Search results for " glioblastoma"

showing 10 items of 24 documents

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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Different immunohistochemical levels of Hsp60 and Hsp70 in a subset of brain tumors and putative role of Hsp60 in neuroepithelial tumorigenesis

2013

In this work we analysed, by immunohistochemistry, a series of brain tumors to detect the levels and cellular distribution of Hsp60 and Hsp70. We found that Hsp60 levels were significantly higher than those of Hsp70 in neuroepithelial tumors, while levels of both molecules were not significantly different from each other in meningeal neoplasms. In particular, Hsp60 immunopositivity was present mainly at the cytoplasmic level, while Hsp70 immunopositivity was found both in the cytoplasm and in the nucleus of tumor cells. The levels of these molecules in healthy control cells were always very low. Finally, Hsp60 and Hsp70 levels did not correlate with the different types (WHO grade) of neopla…

AdultMalePathologymedicine.medical_specialtyanimal structuresHistologyAdolescentNeuroepithelial CellsBiophysicschemical and pharmacologic phenomenaBiologymedulloblastomamedicine.disease_causemeningiomacomplex mixturesHsp60 Hsp70 astrocytoma glioblastoma multiformae medulloblastoma meningiomaHsp70Meningeal NeoplasmsmedicineHumansHSP70 Heat-Shock ProteinsMeningeal NeoplasmChildastrocytomalcsh:QH301-705.5AgedAged 80 and overMedulloblastomaHsp60 Hsp70 astrocytoma glioblastoma multiformae medulloblastoma meningioma.Brain NeoplasmsBrief ReportfungiAstrocytomaChaperonin 60Cell BiologyMiddle AgedHsp60medicine.diseaseImmunohistochemistryNeoplasms NeuroepithelialNeuroepithelial cellglioblastoma multiformaelcsh:Biology (General)Tumor progressionChild PreschoolCancer cellImmunohistochemistryFemaleCarcinogenesisEuropean Journal of Histochemistry
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Spinal Intradural Intramedullary Dissemination in the Absence of Intracranial Relapse of a Previously Radically Treated Temporal Lobe Glioblastoma Mu…

2017

Intracranial glioblastoma multiforme (GBM) constitutes the most frequent and unfortunately aggressive primary central nervous system malignancy. Despite the high tendency of these tumors to show local relapse within the brain after primary therapy, dissemination into the spinal axis is an infrequent event. If spinal metastases occur they are leptomeningeal in the vast majority of cases and always in the context of intracranial progressive disease. Spinal intramedullary metastases of intracranial GBM have rarely been described to date. We report the unique case of a young woman with subacute progressive paraparesis due to spinal intramedullary metastases of a temporal lobe GBM despite the re…

medicine.medical_specialtyPathologymedicine.medical_treatmentCentral nervous systemSpinal intradural intramedullary disseminationContext (language use)Case ReportMalignancylcsh:RC254-282Temporal lobelaw.inventionIntramedullary rod03 medical and health sciences0302 clinical medicinelawmedicineChemotherapybusiness.industrymedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.anatomical_structureOncology030220 oncology & carcinogenesisTemporal lobe glioblastoma multiformeRadiologybusiness030217 neurology & neurosurgeryProgressive diseaseGlioblastomaCase Reports in Oncology
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Blood baseline neutrophil count predicts bevacizumab efficacy in glioblastoma

2016

// Aurelie Bertaut 1 , Caroline Truntzer 2 , Rachid Madkouri 3 , Coureche Guillaume Kaderbhai 4 , Valentin Derangere 5 , Julie Vincent 4 , Bruno Chauffert 6 , Marie Helene Aubriot-Lorton 7 , Wahlid Farah 3 , Klaus Luc Mourier 3 , Romain Boidot 5,8 and Francois Ghiringhelli 4,5,8,9 1 Biostatistics unit Georges Francois Leclerc Cancer Center, Dijon, France 2 CLIPP, Research Center, University of Burgundy, Dijon, France 3 Department of Neurosurgery, CHU, Dijon, France 4 Department of Medical Oncology, Georges Francois Leclerc Cancer Center, Dijon, France 5 Platform of Transfer in Cancer Biology Genetic and histology, Georges Francois Leclerc Cancer Center, Dijon, France 6 Department of Medical…

0301 basic medicineOncologyMaleVascular Endothelial Growth Factor Agenetic structuresNeutrophilsmedicine.medical_treatmentAngiogenesis InhibitorsBiomarkers Pharmacological[ SDV.CAN ] Life Sciences [q-bio]/CancerLeukocyte Count0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsGranulocyte Colony-Stimulating FactorEndothelial Growth-Factorprognostic factorNeoadjuvant therapyRandomized Controlled Trials as TopicNeovascularization PathologicBrain NeoplasmsColony-Stimulating FactorAge FactorsChemoradiotherapyMiddle AgedPrognosisNeoadjuvant Therapy3. Good healthTreatment OutcomeOncology030220 oncology & carcinogenesisTo-Lymphocyte RatioAbsolute neutrophil countFemalemedicine.drugmedicine.medical_specialtyBevacizumabMalignant Glioma[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologybevacizumabDisease-Free Survival03 medical and health sciencesInternal medicinemedicineHumansPretreatment NeutrophilKarnofsky Performance StatusSingle-Agent BevacizumabRetrospective StudiesNewly-Diagnosed GlioblastomaRecurrent Glioblastomabusiness.industry[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyGene Expression ProfilingglioblastomaCancerRetrospective cohort studyLomustinemedicine.diseasePhase-Ii Trialeye diseasesSurgeryIrinotecan030104 developmental biologyprognosistic factorBrain-Tumorssense organsClinical Research PaperNeoplasm Recurrence LocalbusinessChemoradiotherapyFollow-Up Studies
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Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Glioblastoma: development of new diagnostic tools based on EV-associated proteins

2021

Glioblastomas multiforme (GBM) are the most common malignant primary brain tumors in adults. They are highly aggressive and have an overall survival of <15 months despite maximal surgical resection and chemoradiation (Ostrom, 2019). GBMs are typically heterogeneous with a wide range of genetic and epigenetic variations among tumor cells. Extracellular vesicles (EVs) represent one of the plausible ways through which can be obtained a better understanding of the heterogeneous subpopulations of GBM / molecular signatures. EVs hold promise for the discovery of potential tumours biomarkers useful in clinical managment for GBM patient diagnosis and follow-up. Isolating EVs from body fluids and sc…

Settore BIO/16 - Anatomia UmanaGeneral overview of the Glioblastoma
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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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Anti-tumor activity of the methanolic extracts of Salvia menthifolia

2012

In the present research we investigated the anti-proliferative activity of Salvia menthifolia Ten. (formerly Salvia menthaefolia), Lamiaceae, on a glioblastoma cell line, since up to date poor therapeutic results have been reported for treatment of malignant glioblastoma. Methanol extracts from different anatomical parts of S. menthifolia were tested on DBTRG-05MG cell line by MTT assay. The most active primary stems extract was also evaluated for apoptosis induction. Results confirmed the anti-tumor property of all the organs and demonstrated that the primary stems extract induced apoptosis after 4 h with the highest values of DNA fragmentation after 6 to 24 h. Some extracts were also HPLC…

lcsh:RS1-441Salvialcsh:Pharmacy and materia medicachemistry.chemical_compoundapoptosis glioblastoma Salvia menthifolia sageCaffeic acidMTT assaySettore BIO/15 - Biologia FarmaceuticaGeneral Pharmacology Toxicology and Pharmaceuticsapoptosis; glioblastoma; Salvia menthifolia; sageapoptosis glioblastomabiologyTraditional medicineRosmarinic acidapoptosisglioblastomaSalvia menthifoliabiology.organism_classificationQuercitrinSettore CHIM/08 - Chimica FarmaceuticasagechemistryBiochemistryPolyphenolSettore BIO/03 - Botanica Ambientale E ApplicataDNA fragmentationLamiaceae
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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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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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