Search results for "expression"

showing 10 items of 5168 documents

Bone marrowVEGFCexpression is associated with multilineage dysplasia and several prognostic markers in adult acute myeloid leukemia, but not with sur…

2018

Vascular endothelial growth factor C (VEGFC) stimulates leukemia cell proliferation and survival, and promotes angiogenesis. We studied VEGFC expression in bone marrow samples from 353 adult acute myeloid leukemia (AML) patients and its relationship with several clinical, cytogenetic, and molecular variables. We also studied the expression of 84 genes involved in VEGF signaling in 24 patients. We found that VEGFC expression was higher in AML patients with myelodysplasia-related changes (AML-MRC) than in patients with non-AML-MRC. We also found an association between VEGFC expression and the patient cytogenetic risk group, with those with a worse prognosis having higher VEGFC expression leve…

AdultMale0301 basic medicineCancer ResearchAdolescentAngiogenesisVascular Endothelial Growth Factor CKaplan-Meier EstimateVEGFC expressionYoung Adult03 medical and health sciences0302 clinical medicineKDRBone Marrowhemic and lymphatic diseasesNeuropilin 1Biomarkers TumormedicineNRP1HumansGeneFLT1AgedChromosome AberrationsAcute myeloid leukemiaVascular Endothelial Growth Factor Receptor-1Cell growthbusiness.industryAdult Acute Myeloid LeukemiaHematologyVEGF signalingMiddle AgedPrognosismedicine.diseaseVascular Endothelial Growth Factor Receptor-2Neuropilin-1Leukemia Myeloid AcuteLeukemia030104 developmental biologymedicine.anatomical_structureOncologyVascular endothelial growth factor CMyelodysplastic Syndromes030220 oncology & carcinogenesisCancer researchFemaleBone marrowbusinessLeukemia & Lymphoma
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MicroRNAs expression associated with aggressive clinicopathological features and poor prognosis in primary cutaneous melanomas

2020

Several studies have focused on identifying microRNAs involved in the pathogenesis of melanoma. However, its association with clinicopathological features has been scarcely addressed. The aim of this study is to identify microRNAs expression profiles related to aggressive clinicopathological and molecular features, and to analyze the association with melanoma survival. A retrospective and observational study was performed in a series of 179 formalin-fixed paraffin embedded primary cutaneous melanomas. First, a screening analysis on a discovery set (n = 22) using miRNA gene chip array (Affymetrix, Santa Clara, California, USA) was performed. Differentially expressed microRNAs were detected e…

AdultMale0301 basic medicineCancer ResearchPoor prognosisSkin NeoplasmsTERT mutationsDermatologyBiologyPathogenesisBreslow Thickness03 medical and health sciences0302 clinical medicinemicroRNAmelanomamedicineHumansMelanomaMitosisSurvival analysisAgedMelanomaMicroRNA Expression ProfileMiddle AgedPrognosismedicine.diseasemicroRNAsMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchFemaleprognosisclinicopathological featuresMelanoma Research
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A Novel MicroRNA Signature for Cholestatic Drugs in Human Hepatocytes and Its Translation into Novel Circulating Biomarkers for Drug-Induced Liver In…

2019

AbstractDrug-induced liver injury (DILI) diagnosis and classification (hepatocellular, cholestatic, and mixed) relies on traditional clinical biomarkers (eg ALT and ALP), despite limitations such as extrahepatic interferences, narrow dynamic ranges, and low mechanistic value. microRNAs may be very useful for complementing traditional DILI biomarkers but most studies in this direction have considered only paracetamol poisoning. Thus the value of microRNAs (miRNAs) as biomarkers for idiosyncratic DILI has not yet been demonstrated. In this study, we first examined the effect of model cholestatic drugs on the human hepatocyte miRNome by RNAseq and RT-qPCR. Results demonstrated that chlorpromaz…

AdultMale0301 basic medicineDrugmedia_common.quotation_subjectToxicologyCell LineCohort Studies03 medical and health sciences0302 clinical medicineCholestasisCyclosporin amicroRNAmedicineHumansChlorpromazinemedia_commonLiver injuryCholestasisReceiver operating characteristicbusiness.industryGene Expression ProfilingLiver DiseasesTranslation (biology)Middle Agedmedicine.diseaseMicroRNAs030104 developmental biologyHepatocytesCancer researchFemale030211 gastroenterology & hepatologyChemical and Drug Induced Liver InjurybusinessBiomarkersmedicine.drugToxicological Sciences
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EPDR1 up-regulation in human colorectal cancer is related to staging and favours cell proliferation and invasiveness

2020

The finding of novel molecular markers for prediction or prognosis of invasiveness in colorectal cancer (CRC) constitutes an appealing challenge. Here we show the up-regulation of EPDR1 in a prospective cohort of 101 CRC patients, in a cDNA array of 43 patients and in in silico analyses. EPDR1 encodes a protein related to ependymins, a family of glycoproteins involved in intercellular contacts. A thorough statistical model allowed us to conclude that the gene is significantly up-regulated in tumour tissues when compared with normal mucosa. These results agree with those obtained by the analysis of three publicly available databases. EPDR1 up-regulation correlates with the TNM staging parame…

AdultMale0301 basic medicineEpithelial-Mesenchymal TransitionColorectal cancerIn silicolcsh:MedicineNerve Tissue ProteinsBiologyArticle//purl.org/becyt/ford/3.3 [https]03 medical and health sciences0302 clinical medicinemedicinecancerHumansNeoplasm InvasivenesshumanProspective StudiesEpithelial–mesenchymal transitionlcsh:ScienceAgedCell ProliferationNeoplasm StagingcolorectalAged 80 and overRegulation of gene expressionMultidisciplinaryCell growthlcsh:RMethylationMiddle Agedmedicine.diseaseColorectal cancerNeoplasm ProteinsUp-RegulationEPDR1Gene Expression Regulation Neoplastic030104 developmental biologyCpG siteCell culture030220 oncology & carcinogenesisCancer research//purl.org/becyt/ford/3 [https]Femalelcsh:QColorectal NeoplasmsTranscriptionScientific Reports
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Integration of a radiation biomarker into modeling of thyroid carcinogenesis and post-Chernobyl risk assessment

2016

Strong evidence for the statistical association between radiation exposure and disease has been produced for thyroid cancer by epidemiological studies after the Chernobyl accident. However, limitations of the epidemiological approach in order to explore health risks especially at low doses of radiation appear obvious. Statistical fluctuations due to small case numbers dominate the uncertainty of risk estimates. Molecular radiation markers have been searched extensively to separate radiation-induced cancer cases from sporadic cases. The overexpression of the CLIP2 gene is the most promising of these markers. It was found in the majority of papillary thyroid cancers (PTCs) from young patients…

AdultMale0301 basic medicineOncologyRisk analysisCancer Researchmedicine.medical_specialtyMedical surveillanceNeoplasms Radiation-InducedAdolescentThyroid GlandOriginal ManuscriptDisease03 medical and health sciences0302 clinical medicineInternal medicineEpidemiologyBiomarkers TumormedicineHumansThyroid NeoplasmsChildThyroid cancerbusiness.industryCarcinomaCancerGeneral Medicinemedicine.diseaseCarcinoma Papillary3. Good healthBiomarker (cell)Gene Expression Regulation Neoplastic030104 developmental biologyChernobyl Nuclear AccidentThyroid Cancer Papillary030220 oncology & carcinogenesisFemaleRisk assessmentbusinessMicrotubule-Associated ProteinsCarcinogenesis
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Hypoxia-Inducible Factor 2α Mutation-Related Paragangliomas Classify as Discrete Pseudohypoxic Subcluster

2016

Contains fulltext : 172720.pdf (Publisher’s version ) (Open Access) Recently, activating mutations of the hypoxia-inducible factor 2alpha gene (HIF2A/EPAS1) have been recognized to predispose to multiple paragangliomas (PGLs) and duodenal somatostatinomas associated with polycythemia, and ocular abnormalities. Previously, mutations in the SDHA/B/C/D, SDHAF2, VHL, FH, PHD1, and PHD2 genes have been associated with HIF activation and the development of pseudohypoxic (cluster-1) PGLs. These tumors overlap in terms of tumor location, syndromic presentation, and noradrenergic phenotype to a certain extent. However, they also differ especially by clinical outcome and by presence of other tumors o…

AdultMale0301 basic medicineOriginal articleCancer ResearchAdolescentMicroarraySDHBSDHABiologylcsh:RC254-282Oxidative PhosphorylationParagangliomaYoung Adult03 medical and health sciences0302 clinical medicineParagangliomaBasic Helix-Loop-Helix Transcription FactorsmedicineJournal ArticleCluster AnalysisHumansChildHypoxiaAgedGeneticsGene Expression ProfilingVascular damage Radboud Institute for Molecular Life Sciences [Radboudumc 16]Middle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePhenotypeGene Expression Regulation NeoplasticGene expression profiling030104 developmental biologyHypoxia-inducible factors030220 oncology & carcinogenesisMutationFemaleSDHDTranscriptomeProtein BindingNeoplasia
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Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis

2017

Bcl-3 is an atypical NF-κB family member that regulates NF-κB-dependent gene expression in effector T cells, but a cell-intrinsic function in regulatory T (Treg) cells and colitis is not clear. Here we show that Bcl-3 expression levels in colonic T cells correlate with disease manifestation in patients with inflammatory bowel disease. Mice with T-cell-specific overexpression of Bcl-3 develop severe colitis that can be attributed to defective Treg cell development and function, leading to the infiltration of immune cells such as pro-inflammatory γδT cells, but not αβ T cells. In Treg cells, Bcl-3 associates directly with NF-κB p50 to inhibit DNA binding of p50/p50 and p50/p65 NF-κB dimers, t…

AdultMale0301 basic medicineP50ScienceGeneral Physics and AstronomyBiologyT-Lymphocytes RegulatoryInflammatory bowel diseaseArticleGeneral Biochemistry Genetics and Molecular BiologyYoung Adult03 medical and health sciences0302 clinical medicineImmune systemB-Cell Lymphoma 3 ProteinProto-Oncogene ProteinsGene expressionmedicineAnimalsHumansColitisMice KnockoutRegulation of gene expressionMultidisciplinaryEffectorHEK 293 cellsQNF-kappa BTranscription Factor RelANF-kappa B p50 SubunitGeneral ChemistryMiddle AgedColitismedicine.diseaseMice Inbred C57BLHEK293 Cells030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisImmunologyFemaleProtein BindingTranscription FactorsNature Communications
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Active paraplegics are protected against exercise-induced oxidative damage through the induction of antioxidant enzymes

2016

Exercise improves functional capacity in spinal cord injury (SCI). However, exhaustive exercise, especially when sporadic, is linked to the production of reactive oxygen species that may have a detrimental effect on SCI. We aimed to study the effect of a single bout of exhaustive exercise on systemic oxidative stress parameters and on the expression of antioxidant enzymes in individuals with paraplegia. The study was conducted in the Physical Therapy department and the Physical Education and Sports department of the University of Valencia. Sixteen paraplegic subjects were submitted to a graded exercise test (GET) until volitional exhaustion. They were divided into active or non-active group…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyAntioxidantNeurologyEnzimasmedicine.medical_treatmentEnzimaPharmacologyAntioxidantsProtein CarbonylationOxidative damage03 medical and health sciences0302 clinical medicineMalondialdehydeAccelerometrymedicineHumansRNA MessengerExerciseSpinal cord injuryAgedParaplegiachemistry.chemical_classificationGlutathione PeroxidaseParaplejíaSuperoxide Dismutasebusiness.industryGeneral MedicineMiddle AgedCatalasemedicine.disease030104 developmental biologyEnzymeGene Expression RegulationNeurologychemistryExercise TestLeukocytes MononuclearFemaleLipid PeroxidationNeurology (clinical)ParaplegiabusinessEnfermedad030217 neurology & neurosurgery
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Low miR200c expression in tumor budding of invasive front predicts worse survival in patients with localized colon cancer and is related to PD-L1 ove…

2018

At the histological level, tumor budding in colon cancer is the result of cells undergoing at least partial epithelial-to-mesenchymal transition. The microRNA 200 family is an important epigenetic driver of this process, mainly by downregulating zinc-finger E-box binding homeobox (ZEB) and transforming growth factor beta (TGF-β) expression. We retrospectively explored the expression of the miR200 family, and ZEB1 and ZEB2, and their relationship with immune resistance mediated through PD-L1 overexpression. For this purpose, we analyzed a series of 125 colon cancer cases and took samples from two different tumor sites: the area of tumor budding at the invasive front and from the tumor center…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionColorectal cancerPD-L1 OverexpressionBiologyB7-H1 AntigenPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineTumor buddingmicroRNAmedicineHumansAgedRetrospective StudiesAged 80 and overBuddingMesenchymal stem cellTransforming growth factor betaMiddle Agedmedicine.disease3. Good healthMicroRNAs030104 developmental biology030220 oncology & carcinogenesisColonic NeoplasmsCancer researchbiology.proteinBiomarker (medicine)FemaleModern Pathology
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Mutations in theMORC2gene cause axonal Charcot–Marie–Tooth disease

2015

Charcot-Marie-Tooth disease (CMT) is a complex disorder with wide genetic heterogeneity. Here we present a new axonal Charcot-Marie-Tooth disease form, associated with the gene microrchidia family CW-type zinc finger 2 (MORC2). Whole-exome sequencing in a family with autosomal dominant segregation identified the novel MORC2 p.R190W change in four patients. Further mutational screening in our axonal Charcot-Marie-Tooth disease clinical series detected two additional sporadic cases, one patient who also carried the same MORC2 p.R190W mutation and another patient that harboured a MORC2 p.S25L mutation. Genetic and in silico studies strongly supported the pathogenicity of these sequence variant…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyGene ExpressionSchwann cellSural nerveBiologyFasciculationMiceYoung Adult03 medical and health sciences0302 clinical medicineAtrophySural NerveCharcot-Marie-Tooth DiseasemedicineAnimalsHumansAxonAgedGenetic heterogeneityInfantSensory lossMiddle Agedmedicine.diseaseSciatic NerveAxonsPedigreePhenotype030104 developmental biologymedicine.anatomical_structureMutationFemaleNeurology (clinical)Myokymiamedicine.symptomNeuroscience030217 neurology & neurosurgeryTranscription FactorsBrain
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