Search results for " tumor"

showing 10 items of 3819 documents

A role for TASK2 channels in the human immunological synapse.

2020

The immunological synapse is a transient junction that occurs when the plasma membrane of a T cell comes in close contact with an APC after recognizing a peptide from the antigen-MHC. The interaction starts when CRAC channels embedded in the T cell membrane open, flowing calcium ions into the cell. To counterbalance the ion influx and subsequent depolarization, Kv 1.3 and KCa3.1 channels are recruited to the immunological synapse, increasing the extracellular K+ concentration. These processes are crucial as they initiate gene expression that drives T cell activation and proliferation. The T cell-specific function of the K2P channel family member TASK2 channels and their role in autoimmune p…

0301 basic medicineMaleCD3 ComplexImmunological SynapsesT cellCD3T-LymphocytesImmunologyCellGene ExpressionStimulationImmunological synapseAutoimmune Diseases03 medical and health sciencesJurkat CellsMice0302 clinical medicinePotassium Channels Tandem Pore DomainCell Line TumorGene expressionmedicineExtracellularImmunology and AllergyAnimalsHumansCells CulturedKv1.3 Potassium Channelbiologyβ-tubulin ; TASK2 ; immunological synapse ; dSTORM ; T cellCell MembraneDepolarizationIntermediate-Conductance Calcium-Activated Potassium ChannelsCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurebiology.proteinCalciumFemale030215 immunologyEuropean journal of immunologyReferences
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Muscle and serum metabolomes are dysregulated in colon-26 tumor-bearing mice despite amelioration of cachexia with activin receptor type 2B ligand bl…

2019

Cancer-associated cachexia reduces survival, which has been attenuated by blocking the activin receptor type 2B (ACVR2B) ligands in mice. The purpose of this study was to unravel the underlying physiology and novel cachexia biomarkers by use of the colon-26 (C26) carcinoma model of cancer cachexia. Male BALB/c mice were subcutaneously inoculated with C26 cancer cells or vehicle control. Tumor-bearing mice were treated with vehicle (C26+PBS) or soluble ACVR2B either before (C26+sACVR/b) or before and after (C26+sACVR/c) tumor formation. Skeletal muscle and serum metabolomics analysis was conducted by gas chromatography-mass spectrometry. Cancer altered various biologically functional groups …

0301 basic medicineMaleCachexiaPhysiologyEndocrinology Diabetes and MetabolismActivin Receptors Type IIlihaksetMyostatinMice0302 clinical medicineAmino Acidsta315Activin Receptor Type-2BbiologyOrganophosphatesRecombinant Proteins3. Good healthmedicine.anatomical_structureribosome030220 oncology & carcinogenesismyostatinColonic NeoplasmsMetabolomesyöpätauditC26Metabolic Networks and Pathwaysmedicine.medical_specialtyPhenylalanineCachexia03 medical and health sciencesribosomitPhysiology (medical)Internal medicineCell Line TumormedicineAnimalsskeletal muscleMuscle SkeletalPI3K/AKT/mTOR pathwaybusiness.industrySkeletal muscleCancermedicine.diseaseta3122BlockadeImmunoglobulin Fc Fragments030104 developmental biologyEndocrinologyProtein Biosynthesisbiology.proteinaineenvaihduntatuotteetPyrimidine NucleotidesproteiinitbusinesslihassurkastumasairaudetACVR2BAmerican journal of physiology. Endocrinology and metabolism
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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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miR-21 antagonism abrogates Th17 tumor promoting functions in multiple myeloma

2020

Multiple myeloma (MM) is tightly dependent on inflammatory bone marrow microenvironment. IL-17 producing CD4+ T cells (Th17) sustain MM cells growth and osteoclasts-dependent bone damage. In turn, Th17 differentiation relies on inflammatory stimuli. Here, we investigated the role of miR-21 in Th17-mediated MM tumor growth and bone disease. We found that early inhibition of miR-21 in naive T cells (miR-21i-T cells) impaired Th17 differentiation in vitro and abrogated Th17-mediated MM cell proliferation and osteoclasts activity. We validated these findings in NOD/SCID-g-NULL mice, intratibially injected with miR-21i-T cells and MM cells. A Pairwise RNAseq and proteome/phosphoproteome analysis…

0301 basic medicineMaleCancer ResearchBone diseaseApoptosisBone NeoplasmsNodMice SCIDBone NeoplasmT-Lymphocytes RegulatoryTh17 Cell03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationgammopathiesMice Inbred NODmedicineTumor Cells CulturedTumor MicroenvironmentBiomarkers TumorAnimalsHumansMultiple myelomaCell ProliferationChemistryCell growthAnimalApoptosiHematologymedicine.diseasePrognosisXenograft Model Antitumor AssaysIn vitroGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCase-Control StudiesCancer researchTh17 CellsBone marrowAntagonismCase-Control StudieMultiple Myeloma
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BRG1/SMARCA4 is essential for neuroblastoma cell viability through modulation of cell death and survival pathways.

2016

Neuroblastoma (NB) is a neoplasm of the sympathetic nervous system, and is the most common solid tumor of infancy. NBs are very heterogeneous, with a clinical course ranging from spontaneous regression to resistance to all current forms of treatment. High-risk patients need intense chemotherapy, and only 30-40% will be cured. Relapsed or metastatic tumors acquire multi-drug resistance, raising the need for alternative treatments. Owing to the diverse mechanisms that are responsible of NB chemoresistance, we aimed to target epigenetic factors that control multiple pathways to bypass therapy resistance. We found that the SWI/SNF-related, matrix-associated, actin-dependent regulator of chromat…

0301 basic medicineMaleCancer ResearchCombination therapyCell SurvivalBiologyMolecular oncologyTranscriptome03 medical and health sciencesNeuroblastomaPhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptorNeuroblastomaCell Line TumorGeneticsmedicineHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayCell ProliferationCell DeathDNA HelicasesNuclear ProteinsCell cyclemedicine.diseaseGene Expression Regulation Neoplastic030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisImmunologyCancer researchFemaleTranscriptomeSignal TransductionTranscription FactorsOncogene
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A multidimensional network approach reveals microRNAs as determinants of the mesenchymal colorectal cancer subtype

2016

Colorectal cancer (CRC) is a heterogeneous disease posing a challenge for accurate classification and treatment of this malignancy. There is no common genetic molecular feature that would allow for the identification of patients at risk for developing recurrences and thus selecting patients who would benefit from more stringent therapies still poses a major clinical challenge. Recently, an international multicenter consortium (CRC Subtyping Consortium) was established aiming at the classification of CRC patients in biologically homogeneous CRC subtypes. Four consensus molecular subtypes (CMSs) were identified, of which the mesenchymal CMS4 presented with worse prognosis signifying the impor…

0301 basic medicineMaleCancer ResearchEpithelial-Mesenchymal TransitionGene regulatory networkComputational biologyBiologymedicine.disease_causeEpigenesis Genetic03 medical and health sciencesMolecular Biology; Cancer Research; GeneticsCell Line TumormicroRNAmedicineGeneticsHumansGene Regulatory NetworksEpigeneticsPromoter Regions GeneticMolecular BiologyRegulation of gene expressionCancerComputational BiologyDNA Methylationmedicine.diseasePrognosisSubtyping3. Good healthGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyPhenotypeMultigene FamilyDNA methylationCancer researchFemaleOriginal ArticleCarcinogenesisColorectal NeoplasmsTranscriptomeOncogene
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Germinal Centers Determine the Prognostic Relevance of Tertiary Lymphoid Structures and Are Impaired by Corticosteroids in Lung Squamous Cell Carcino…

2018

Abstract In solid tumors, the presence of lymph node–like structures called tertiary lymphoid structures (TLS) is associated with improved patient survival. However, little is known about how TLS develop in cancer, how their function affects survival, and whether they are affected by cancer therapy. In this study, we used multispectral microscopy, quantitative pathology, and gene expression profiling to analyze TLS formation in human lung squamous cell carcinoma (LSCC) and in an experimental model of lung TLS induction. We identified a niche of CXCL13+ perivascular and CXCL12+LTB+ and PD-L1+ epithelial cells supporting TLS formation. We also characterized sequential stages of TLS maturation…

0301 basic medicineMaleCancer ResearchLung Neoplasmsmedicine.medical_treatmentApoptosis03 medical and health sciencesMiceLymphocytes Tumor-InfiltratingAdrenal Cortex HormonesCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsCarcinomaTumor Cells CulturedTumor MicroenvironmentMedicineAnimalsHumansCXCL13Lung cancerSurvival rateAgedCell ProliferationChemotherapyTumor microenvironmentbusiness.industryGene Expression ProfilingCancerGerminal centerMiddle Agedmedicine.diseaseGerminal CenterPrognosisXenograft Model Antitumor Assays3. Good healthMice Inbred C57BLSurvival Rate030104 developmental biologyTertiary Lymphoid StructuresOncologyCancer researchCarcinoma Squamous CellFemalebusinessFollow-Up StudiesCancer research
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Antibody–Fc/FcR Interaction on Macrophages as a Mechanism for Hyperprogressive Disease in Non–small Cell Lung Cancer Subsequent to PD-1/PD-L1 Blockade

2019

Abstract Purpose: Hyperprogression (HP), a paradoxical boost in tumor growth, was described in a subset of patients treated with immune checkpoint inhibitors (ICI). Neither clinicopathologic features nor biological mechanisms associated with HP have been identified. Experimental Design: Among 187 patients with non–small cell lung cancer (NSCLC) treated with ICI at our institute, cases with HP were identified according to clinical and radiologic criteria. Baseline histologic samples from patients treated with ICI were evaluated by IHC for myeloid and lymphoid markers. T-cell–deficient mice, injected with human lung cancer cells and patient-derived xenografts (PDX) belonging to specific mutat…

0301 basic medicineMaleCancer ResearchMyeloidLung NeoplasmsCD33Programmed Cell Death 1 ReceptorFc receptorMice NudeMice SCIDReceptors Fcnon-small cell lung cancer Hyperprogression immune checkpoint inhibitors.B7-H1 AntigenArticle03 medical and health sciences0302 clinical medicineImmunophenotypingAntineoplastic Agents ImmunologicalPD-L1Carcinoma Non-Small-Cell LungCell Line TumormedicineAnimalsHumansLung cancerAntibodies Blockingbiologybusiness.industryMacrophagesmedicine.diseaseXenograft Model Antitumor Assays3. Good healthImmunoglobulin Fc FragmentsTumor Burden030104 developmental biologymedicine.anatomical_structureNivolumabOncology030220 oncology & carcinogenesisbiology.proteinCancer researchImmunohistochemistryFemaleAntibodybusinessClinical Cancer Research
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The prognostic value of the myeloid-mediated immunosuppression marker Arginase-1 in classic Hodgkin lymphoma

2016

// Alessandra Romano 1 , Nunziatina Laura Parrinello 1 , Calogero Vetro 1 , Daniele Tibullo 1 , Cesarina Giallongo 1 , Piera La Cava 1 , Annalisa Chiarenza 1 , Giovanna Motta 1 , Anastasia L. Caruso 1 , Loredana Villari 2 , Claudio Tripodo 3 , Sebastiano Cosentino 4 , Massimo Ippolito 4 , Ugo Consoli 5 , Andrea Gallamini 6 , Stefano Pileri 7 , Francesco Di Raimondo 1 1 Division of Hematology, AOU “Policlinico - Vittorio Emanuele”, University of Catania, Catania, Italy 2 Division of Pathology, AOU “Policlinico - Vittorio Emanuele”, Catania, Italy 3 Tumor Immunology Unit, Department of Health Science, University of Palermo, Palermo, Italy 4 Nuclear Medicine Center, Azienda Ospedaliera Cannizz…

0301 basic medicineMaleCancer ResearchMyeloidNeutrophilsmedicine.medical_treatmentArginase-1Treatment outcomeKaplan-Meier EstimateGastroenterology0302 clinical medicineHematologyHealthy subjectsImmunosuppressionHematologyMiddle AgedPrognosisHodgkin DiseaseTreatment Outcomemedicine.anatomical_structureOncology030220 oncology & carcinogenesisFemaleArginase-1; Hodgkin Lymphoma; PET-2Tumor immunologyResearch PaperAdultmedicine.medical_specialtyPrognostic variableAdolescentAntineoplastic AgentsPET-2Sensitivity and SpecificityDisease-Free SurvivalYoung Adult03 medical and health sciencesInternal medicineBiomarkers TumormedicineHumansProgression-free survivalAgedArginasebusiness.industryMyeloid-Derived Suppressor Cells030104 developmental biologyPotential biomarkersImmunologyHodgkin lymphomabusinessHodgkin lymphoma030215 immunologyOncotarget
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Galectin-3 is a marker of favorable prognosis and a biologically relevant molecule in neuroblastic tumors

2014

Childhood neuroblastic tumors are characterized by heterogeneous clinical courses, ranging from benign ganglioneuroma (GN) to highly lethal neuroblastoma (NB). Although a refined prognostic evaluation and risk stratification of each tumor patient is becoming increasingly essential to personalize treatment options, currently only few biomolecular markers (essentially MYCN amplification, chromosome 11q status and DNA ploidy) are validated for this purpose in neuroblastic tumors. Here we report that Galectin-3 (Gal-3), a β-galactoside-binding lectin involved in multiple biological functions that has already acquired diagnostic relevance in specific clinical settings, is variably expressed in m…

0301 basic medicineMaleCancer ResearchPathologyTime FactorsCellular differentiationGalectin 3ApoptosisPredictive Value of TestKaplan-Meier EstimateNeuroblastoma0302 clinical medicineRisk FactorsChildGanglioneuroblastomaGanglioneuroblastomaCell DifferentiationBlood ProteinsNeuroblastic TumorPhenotypeImmunohistochemistry3. Good healthGalectin-3030220 oncology & carcinogenesisChild PreschoolImmunohistochemistryOriginal ArticleFemaleHumanmedicine.medical_specialtyAdolescentTime FactorSchwannian stromaGalectinsImmunologyBiologyTransfectionNeural cell differentiationschwannian stroma; neuroblastoma prognostic factor; neural cell differentiation; neuroblastoma03 medical and health sciencesCellular and Molecular NeurosciencePredictive Value of TestsNeuroblastomaCell Line TumormedicineBiomarkers TumorCell AdhesionHumansGanglioneuromaNeuroblastoma prognostic factorCell ProliferationNeoplasm StagingRisk FactorInfant NewbornApoptosiInfantGanglioneuromaCell Biologymedicine.disease030104 developmental biologyCancer research
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