Search results for "Proband"

showing 10 items of 99 documents

Whole-exome sequencing and targeted gene sequencing provide insights into the role ofPALB2as a male breast cancer susceptibility gene

2016

BACKGROUND Male breast cancer (MBC) is a rare disease whose etiology appears to be largely associated with genetic factors. BRCA1 and BRCA2 mutations account for about 10% of all MBC cases. Thus, a fraction of MBC cases are expected to be due to genetic factors not yet identified. To further explain the genetic susceptibility for MBC, whole-exome sequencing (WES) and targeted gene sequencing were applied to high-risk, BRCA1/2 mutation–negative MBC cases. METHODS Germ-line DNA of 1 male and 2 female BRCA1/2 mutation–negative breast cancer (BC) cases from a pedigree showing a first-degree family history of MBC was analyzed with WES. Targeted gene sequencing for the validation of WES results w…

0301 basic medicineCancer genome sequencingProbandGeneticsCancer ResearchPALB2Nonsense mutationCancerBiologymedicine.disease03 medical and health sciences030104 developmental biology0302 clinical medicineBreast cancerOncology030220 oncology & carcinogenesisMale breast cancermedicineskin and connective tissue diseasesExome sequencingCancer
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Further delineation of the female phenotype with KDM5C disease causing variants: 19 new individuals and review of the literature.

2020

X-linked intellectual disability (XLID) is a genetically heterogeneous condition involving more than 100 genes. To date, 35 pathogenic variants have been reported in the lysine specific demethylase 5C (KDM5C) gene. KDM5C variants are one of the major causes of moderate to severe XLID. Affected males present with short stature, distinctive facial features, behavioral disorders, epilepsy, and spasticity. For most of these variants, related female carriers have been reported, but phenotypic descriptions were poor. Here, we present clinical and molecular features of 19 females carrying 10 novel heterozygous variants affecting KDM5C function, including five probands with de novo variants. Four h…

0301 basic medicineProbandAdultMaleHeterozygoteX-linked intellectual disabilityGenetic counselingDisease030105 genetics & heredityBiologyShort stature03 medical and health sciencesYoung AdultGenes X-LinkedIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumans10. No inequalityExomeGenetics (clinical)GeneticsHistone DemethylasesEpilepsyGenetic heterogeneityGenetic Variationmedicine.disease3. Good health030104 developmental biologyPhenotypeChild PreschoolMental Retardation X-LinkedFemalemedicine.symptomClinical geneticsREFERENCES
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Diagnostic Targeted Resequencing in 349 Patients with Drug-Resistant Pediatric Epilepsies Identifies Causative Mutations in 30 Different Genes

2017

Targeted resequencing gene panels are used in the diagnostic setting to identify gene defects in epilepsy. We performed targeted resequencing using a 30-genes panel and a 95-genes panel in 349 patients with drug-resistant epilepsies beginning in the first years of life. We identified 71 pathogenic variants, 42 of which novel, in 30 genes, corresponding to 20.3% of the probands. In 66% of mutation positive patients seizures onset occurred before age 6 months. The 95-genes panel allowed a genetic diagnosis in 22 (6.3%) patients that would have otherwise been missed using the 30-gene panel. About 50% of mutations were identified in genes coding for sodium and potassium channel components. SCN2…

0301 basic medicineProbandMaleCDKL5Drug Resistancemedicine.disease_causeBioinformaticsEpilepsyAnticonvulsantSTXBP1Age of OnsetChildGenetics (clinical)AlleleMutationepilepsy; next-generation sequencing; gene panel; mutationPhenotypeMagnetic Resonance ImagingSettore MED/39 - Neuropsichiatria Infantile3. Good healthPhenotypeChild PreschoolAnticonvulsantsFemaleSequence AnalysisHumanAdolescentGenotypeGenetic Association StudieBiologyMECP203 medical and health sciencesGeneticgene panelGeneticsmedicineHumansGenetic Predisposition to DiseasePreschoolGeneAllelesGenetic Association StudiesGene Expression ProfilingInfant NewbornComputational BiologyInfantMolecular Sequence AnnotationDNASequence Analysis DNANewbornmedicine.disease030104 developmental biologyepilepsynext-generation sequencingmutation
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A systematic variant screening in familial cases of congenital heart defects demonstrates the usefulness of molecular genetics in this field

2016

International audience; The etiology of congenital heart defect (CHD) combines environmental and genetic factors. So far, there were studies reporting on the screening of a single gene on unselected CHD or on familial cases selected for specific CHD types. Our goal was to systematically screen a proband of familial cases of CHD on a set of genetic tests to evaluate the prevalence of disease-causing variant identification. A systematic screening of GATA4, NKX2-5, ZIC3 and Multiplex ligation-dependent probe amplification (MLPA) P311 Kit was setup on the proband of 154 families with at least two cases of non-syndromic CHD. Additionally, ELN screening was performed on families with supravalvula…

0301 basic medicineProbandMaleCardiomyopathy22q11.2Disease030204 cardiovascular system & hematologyBioinformatics0302 clinical medicinede-novoEpidemiology3 large registriesGenetics (clinical)zic3 mutationsGeneticsHigh-Throughput Nucleotide Sequencing3. Good healthPedigreeHomeobox Protein Nkx-2.5malformationsFemaleepidemiologyHeart Defects Congenitalmedicine.medical_specialtyGenetic counselingArticle03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationGenetic TestingHomeodomain Proteinsdiseasebusiness.industryvariabilityGenetic Variationmedicine.diseaseGATA4 Transcription Factor030104 developmental biologyMutationEtiologycardiovascular defectsbusinessMultiplex Polymerase Chain Reactioncardiomyopathy[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyTranscription Factors
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Mutations in the GLA Gene and LysoGb3: Is It Really Anderson-Fabry Disease?

2018

Anderson-Fabry disease (FD) is a rare, progressive, multisystem storage disorder caused by the partial or total deficit of the lysosomal enzyme &alpha

0301 basic medicineProbandMaleDiseasemedicine.disease_causeSphingolipidCatalysilcsh:Chemistry0302 clinical medicineGla geneFabry disease; GLA gene; LysoGb3MedicineChildlcsh:QH301-705.5Spectroscopychemistry.chemical_classificationGeneticsAlleleAged 80 and overMutationComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineMiddle AgedPhenotype3. Good healthComputer Science ApplicationsPhenotypeChild PreschoolFemaleHumanAdultAdolescentGenotypeGlycolipidCatalysisArticleInorganic Chemistry03 medical and health sciencesYoung Adultotorhinolaryngologic diseasesHumansPhysical and Theoretical ChemistryMolecular BiologyGeneGLA geneAllelesAgedFabry diseaseSphingolipidsbusiness.industryOrganic ChemistryInfant NewbornLysoGb3InfantBiomarkerFabry disease; gla gene; lysogb3; adolescent; adult; aged; aged 80 and over; alleles; amino acid substitution; biomarkers; child; child preschool; fabry disease; female; genotype; glycolipids; humans; infant; infant newborn; male; middle aged; phenotype; sphingolipids; young adult; alpha-galactosidase; mutationmedicine.diseaseFabry disease030104 developmental biologyEnzymechemistrylcsh:Biology (General)lcsh:QD1-999Amino Acid Substitutionalpha-GalactosidaseMutationGlycolipidsbusiness030217 neurology & neurosurgeryBiomarkersInternational Journal of Molecular Sciences
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Analysis of Plasminogen Genetic Variants in Multiple Sclerosis Patients.

2016

Multiple sclerosis (MS) is a prevalent neurological disease of complex etiology. Here, we describe the characterization of a multi-incident MS family that nominated a rare missense variant (p.G420D) in plasminogen (PLG) as a putative genetic risk factor for MS. Genotyping of PLG p.G420D (rs139071351) in 2160 MS patients, and 886 controls from Canada, identified 10 additional probands, two sporadic patients and one control with the variant. Segregation in families harboring the rs139071351 variant, identified p.G420D in 26 out of 30 family members diagnosed with MS, 14 unaffected parents, and 12 out of 30 family members not diagnosed with disease. Despite considerably reduced penetrance, lin…

0301 basic medicineProbandMaleGene ExpressionQH426-470multiple sclerosis0302 clinical medicineRisk FactorsGenotypeMissense mutationExomegeneticsguidelinesGenetics (clinical)degradationriskGeneticsLinkagedeficiencyMiddle AgedPenetrance3. Good healthPedigreeplasminogenChromosomes Human Pair 6FemalelinkageAdultGenotype610 Medicine & healthInvestigationsBiologysystemPolymorphism Single Nucleotideblood-brain-barrieractivatorMultiple sclerosisAssociation03 medical and health scienceslamininGenetic linkagemedicineGeneticsHumansAmino Acid Sequenceddc:610Molecular BiologyGenotypingAgeddiseaseSequence Homology Amino AcidMultiple sclerosisCase-control studyassociationPlasminogenmedicine.diseasediagnostic-criteria030104 developmental biologyCase-Control StudiesImmunologySequence Alignment030217 neurology & neurosurgery
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HCN1 mutation spectrum: from neonatal epileptic encephalopathy to benign generalized epilepsy and beyond

2018

International audience; Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels control neuronal excitability and their dysfunction has been linked to epileptogenesis but few individuals with neurological disorders related to variants altering HCN channels have been reported so far. In 2014, we described five individuals with epileptic encephalopathy due to de novo HCN1 variants. To delineate HCN1-related disorders and investigate genotype-phenotype correlations further, we assembled a cohort of 33 unpublished patients with novel pathogenic or likely pathogenic variants: 19 probands carrying 14 different de novo mutations and four families with dominantly inherited variants segre…

0301 basic medicineProbandMaleModels MolecularPotassium Channels[SDV]Life Sciences [q-bio]Medizinmedicine.disease_causeEpileptogenesisMembrane PotentialsEpilepsy0302 clinical medicineHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsMissense mutationChildGeneticsMutationMiddle AgedPhenotype3. Good healthTransmembrane domainclinical spectrum; epilepsy; HCN1; intellectual disability; ion channelintellectual disabilityChild PreschoolEpilepsy GeneralizedFemaleSpasms InfantileAdultAdolescentCHO CellsBiology03 medical and health sciencesYoung AdultCricetulusHCN1medicineAnimalsHumansGeneralized epilepsyGenetic Association StudiesAgedInfantmedicine.diseaseElectric Stimulationclinical spectrum030104 developmental biologyMutationion channelMutagenesis Site-DirectedepilepsyNeurology (clinical)030217 neurology & neurosurgery
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Familial Central Hypothyroidism Caused by a Novel IGSF1 Gene Mutation.

2016

Congenital hypothyroidism of central origin (CH-C) is a rare disease in which thyroid hormone deficiency is caused by insufficient thyrotropin stimulation of a normal thyroid gland. A recently described syndrome of isolated CH-C and macroorchidism was attributed to loss-of-function mutations of the immunoglobulin superfamily, member 1 gene (IGSF1).CH-C was diagnosed in three siblings. The TRH, TRHR, and TSHB genes were sequenced followed by whole-exome sequencing in the proband. A mutation identified in IGSF1 was analyzed by direct PCR sequencing in family members. The effects of the mutation were assessed by in vitro studies in HEK293 cells.The index case was negative for mutations in TRH,…

0301 basic medicineProbandMaleendocrine systemEndocrinology Diabetes and MetabolismDNA Mutational AnalysisImmunoglobulinsThyrotropin030209 endocrinology & metabolismBiology03 medical and health sciences0302 clinical medicineEndocrinologyHypothyroidismmedicineCentral hypothyroidismCongenital HypothyroidismHumansInsertionThyrotropin-Releasing HormoneGeneticsMacroorchidismReceptors Thyrotropin-Releasing HormoneSiblingsThyroidInfant NewbornInfantMembrane Proteinsmedicine.diseaseMolecular biologyCongenital hypothyroidismIGSF1030104 developmental biologymedicine.anatomical_structureHEK293 CellsChild PreschoolMutation (genetic algorithm)MutationThyroid : official journal of the American Thyroid Association
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Confirmation of PDZD7 as a Nonsyndromic Hearing Loss Gene.

2016

Objective PDZD7 was identified in 2009 in a family with apparent nonsyndromic sensorineural hearing loss. However, subsequent clinical reports have associated PDZD7 with digenic Usher syndrome, the most common cause of deaf-blindness, or as a modifier of retinal disease. No further reports have validated this gene for nonsyndromic hearing loss, intuitively calling correct genotype-phenotype association into question. This report describes a validating second case for biallelic mutations in PDZD7 causing nonsyndromic mild to severe sensorineural hearing loss. It also provides detailed audiometric and ophthalmologic data excluding Usher syndrome in both the present proband (proband 1) and the…

0301 basic medicineProbandMalemedicine.medical_specialtyHeterozygoteAdolescentHearing lossUsher syndromeHearing Loss SensorineuralOtoacoustic Emissions SpontaneousAudiologyCompound heterozygosity03 medical and health sciencesSpeech and Hearing0302 clinical medicineotorhinolaryngologic diseasesmedicineEvoked Potentials Auditory Brain StemHumansGenetic Predisposition to DiseaseChildAllelesmedicine.diagnostic_testbusiness.industryAudiogramSequence Analysis DNAmedicine.diseaseMinor allele frequency030104 developmental biologyOtorhinolaryngologyMutationAudiometry Pure-ToneSensorineural hearing lossFemaleAudiometrymedicine.symptombusinessCarrier Proteins030217 neurology & neurosurgeryEar and hearing
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Association between familial hypobetalipoproteinemia and the risk of diabetes. Is this the other side of the cholesterol-diabetes connection? A syste…

2017

Statin therapy is beneficial in reducing LDL cholesterol (LDL-C) levels and cardiovascular events, but it is associated with the risk of incident diabetes mellitus (DM). Familial hypercholesterolemia (FH) is characterized by genetically determined high levels of plasma LDL-C and a low prevalence of DM. LDL-C levels seem then inversely correlated with prevalence of DM. Familial hypobetalipoproteinemia (FHBL) represents the genetic mirror of FH in terms of LDL-C levels, very low in subjects carrying mutations of APOB, PCSK9 (FHBL1) or ANGPTL3 (FHBL2). This review explores the hypothesis that FHBL might represent also the genetic mirror of FH in terms of prevalence of DM and that it is expecte…

0301 basic medicineProbandMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and MetabolismPopulationPrevalenceFamilial hypercholesterolemia030204 cardiovascular system & hematologyHypobetalipoproteinemias03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyInternal medicineDiabetes mellitusInternal MedicinemedicineDiabetes MellitusPrevalenceHumansFamilial hypobetalipoproteinemiaDiabetes mellitus riskeducationeducation.field_of_studybiologyCholesterolbusiness.industryPCSK9StatinsStatinGeneral MedicineCholesterol LDLFamilial hypobetalipoproteinemia; Cholesterol; Diabetes mellitus risk ;Statinsmedicine.diseaseFamilial hypobetalipoproteinemia-Cholesterol- Diabetes mellitus risk- Statins030104 developmental biologyEndocrinologyCholesterolchemistrybiology.proteinlipids (amino acids peptides and proteins)Femalebusiness
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