Search results for "norm"

showing 10 items of 4018 documents

Expanding the phenotype of reciprocal 1q21.1 deletions and duplications: a case series

2017

Abstract Background Recurrent reciprocal 1q21.1 deletions and duplications have been associated with variable phenotypes. Phenotypic features described in association with 1q21.1 microdeletions include developmental delay, craniofacial dysmorphism and congenital anomalies. The 1q21.1 reciprocal duplication has been associated with macrocephaly or relative macrocephaly, frontal bossing, hypertelorism, developmental delay, intellectual disability and autism spectrum disorder. Methods Our study describes seven patients, who were referred to us for developmental delay/intellectual disability, dysmorphic features and, in some cases, congenital anomalies, in whom we identified 1q21.1 CNVs by arra…

0301 basic medicineMalePediatricsmedicine.medical_specialtyArray-CGHDevelopmental delayTrigonocephaly03 medical and health sciencesFrontal BossingPregnancyPrenatal DiagnosisGene duplicationIntellectual disabilityMedicineHumansAbnormalities MultipleMegalencephalyHypertelorismChild1q21.1 deletionGeneticsbusiness.industryResearchMacrocephalylcsh:RJ1-570Infantlcsh:Pediatricsmedicine.diseaseMegalencephalyDysmorphism030104 developmental biologyPhenotypeAutism spectrum disorderChromosomes Human Pair 1Female1q21.1 duplicationmedicine.symptomChromosome DeletionbusinessItalian Journal of Pediatrics
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Autosomal recessive variations of TBX6 , from congenital scoliosis to spondylocostal dysostosis

2017

International audience; Proximal 16p11.2 microdeletions are recurrent microdeletions with an overall prevalence of 0.03%. In patients with segmentation defects of the vertebra (SDV), a burden of this microdeletion was observed with TBX6 as a candidate gene for SDV. In a published cohort of patients with congenital scoliosis (CS), TBX6 haploinsufficiency was compound heterozygous with a common haplotype. Besides, a single three-generation family with spondylocostal dysostosis (SCD) was reported with a heterozygous stop-loss of TBX6. These observations questioned both on the inheritance mode and on the variable expressivity associated with TBX6-associated SDV. Based on a national recruitment …

0301 basic medicineMalePediatricsmedicine.medical_specialtyCandidate geneGenotypeScoliosis030105 genetics & heredityCompound heterozygosity03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineInheritance ModeMissense mutationHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildGenetics (clinical)GeneticsHernia Diaphragmaticbusiness.industryHaplotypeInfantmedicine.diseaseSpondylocostal dysostosisSpine3. Good healthPedigree030104 developmental biologyHaplotypesScoliosisChild PreschoolMutationFemalebusinessHaploinsufficiencyT-Box Domain Proteins[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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DNA methylation changes and somatic mutations as tumorigenic events in Lynch syndrome-associated adenomas retaining mismatch repair protein expression

2018

Background: DNA mismatch repair (MMR) defects are a major factor in colorectal tumorigenesis in Lynch syndrome (LS) and 15% of sporadic cases. Some adenomas from carriers of inherited MMR gene mutations have intact MMR protein expression implying other mechanisms accelerating tumorigenesis. We determined roles of DNA methylation changes and somatic mutations in cancer-associated genes as tumorigenic events in LS-associated colorectal adenomas with intact MMR. Methods: We investigated 122 archival colorectal specimens of normal mucosae, adenomas and carcinomas from 57 LS patients. MMR-deficient (MMR-D, n 49) and MMR-proficient (MMR-P, n 18) adenomas were of particular interest and were inter…

0301 basic medicineMaleResearch paperMICROSATELLITE INSTABILITYHYPOMETHYLATIONDNA mismatch repairPHENOTYPEmedicine.disease_causeEpigenesis Genetic0302 clinical medicineCOLORECTAL ADENOMASCDKN2APromoter Regions Geneticcolorectal adenomaDNA methylationLINE-1 methylationTumor suppressorGeneral MedicineMethylationMiddle AgedCANCERTUMORSLynch syndromeDNA-metylaatio3. Good healthDEFICIENCY030220 oncology & carcinogenesisDNA methylationsyöpätauditFemaleColorectal adenomaAdultcongenital hereditary and neonatal diseases and abnormalitiesAdenomatumor suppressorsuolistosyövätColorectal adenomaBiologycomplex mixturesGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesBRAF MUTATIONmedicineHumansLynchin oireyhtymäAgedTumor Suppressor ProteinsMicrosatellite instabilityDNAUNE-1 methylationta3122medicine.diseaseGENEColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasestumorigenesisCOPY NUMBER030104 developmental biologyLynch syndromeLong Interspersed Nucleotide Elements3121 General medicine internal medicine and other clinical medicineMutationTumorigenesisCancer research3111 BiomedicineTumotigenesismutationCarcinogenesisEBioMedicine
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Facial cutaneo-mucosal venous malformations can develop independently of mutation of TEK gene but may be associated with excessive expression of Src…

2017

International audience; We aimed to search for mutations in the germline and somatic DNA of the TEK gene and to analyze the expression level of Src and phospho- Src (p-Src) in tumor and healthy tissues from patients with facial cutaneo-mucosal venous malformations (VMCM). Eligible patients from twelve families and thirty healthy controls were recruited respectively at the Departments of Stomatology and Oral Surgery, and Transfusion Medicine of Tlemcen University Medical Centre. Immunoblot analyses of Src and p-Src were performed after direct DNA sequencing. No somatic or germline mutations were found in all the 23 exons and their 5' and 3' intronic flanking regions, except for one case in w…

0301 basic medicineMaleSomatic cellVascular MalformationsCutaneo-mucosal venous malformationsTyrosine Kinase Tie2Bioinformaticsmedicine.disease_causeGermlineMetastasisp-SrcExonPharmacology Toxicology and Pharmaceutics(all)General Pharmacology Toxicology and PharmaceuticsPhosphorylationCancerMedicine(all)MutationBrief ReportGeneral MedicineReceptor TIE-2[SDV.BDD.MOR] Life Sciences [q-bio]/Development Biology/Morphogenesis3. Good healthsrc-Family Kinases[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]FemaleProto-oncogene tyrosine-protein kinase SrcReceptorSrc[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]AdolescentDirect sequencingContext (language use)BiologyVegfGeneral Biochemistry Genetics and Molecular BiologyPermeability03 medical and health sciencesGermline mutationTEK gene[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN][ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansAmino Acid SequenceGeneMucous MembraneCell-Lines[ SDV ] Life Sciences [q-bio]Base SequenceBiochemistry Genetics and Molecular Biology(all)[SDV.BDD.MOR]Life Sciences [q-bio]/Development Biology/MorphogenesisGermline and somatic DNA030104 developmental biologyFaceMutationCancer researchSkin AbnormalitiesAngiogenesisPathwayJournal of negative results in biomedicine
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9q33.3q34.11 microdeletion: new contiguous gene syndrome encompassing STXBP1, LMX1B and ENG genes assessed using reverse phenotyping

2016

International audience; The increasing use of array-CGH in malformation syndromes with intellectual disability could lead to the description of new contiguous gene syndrome by the analysis of the gene content of the microdeletion and reverse phenotyping. Thanks to a national and international call for collaboration by Achropuce and Decipher, we recruited four patients carrying de novo overlapping deletions of chromosome 9q33.3q34.11, including the STXBP1, the LMX1B and the ENG genes. We restrained the selection to these three genes because the effects of their haploinsufficency are well described in the literature and easily recognizable clinically. All deletions were detected by array-CGH …

0301 basic medicineMale[ SDV.MHEP.PED ] Life Sciences [q-bio]/Human health and pathology/PediatricsHaploinsufficiencycerebral hypomyelinationwest-syndromeBioinformaticsCraniofacial Abnormalities0302 clinical medicineIntellectual disabilitySTXBP1ChildGenetics (clinical)Nail patella syndromeGeneticsEndoglinSyndrome3. Good healthdevelopmental delayPhenotypeintellectual disabilityMedical geneticsFemaleChromosome DeletionHaploinsufficiencyChromosomes Human Pair 9medicine.medical_specialtyAdolescentLIM-Homeodomain ProteinsBiologyContiguous gene syndromeArticle03 medical and health sciencesMunc18 ProteinsGenetic linkageGeneticsmedicineHumansde-novo mutations[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/PediatricsdiseaseEpilepsyinfantile epileptic encephalopathyassociationdeletionsmedicine.diseaseHuman genetics030104 developmental biologynail-patella syndrome030217 neurology & neurosurgeryTranscription Factors
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Total colonic aganglionosis and cleft palate in a newborn with Janus-cysteine 618 mutation of RET proto-oncogene: a case report.

2020

Abstract Background Hirschsprung disease, the most important congenital colonic dysmotility in children results from neural crest migration, differentiation, proliferation, or apoptosis defects where the rearranged during transfection (RET)-Protooncogene pathway has a central role. Although palatal and retinal anomalies in the context of chromosomopathies and some mono−/oligogenic syndromes are reported associated with Hirschsprung disease the role of inactivating RET mutations in these cases is not clarified. Case presentation We report on a dysmorphic newborn with cleft palate and palatal synechia, who showed intestinal obstruction after 24 h of life. Transient ileostomy and surgical biop…

0301 basic medicineMalecongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyCongenital digestive system abnormalitieNeurocristopathyCase ReportContext (language use)RET proto-oncogenemedicine.disease_causeProto-Oncogene MasCongenital digestive system abnormalities03 medical and health sciences0302 clinical medicineGermline mutationCase-reportmedicineCarcinomaHumansCysteineHirschsprung DiseaseTotal colonic aganglionosisLoss functionGerm-Line MutationJanus KinasesNeurocristopathyMutationbusiness.industryProto-Oncogene Proteins c-retlcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseCleft Palate030104 developmental biologyItaly030220 oncology & carcinogenesisREarranged during TransfectionbusinessItalian journal of pediatrics
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Determinants of the Quality of Warfarin Control after Venous Thromboembolism and Validation of the SAMe-TT2-R2 Score: An Analysis of Hokusai-VTE.

2019

Background Time in therapeutic range (TTR) measures the quality of vitamin K antagonist (VKA) anticoagulation. In patients with atrial fibrillation, the dichotomized SAMe-TT2-R2 score (≥2 vs. < 2 points) can predict if adequate TTR is unlikely to be achieved. Aims We validated the SAMe-TT2-R2 score in patients with venous thromboembolism (VTE) randomized to the warfarin arm of the Hokusai-VTE trial. Patients and Methods A total of 3,874 patients were included in the primary analysis (day 31–180 from randomization). The efficacy and safety outcomes were symptomatic recurrent VTE and major or clinically relevant non-major bleeding. Results The rates of recurrent VTE and bleeding events we…

0301 basic medicineMalevitamin K antagonistEXTERNAL VALIDATIONTime FactorsVitamin KWarfarin/therapeutic use030204 cardiovascular system & hematologyTHERAPYSeverity of Illness Indexlaw.inventionchemistry.chemical_compound0302 clinical medicineRandomized controlled trialEdoxabanlawRecurrenceAtrial FibrillationVitamin K/antagonists & inhibitorsStrokeRISKAtrial fibrillationHematologyVenous ThromboembolismVitamin K antagonistMiddle Agedrisk assessment modelTIMEPREDICTSTreatment OutcomeAnticoagulants/therapeutic useResearch DesignANTICOAGULATION CONTROLFemaleLife Sciences & Biomedicinemedicine.drugHemorrhage/drug therapyAdultmedicine.medical_specialtyRandomizationmedicine.drug_classvenous thromboembolismHemorrhageRisk AssessmentSensitivity and SpecificityEDOXABAN03 medical and health sciencesDouble-Blind MethodVITAMIN-K ANTAGONISTSInternal medicinemedicineNONVALVULAR ATRIAL-FIBRILLATIONORAL ANTICOAGULANTHumansInternational Normalized RatioBlood CoagulationScience & Technologybusiness.industryquality of treatmentWarfarinAnticoagulantsmedicine.diseasewarfarinClinical trial030104 developmental biologyPeripheral Vascular DiseasechemistryBlood Coagulation/drug effectsAtrial Fibrillation/bloodCardiovascular System & CardiologyLinear ModelsWarfarinbusinessVenous Thromboembolism/drug therapyThrombosis and haemostasis
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Comprehensive evaluation of coding region point mutations in microsatellite-unstable colorectal cancer

2018

Microsatellite instability (MSI) leads to accumulation of an excessive number of mutations in the genome, mostly small insertions and deletions. MSI colorectal cancers (CRCs), however, also contain more point mutations than microsatellite-stable (MSS) tumors, yet they have not been as comprehensively studied. To identify candidate driver genes affected by point mutations in MSI CRC, we ranked genes based on mutation significance while correcting for replication timing and gene expression utilizing an algorithm, MutSigCV. Somatic point mutation data from the exome kit-targeted area from 24 exome-sequenced sporadic MSI CRCs and respective normals, and 12 whole-genome-sequenced sporadic MSI CR…

0301 basic medicineMedicine (General)Candidate geneclinical evaluationgenetic identificationgenetic analysisQH426-470medicine.disease_causeChromatin Epigenetics Genomics & Functional Genomicswhole exome sequencingddc:590mutator genesingle nucleotide polymorphismddc:576.5Gene Regulatory NetworksExomeExome sequencingCancercancer cellGeneticsMutation1184 Genetics developmental biology physiology3. Good healthgenetic codesyöpägeenitpriority journalMolecular Medicinewild typepoint mutationSystems MedicineColorectal Neoplasmscongenital hereditary and neonatal diseases and abnormalitiesddc:025.063/5703122 Cancerscancer geneticsSingle-nucleotide polymorphismcolorectal cancerBiologygene frequencyta3111mikrosatelliititcolony formationR105W geneArticle03 medical and health sciencesR5-920Gene interactionReportGeneticsmedicineHumanscontrolled studyhumanneoplasmspaksusuolisyöpäPoint mutationgene interactionhuman celltumor-related geneMicrosatellite instabilityMolecular Sequence AnnotationSequence Analysis DNAmedicine.diseaseta3122digestive system diseaseshuman tissueSTK38L gene030104 developmental biologyvalidation processgene expressionSMARCB1 genemicrosatellite instability3111 Biomedicinegene replicationReports
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Apoptotic Activity of MeCP2 Is Enhanced by C-Terminal Truncating Mutations.

2016

Methyl-CpG binding protein 2 (MeCP2) is a widely abundant, multifunctional protein most highly expressed in post-mitotic neurons. Mutations causing Rett syndrome and related neurodevelopmental disorders have been identified along the entire MECP2 locus, but symptoms vary depending on mutation type and location. C-terminal mutations are prevalent, but little is known about the function of the MeCP2 C-terminus. We employ the genetic efficiency of Drosophila to provide evidence that expression of p.Arg294* (more commonly identified as R294X), a human MECP2 E2 mutant allele causing truncation of the C-terminal domains, promotes apoptosis of identified neurons in vivo. We confirm this novel find…

0301 basic medicineMethyl-CpG-Binding Protein 2lcsh:MedicineApoptosisBiochemistryPhosphoserine0302 clinical medicineAnimal CellsDrosophila ProteinsPost-Translational ModificationPhosphorylationlcsh:ScienceNeuronsMotor NeuronsGeneticsMultidisciplinaryCell DeathbiologyDrosophila MelanogasterAnimal ModelsInsectsFOXG1Cell ProcessesCaspasesPhosphorylationDrosophilaBiological CulturesCellular TypesDrosophila melanogasterResearch ArticleGene isoformcongenital hereditary and neonatal diseases and abnormalitiesArthropodaProtein domainMouse ModelsMotor ActivityResearch and Analysis MethodsTransfectionModels BiologicalMECP203 medical and health sciencesModel OrganismsProtein Domainsmental disordersAnimalsHumansMolecular Biology TechniquesImmunohistochemistry TechniquesMolecular BiologyTranscription factorBinding proteinlcsh:ROrganismsBiology and Life SciencesProteinsCell BiologyCell Culturesbiology.organism_classificationInvertebratesHistochemistry and Cytochemistry TechniquesHEK293 Cells030104 developmental biologyCellular NeuroscienceMutationImmunologic TechniquesMutant Proteinslcsh:Q030217 neurology & neurosurgeryNeuroscienceTranscription FactorsPLoS ONE
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Towards development of a statistical framework to evaluate myotonic dystrophy type 1 mRNA biomarkers in the context of a clinical trial

2020

AbstractMyotonic dystrophy type 1 (DM1) is a rare genetic disorder, characterised by muscular dystrophy, myotonia, and other symptoms. DM1 is caused by the expansion of a CTG repeat in the 3’-untranslated region of DMPK. Longer CTG expansions are associated with greater symptom severity and earlier age at onset. The primary mechanism of pathogenesis is thought to be mediated by a gain of function of the CUG-containing RNA, that leads to trans-dysregulation of RNA metabolism of many other genes. Specifically, the alternative splicing (AS) and alternative polyadenylation (APA) of many genes is known to be disrupted. In the context of clinical trials of emerging DM1 treatments, it is important…

0301 basic medicineMicroarrayPhysiologyMicroarraysBioinformaticsBiochemistryMachine Learning0302 clinical medicineMathematical and Statistical TechniquesMedicine and Health SciencesMyotonic DystrophyMuscular dystrophyOligonucleotide Array Sequence AnalysisClinical Trials as TopicMultidisciplinaryMusclesQStatisticsRGenetic disorderMuscle AnalysisBody FluidsNucleic acidsBloodBioassays and Physiological AnalysisTreatment OutcomeGenetic DiseasesPhysical SciencesMedicineRegression AnalysisAnatomyDatabases Nucleic AcidResearch Articlemusculoskeletal diseasesGenetic Markerscongenital hereditary and neonatal diseases and abnormalitiesScienceContext (language use)Linear Regression AnalysisBiostatisticsResearch and Analysis MethodsPolyadenylationMyotonic dystrophyMyotonin-Protein Kinase03 medical and health sciencesmedicineGeneticsHumansRNA MessengerStatistical MethodsLeast-Squares AnalysisGeneClinical GeneticsModels Geneticbusiness.industryAlternative splicingBiology and Life Sciencesmedicine.diseaseMyotoniaAlternative Splicing030104 developmental biologyRNA processingRNAGene expressionbusinessTrinucleotide repeat expansionTrinucleotide Repeat Expansion030217 neurology & neurosurgeryBiomarkersMathematicsForecastingPLoS ONE
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