Search results for "Pedigree"

showing 10 items of 313 documents

Hereditary common cancers: molecular and clinical genetics.

2001

This review focuses on the functional role and structural features of the genes involved in common hereditary cancers. Most of these tumors are sporadic and the genetic alterations responsible for their genesis take place over several cell generations; nevertheless, 5 to 10% of the human tumors are hereditary, with a rapid development. Cancer susceptibility genes have been classified as "gatekeepers" (e.g. RB1, ki-ras) and "caretakers" (e.g. hMLH1 and hMSH2, BRCA1). The first step in identifying individuals at high risk of developing a specific inherited form of cancer, and who should therefore undergo genetic tests, is the detailed construction of family history (an accurate cancer family …

MaleModels GeneticSettore MED/06 - Oncologia MedicaBRCA geneRisk AssessmentHereditary cancerPedigreeAPC geneNeoplasmsBiomarkers TumorAnimalsHumansFemaleGenes Tumor SuppressorGenetic Predisposition to DiseaseMMR genesAnticancer research
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TBC1D24-TLDc-related epilepsy exercise-induced dystonia: rescue by antioxidants in a disease model

2019

Genetic mutations in TBC1D24 have been associated with multiple phenotypes, with epilepsy being the main clinical manifestation. The TBC1D24 protein consists of the unique association of a Tre2/Bub2/Cdc16 (TBC) domain and a TBC/lysin motif domain/catalytic (TLDc) domain. More than 50 missense and loss-of-function mutations have been described and are spread over the entire protein. Through whole genome/exome sequencing we identified compound heterozygous mutations, R360H and G501R, within the TLDc domain, in an index family with a Rolandic epilepsy exercise-induced dystonia phenotype (http://omim.org/entry/608105). A 20-year long clinical follow-up revealed that epilepsy was self-limited in…

MaleModels Molecular0301 basic medicineProtein ConformationAmino Acid Motifsalpha-TocopherolMutantCrystallography X-RayPHENOTYPECompound heterozygosityAntioxidantsAnimals Genetically ModifiedEpilepsy0302 clinical medicineCatalytic DomainDrosophila ProteinsMissense mutationoxidative stressChildTLDC DOMAINVITAMIN-EExome sequencingSequence DeletionNeuronsDystoniaGeneticsexercise-induced dystoniaTBC1D24GTPase-Activating ProteinsANNOTATIONSEpilepsy RolandicPhenotypeRecombinant ProteinsPedigree3. Good healthRolandic epilepsyDystoniaDrosophila melanogasterChild PreschoolFemaleSettore MED/26 - NeurologiaSynaptic VesiclesDrosophila melanogasterPROTEIN STABILITYLife Sciences & BiomedicineLocomotionAdolescentPhysical ExertionMutation MissenseClinical NeurologyPREDICTIONSBiology03 medical and health sciencesmedicineAnimalsHumansAmino Acid SequenceCOMPARTMENToxidative streScience & TechnologySequence Homology Amino AcidMUTATIONSNeurosciencesInfantBiological TransportDEGRADATIONmedicine.diseasebiology.organism_classificationAcetylcysteineDisease Models AnimalOxidative Stress030104 developmental biologyrab GTP-Binding ProteinsSEIZURESNeurosciences & NeurologyNeurology (clinical)Reactive Oxygen SpeciesSequence Alignment030217 neurology & neurosurgery
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20 ans après: a second mutation in MAOA identified by targeted high-throughput sequencing in a family with altered behavior and cognition

2013

Intellectual disability (ID) is characterized by an extraordinary genetic heterogeneity, with >250 genes that have been implicated in monogenic forms of ID. Because this complexity precluded systematic testing for mutations and because clinical features are often non-specific, for some of these genes only few cases or families have been unambiguously documented. It is the case of the X-linked gene encoding monoamine oxidase A (MAOA), for which only one nonsense mutation has been identified in Brunner syndrome, characterized in a single family by mild non-dysmorphic ID and impulsive, violent and aggressive behaviors. We have performed targeted high-throughput sequencing of 220 genes, includi…

MaleModels MolecularBrunner syndromeNonsense mutationMutation MissenseArticleIntellectual DisabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseAmino Acid SequenceMonoamine OxidaseGenetics (clinical)GeneticsFamily HealthbiologyBase SequenceGenetic heterogeneityPoint mutationHigh-Throughput Nucleotide Sequencingmedicine.diseasePedigreeProtein Structure TertiaryAutism spectrum disorderAttention Deficit and Disruptive Behavior DisordersChild Development Disorders Pervasivebiology.proteinAutismFemaleMonoamine oxidase A
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Haploinsufficiency of the NOTCH1 receptor as a cause of Adams-Oliver syndrome with variable cardiac anomalies

2015

Background— Adams–Oliver syndrome (AOS) is a rare disorder characterized by congenital limb defects and scalp cutis aplasia. In a proportion of cases, notable cardiac involvement is also apparent. Despite recent advances in the understanding of the genetic basis of AOS, for the majority of affected subjects, the underlying molecular defect remains unresolved. This study aimed to identify novel genetic determinants of AOS. Methods and Results— Whole-exome sequencing was performed for 12 probands, each with a clinical diagnosis of AOS. Analyses led to the identification of novel heterozygous truncating NOTCH1 mutations (c.1649dupA and c.6049_6050delTC) in 2 kindreds in which AOS was segregat…

MaleModels MolecularProbandreceptorGene ExpressionHaploinsufficiencyNOTCH1Ectodermal DysplasiaMissense mutationExomeReceptor Notch1ChildExomeGenetics (clinical)GeneticsReverse Transcriptase Polymerase Chain ReactionAutosomal dominant traitMiddle AgedPedigreeembryonic structuresheart defectscardiovascular systemFemaleCardiology and Cardiovascular MedicineHaploinsufficiencySignal TransductionAdultHeart Defects CongenitalAdolescentLimb Deformities CongenitalNotch signaling pathwayBiologyArticleYoung AdultAdams-Oliver syndromeGeneticsmedicineHumansGenetic Predisposition to DiseaseGeneFamily HealthBase SequencecongenitalAdams-Oliver syndrome; genetics; haploinsufficiency; heart defects; congenital; receptor; NOTCH1; Cardiology and Cardiovascular Medicine; Genetics (clinical); GeneticsSequence Analysis DNAmedicine.diseaseProtein Structure TertiaryScalp DermatosesHuman medicineAdams–Oliver syndromeCirculation. Cardiovascular genetics
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Pseudodominant inheritance of goitrous congenital hypothyroidism caused by TPO mutations: molecular and in silico studies.

2007

CONTEXT AND OBJECTIVE: Most cases of goitrous congenital hypothyroidism (CH) from thyroid dyshormonogenesis 1) follow a recessive mode of inheritance and 2) are due to mutations in the thyroid peroxidase gene (TPO). We report the genetic mechanism underlying the apparently dominant inheritance of goitrous CH in a nonconsanguineous family of French Canadian origin. DESIGN, SETTING, AND PARTICIPANTS: Two brothers identified by newborn TSH screening had severe hypothyroidism and a goiter with increased (99m)Tc uptake. The mother was euthyroid, but the father and two paternal uncles had also been diagnosed with goitrous CH. After having excluded PAX8 gene mutations, we hypothesized that the und…

MaleModels Molecularendocrine systemmedicine.medical_specialtySurface PropertiesEndocrinology Diabetes and MetabolismClinical BiochemistryMolecular Sequence DataStatic ElectricityContext (language use)Gene mutationCompound heterozygosityBiochemistryIodide PeroxidasePolymerase Chain ReactionEndocrinologyThyroid dyshormonogenesisInternal medicineCongenital HypothyroidismMedicineMissense mutationHumansEuthyroidAmino Acid SequenceAlleleGeneticsBase Sequencebusiness.industryGoiterBiochemistry (medical)Infant NewbornDNAmedicine.diseaseCongenital hypothyroidismPedigreeEndocrinologyMutationFemalebusinessSequence AlignmentThe Journal of clinical endocrinology and metabolism
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In-Frame Mutations in Exon 1 of SKI Cause Dominant Shprintzen-Goldberg Syndrome

2012

International audience; Shprintzen-Goldberg syndrome (SGS) is characterized by severe marfanoid habitus, intellectual disability, camptodactyly, typical facial dysmorphism, and craniosynostosis. Using family-based exome sequencing, we identified a dominantly inherited heterozygous in-frame deletion in exon 1 of SKI. Direct sequencing of SKI further identified one overlapping heterozygous in-frame deletion and ten heterozygous missense mutations affecting recurrent residues in 18 of the 19 individuals screened for SGS; these individuals included one family affected by somatic mosaicism. All mutations were located in a restricted area of exon 1, within the R-SMAD binding domain of SKI. No mut…

MaleModels Molecularmedicine.disease_cause[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMarfan SyndromeArachnodactylyExon0302 clinical medicineGene OrderMissense mutationGenetics(clinical)Child[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)Exome sequencingGenes DominantGenetics0303 health sciencesMutationShprintzen–Goldberg syndromeExonsPhenotypePedigreeDNA-Binding ProteinsPhenotypeChild PreschoolFemalemedicine.symptomAdultAdolescentMolecular Sequence Data[ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics03 medical and health sciencesCamptodactylyCraniosynostosesYoung Adultstomatognathic systemReportProto-Oncogene ProteinsmedicineGeneticsHumansAmino Acid Sequence030304 developmental biologyFacies[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseMolecular biologyProtein Structure TertiaryArachnodactyly[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationSequence Alignmenthuman activities030217 neurology & neurosurgery
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Rare variants in the genetic background modulate cognitive and developmental phenotypes in individuals carrying disease-associated variants

2019

Purpose: To assess the contribution of rare variants in the genetic background toward variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive variants. Methods: We analyzed quantitative clinical information, exome sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated variants. Results: The number of rare likely deleterious variants in functionally intolerant genes (“other hits”) correlated with expression of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in autism probands carrying gene-disruptive variants (n=184, p=0.03) compared with thei…

MaleParents0301 basic medicineProbandNeuronalGenetic Carrier Screening16p11.2 deletion030105 genetics & heredityCognitionFamily historyNeural Cell Adhesion MoleculesGenetics (clinical)Exome sequencingSequence DeletionGeneticsGenetic Carrier ScreeningPhenotypePenetrancePedigreePhenotypeAutistic Disorder/genetics; Autistic Disorder/physiopathology; Cell Adhesion Molecules Neuronal/genetics; Chromosomes Human Pair 16/genetics; Cognition/physiology; DNA Copy Number Variations/genetics; Female; Gene Expression Regulation/genetics; Genetic Background; Genetic Carrier Screening; Humans; Male; Methyltransferases/genetics; Nerve Tissue Proteins/genetics; Parents; Pedigree; Phenotype; Proteins/genetics; Sequence Deletion/genetics; Siblings; 16p11.2 deletion; CNV; autism; modifier; phenotypic variabilityFemaleGenetic BackgroundHumanDNA Copy Number VariationsCell Adhesion Molecules NeuronalCNVautismNerve Tissue ProteinsBiologyChromosomesArticle03 medical and health sciencesmental disordersmedicineHumansAutistic DisorderBiologyGenemodifierPair 16SiblingsCalcium-Binding ProteinsProteinsMethyltransferasesmedicine.disease16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Genetics (clinical)Cytoskeletal Proteins030104 developmental biologyGene Expression Regulation[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutismphenotypic variabilityHuman medicine16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Autistic Disorder; Cell Adhesion Molecules Neuronal; Chromosomes Human Pair 16; Cognition; DNA Copy Number Variations; Female; Gene Expression Regulation; Genetic Background; Humans; Male; Methyltransferases; Nerve Tissue Proteins; Parents; Pedigree; Phenotype; Proteins; Sequence Deletion; Siblings; Genetic Carrier ScreeningCell Adhesion MoleculesChromosomes Human Pair 16Transcription FactorsGenetics in Medicine
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Clinical characteristics of patients with familial amyotrophic lateral sclerosis carrying the pathogenic GGGGCC hexanucleotide repeat expansion of C9…

2012

A large hexanucleotide (GGGGCC) repeat expansion in the first intron of C9ORF72, a gene located on chromosome 9p21, has been recently reported to be responsible for 40% of familial amyotrophic lateral sclerosis cases of European ancestry. The aim of the current article was to describe the phenotype of amyotrophic lateral sclerosis cases carrying the expansion by providing a detailed clinical description of affected cases from representative multi-generational kindreds, and by analysing the age of onset, gender ratio and survival in a large cohort of patients with familial amyotrophic lateral sclerosis. We collected DNA and analysed phenotype data for 141 index Italian familial amyotrophic l…

MaleParentsPathologyphenotype-genotype correlationCohort Studies0302 clinical medicineC9orf72amyotrophic lateral sclerosigeneticsAmyotrophic lateral sclerosisAge of Onsetamyotrophic lateral sclerosis; familial als; C9Orf72; phenotype-genotype correlation0303 health sciencesSex CharacteristicsDNA Repeat ExpansionAdult Age of Onset Aged Amyotrophic Lateral Sclerosis; genetics/pathology Cohort Studies DNA Repeat Expansion DNA; genetics Female Humans Italy Male Middle Aged Mutation; genetics Parents Pedigree Phenotype Proteins; genetics Sex Characteristics Survival AnalysisMiddle Aged3. Good healthPedigreeSettore MED/26 - NEUROLOGIAPhenotypeItalyC9Orf72Settore MED/26 - NeurologiaFemaleFrontotemporal dementiaAdultmedicine.medical_specialtySOD1BiologyTARDBP03 medical and health sciencesInternal medicinemedicineHumans030304 developmental biologyAgedamyotrophic lateral sclerosis familial ALS C9ORF72 gene phenotype–genotype correlationC9orf72 ProteinAmyotrophic Lateral Sclerosisgenetics/pathologyProteinsOriginal ArticlesDNAmedicine.diseaseSurvival AnalysisC9orf72 ProteinSettore BIO/18 - Geneticaamyotrophic lateral sclerosis; familial ALS C9ORF72 gene; phenotype-genotype correlation;MutationNeurology (clinical)Age of onsetTrinucleotide repeat expansionfamilial al030217 neurology & neurosurgery
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Identification of the novel D297fsX318 PINK1 mutation and phenotype variation in a family with early-onset Parkinson's disease

2008

Herein we first describe a novel homozygous single nucleotide deletion in PINK1 exon 4 (889delG) which results in a loss of kinase domain on the PINK1 protein (D297fsX318). This mutation was identified in two brothers with early-onset Parkinson disease (EOPD) from a Sicilian consanguineous family. Of note, while one of the two patients developed mental deterioration and psychiatric problems, the other showed no cognitive decline. The present study supports the view that PINK1 is a pathogenic gene in some Italian families with EOPD and contributes to define the PINK1-associated phenotype. Herein we first describe a novel homozygous single nucleotide deletion in PINK1 exon 4 (889delG) which r…

MaleParkinson's diseaseGenotypeParkinson's diseaseMolecular Sequence DataPINK1DiseaseBiologyAntiparkinson AgentsLevodopaExonmedicineHumansAmino Acid SequenceAge of OnsetCognitive declineGeneAgedGeneticsGenotype–phenotype correlationPINK1Parkinson DiseaseExonsFamilial formmedicine.diseasePhenotypePedigreeSettore BIO/18 - GeneticaPhenotypeNeurologyMutationMutation (genetic algorithm)Settore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyCognition DisordersProtein KinasesGene DeletionParkinsonism & Related Disorders
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Prenatal diagnosis of infantile neuronal ceroid-lipofuscinosis: a combined electron microscopic and molecular genetic approach.

1995

Based on two unrelated index patients afflicted with INCL, fetal chorion tissues were studied from subsequent pregnancies of the two respective mothers resulting in the prenatal diagnosis of INCL in two of the three pregnancies. Documentation of INCL was based on electron microscopy and DNA studies of the biopsied chorion tissue, later confirmed in the two affected fetuses after termination of their pregnancies by demonstrating INCL-specific lipopigments in post-mortem tissues, in the liver of both aborted fetuses and, additionally, in spleen and skeletal muscle of one of the affected fetuses. The autolysis of the aborted tissues, however, precluded a systematic documentation of all affecte…

MalePathologymedicine.medical_specialtyCell typeBiopsyInfantile neuronal ceroid lipofuscinosisSpleenPrenatal diagnosisBiologyConsanguinityDevelopmental NeuroscienceNeuronal Ceroid-LipofuscinosesPregnancyPrenatal DiagnosisBiopsymedicineHumansreproductive and urinary physiologyFetusmedicine.diagnostic_testAborted FetusSkeletal muscleInfantAbortion InducedGeneral MedicineChorionDNAmedicine.diseasePedigreeMicroscopy Electronmedicine.anatomical_structureLiverembryonic structuresPediatrics Perinatology and Child HealthFemaleNeurology (clinical)Braindevelopment
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