Search results for "Brain Neoplasm"

showing 10 items of 249 documents

Long-term freedom from recurrence in 2 stage IV melanoma patients following vaccination with tyrosinase peptides.

2002

We report here on 2 patients who received adjuvant vaccination with an HLA-A2- or HLA-A24-restricted tyrosinase peptide, respectively, and GM-CSF for frequently relapsing stage IV melanoma. Following resection of metastases and irradiation of brain metastases in 1 patient, both patients were without evidence of disease when receiving the first vaccination. While the patients had had 9 and 12, respectively, mostly s.c., relapses during the 3 years before vaccination, they experienced freedom from relapse for more than 2 years after vaccination. We found a T-cell response to the vaccine peptide in both patients in the peripheral blood by ex vivo IFN-gamma ELISPOT assay. The T-cell population …

Cancer ResearchTime FactorsCD3 Complexmedicine.medical_treatmentCD8 AntigensT-LymphocytesPopulationTyrosinase PeptideCancer VaccinesPolymerase Chain ReactionDisease-Free SurvivalEpitopesInterferon-gammaRecurrencemedicineHumansRNA MessengerNeoplasm MetastasiseducationMelanomaeducation.field_of_studybiologybusiness.industryBrain NeoplasmsMonophenol MonooxygenaseMelanomaELISPOTImmunotherapymedicine.diseaseFlow CytometryImmunohistochemistryVaccinationOncologyGranzymeImmunologybiology.proteinbusinessPeptidesCD8International journal of cancer
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Bmi1 and Cell of Origin Determinants of Brain Tumor Phenotype

2007

Glioblastomas frequently express oncogenic EGFR and loss of the Ink4a/Arf locus. Bmi1, a positive regulator of stem cell self renewal, may be critical to drive brain tumor growth. In this issue of Cancer Cell, Bruggeman and colleagues suggest that brain tumors with these molecular alterations can be initiated in both neural precursor and differentiated cell compartments in the absence of Bmi1; however, tumorigenicity is reduced, and tumors contain fewer precursor cells. Surprisingly, tumors appear less malignant when initiated in precursor cells. Bmi1-deficient tumors also had fewer neuronal lineage cells, suggesting a role for Bmi1 in determination of cell lineage and tumor phenotype.

Cancer ResearchTime FactorsCell of originCellular differentiationBrain tumormacromolecular substancesBiologyMiceProto-Oncogene ProteinsPrecursor cellmedicineAnimalsHumansCyclin-Dependent Kinase Inhibitor p16Cell ProliferationNeoplasm StagingMice KnockoutNeuronsPolycomb Repressive Complex 1Brain NeoplasmsCell growthStem CellsNuclear ProteinsCell DifferentiationNeoplasms ExperimentalCell Biologymedicine.diseaseStem Cell Self-RenewalErbB ReceptorsGene Expression Regulation NeoplasticRepressor ProteinsCell Transformation NeoplasticPhenotypeOncologyBMI1AstrocytesMutationCancer cellCancer researchGlioblastomaSignal TransductionCancer Cell
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Blood flow and metabolic microenvironment of brain tumors

1994

Summarizing thesein vivo data in the context of brain tumor therapy, the following aspects are of particular importance: Low and heterogeneous tumor blood flow may — in addition to the limiting effects of the blood-brain barrier — result in compromised delivery of drugs from blood to the tissue. Low tumor pO2 reduces sensitivity to standard radiation and ‘O2-dependent’ anticancer drugs. Treatment efficacy may be further altered by changes of tumor pH. Particularly acidosis can decrease radiation sensitivity and modulate the cytotoxicity of anticancer drugs. In the following presentations, these aspects will be discussed regardingin vivo data obtained with positron emission tomography.

Cancer Researchmedicine.medical_specialtyNeurologyPartial PressureBrain tumorContext (language use)AstrocytomaPharmacologyOxygen ConsumptionRadiation sensitivitymedicineAnimalsHumansCytotoxicityAcidosismedicine.diagnostic_testBrain Neoplasmsbusiness.industryGliomaBlood flowmedicine.diseaseOxygenNeurologyOncologyRegional Blood FlowPositron emission tomographyCerebrovascular CirculationNeurology (clinical)medicine.symptombusinessJournal of Neuro-Oncology
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MGMT activity, promoter methylation and immunohistochemistry of pretreatment and recurrent malignant gliomas: a comparative study on astrocytoma and …

2010

The DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) is a key player in tumor cell resistance. Promoter methylation, MGMT activity and immunohistochemistry are used for determining the MGMT status. However, it is unclear whether MGMT promoter methylation correlates with MGMT activity and whether MGMT promoter methylation of the pretreatment tumor predicts the MGMT status of recurrences. To address these questions, we determined MGMT activity promoter methylation and immunoreactivity in pretreatment and recurrent glioblastomas (GB, WHO Grade IV), and in astrocytomas (WHO Grade III). We show that GB that were promoter methylated display a range of 0-62 fmol/mg MGMT and tumor…

Cancer Researchmedicine.medical_specialtyPathologyMethyltransferaseDNA repairAstrocytomaBiologyRecurrenceCell Line TumormedicineHumansPromoter Regions GeneticDNA Modification MethylasesneoplasmsBrain NeoplasmsTumor Suppressor ProteinsAstrocytomaCancerAnatomical pathologyBiological activityMethylationDNA Methylationmedicine.diseaseImmunohistochemistrydigestive system diseasesDNA Repair EnzymesOncologyCancer researchImmunohistochemistryGlioblastomaInternational Journal of Cancer
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Cerebral metastases of an endometrial stromal sarcoma: report of the first case.

2012

Endometrial stromal sarcomas (ESSs) of the uterus are rare gynecological malignancies. Common locations of distant metastases are vagina, vulva, lung, mediastinum, abdomen, bones and ovaries.We present the case of a 69-year-old woman with a Federation of Gynecology and Obstetrics (FIGO) IIb (classification 2009) ESS of the uterus of high-grade malignancy. Initially, a hysterectomy Piver II and total colpectomy were performed, followed by pelvic field irradiation. 8 months later, the patient suffered seizures and hemiparesis. A computed tomography (CT) scan revealed cerebral metastases, and irradiation of the brain was initiated. After completion of the staging examinations, additional metas…

Cancer Researchmedicine.medical_specialtyPathologyStromal cellSarcoma Endometrial StromalUterusVulvamedicineHumansAgedEndometrial stromal sarcomaLungUterine sarcomaurogenital systembusiness.industryBrain NeoplasmsHematologyGeneral Medicinemedicine.diseaseEndometrial Neoplasmsmedicine.anatomical_structureTreatment OutcomeOncologyVaginaFemaleRadiologybusinessOnkologie
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Novel Approaches for Glioblastoma Treatment: Focus on Tumor Heterogeneity, Treatment Resistance, and Computational Tools

2019

BACKGROUND: Glioblastoma (GBM) is a highly aggressive primary brain tumor. Currently, the suggested line of action is the surgical resection followed by radiotherapy and treatment with the adjuvant temozolomide (TMZ), a DNA alkylating agent. However, the ability of tumor cells to deeply infiltrate the surrounding tissue makes complete resection quite impossible, and in consequence, the probability of tumor recurrence is high, and the prognosis is not positive. GBM is highly heterogeneous and adapts to treatment in most individuals. Nevertheless, these mechanisms of adaption are unknown. RECENT FINDINGS: In this review, we will discuss the recent discoveries in molecular and cellular heterog…

Cancer Researchmedicine.medical_treatmentDNA Mutational AnalysisBrain tumorBioinformaticsComplete resectionTumor heterogeneityCancer VaccinesMicrotubulesArticleClonal EvolutionMachine LearningGenetic HeterogeneityCancer stem cellAntineoplastic Combined Chemotherapy ProtocolsTumor MicroenvironmentMedicineHumansTreatment resistancePrecision MedicineDNA Modification MethylasesImmune Checkpoint InhibitorsTemozolomideModels Geneticbusiness.industryBrain NeoplasmsTumor Suppressor ProteinsBrainComputational BiologyChemoradiotherapy Adjuvantmedicine.diseasePrognosisRadiation therapyDNA Repair EnzymesOncologyDrug Resistance NeoplasmMutationTumor Suppressor Protein p53businessGlioblastomaGlioblastomamedicine.drug
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Rad51 and BRCA2 - New Molecular Targets for Sensitizing Glioma Cells to Alkylating Anticancer Drugs

2011

First line chemotherapeutics for brain tumors (malignant gliomas) are alkylating agents such as temozolomide and nimustine. Despite growing knowledge of how these agents work, patients suffering from this malignancy still face a dismal prognosis. Alkylating agents target DNA, forming the killing lesion O(6)-alkylguanine, which is converted into DNA double-strand breaks (DSBs) that trigger apoptosis. Here we assessed whether inhibiting repair of DSBs by homologous recombination (HR) or non-homologous end joining (NHEJ) is a reasonable strategy for sensitizing glioma cells to alkylating agents. For down-regulation of HR in glioma cells, we used an interference RNA (iRNA) approach targeting Ra…

Cancer Treatmentlcsh:MedicineApoptosisToxicologyBiochemistrychemistry.chemical_compoundDrug DiscoveryRNA Small Interferinglcsh:ScienceHomologous RecombinationNeurological TumorsGene knockdownMultidisciplinaryBrain NeoplasmsGliomaFlow CytometryNon-homologous end joiningOncologyPARP inhibitorMedicinemedicine.drugResearch ArticleBiotechnologyDrugs and DevicesDrug Research and DevelopmentDNA damageMorpholinesToxic AgentsOlaparibGliomaCell Line TumormedicineHumansBiologyAntineoplastic Agents AlkylatingProtein Kinase InhibitorsBRCA2 ProteinTemozolomideBase SequenceNimustinelcsh:RCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseasechemistryMicroscopy FluorescenceChromonesCancer researchlcsh:QRad51 RecombinaseDNA DamagePLoS ONE
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Immunoproteomic studies on paediatric opsoclonus-myoclonus associated with neuroblastoma

2016

We aimed to identify new cell-membrane antigens implicated in opsoclonus-myoclonus with neuroblastoma. The sera of 3 out of 14 patients showed IgG electron-microscopy immunogold reactivity on SH-SY5Y neuroblastoma cells. Immunoprecipitation experiments using rat brain synaptosomes and SH-SY5Y cells led to the identification of: (1) thirty-one nuclear/cytoplasmic proteins (including antigens HuB, HuC); (2) seven neuronal membrane proteins, including the Shaw-potassium channel Kv3.3 (KCNC3), whose genetic disruption in mice causes ataxia and generalized muscle twitching. Although cell-based assays did not demonstrate direct antigenicity, our findings point to Shaw-related subfamily of the pot…

Central Nervous SystemMale0301 basic medicineAntigenicityDatabases FactualThymomaImmunoprecipitationKCTD7Cell Adhesion Molecules NeuronalImmunologyNerve Tissue ProteinsBiologyNeuroblastoma03 medical and health sciences0302 clinical medicineAntigenCell Line TumorNeuroblastomaOpsoclonus myoclonus syndromemedicineAnimalsHumansImmunology and AllergyRats WistarChildOpsoclonus-Myoclonus SyndromeBrain NeoplasmsMembrane ProteinsNuclear ProteinsImmunogold labellingmedicine.diseaseMolecular biologyRatsHEK293 Cells030104 developmental biologyShaw Potassium ChannelsNeurologyMembrane proteinEncephalitisFemaleNeurology (clinical)030217 neurology & neurosurgerySynaptosomesJournal of Neuroimmunology
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Immunohistochemistry of primary central nervous system malignant rhabdoid tumors: report of five cases and review of the literature

1996

Malignant rhabdoid tumors (MRT) are characterized by a typical light microscopic morphology with uniformly round tumor cells, vacuolated cytoplasm with occasional round, hyaline intracytoplasmic, periodic acid-Schiff-positive inclusions, vesicular nuclei with prominent nucleoli and positive immunoreactivity for vimentin. The histogenesis of MRT is controversial. Five cases of primary central nervous system (CNS) rhabdoid tumors in children are presented. Immunohistochemical, light and electron microscopic features are compared with primary CNS malignant rhabdoid tumors reported in the literature. Expression of various neurofilaments in our cases of primary CNS rhabdoid tumors was prominent …

Central Nervous SystemMalePathologymedicine.medical_specialtyNeurofilamentCentral nervous systemVimentinHistogenesisBiologyPathology and Forensic MedicineCentral nervous system disease03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineHumansRhabdoid TumorHyalineBrain NeoplasmsRhabdoid tumorsInfantmedicine.diseaseImmunohistochemistry3. Good healthMicroscopy Electronmedicine.anatomical_structureChild Preschool030220 oncology & carcinogenesisbiology.proteinImmunohistochemistryFemaleNeurology (clinical)030217 neurology & neurosurgeryActa Neuropathologica
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Aspartate aminotransferase in brain tissue cultures

1969

Cerebral CortexEpendymomaPathologymedicine.medical_specialtyBrain NeoplasmsChemistryAge FactorsCentrifugationNeoplasms ExperimentalBrain tissueAspartate Aminotransferasesmedicine.diseaseBiochemistryRatsCellular and Molecular Neurosciencemedicine.anatomical_structureAnimals NewbornEpendymomaSpectrophotometryCerebral cortexCulture TechniquesmedicineAnimalsCentrifugationAspartate AminotransferasesJournal of Neurochemistry
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