Search results for "abnormalities"

showing 10 items of 638 documents

Molecular Basis of Mismatch Repair Protein Deficiency in Tumors from Lynch Suspected Cases with Negative Germline Test Results

2020

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0301 basic medicineCancer Researchcongenital hereditary and neonatal diseases and abnormalitiesCARCINOMADNA mismatch repair3122 Cancerscolorectal cancersuolistosyövätBiologyGene mutationMLH1DIAGNOSISlcsh:RC254-282Article03 medical and health sciencesdeep sequencing0302 clinical medicineGermline mutationFREQUENT CAUSEMANAGEMENTLynchin oireyhtymäneoplasmspaksusuolisyöpäMUTATIONSPoint mutationMLH1METHYLATIONnutritional and metabolic diseasesNONPOLYPOSIS COLORECTAL-CANCERDEFECTSdiagnostiikkalcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensdigestive system diseases3. Good healthDNA-metylaatioMSH2MSH6030104 developmental biologyLynch syndromeOncologyMSH3syöpägeenitMSH2030220 oncology & carcinogenesisCancer researchDNA mismatch repairsyöpätauditCancers
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SLC20A1 Is Involved in Urinary Tract and Urorectal Development

2020

Previous studies in developing Xenopus and zebrafish reported that the phosphate transporter slc20a1a is expressed in pronephric kidneys. The recent identification of SLC20A1 as a monoallelic candidate gene for cloacal exstrophy further suggests its involvement in the urinary tract and urorectal development. However, little is known of the functional role of SLC20A1 in urinary tract development. Here, we investigated this using morpholino oligonucleotide knockdown of the zebrafish ortholog slc20a1a. This caused kidney cysts and malformations of the cloaca. Moreover, in morphants we demonstrated dysfunctional voiding and hindgut opening defects mimicking imperforate anus in human cloacal exs…

0301 basic medicineCandidate genePathologyMorpholinoPediatricsEmbryonalentwicklungBlasenekstrophieBladder exstrophyZebrabärbling0302 clinical medicinebladder exstrophy-epispadias complex; CAKUT; cloacal malformation; functional genetics; kidney formation; SLC20A1; urinary tract development; zebrafish developmentbladder exstrophy-epispadias complexUrinary tract; Growth and developmentZebrafishlcsh:QH301-705.5ZebrafishNiereOriginal Researchcloacal malformationKidney; EmbryologyPediatrikzebrafish developmentKidney; Growth and developmentReconstructive and regenerative medicine Radboud Institute for Molecular Life Sciences [Radboudumc 10]030220 oncology & carcinogenesisembryonic structuresfunctional geneticsmedicine.symptomSLC20A1medicine.medical_specialtyEpispadiasanimal structuresUrinary systemBiologyKidney cystsCell and Developmental Biology03 medical and health sciencesAll institutes and research themes of the Radboud University Medical Centermedicineddc:610CAKUTNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Cloaca; Abnormalitieskidney formationCell Biologymedicine.diseaseCloacal exstrophybiology.organism_classificationurinary tract developmentReconstructive and regenerative medicine Radboud Institute for Health Sciences [Radboudumc 10]Bladder exstrophy030104 developmental biologyCloaca (embryology)lcsh:Biology (General)Developmental BiologyFrontiers in Cell and Developmental Biology
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Daunorubicin reduces MBNL1 titration by expanded CUG repeat RNA and rescues cardiac dysfunctions in a Drosophila model of myotonic dystrophy

2018

International audience; Myotonic dystrophy (DM) is a dominantly inherited neuromuscular disorder caused by expression of mutant DMPK transcripts containing expanded CUG repeats. Pathogenic RNA sequesters the muscleblind-like (MBNL) proteins, causing alterations of RNA metabolism. Cardiac dysfunction represents the second most common cause of death in DM1 patients. However, the contribution of MBNL titration in DM1 cardiac dysfunction is unclear. We overexpressed Muscleblind (Mbl), Drosophila MBNL orthologue, in cardiomyocytes of DM1 model flies and observed a rescue of heart dysfunctions, which are characteristic of these model flies and resemble cardiac defects observed in patients. We als…

0301 basic medicineCardiac function curvecongenital hereditary and neonatal diseases and abnormalitiesDaunorubicin[SDV]Life Sciences [q-bio]Neuroscience (miscellaneous)Medicine (miscellaneous)BiologyMyotonic dystrophyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmunology and Microbiology (miscellaneous)medicineMBNL1Daunorubicin HydrochlorideRNAmedicine.diseaseTrinucleotide repeat disorder3. Good healthCell biology[SDV] Life Sciences [q-bio]030104 developmental biologychemistryTrinucleotide repeat expansion030217 neurology & neurosurgerymedicine.drug
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A High Throughput Phenotypic Screening reveals compounds that counteract premature osteogenic differentiation of HGPS iPS-derived mesenchymal stem ce…

2016

AbstractHutchinson-Gilford progeria syndrome (HGPS) is a rare fatal genetic disorder that causes systemic accelerated aging in children. Thanks to the pluripotency and self-renewal properties of induced pluripotent stem cells (iPSC), HGPS iPSC-based modeling opens up the possibility of access to different relevant cell types for pharmacological approaches. In this study, 2800 small molecules were explored using high-throughput screening, looking for compounds that could potentially reduce the alkaline phosphatase activity of HGPS mesenchymal stem cells (MSCs) committed into osteogenic differentiation. Results revealed seven compounds that normalized the osteogenic differentiation process an…

0301 basic medicineCell typecongenital hereditary and neonatal diseases and abnormalitiesPhenotypic screeningInduced Pluripotent Stem CellsRetinoic acidTretinoinBiologyArticle03 medical and health scienceschemistry.chemical_compoundProgeriaOsteogenesis[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]medicineHumansInduced pluripotent stem cellChildIsotretinoinGeneticsProgeriaMultidisciplinaryintegumentary systemGuided Tissue RegenerationMesenchymal stem cellnutritional and metabolic diseasesAging PrematureCell DifferentiationMesenchymal Stem Cellsmedicine.diseaseProgerinAlkaline PhosphataseLamin Type A3. Good healthCell biologyHigh-Throughput Screening Assays030104 developmental biologychemistryGene Expression Regulation[ SDV.BBM.GTP ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]Alkaline phosphataseScientific Reports
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The why, the how and the when of PGS 2.0

2016

STUDY QUESTION: We wanted to probe the opinions and current practices on preimplantation genetic screening (PGS), and more specifically on PGS in its newest form: PGS 2.0? STUDY FINDING: Consensus is lacking on which patient groups, if any at all, can benefit from PGS 2.0 and, a fortiori, whether all IVF patients should be offered PGS. WHAT IS KNOWN ALREADY: It is clear from all experts that PGS 2.0 can be defined as biopsy at the blastocyst stage followed by comprehensive chromosome screening and possibly combined with vitrification. Most agree that mosaicism is less of an issue at the blastocyst stage than at the cleavage stage but whether mosaicism is no issue at all at the blastocyst st…

0301 basic medicineEmbryologymedia_common.quotation_subjectFertilityBiology03 medical and health sciences0302 clinical medicinePregnancyGeneticsCleavage stagemedicineHumansGenetic TestingMolecular BiologyPreimplantation Diagnosismedia_commonGenetic testingGeneticsMedical educationblastocyst biopsy030219 obstetrics & reproductive medicinemedicine.diagnostic_testCompeting interestsurogenital systempreimplantation embryoObstetrics and Gynecologymassive parallel sequencingCell BiologyLarge scale dataEmbryo biopsyRedactionAneuploidyNew Research Horizon ReviewReproductive geneticsvitrification030104 developmental biologychromosomal abnormalitiesReproductive Medicinearray comparative genomic hybridizationFemalelipids (amino acids peptides and proteins)Developmental Biologypreimplantation genetic screeningMolecular Human Reproduction
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Rett‐like phenotypes: expanding the genetic heterogeneity to the KCNA2 gene and first familial case of CDKL5 ‐related disease

2016

Several genes have been implicated in Rett syndrome (RTT) in its typical and variant forms. We applied next-generation sequencing (NGS) to evaluate for mutations in known or new candidate genes in patients with variant forms of Rett or Rett-like phenotypes of unknown molecular aetiology. In the first step, we used NGS with a custom panel including MECP2, CDKL5, FOXG1, MEF2C and IQSEC2. In addition to a FOXG1 mutation in a patient with all core features of the congenital variant of RTT, we identified a missense (p.Ser240Thr) in CDKL5 in a patient who appeared to be seizure free. This missense was maternally inherited with opposite allele expression ratios in the proband and her mother. In th…

0301 basic medicineGeneticscongenital hereditary and neonatal diseases and abnormalitiesCandidate geneGenetic heterogeneityCDKL5Rett syndromeBiologymedicine.disease3. Good healthMECP203 medical and health sciences030104 developmental biology0302 clinical medicineGeneticsmedicineMissense mutationExome030217 neurology & neurosurgeryGenetics (clinical)Exome sequencingClinical Genetics
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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Clinical and molecular characterization of 112 single-center patients with Neurofibromatosis type 1.

2018

Abstract Background The aim of this retrospective study was to define clinical and molecular characteristics of a large sample of neurofibromatosis type 1 (NF1) patients, as well as to evaluate mutational spectrum and genotype-phenotype correlation. NF1 is a relatively common neurogenetic disorder (1:2500–1:3000 individuals). It is caused by mutations of the NF1 gene on chromosome 17ql1.2, with autosomal dominant pattern of inheritance and wide phenotypical variability. Café-au-lait spots (CALs), cutaneous and/or subcutaneous neurofibromas (CNFs/SCNFs), skinfold freckling, skeletal abnormalities, Lisch nodules of the iris and increased risk of learning and intellectual disabilities, as well…

0301 basic medicineGenotype-phenotype correlation; New mutation; NF1 gene; NF1 microdeletion syndrome; Adolescent; Adult; Age Factors; Child; Child Preschool; Cohort Studies; DNA Mutational Analysis; Female; Genes Neurofibromatosis 1; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Neurofibromatosis 1; Prevalence; Prognosis; Retrospective Studies; Risk Assessment; Sex Factors; Young Adult; Mutation MissenseMaleGenotype-phenotype correlationDNA Mutational AnalysisDiseaseCohort Studies0302 clinical medicineDNA Mutational AnalysisGenotypePrevalenceMedicineYoung adultChildNew mutationlcsh:RJ1-570Age FactorsMiddle AgedPrognosisItalyNF1 geneChild PreschoolCohortFemaleNF1 microdeletion syndromeCohort studyAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosis 1AdolescentMutation MissenseRisk Assessment03 medical and health sciencesYoung AdultSex FactorsGenes Neurofibromatosis 1HumansGenetic Predisposition to DiseaseNeurofibromatosisPreschoolGenetic Association StudiesRetrospective Studiesbusiness.industryResearchRetrospective cohort studylcsh:Pediatricsmedicine.diseaseDermatology030104 developmental biologyGenesPediatrics Perinatology and Child HealthMutationMissensebusiness030217 neurology & neurosurgeryItalian journal of pediatrics
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Neonatal hyperinsulinemic hypoglycemia: case report of kabuki syndrome due to a novel KMT2D splicing-site mutation

2020

Abstract Background Persistent neonatal hypoglycemia, owing to the possibility of severe neurodevelopmental consequences, is a leading cause of neonatal care admission. Hyperinsulinemic hypoglycemia is often resistant to dextrose infusion and needs rapid diagnosis and treatment. Several congenital conditions, from single gene defects to genetic syndromes should be considered in the diagnostic approach. Kabuki syndrome type 1 (MIM# 147920) and Kabuki syndrome type 2 (MIM# 300867), can be associated with neonatal hyperinsulinemic hypoglycemia. Patient presentation We report a female Italian (Sicilian) child, born preterm at 35 weeks gestation, with persistent hypoglycemia. Peculiar facial dys…

0301 basic medicineHeterozygotePediatricsmedicine.medical_specialtyFacial dysmorphismNeonatal hypotoniaCase ReportHypoglycemiamedicine.disease_causeDiagnosis DifferentialNervous system malformation03 medical and health sciences0302 clinical medicineHyperinsulinismmedicineHumansAbnormalities MultipleHyperinsulinemic hypoglycemiaPathologicalbusiness.industryNeonatal hypoglycemiaInfant Newbornlcsh:RJ1-570lcsh:Pediatricsmedicine.diseaseHematologic DiseasesNeoplasm ProteinsDNA-Binding ProteinsPhenotype030104 developmental biologyNeonatal hypotoniaItalyVestibular DiseasesFaceMutationGestationFemalebusinessHyperinsulinismKabuki syndromeInfant PrematureNeonatal hypoglycemia030217 neurology & neurosurgeryItalian Journal of Pediatrics
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Clinical and hormonal characteristics in heterozygote carriers of congenital adrenal hyperplasia

2020

Abstract Non-classical congenital adrenal hyperplasia (NC-CAH) includes a group of genetic disorders due to a broad class of CYP21A2 variants identifying a disease-causing ‘C’ genotype. The heterozygous carriers of CYP21 mutations are at increased risk of developing clinically evident hyperandrogenism, even though clinical and laboratory characteristics are still underestimated. With the aim of obtaining a more accurate delineation of the phenotype of heterozygous carrier of CAH, we analyzed clinical, biochemical and molecular characteristics in a cohort of Sicilian subjects. Fifty-seven females with biallelic and monoallelic CYP21A2 variants classifying NC-CAH (24) and heterozygous carrier…

0301 basic medicineHirsutismHydrocortisoneendocrine system diseasesEndocrinology Diabetes and MetabolismClinical BiochemistryPhysiologyOverweighturologic and male genital diseasesBiochemistrySettore MED/13 - Endocrinologia0302 clinical medicineEndocrinologySettore BIO/10 - BiochimicaGenotypeMedicineChildhirsutismPolycystic ovaryfemale genital diseases and pregnancy complications030220 oncology & carcinogenesisCohortMolecular MedicineFemalemedicine.symptomAdultHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAdolescentYoung Adult03 medical and health sciencesHumansCongenital adrenal hyperplasiaMolecular BiologyHeterozygous carrierAdrenal Hyperplasia Congenitalbusiness.industryHyperandrogenismCongenital adrenal hyperplasianutritional and metabolic diseasesHeterozygote advantageCell BiologyOverweightmedicine.diseaseOligomenorrhea17OHProgesterone deficiency030104 developmental biologyMutationSteroid 21-HydroxylaseHyperandrogenismbusinessThe Journal of Steroid Biochemistry and Molecular Biology
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