Search results for "DELE"

showing 10 items of 631 documents

Genomic Amplifications and Distal 6q Loss: Novel Markers for Poor Survival in High-risk Neuroblastoma Patients.

2018

Abstract Background Neuroblastoma is characterized by substantial clinical heterogeneity. Despite intensive treatment, the survival rates of high-risk neuroblastoma patients are still disappointingly low. Somatic chromosomal copy number aberrations have been shown to be associated with patient outcome, particularly in low- and intermediate-risk neuroblastoma patients. To improve outcome prediction in high-risk neuroblastoma, we aimed to design a prognostic classification method based on copy number aberrations. Methods In an international collaboration, normalized high-resolution DNA copy number data (arrayCGH and SNP arrays) from 556 high-risk neuroblastomas obtained at diagnosis were coll…

0301 basic medicineOncologyCancer ResearchSomatic cellNeuroblastoma0302 clinical medicineGene duplicationMedicine and Health SciencesHigh risk neuroblastomaN-Myc Proto-Oncogene ProteinABNORMALITIESIntensive treatmentGenomicsArticlesPrognosis3. Good healthOncologyChild Preschool030220 oncology & carcinogenesisChromosomes Human Pair 6Chromosome DeletionINTEGRATIONmedicine.medical_specialtyDNA Copy Number VariationsCLASSIFICATION03 medical and health sciencesAGEInternal medicineNeuroblastomaSTRATIFICATIONClinical heterogeneityBiomarkers TumormedicineHumansGenetic Predisposition to DiseaseCopy number aberrationneoplasmsGenetic Association StudiesNeoplasm StagingACCUMULATIONbusiness.industryOUTCOME PREDICTIONGene AmplificationInfantBiology and Life SciencesDNAmedicine.diseaseDELINEATION030104 developmental biologyCOPY NUMBEROutcome predictionbusiness
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Comprehensive cross-platform comparison of methods for non-invasive EGFR mutation testing : results of the RING observational trial

2020

Plasma samples from 72 EGFR‐mutant advanced NSCLC patients, collected upon progression to first‐line TKI, were analyzed by seven methodologies (two NGS‐based methods, three high‐sensitivity PCR‐based platforms, and two FDA‐approved methods). Our study demonstrates a good to excellent agreement between methodologies and supports the use of liquid biopsies for therapy decision‐making.

0301 basic medicineOncologyMaleCancer Researchcell lung cancerIntraclass correlationBiopsyDNA Mutational Analysisnon-small cell lung cancer (NSCLC)Tyrosine kinase inhibitorTyrosine-kinase inhibitorCohort Studies*circulating free DNAT790M0302 clinical medicinetyrosine kinase inhibitorGene FrequencyOsimertinibProspective cohort studyCàncernon‐small‐cell lung cancerCirculating free DNARC254-282Research ArticlesSequence DeletionAged 80 and overNeoplasms. Tumors. Oncology. Including cancer and carcinogensHigh-Throughput Nucleotide Sequencingnon&#8208General MedicineDNA NeoplasmExonsMiddle AgedErbB ReceptorsEpidermal growth factor receptor (EGFR) NGS Non-small cell lung cancer (NSCLC) PCR Tyrosine Kinase Inhibitor (TKI) circulating free DNA (cfDNA) osimertinibOncology030220 oncology & carcinogenesisosimertinibNGSMolecular Medicinesmall&#8208FemaleResearch Article*NGSAdultmedicine.medical_specialtymedicine.drug_classSensitivity and Specificity03 medical and health sciencesPredictive Value of TestsInternal medicineGeneticsmedicineHumansAged*non-small-cell lung cancerbusiness.industryEpidermal growth factor receptorNon invasive*epidermal growth factor receptormedicine.disease*tyrosine kinase inhibitorrespiratory tract diseases030104 developmental biologyEgfr mutationPulmonsMutationcirculating free DNAbusinessepidermal growth factor receptorNon-small-cell lung cancer*osimertinibOsimertinib
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NF1 microdeletion syndrome: case report of two new patients

2019

Abstract Background 17q11.2 microdeletions, which include the neurofibromatosis type 1 (NF1) gene region, are responsible for the NF1 microdeletion syndrome, observed in 4.2% of all NF1 patients. Large deletions of the NF1 gene and its flanking regions are associated with a more severe NF1 phenotype than the NF1 general population. Case presentation We hereby describe the clinical and molecular features of two girls (aged 2 and 4 years, respectively), with non-mosaic atypical deletions. Patient 1 showed fifteen café-au-lait spots and axillary freckling, as well as a Lisch nodule in the left eye, strabismus, high-arched palate, malocclusion, severe kyphoscoliosis, bilateral calcaneovalgus fo…

0301 basic medicinePathologymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesGenotype-phenotype correlationNeurofibromatosesLisch noduleContiguous gene syndromePopulationCase ReportContiguous gene syndromeChromosomesCraniofacial Abnormalities03 medical and health sciences0302 clinical medicineAtypical deletionIntellectual DisabilitymedicineHumansMultiplex ligation-dependent probe amplificationNeurofibromatosiseducationChildPreschoolNeurofibromatoseseducation.field_of_studybusiness.industryLearning DisabilitiesPair 17lcsh:RJ1-570Axillary frecklinglcsh:Pediatricsmedicine.diseaseeye diseasesMLPA030104 developmental biologyNF1 geneChild PreschoolFemalemedicine.symptomChromosome DeletionbusinessAtypical deletion; Contiguous gene syndrome; Genotype-phenotype correlation; MLPA; NF1 gene; Child Preschool; Chromosome Deletion; Chromosomes Human Pair 17; Craniofacial Abnormalities; Female; Humans; Intellectual Disability; Learning Disabilities; Neurofibromatoses030217 neurology & neurosurgeryChromosomes Human Pair 17Comparative genomic hybridizationHumanItalian Journal of Pediatrics
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Jacobsen syndrome and neonatal bleeding: report on two unrelated patients

2021

Abstract Introduction In 1973, Petrea Jacobsen described the first patient showing dysmorphic features, developmental delay and congenital heart disease (atrial and ventricular septal defect) associated to a 11q deletion, inherited from the father. Since then, more than 200 patients have been reported, and the chromosomal critical region responsible for this contiguous gene disorder has been identified. Patients’ presentation We report on two unrelated newborns observed in Italy affected by Jacobsen syndrome (JBS, also known as 11q23 deletion). Both patients presented prenatal and postnatal bleeding, growth and developmental delay, craniofacial dysmorphisms, multiple congenital anomalies, a…

0301 basic medicinePediatricsmedicine.medical_specialtyGenotype-phenotype correlationHeart diseaseGenetic counselingCase ReportIn situ hybridization030105 genetics & heredityPediatricsRJ1-57003 medical and health sciences0302 clinical medicineaCGHJBSmedicineHumansJacobsen Distal 11q Deletion SyndromeJacobsen syndromeCraniofacialGenetic Association StudiesCerebral Hemorrhage11q23 deletionbusiness.industryInfant NewbornEarly diagnosimedicine.diseaseEarly diagnosisPancytopeniaThrombocytopeniaItalyFemalePresentation (obstetrics)business030217 neurology & neurosurgeryComparative genomic hybridizationItalian Journal of Pediatrics
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Quantitative analysis of the impact of a human pathogenic mutation on the CCT5 chaperonin subunit using a proxy archaeal ortholog

2017

The human chaperonin complex is a ~ 1 MDa nanomachine composed of two octameric rings formed from eight similar but non-identical subunits called CCT. Here, we are elucidating the mechanism of a heritable CCT5 subunit mutation that causes profound neuropathy in humans. In previous work, we introduced an equivalent mutation in an archaeal chaperonin that assembles into two octameric rings like in humans but in which all subunits are identical. We reported that the hexadecamer formed by the mutant subunit is unstable with impaired chaperoning functions. This study quantifies the loss of structural stability in the hexadecamer due to the pathogenic mutation, using differential scanning calorim…

0301 basic medicineProtein subunitMutantBiophysicsHeterologousBiochemistryChaperoninChaperoninlcsh:Biochemistry03 medical and health sciencesDSC differential scanning calorimetryCCT% chaperoninPf Pyrococcus furiosusDenaturation (biochemistry)lcsh:QD415-436Molecular Biologylcsh:QH301-705.5DLS dynamic light scatteringbiologyITC isothermal titration calorimetryWild typeIsothermal titration calorimetryCell BiologyChaperonopathiesbiology.organism_classificationProtein calorimetryNeuropathyPyrococcus furiosus030104 developmental biologyBiochemistryBiophysiclcsh:Biology (General)Pyrococcus furiosusChaperonopathieCCT5; Chaperonin; Chaperonopathies; Neuropathy; Protein calorimetry; Pyrococcus furiosus; Biophysics; Biochemistry; Molecular Biology; Cell BiologyCCT5Pyrococcus furiosuResearch ArticlePf-CD1 Pyrococcus furiosus chaperonin subunit with the last 22 amino acids deletedBiochemistry and Biophysics Reports
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Fungicide resistance towards fludioxonil conferred by overexpression of the phosphatase gene Mo PTP 2 in Magnaporthe oryzae

2018

The fungicide fludioxonil causes hyperactivation of the Hog1p MAPK within the high-osmolarity glycerol signaling pathway essential for osmoregulation in pathogenic fungi. The molecular regulation of MoHog1p phosphorylation is not completely understood in pathogenic fungi. Thus, we identified and characterized the putative MoHog1p-interacting phosphatase gene MoPTP2 in the filamentous rice pathogen Magnaporthe oryzae. We found overexpression of MoPTP2 conferred fludioxonil resistance in M. oryzae, whereas the 'loss of function' mutant ΔMoptp2 was more susceptible toward the fungicide. Additionally, quantitative phosphoproteome profiling of MoHog1p phosphorylation revealed lower phosphorylati…

0301 basic medicineProteomeMutantPhosphataseGene ExpressionDioxolesBiologyFludioxonilMicrobiologyMicrobiologyFungal Proteins03 medical and health sciencesDrug Resistance FungalGene expressionPyrrolesPhosphorylationMolecular BiologyGenePlant DiseasesOryzaPhosphoproteinsFungicides IndustrialFungicideMagnaporthe030104 developmental biologyPhosphorylationMitogen-Activated Protein KinasesProtein Tyrosine PhosphatasesSignal transductionProtein Processing Post-TranslationalGene DeletionMolecular Microbiology
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SPEN haploinsufficiency causes a neurodevelopmental disorder overlapping proximal 1p36 deletion syndrome with an episignature of X chromosomes in fem…

2021

Contains fulltext : 231702.pdf (Publisher’s version ) (Closed access) Deletion 1p36 (del1p36) syndrome is the most common human disorder resulting from a terminal autosomal deletion. This condition is molecularly and clinically heterogeneous. Deletions involving two non-overlapping regions, known as the distal (telomeric) and proximal (centromeric) critical regions, are sufficient to cause the majority of the recurrent clinical features, although with different facial features and dysmorphisms. SPEN encodes a transcriptional repressor commonly deleted in proximal del1p36 syndrome and is located centromeric to the proximal 1p36 critical region. Here, we used clinical data from 34 individuals…

0301 basic medicineSHARPMaleobesitygenotype-phenotype correlationsAutism Spectrum DisorderPROTEINChromosome DisordersHaploinsufficiencyRNA-Binding ProteinPHENOTYPE CORRELATIONS1p36; distal 1p36 deletion syndrome; DNA methylome analysis; episignature; genotype-phenotype correlations; neurodevelopmental disorder; obesity; proximal 1p36 deletion syndrome; SPEN; X chromosome; Adolescent; Autism Spectrum Disorder; Child; Child Preschool; Chromosome Deletion; Chromosome Disorders; Chromosomes Human Pair 1; Chromosomes Human X; DNA Methylation; DNA-Binding Proteins; Epigenesis Genetic; Female; Haploinsufficiency; Humans; Intellectual Disability; Male; Neurodevelopmental Disorders; Phenotype; RNA-Binding Proteins; Young AdultEpigenesis GeneticX chromosome0302 clinical medicineNeurodevelopmental disorderNeurodevelopmental DisorderIntellectual disabilityMOLECULAR CHARACTERIZATIONdistal 1p36 deletion syndromeChildGenetics (clinical)X chromosomeGeneticsXDNA methylome analysiRNA-Binding ProteinsSPLIT-ENDSHypotoniaDNA-Binding ProteinsPhenotypeAutism spectrum disorderChromosomes Human Pair 1Child PreschoolDNA methylome analysisMONOSOMY 1P36Pair 1SPENFemalemedicine.symptomChromosome DeletionHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]HumanAdolescentDNA-Binding ProteinBiologygenotype-phenotype correlationChromosomes03 medical and health sciencesYoung AdultGeneticSDG 3 - Good Health and Well-beingReportIntellectual DisabilityREVEALSGeneticsmedicineHumansEpigeneticsPreschoolChromosomes Human XNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]1p361p36 deletion syndromeIDENTIFICATIONMUTATIONSproximal 1p36 deletion syndromeDNA Methylationmedicine.diseaseneurodevelopmental disorderGENEepisignature030104 developmental biologyChromosome DisorderNeurodevelopmental Disorders030217 neurology & neurosurgeryEpigenesis
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Characterization of a mutant form of human apolipoprotein B (Thr26_Tyr27del) associated with familial hypobetalipoproteinemia

2016

We have previously identified a deletion mutant of human apoB [apoB (Thr26_Tyr27del)] in a subject with primary hypobetalipoproteinemia. The present study determined the effect of Thr26_Tyr27del mutation on apoB secretion using transfected McA-RH7777 cells. Transient or stable transfection of apoB-48 containing the Thr26_Tyr27del mutation showed drastically reduced secretion of the mutant as compared to wild-type apoB-48. No lipoproteins containing the mutant apoB-48 were secreted into the medium. Incubation of transfected cells in a lipid-rich medium in the presence of cycloheximide showed rapid turnover of cell-associated mutant apoB-48 as compared to that of wild-type apoB-48. Immunofluo…

0301 basic medicineSettore MED/09 - Medicina InternaTime FactorsApolipoprotein B-48 secretionApolipoprotein BMutantDNA Mutational AnalysisApolipoprotein B mutation Apolipoprotein B-48 secretion Hypobetalipoproteinemia Proteasomal degradation030204 cardiovascular system & hematologymedicine.disease_causeEndoplasmic ReticulumHypobetalipoproteinemiaschemistry.chemical_compound0302 clinical medicineProteasomal degradationProteolysiSequence DeletionMutationbiologyMedicine (all)TransfectionProteasome InhibitorPhenotypeBiochemistryApolipoprotein B-100lipids (amino acids peptides and proteins)Proteasome InhibitorsHumanHeterozygoteProteasome Endopeptidase ComplexTime FactorCycloheximideTransfectiondigestive systemCell LineDNA Mutational Analysi03 medical and health sciencesmedicineHumansSecretionGenetic Predisposition to DiseaseMolecular BiologyEndoplasmic reticulumnutritional and metabolic diseasesCell Biologymedicine.diseaseMolecular biology030104 developmental biologychemistryProteolysisbiology.proteinHypobetalipoproteinemiaApolipoprotein B mutationApolipoprotein B-48Hypobetalipoproteinemia
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Null mutants of Candida albicans for cell-wall-related genes form fragile biofilms that display an almost identical extracellular matrix proteome.

2016

By two-dimensional gel electrophoresis (2-DE) and mass spectrometry, we have characterized the polypeptide species present in extracts obtained by 60% ethanol treatment of whole mature (48 h) biofilms formed by a reference strain (CAI4- URA3 ) and four Candida albicans null mutants for cell-wall-related genes ( ALG5, CSA1, MNN9 and PGA10) . Null mutants form fragile biofilms that appeared partially split and weakly attached to the substratum contrary to those produced by the reference strain. An almost identical, electrophoretic profile consisting of about 276 spots was visualized in all extracts examined. Proteomic analysis led to the identification of 131 polypeptides, corresponding to 86…

0301 basic medicineSignal peptideProteomeMutantGenes FungalBiologyApplied Microbiology and BiotechnologyMicrobiologyMass SpectrometryCell wallFungal Proteins03 medical and health sciencesCell WallCandida albicansElectrophoresis Gel Two-DimensionalCandida albicansGel electrophoresisMolecular massBiofilmGeneral Medicinebiology.organism_classificationMolecular biologyExtracellular Matrix030104 developmental biologyBiofilmsProteomeGene DeletionFEMS yeast research
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Identification of control targets in Boolean molecular network models via computational algebra

2015

Motivation: Many problems in biomedicine and other areas of the life sciences can be characterized as control problems, with the goal of finding strategies to change a disease or otherwise undesirable state of a biological system into another, more desirable, state through an intervention, such as a drug or other therapeutic treatment. The identification of such strategies is typically based on a mathematical model of the process to be altered through targeted control inputs. This paper focuses on processes at the molecular level that determine the state of an individual cell, involving signaling or gene regulation. The mathematical model type considered is that of Boolean networks. The pot…

0301 basic medicineTheoretical computer scienceComputer scienceProcess (engineering)Molecular Networks (q-bio.MN)Systems biologySystem of polynomial equationsENCODEBoolean networksSet (abstract data type)03 medical and health sciences0302 clinical medicineStructural BiologyModelling and SimulationQuantitative Biology - Molecular NetworksMolecular BiologyEdge deletionsApplied MathematicsComputer Science ApplicationsNetwork controlIdentification (information)030104 developmental biologyBoolean networkBlocking transitionsFOS: Biological sciencesModeling and SimulationAlgebraic controlState (computer science)030217 neurology & neurosurgeryResearch ArticleBMC Systems Biology
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