Search results for "hrom"

showing 10 items of 11836 documents

EBI2 Is Highly Expressed in Multiple Sclerosis Lesions and Promotes Early CNS Migration of Encephalitogenic CD4 T Cells

2017

Arrival of encephalitogenic T cells at inflammatory foci represents a critical step in development of experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. EBI2 and its ligand, 7{alpha},25-OHC, direct immune cell localization in secondary lymphoid organs. CH25H and CYP7B1 hydroxylate cholesterol to 7{alpha},25-OHC. During EAE, we found increased expression of CH25H by microglia and CYP7B1 by CNS-infiltrating immune cells elevating the ligand concentration in the CNS. Two critical pro-inflammatory cytokines, interleukin-23 (IL-23) and interleukin-1 beta (IL-1{beta}), maintained expression of EBI2 in differentiating Th17 cells. In line with this, EBI2 enhan…

0301 basic medicineCD4-Positive T-LymphocytesCentral Nervous SystemMaleGPR183Cancer ResearchEncephalomyelitis Autoimmune ExperimentalOxysterolCentral nervous systemInterleukin-1betaCytochrome P450 Family 7CH25HmicrogliaAutoimmunityBiologymedicine.disease_causemultiple sclerosisInterleukin-23General Biochemistry Genetics and Molecular BiologyAutoimmunityReceptors G-Protein-Coupled03 medical and health sciencesMiceImmune systemCell MovementmedicineAnimalsEBI2lcsh:QH301-705.5MicrogliaEAEMultiple sclerosisExperimental autoimmune encephalomyelitisGPR18325-OHCmedicine.diseaseMice Inbred C57BLDisease Models Animal030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)ImmunologySteroid HydroxylasesTh17 CellsFemaleTh17CNSoxysterolCell Reports
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The NSL Chromatin-Modifying Complex Subunit KANSL2 Regulates Cancer Stem-like Properties in Glioblastoma That Contribute to Tumorigenesis.

2016

KANSL2 is an integral subunit of the nonspecific lethal (NSL) chromatin-modifying complex that contributes to epigenetic programs in embryonic stem cells. In this study, we report a role for KANSL2 in regulation of stemness in glioblastoma (GBM), which is characterized by heterogeneous tumor stem-like cells associated with therapy resistance and disease relapse. KANSL2 expression is upregulated in cancer cells, mainly at perivascular regions of tumors. RNAi-mediated silencing of KANSL2 in GBM cells impairs their tumorigenic capacity in mouse xenograft models. In clinical specimens, we found that expression levels of KANSL2 correlate with stemness markers in GBM stem-like cell populations. M…

0301 basic medicineCHROMATINMaleCancer ResearchCarcinogenesisCellCell SeparationMice SCIDmedicine.disease_causeMiceCANCER STEM CELLMice Inbred NODHistone AcetyltransferasesOligonucleotide Array Sequence AnalysisBrain NeoplasmsNuclear ProteinsMiddle AgedFlow CytometryImmunohistochemistryChromatinUp-Regulationmedicine.anatomical_structureOncologyGene Knockdown TechniquesNeoplastic Stem CellsHeterograftsFemaleCIENCIAS NATURALES Y EXACTASAdultKANSLOtras Ciencias BiológicasBlotting WesternGLIOBLASTOMABiologyReal-Time Polymerase Chain ReactionArticleCiencias Biológicas03 medical and health sciencesCancer stem cellmedicineBiomarkers TumorGene silencingAnimalsHumansEpigeneticsAgedEmbryonic stem cell030104 developmental biologyCancer cellImmunologyCancer researchCarcinogenesisGlioblastomaCancer research
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Impact of plant sterols enrichment dose on gut microbiota from lean and obese subjects using TIM-2 in vitro fermentation model

2019

There are scarce data on plant sterols (PS) and gut microbiota relationship. The purpose of this study is to compare the interaction between PS and gut microbiota through in vitro colonic fermentation studies using a validated system (TIM-2) with a PS-enriched dose (similar to 2 g/day) from two sources (food PS-source ingredient and commercial standard) using microbiota from lean and obese populations. Fecal sterols, short chain fatty acids (SCFA) and microbiota composition were determined by GC/MS, IEC, and 16S-sequencing, respectively.PS-feeding decreased coprostanol and ethylcoprostanol concentration and increased the production of acetate and butyrate (mainly with lean microbiota). In a…

0301 basic medicineCHROMATOGRAPHYMedicine (miscellaneous)ButyrateGut microbiotaGut floradigestive systemPlant sterolsNEUTRAL STEROLS03 medical and health sciencesIngredientchemistry.chemical_compoundBUTYRATE0404 agricultural biotechnologyfluids and secretionsTX341-641Food scienceFecesBILE-ACIDS030109 nutrition & dieteticsNutrition and DieteticsbiologyPHYTOSTEROLSCholesterolNutrition. Foods and food supplyCHOLESTEROLHUMANSShort chain fatty acids04 agricultural and veterinary sciencesbiology.organism_classificationCANCER040401 food scienceIn vitroPRODUCTSCoprostanolCHAIN FATTY-ACIDSchemistryFermentationTIM-2 in vitro modelFecal sterolsFood ScienceJournal of Functional Foods
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Case report : partial uniparental disomy unmasks a novel recessive mutation in the LYST gene in a patient with a severe phenotype of Chediak-Higashi …

2021

Síndrome de Chédiak-Higashi; LYST; Disomia uniparental Síndrome de Chédiak-Higashi; LYST; Disomía uniparental Chédiak-Higashi syndrome; LYST; Uniparental disomy Chédiak-Higashi syndrome (CHS) is a rare autosomal recessive (AR) immune disorder that has usually been associated to missense, nonsense or indels mutations in the LYST gene. In this study, we describe for the first time the case of a CHS patient carrying a homozygous mutation in the LYST gene inherited as a result of a partial uniparental isodisomy (UPiD) of maternal origin. Sanger sequencing of the LYST cDNA and single nucleotide polymorphism (SNP)-arrays were performed to identify the causative mutation and to explain the molecul…

0301 basic medicineCHSLYSTCase ReportHemophagocytic lymphohistiocytosis030105 genetics & hereditymedicine.disease_causeLoss of heterozygosityExonCh&#233diak-Higashi syndromeImmunology and AllergyMissense mutation:Genetic Phenomena::Genetic Phenomena::Inheritance Patterns::Genes Recessive [PHENOMENA AND PROCESSES]Genetics:fenómenos genéticos::fenómenos genéticos::patrones de herencia::genes recesivos [FENÓMENOS Y PROCESOS]MutationPrimary immunodeficiencySistema inmune - Enfermedades - Diagnóstico.Loss of heterozygosityChédiak-Higashi Síndrome de - Diagnóstico.:enfermedades del sistema inmune::síndromes de inmunodeficiencia::disfunción bactericida del fagocito::síndrome de Chediak-Higashi [ENFERMEDADES]Uniparental disomyImmune system - Diseases - Diagnosis.Chromosome abnormalities.loss of heterozygositySNP array:fenómenos genéticos::variación genética::mutación::aberraciones cromosómicas::disomía uniparental [FENÓMENOS Y PROCESOS]lcsh:Immunologic diseases. AllergyAnomalías y malformaciones cromosómicas.disomia uniparentaluniparental disomy:Immune System Diseases::Immunologic Deficiency Syndromes::Phagocyte Bactericidal Dysfunction::Chediak-Higashi Syndrome [DISEASES]ImmunologyChédiak-Higashi syndromeSingle-nucleotide polymorphismBiologyprimary immunodeficiency03 medical and health sciencesMalalties immunològiquesmedicineGenetic disorders - Diagnosis.Béguez-Chédiak-Higashi syndrome - Diagnosis.Uniparental disomymedicine.diseaseSNP-array030104 developmental biologyAnomalies cromosòmiquesUniparental Isodisomyhemophagocytic lymphohistiocytosisEnfermedades genéticas - Diagnóstico.lcsh:RC581-607:Genetic Phenomena::Genetic Variation::Mutation::Chromosome Aberrations::Uniparental Disomy [PHENOMENA AND PROCESSES]
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Extracellular Vesicles Shed by Melanoma Cells Contain a Modified Form of H1.0 Linker Histone and H1.0 mRNA-binding Proteins

2016

Extracellular vesicles (EVs) are shed in the extracellular environment by both prokaryotes and eukaryotes. Although produced from both normal and cancer cells, malignant cells release a much higher amount of EVs, which also contain tumor-specific proteins and RNAs. We previously found that G26/24 oligodendroglioma cells shed EVs that contain the pro-apoptotic factors FasL and TRAIL1-2. Interestingly, G26/24 release, via EVs, extracellular matrix remodelling proteases3, and H1° histone protein4, and mRNA. To shed further light on the role of EVs in discarding proteins and mRNAs otherwise able to counteract proliferative signals, we studied a melanoma cell line (A375). We found that also thes…

0301 basic medicineCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueMYEF2ApoptosisRNA-binding proteinexosomesmembrane vesiclesReal-Time Polymerase Chain ReactionChromatography AffinityHistones03 medical and health sciencesH1.0 linker histone; RNA-binding proteins (RBPs); extracellular vesicles (EVs) membrane vesicles (MVs); exosomes; MYEF2Settore BIO/10 - BiochimicaTumor Cells CulturedHumansexosomeSecretionRNA MessengerSettore BIO/06 - Anatomia Comparata E Citologiamelanoma cell line (A375) myelin expression factor-2 (MYEF2)MelanomaTranscription factorCell ProliferationH1.0 linker histonebiologyReverse Transcriptase Polymerase Chain ReactionEXTRACELLULAR VESICLESRNA-Binding ProteinsRNACell DifferentiationArticlesCell biologyBlotCell Transformation Neoplastic030104 developmental biologyHistoneOncologySpectrometry Mass Matrix-Assisted Laser Desorption-IonizationCancer cellbiology.proteinRNA-binding proteins (RBPs)extracellular vesicles (EVs) membrane vesicles (MVs)
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Spontaneous and Radiation-Induced Chromosome Aberrations in Primary Fibroblasts of Patients With Pediatric First and Second Neoplasms

2020

Frontiers in oncology 10, 1338 (2020). doi:10.3389/fonc.2020.01338

0301 basic medicineCancer ResearchDNA repairSomatic cell610Chromosomal translocationlcsh:RC254-28203 medical and health sciences0302 clinical medicineRadiation sensitivityChromosome instabilitymedicinechildhood cancerddc:610spontaneous chromosomal instabilityOriginal Researchmedicine.diagnostic_testbusiness.industryChromosomeradiation sensitivitysecond primary malignancieslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrimary Neoplasm030104 developmental biologychromosome aberrationsOncology030220 oncology & carcinogenesisCancer researchbusinessionizing radiationSecond primary malignancies ; Radiation sensitivity ; Chromosome aberrations ; Childhood cancer ; Spontaneous chromosomal instability ; Ionizing radiationFluorescence in situ hybridization
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Targeting the chromosomal passenger complex subunit INCENP induces polyploidization, apoptosis and senescence in neuroblastoma

2019

Abstract Chromosomal passenger complex (CPC) has been demonstrated to be a potential target of cancer therapy by inhibiting Aurora B or survivin in different types of cancer including neuroblastoma. However, chemical inhibition of either Aurora B or survivin does not target CPC specifically due to off-target effects or CPC-independent activities of these two components. In a previous chromatin-focused siRNA screen, we found that neuroblastoma cells were particularly vulnerable to loss of INCENP, a gene encoding a key scaffolding component of the CPC. In this study, INCENP was highly expressed by neuroblastoma cells, and its expression decreased following retinoic acid–induced neuroblastoma …

0301 basic medicineCancer ResearchINCENP/CPC/Polyploidy/DNA damage/Apoptosis/SenescenceCarcinogenesisChromosomal Proteins Non-HistoneAurora B kinaseApoptosisBiologymedicine.disease_causeArticlePolyploidy03 medical and health sciencesMiceNeuroblastoma0302 clinical medicineNeuroblastomaSurvivinmedicineGene silencingAnimalsHumansneoplasmsCellular SenescenceINCENPmedicine.disease030104 developmental biologyOncologyApoptosisTumor progression030220 oncology & carcinogenesisCancer researchHeterograftsCarcinogenesis
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An Algorithm Combining Patient Performance Status, Second Hit Analysis, PROVEAN and Dann Prediction Tools Could Foretell Sensitization to PARP Inhibi…

2021

Simple Summary PARP inhibitors, a family of targeted cancer therapeutics, have been shown to be efficient in patients with some deficiencies in the homologous recombination machinery. However, a quick and reliable identification of patients who would benefit from such therapies remains a challenge. In particular, patients with tumors carrying variants of unknown significance (VUS) in homologous recombination genes do not currently benefit from PARP inhibitor treatments. In this study, we present an algorithm that may allow classification of these variants with regard to their impact on tumor responsiveness to PARP inhibitors. If validated on a larger patient sample, our algorithm would allo…

0301 basic medicineCancer ResearchIn silicohomologous recombinationArticleOlaparib03 medical and health scienceschemistry.chemical_compound0302 clinical medicineHomologous chromosomeMedicineProgression-free survivalAllele frequencyPARP inhibitorsSensitizationRC254-282responsePerformance statusbusiness.industryNeoplasms. Tumors. Oncology. Including cancer and carcinogensVUS030104 developmental biologymedicine.anatomical_structureOncologychemistry030220 oncology & carcinogenesisPARP inhibitorbusinessAlgorithmprogression-free survivalCancers
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Quantitative Imaging of D-2-Hydroxyglutarate in Selected Histological Tissue Areas by a Novel Bioluminescence Technique

2016

Abstract Patients with malignant gliomas have a poor prognosis with average survival of less than one year. Whereas in other tumor entities the characteristics of tumor metabolism are successfully used for therapeutic approaches, such developments are very rare in brain tumors, notably in gliomas. One metabolic feature characteristic of gliomas, in particular diffuse astrocytomas and oligodendroglial tumors, is the variable content of D-2-hydroxyglutarate (D2HG), a metabolite, which was discovered first in this tumor entity. D2HG is generated in large amounts due to various “gain-of–function” mutations in the isocitrate dehydrogenases IDH-1 and IDH-2. Meanwhile, D2HG has been detected in se…

0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyMetabolite610 MedizinBiology03 medical and health scienceschemistry.chemical_compoundmedicineBioluminescence imagingBioluminescenceOligodendroglial TumorOriginal Researchddc:610D-2 hydroxyglutarateglioblastomaMyeloid leukemiaCancerACUTE MYELOID-LEUKEMIA; ISOCITRATE DEHYDROGENASE 1; IDH2 MUTATIONS; CHROMATOGRAPHY/MASS SPECTROMETRY; MAGNETIC-RESONANCE; 2-HYDROXYGLUTARATE; CANCER; GLIOMAS; L-2-HYDROXYGLUTARATE; METABOLITES; D-2 hydroxyglutarate; IDH mutations; bioluminescence imaging; oncometabolite; glioblastomabioluminescence imagingIDH mutationsmedicine.diseaseoncometaboliteLymphoma030104 developmental biologychemistryOncologyChondrosarcoma
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Frequency and prognostic impact of ALK amplifications and mutations in the European Neuroblastoma Study Group (SIOPEN) high-risk neuroblastoma trial …

2021

Purpose: In neuroblastoma (NB), the ALK receptor tyrosine kinase can be constitutively activated through activating point mutations or genomic amplification. We studied ALK genetic alterations in high-risk (HR) patients on the HR-NBL1/SIOPEN trial to determine their frequency, correlation with clinical parameters, and prognostic impact. Materials and methods: Diagnostic tumor samples were available from 1,092 HR-NBL1/SIOPEN patients to determine ALK amplification status (n = 330), ALK mutational profile (n = 191), or both (n = 571). Results: Genomic ALK amplification (ALKa) was detected in 4.5% of cases (41 out of 901), all except one with MYCN amplification (MNA). ALKa was associated with …

0301 basic medicineCancer ResearchPrognostic ImpactAnaplastic Lymphoma Kinase/genetics; Child Preschool; Clinical Trials Phase III as Topic; Europe; Female; Follow-Up Studies; Gene Amplification; Humans; Infant; Male; Mutation Rate; N-Myc Proto-Oncogene Protein/genetics; Neuroblastoma/genetics; Prognosis; Randomized Controlled Trials as Topic; Risk Factors; Survival RateEuropean Neuroblastoma Study GroupSIOPENRELAPSE03 medical and health sciencesNeuroblastoma0302 clinical medicineText miningNeuroblastomahemic and lymphatic diseasesREVEALSMedicine and Health SciencesKINASEMedicineHigh risk neuroblastomaHETEROGENEITYCRIZOTINIBSEGMENTAL CHROMOSOMAL ALTERATIONSACTIVATING MUTATIONSPEDIATRIC-PATIENTSbusiness.industryALK receptor tyrosine kinasePoint mutationREARRANGEMENTSCHEMOTHERAPYmedicine.diseaseDoenças Genéticas030104 developmental biologyALKOncology030220 oncology & carcinogenesisCancer researchbusiness
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