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Substantial deficiency of free sialic acid in muscles of patients with GNE myopathy and in a mouse model

2017

GNE myopathy (GNEM), also known as hereditary inclusion body myopathy (HIBM), is a late- onset, progressive myopathy caused by mutations in the GNE gene encoding the enzyme responsible for the first regulated step in the biosynthesis of sialic acid (SA). The disease is characterized by distal muscle weakness in both the lower and upper extremities, with the quadriceps muscle relatively spared until the late stages of disease. To explore the role of SA synthesis in the disease, we conducted a comprehensive and systematic analysis of both free and total SA levels in a large cohort of GNEM patients and a mouse model. A sensitive LC/MS/MS assay was developed to quantify SA in serum and muscle h…

0301 basic medicineMaleBiopsylcsh:MedicineMuscle ProteinsBiochemistryPathogenesischemistry.chemical_compoundMice0302 clinical medicineTandem Mass SpectrometryMedicine and Health Scienceslcsh:ScienceMusculoskeletal SystemMultidisciplinarymedicine.diagnostic_testOrganic CompoundsMusclesGastrocnemius MusclesAnimal ModelsMuscle AnalysisMiddle AgedChemistrymedicine.anatomical_structureBioassays and Physiological AnalysisBiochemistryExperimental Organism SystemsPhysical SciencesFemalemedicine.symptomAnatomyResearch ArticleMuscle tissueAdultmedicine.medical_specialtyAdolescentMuscle TissueMouse ModelsSurgical and Invasive Medical ProceduresCreatineResearch and Analysis Methods03 medical and health sciencesYoung AdultModel OrganismsInternal medicineBiopsymedicineAnimalsHumansMyopathyMuscle SkeletalAgedHereditary inclusion body myopathybusiness.industrylcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsmedicine.diseaseCreatineN-Acetylneuraminic AcidSialic acidDistal MyopathiesDisease Models Animal030104 developmental biologyEndocrinologyBiological TissuechemistrySkeletal Muscleslcsh:QbusinessN-Acetylneuraminic acid030217 neurology & neurosurgeryBiomarkersChromatography LiquidPLoS ONE
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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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Bone marrow B lymphocytes in multiple myeloma and MGUS: Focus on distribution of naïve cells and memory subsets.

2016

Multiple myeloma (MM) is caused by proliferation of clonal plasma cells (cPCs) in bone marrow (BM), associated with numerical and functional defects in immune subsets. An impairment of B cell compartment is involved in onset/progression of the disease.By flow cytometry, we studied distribution of naïve/transitional (IgD(+)CD27(-)), memory unswitched (IgD(+)CD27(+)), memory switched (IgD(-)CD27(+)) and double negative (DN) (IgD(-)CD27(-)) B lymphocytes in BM of control subjects, and responding and relapsing patients.We observed an increased percentage of IgD(+)CD27(+) B cells in healthy controls vs responding patients (p0.05). Treated non complete responders exhibited an expanded DN compartm…

0301 basic medicineMaleCancer ResearchB-Lymphocyte Subsetschemical and pharmacologic phenomenaBone Marrow CellsImmunoglobulin DMonoclonal Gammopathy of Undetermined SignificanceFlow cytometry03 medical and health sciencesImmune systemstomatognathic systemimmune system diseaseshemic and lymphatic diseasesmedicineHumansB cellMultiple myelomaB-Lymphocyte SubsetsB cellB-Lymphocytesmedicine.diagnostic_testbiologyhemic and immune systemsHematologyImmunoglobulin Dmedicine.diseaseFlow CytometryTumor Necrosis Factor Receptor Superfamily Member 7030104 developmental biologymedicine.anatomical_structureOncologyCase-Control StudiesImmunologybiology.proteinMGUSFemaleBone marrowMultiple MyelomaMonoclonal gammopathy of undetermined significanceLeukemia research
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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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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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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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JC Virus and Lung Adenocarcinoma: Fact or Myth?

2017

Background/aim An association has been reported between lung cancer and John Cunningham (JC) virus infection. The aim of this study was to evaluate the prevalence of JC virus in a small cohort of patients with lung adenocarcinoma and assess its presence in nodal metastasis. Materials and methods Consecutive samples of 13 surgically-removed lung tumors and 13 surrounding normal cancer-free tissues were selected. Five cases included metastatic lymph nodes. JC virus infection was assessed through nested PCR. Results Seven out of thirteen patients with lung adenocarcinoma had a positive PCR test for JC virus. One of the five patients with nodal metastasis had a positive PCR test for JC virus. N…

0301 basic medicineMaleCancer ResearchPathologymedicine.medical_specialtyTumor Virus InfectionsLung NeoplasmsvirusesJC virusAdenocarcinoma of Lung030230 surgeryAdenocarcinomamedicine.disease_causePolymerase Chain ReactionVirus03 medical and health sciences0302 clinical medicinemedicineHumansLung cancerAgedPolyomavirus InfectionsLungbusiness.industryJC Virus InfectionGeneral Medicinemedicine.diseaseJC VirusTumor Virus Infections030104 developmental biologymedicine.anatomical_structureOncologyCase-Control StudiesLymphatic MetastasisDNA ViralAdenocarcinomaFemalebusinessPolyomavirus InfectionsAnticancer research
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Investigation of SOSTDC1 gene in non-syndromic patients with supernumerary teeth

2018

WOS: 000443304400005 PubMed: 30148467 Background: The etiology of supernumerary teeth is still unclear however heredity is believed to be a major factor and this idea was supported by several case reports. Recently, a relationship between supernumerary tooth formation and deficiency of Uterine Sensitization Associated Gene-1 (Usag-1), a rat gene that is expressed in sensitized endometrium, was reported in mice. The human homolog gene for Usag-1, Sclerostin Domain Containing 1 (SOSTDC1), shows 85% identity with mouse Usag-1. The present study aimed to investigate SOSTDC1 coding regions in non-syndromic patients with one or more supernumerary teeth. Material and Methods: Twenty-five non-syndr…

0301 basic medicineMaleCandidate geneAdolescentBiologymesiodensmedicine.disease_cause03 medical and health sciences0302 clinical medicineHeredityGeneticsmedicineCoding regionHumansSupernumeraryDNA sequencingChildGeneral DentistryGeneAdaptor Proteins Signal TransducingGeneticsOral Medicine and PathologyResearchIntracellular Signaling Peptides and ProteinsProteins030206 dentistry:CIENCIAS MÉDICAS [UNESCO]Phenotypepediatric dentistryPCR030104 developmental biologyOtorhinolaryngologyTooth SupernumeraryUsag-1Child PreschoolUNESCO::CIENCIAS MÉDICASEtiologySurgeryHuman genomeFemaleMedicina Oral, Patología Oral y Cirugía Bucal
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