Search results for "Neoplasm Protein"

showing 10 items of 247 documents

Diffuse Type of Giant-Cell Tumor of Tendon Sheath: An Ultrastructural Study of Two Cases With Cytogenetic Support

2002

Two cases of the diffuse type of giant-cell tumor of the tendon sheath (GCTTS) are described. Both tumors arose in the vicinity of large joints of the lower extremity, showing similar clinical and radiological features. Histologically, a proliferation of polygonal mononuclear cells was seen, together with osteoclastlike giant cells, foam cells, and siderophages. The tumors were poorly delineated, displaying an infiltrative pattern into the neighboring soft tissues. Immunohistochemically, strong expression of vimentin, neuron-specific enolase, A1-antitrypsin, and CD68 was found in both mono- and multinucleated tumor cells. At the ultrastructural level, mononuclear cells revealed a diverse mo…

AdultMalePathologymedicine.medical_specialtySoft Tissue NeoplasmsVimentinBiologyGiant CellsPeripheral blood mononuclear cellTranslocation GeneticChromosome PaintingPathology and Forensic MedicineImmunoenzyme TechniquesTendonsMultinucleateStructural BiologyBiomarkers TumorTumor Cells CulturedmedicineHumansCD68Giant Cell TumorsDNA NeoplasmNeurosecretory SystemsNeoplasm ProteinsTendon sheathCytoplasmGiant cellKaryotypingUltrastructurebiology.proteinFemaleUltrastructural Pathology
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Generation of cytotoxic T-cell responses with synthetic melanoma-associated peptidesin vivo: Implications for tumor vaccines with melanoma-associated…

1996

Peptide epitopes derived from differentiation antigens of the melanocyte lineage have been identified in human melanomas and normal cultured melanocytes as targets for MHC-restricted cytotoxic T lymphocytes (CTL). Characterization of multiple CTL-defined antigenic determinants and the presence of corresponding precursor CTL open perspectives for the development of antigen-based vaccines. In the present study, we determined the CTL reactivity against melanoma-associated peptides derived from Melan A/MART-1, tyrosinase and gp100/Pmel17 in 10 HLA-A2+ melanoma patients and 10 healthy individuals. Then, we examined the immunological effects and toxicity of intradermal inoculation of synthetic me…

AdultMaleSignal peptideCancer ResearchInjections IntradermalMolecular Sequence DataTyrosinase Peptide10050 Institute of Pharmacology and Toxicology610 Medicine & healthchemical and pharmacologic phenomenaPeptideEpitopeImmune systemAntigenAntigens NeoplasmHumansCytotoxic T cellMedicine1306 Cancer ResearchHypersensitivity DelayedAmino Acid SequenceMelanomaCells CulturedAgedchemistry.chemical_classificationVaccinesbusiness.industryMiddle AgedNeoplasm ProteinsCTL*OncologychemistryImmunology570 Life sciences; biology2730 OncologyFemalebusinessMelanoma-Specific AntigensT-Lymphocytes CytotoxicInternational Journal of Cancer
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Deficiency of the autoimmune regulator AIRE in thymomas is insufficient to elicit autoimmune polyendocrinopathy syndrome type 1 (APS‐1)

2007

Thymomas are thymic epithelial neoplasms, associated with a variety of autoimmune disorders (especially myasthenia gravis), that apparently result from aberrant intra-tumourous thymopoiesis and export of inefficiently tolerized T-cells to the periphery. The autoimmune regulator (AIRE) drives the expression of self-antigens in the thymic medulla and plays an essential role in ‘central’ tolerance in both humans and mice. However, while inactivating AIRE mutations result in the ‘autoimmune polyendocrinopathy syndrome type 1’ (APS-1), its major features are not well reproduced in AIRE-knock-out mice. Therefore, alternative human disease scenarios with concomitant AIRE deficiency may be valuable…

AdultMaleThymomaAdolescentThymomaAntibodies NeoplasmThymus Glandmedicine.disease_causeAutoantigensAutoimmune DiseasesPathology and Forensic MedicineAutoimmunity03 medical and health sciences0302 clinical medicineAntigens NeoplasmInterferonMyasthenia GravismedicineHumansPolyendocrinopathies AutoimmuneAgedAutoantibodies030304 developmental biologyAged 80 and over0303 health sciencesbiologybusiness.industryAutoantibodyThymus NeoplasmsMiddle AgedAutoimmune regulatormedicine.diseaseImmunohistochemistryMyasthenia gravisNeoplasm Proteins3. Good healthThymic Tissue030220 oncology & carcinogenesisInterferon Type IImmunologybiology.proteinCytokinesFemaleAntibodybusinessTranscription Factorsmedicine.drugThe Journal of Pathology
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Heat shock protein-27 protects human bronchial epithelial cells against oxidative stress-mediated apoptosis: possible implication in asthma.

2002

Inflammation of the human bronchial epithelium, as observed in asthmatics, is characterized by the selective death of the columnar epithelial cells, which desquamate from the basal cells. Tissue repair initiates from basal cells that resist inflammation. Here, we have evaluated the extent of apoptosis as well as the Hsp27 level of expression in epithelial cells from bronchial biopsy samples taken from normal and asthmatic subjects. Hsp27 is a chaperone whose expression protects against oxidative stress. We report that in asthmatic subjects the basal epithelium cells express a high level of Hsp27 but no apoptotic morphology. In contrast, apoptotic columnar cells are devoid of Hsp27 expressio…

Adultendocrine systemanimal structuresHSP27 Heat-Shock ProteinsInflammationApoptosisBronchiColumnar CellRespiratory MucosaBiologymedicine.disease_causeBiochemistryGene Expression Regulation EnzymologicHsp27Heat shock proteinmedicineBronchial BiopsyHumansHeat-Shock ProteinsEpithelial CellsCell BiologyHydrogen PeroxideOriginal ArticlesMiddle AgedOxidantsEpitheliumAsthmaCell biologyNeoplasm ProteinsOxidative Stressmedicine.anatomical_structureApoptosisImmunologybiology.proteinmedicine.symptomOxidative stressMolecular ChaperonesCell stresschaperones
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5-HT3 receptor-channels coupled with Na+ influx in human T cells: role in T cell activation.

1999

The study was conducted on a human (Jurkat) T cell line, loaded with a Na+ fluorescent probe, SBFI/AM. Serotonin and an agonist of 5-HT3 receptor-channels, 2-methyl-5HT, evoked Na+ influx, whereas the agonists of other serotonergic receptor subtypes, i.e., 5-HT1A and 5-HT1B receptors, failed to induce Na+ influx in these cells. By using 3H-BRL43694, an agonist of 5-HT3 receptor-channels, we characterized 5-HT3 lymphocyte receptors which exhibited a density (Bmax) of 300 +/- 20 fmol/10(6) cells and a Kd of 30 nM in Jurkat T cells. The T-cell 5-HT3 receptor-channel is not regulated either by the protein kinase C or by the free intracellular calcium concentrations as the agents known to activa…

AgonistSerotoninmedicine.drug_classMetoclopramideT cellT-LymphocytesImmunologyBiologyLymphocyte ActivationJurkat cellsCalcium in biologyPiperazinesSodium ChannelsGranisetronJurkat CellsQuinoxalinesmedicineImmunology and AllergyHumansCalcium SignalingPhytohemagglutininsReceptorProtein kinase C5-HT receptorProtein Kinase C8-Hydroxy-2-(di-n-propylamino)tetralinIon TransportRyanodineCell CycleSodiumCell biologyNeoplasm ProteinsSerotonin Receptor AgonistsEnzyme Activationmedicine.anatomical_structureNeurologyReceptors SerotoninReceptor Serotonin 5-HT1BThapsigarginNeurology (clinical)Serotonin AntagonistsReceptors Serotonin 5-HT3Ion Channel GatingReceptors Serotonin 5-HT1IntracellularJournal of neuroimmunology
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Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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Wnt activity defines colon cancer stem cells and is regulated by the microenvironment.

2010

Despite the presence of mutations in APC or beta-catenin, which are believed to activate the Wnt signalling cascade constitutively, most colorectal cancers show cellular heterogeneity when beta-catenin localization is analysed, indicating a more complex regulation of Wnt signalling. We explored this heterogeneity with a Wnt reporter construct and observed that high Wnt activity functionally designates the colon cancer stem cell (CSC) population. In adenocarcinomas, high activity of the Wnt pathway is observed preferentially in tumour cells located close to stromal myofibroblasts, indicating that Wnt activity and cancer stemness may be regulated by extrinsic cues. In agreement with this noti…

Beta-cateninColorectal cancerTransplantation HeterologousMice NudeBiologyMiceCancer stem cellParacrine CommunicationmedicineAnimalsHumansAPC microenvironmentbeta CateninHepatocyte Growth FactorWnt signaling pathwayLRP6LRP5Cell BiologyNeoplasms ExperimentalFibroblastsmedicine.diseaseCoculture TechniquesCell biologyNeoplasm ProteinsWnt ProteinsColonic Neoplasmsbiology.proteinNeoplastic Stem CellsHepatocyte growth factorStem cellmedicine.drugSignal Transduction
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CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis.

2014

SummaryCancer stem cells drive tumor formation and metastasis, but how they acquire metastatic traits is not well understood. Here, we show that all colorectal cancer stem cells (CR-CSCs) express CD44v6, which is required for their migration and generation of metastatic tumors. CD44v6 expression is low in primary tumors but demarcated clonogenic CR-CSC populations. Cytokines hepatocyte growth factor (HGF), osteopontin (OPN), and stromal-derived factor 1α (SDF-1), secreted from tumor associated cells, increase CD44v6 expression in CR-CSCs by activating the Wnt/β-catenin pathway, which promotes migration and metastasis. CD44v6− progenitor cells do not give rise to metastatic lesions but, when…

CA15-3Animals; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Hyaluronan Receptors; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Molecular Medicine; Genetics; Cell BiologyCarcinogenesisWnt ProteinMice SCIDmedicine.disease_causeAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular ReprogrammingMetastasisMicePhosphatidylinositol 3-KinasesCD44Neoplasm MetastasisCarcinogenesiPhosphoinositide-3 Kinase InhibitorsColonic NeoplasmTumorbiologyProto-Oncogene Proteins c-metCellular ReprogrammingPrognosisAntigens CD44Neoplasm ProteinsNeoplasm MetastasiAnimals; Antigens CD44; Biomarkers Tumor; Bone Morphogenetic Proteins; Carcinogenesis; Colonic Neoplasms; Fibroblasts; Humans; Mice SCID; Neoplasm Metastasis; Neoplasm Proteins; Neoplastic Stem Cells; Phosphatidylinositol 3-Kinases; Prognosis; Protein Kinase Inhibitors; Proto-Oncogene Proteins c-met; Signal Transduction; Treatment Outcome; Wnt Proteins; Cellular Reprogramming; Cell Biology; Molecular Medicine; GeneticsHyaluronan ReceptorsTreatment OutcomeBone Morphogenetic ProteinsColonic NeoplasmsNeoplastic Stem CellsFibroblastMolecular MedicineHepatocyte growth factorStem cellHumanmedicine.drugSignal TransductionPrognosiProtein Kinase InhibitorSCIDNeoplasm ProteinCancer stem cellSettore MED/04 - PATOLOGIA GENERALEmedicineGeneticsBiomarkers TumorAnimalsHumansAntigensProgenitor cellProtein Kinase InhibitorsSettore MED/04 - Patologia GeneraleAnimalBone Morphogenetic Proteincancer metastasisCD44Cell BiologyFibroblastsmedicine.diseaseWnt ProteinsSettore MED/18 - Chirurgia GeneraleImmunologyCancer researchbiology.proteinNeoplastic Stem CellPhosphatidylinositol 3-KinaseCarcinogenesisBiomarkersCell stem cell
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Expression of stress protein gp96, a tumor rejection antigen, in human colorectal cancer

2000

Preparations of stress protein gp96 from tumor cells are active as tumor vaccines by eliciting immune responses against mixtures of individual tumor peptide antigens which are complexed to gp96. Due to the individual antigenicity of tumors, a vaccine consisting of tumor-derived gp96 has to be prepared individually for each patient from autologous tumor tissue. So far, gp96 expression by human tumors has not been analyzed. Here, we report stable and mostly homogenous expression of gp96 by colorectal cancer, which was enhanced compared to surrounding tumor stroma in 70% to 80% of colorectal cancer specimens. Fewer non-metastatic than metastatic primary cancer specimens showed enhanced gp96 ex…

CA15-3Cancer ResearchColorectal cancerbusiness.industryTumor M2-PKMouse model of colorectal and intestinal cancermedicine.diseaseImmunohistochemistryNeoplasm ProteinsImmune systemOncologyAntigenCell cultureImmunologymedicineHumansCA19-9Colorectal NeoplasmsbusinessHT29 CellsHeat-Shock ProteinsInternational Journal of Cancer
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Cell mechanisms of gustatory lipids perception and modulation of the dietary fat preference.

2014

Dietary lipids are usually responsible of several metabolic disorders. Recent compelling evidences suggest that there is a sixth taste modality, destined for the detection of oro-gustatory fats. The lipid-binding glycoprotein CD36, expressed by circumvallate papillae (CVP) of the mouse tongue, has been shown to be implicated in oro-gustatory perception of dietary lipids. We demonstrate that linoleic acid (LA) by activating sPLA2, cPLA2 and iPLA2 via CD36, produced arachidonic acid (AA) and lyso-phosphatidylcholine (Lyso-PC) which triggered Ca(2+) influx in CD36-positive taste bud cells (TBC), purified from mouse CVP. LA induced the production of Ca(2+) influx factor (CIF). CIF, AA and Lyso-…

CD36 AntigensTasteCD36Linoleic acidBiochemistryModels Biologicalchemistry.chemical_compoundFood PreferencesAnimalsHumansStromal Interaction Molecule 1Calcium signalingbiologyORAI1Endoplasmic reticulumMembrane ProteinsTaste PerceptionSTIM1General MedicineTaste BudsDietary FatsCell biologyNeoplasm ProteinschemistryBiochemistrybiology.proteinArachidonic acidCalciumBiochimie
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