor ADrug CombinationsAdipose TissueAdipose Tissue; Animals; Bone Morphogenetic Protein 7; Cell Death; Cell Line Tumor; Cell Movement; Cell Proliferation; Collagen; Drug Combinations; Endothelial Cells; Fibroblast Growth Factor 2; Glioblastoma; Human Umbilical Vein Endothelial Cells; Humans; Laminin; Male; Mice Nude; Neoplastic Stem Cells; Neovascularization Pathologic; Neovascularization Physiologic; Proteoglycans; Receptor Fibroblast Growth Factor Type 1; Signal Transduction; Smad Proteins; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Xenograft Model Antitumor Assays; Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Neoplastic Stem CellsFibroblast Growth Factor 2ProteoglycansCollagenmedicine.symptomReceptorType 1Research ArticleSignal TransductionMice NudeNeovascularization PhysiologicBMP7BiologyCell LineSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansAgricultural and Biological Sciences (all); Biochemistry Genetics and Molecular Biology (all); Medicine (all)Receptor Fibroblast Growth Factor Type 1PhysiologicNeovascularizationCell ProliferationPathologicMatrigelBiochemistry Genetics and Molecular Biology (all)lcsh:REndothelial CellsKinase insert domain receptorVascular Endothelial Growth Factor Receptor-2Xenograft Model Antitumor AssaysAgricultural and Biological Sciences (all)lcsh:QAngiogenesisLamininGlioblastomaPLoS ONE
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Quaking and miR-155 interactions in inflammation and leukemogenesis.

2015

Quaking (QKI) is a tumor-suppressor gene encoding a conserved RNA-binding protein, whose expression is downregulated in several solid tumors. Here we report that QKI plays an important role in the immune response and suppression of leukemogenesis. We show that the expression of Qki is reduced in lipopolysaccharide (LPS)-challenged macrophages, suggesting that Qki is a key regulator of LPS signaling pathway. Furthermore, LPS-induced downregulation of Qki expression is miR-155-dependent. Qki overexpression impairs LPS-induced phosphorylation of JNK and particularly p38 MAPKs, in addition to increasing the production of anti-inflammatory cytokine IL-10. In contrast, Qki ablation decreases Fas …

LipopolysaccharidesTime Factorsmedicine.medical_treatmentmedicine.disease_causeTransgenicMiceInnatePhosphorylationChronicB-LymphocytesLeukemiaRNA-Binding ProteinsU937 CellsLymphocyticCell biologyCytokineOncologyPhosphorylationCytokinesCLL; Glioblastoma; Inflammation; MiR-155; QKI; Animals; Apoptosis Regulatory Proteins; B-Lymphocytes; Case-Control Studies; Cytokines; Humans; Immunity Innate; Inflammation; Leukemia Lymphocytic Chronic B-Cell; Lipopolysaccharides; Macrophages; Mice; Mice Transgenic; MicroRNAs; Mitogen-Activated Protein Kinases; Phosphorylation; RAW 264.7 Cells; RNA-Binding Proteins; Signal Transduction; Time Factors; Transfection; U937 Cells; OncologySignal transductionMitogen-Activated Protein KinasesSignal Transductionp38 mitogen-activated protein kinasesOncology and CarcinogenesisMice TransgenicTransfectionNOmiR-155miR-155Downregulation and upregulationmicroRNAmedicineAnimalsHumansInflammationQKIbusiness.industryMacrophagesB-CellImmunityglioblastomaLeukemia Lymphocytic Chronic B-CellImmunity InnateMicroRNAsRAW 264.7 CellsCase-Control StudiesImmunologyCarcinogenesisbusinessApoptosis Regulatory ProteinsCLLPriority Research Paper
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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ERGO: A pilot study of ketogenic diet in recurrent glioblastoma

2014

Limiting dietary carbohydrates inhibits glioma growth in preclinical models. Therefore, the ERGO trial (NCT00575146) examined feasibility of a ketogenic diet in 20 patients with recurrent glioblastoma. Patients were put on a low-carbohydrate, ketogenic diet containing plant oils. Feasibility was the primary endpoint, secondary endpoints included the percentage of patients reaching urinary ketosis, progression-free survival (PFS) and overall survival. The effects of a ketogenic diet alone or in combination with bevacizumab was also explored in an orthotopic U87MG glioblastoma model in nude mice. Three patients (15%) discontinued the diet for poor tolerability. No serious adverse events attri…

MaleCancer ResearchStatement (logic)medicine.medical_treatmentSalvage treatmentPilot ProjectsBioinformaticsGastroenterologyMicegliomaClinical endpoint1306 Cancer ResearchglucoseArticlesMiddle AgedCombined Modality TherapyBevacizumabTreatment OutcomeTolerabilityOncologyketogenic dietFemale2730 OncologyDiet Ketogenicmedicine.drugAdultmedicine.medical_specialtyBevacizumabMice NudeAntineoplastic Agents610 Medicine & healthMistakeRecurrent GliomaBiologyAntibodies Monoclonal HumanizedInternal medicineGliomamedicineAnimalsHumansddc:610Adverse effectAgedbusiness.industryRecurrent glioblastomaGeneral surgeryKetosisNeoplasms Experimentalmedicine.diseaseSurvival Analysis10040 Clinic for NeurologySurgeryQuality of LifeNeoplasm Recurrence LocalKetosisGlioblastomabusinessmetabolismfeasibilityKetogenic dietInternational Journal of Oncology
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Higher vascularity at infiltrated peripheral edema differentiates proneural glioblastoma subtype

2020

[EN] Background and purpose Genetic classifications are crucial for understanding the heterogeneity of glioblastoma. Recently, perfusion MRI techniques have demonstrated associations molecular alterations. In this work, we investigated whether perfusion markers within infiltrated peripheral edema were associated with proneural, mesenchymal, classical and neural subtypes. Materials and methods ONCOhabitats open web services were used to obtain the cerebral blood volume at the infiltrated peripheral edema for MRI studies of 50 glioblastoma patients from The Cancer Imaging Archive: TCGA-GBM. ANOVA and Kruskal-Wallis tests were carried out in order to assess the association between vascular fea…

MalePathologyMolecular compositionPhysiologyPeripheral edemaBrain Edema030218 nuclear medicine & medical imagingDiagnostic Radiology0302 clinical medicineVascularityMedicine and Health SciencesMedicine03.- Garantizar una vida saludable y promover el bienestar para todos y todas en todas las edadesEdemaCerebral Blood VolumeNeurological TumorsProneural GlioblastomaAged 80 and overMultidisciplinaryBlood VolumeBrain NeoplasmsRadiology and ImagingQRMiddle AgedPrognosisMagnetic Resonance Imaging3. Good healthBody FluidsBloodOncologyNeurology030220 oncology & carcinogenesisMedicineFemaleAnalysis of variancemedicine.symptomAnatomyPerfusionResearch ArticleAdultmedicine.medical_specialtyAdolescentImaging TechniquesBlastomaScienceResearch and Analysis Methods03 medical and health sciencesYoung AdultText miningSigns and SymptomsMalignant TumorsDiagnostic MedicineGeneticsHumansAgedRetrospective StudiesMri techniquesCancer och onkologibusiness.industryProportional hazards modelMesenchymal stem cellCancers and NeoplasmsBiology and Life Sciencesmedicine.diseaseSurvival AnalysisCancer and OncologyFISICA APLICADAClinical MedicinebusinessGlioblastoma030217 neurology & neurosurgeryGlioblastoma MultiformeMagnetic Resonance AngiographyGlioblastomaPLoS ONE
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Cancer stem cell analysis and clinical outcome in patients with glioblastoma multiforme

2008

Abstract Purpose: Cancer stem cells (CSC) are thought to represent the population of tumorigenic cells responsible for tumor development. The stem cell antigen CD133 identifies such a tumorigenic population in a subset of glioblastoma patients. We conducted a prospective study to explore the prognostic potential of CSC analysis in glioblastoma patients. Experimental Design: We investigated the relationship between the in vitro growth potential of glioblastoma CSCs and patient death or disease progression in tumors of 44 consecutive glioblastoma patients treated with complete or partial tumorectomy followed by radiotherapy combined with temozolomide treatment. Moreover, we evaluated by immun…

OncologyAdultMaleCancer Researchmedicine.medical_specialtyPathologyAC133 Antigen; Adult; Aged; Antigens CD; Brain Neoplasms; Female; Glioblastoma; Glycoproteins; Humans; Ki-67 Antigen; Male; Middle Aged; Multivariate Analysis; Neoplastic Stem Cells; Peptides; Prospective Studiesmedicine.medical_treatmentPopulationAntigens CDCancer stem cellInternal medicinemedicineHumansAC133 AntigenProspective StudiesAntigensProspective cohort studyeducationAgedGlycoproteinseducation.field_of_studyTemozolomideSettore MED/08 - ANATOMIA PATOLOGICAbusiness.industryBrain NeoplasmsHazard ratioMiddle AgedGliobastoma MultiformeCDRadiation therapyKi-67 AntigenOncologyMultivariate AnalysisNeoplastic Stem CellsImmunohistochemistryFemaleStem cellbusinessGlioblastomaPeptidesmedicine.drug
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The Role of Medicinal Mushrooms in Brain Cancer Therapies: Review.

2021

Medicinal mushrooms are considered an unlimited source of polysaccharides (mainly β-glucans) and polysaccharide-protein complexes and possess various immunological and anticancer properties. In addition, their use in integrative medicine leads to a clear reduction of side effects in patients undergoing chemotherapy or radiotherapy. The literature reports a number of beneficial effects of using mushrooms as health supplements in patients affected by high-grade glioma. The effects of medicinal mushrooms on side effects in patients with brain cancer and a case study report are also described in this review.

Oncologymedicine.medical_specialtymedicine.medical_treatmentMEDLINEApplied Microbiology and BiotechnologyBrain cancerStudy reportPolysaccharidesInternal medicineGliomaDrug DiscoverymedicineHumansIn patientintegrative therapies brain cancer glioblastoma medicinal mushrooms mycotherapeutic supportPharmacologyChemotherapybusiness.industryBrain Neoplasmsmedicine.diseaseRadiation therapySettore BIO/03 - Botanica Ambientale E ApplicataDietary SupplementsIntegrative medicinebusinessAgaricalesInternational journal of medicinal mushrooms
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Integrated approach to delineating molecular traits of recurrent glioblastoma using glioma stem cell models and tumor tissue profiling

2018

Recurrent glioblastomaGliomamedicineCancer researchProfiling (information science)BiologyIntegrated approachStem cellmedicine.diseaseTumor tissue27th Annual Meeting of the working group “Experimental Neuro-Oncology”
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