Search results for "carrier screening"

showing 8 items of 28 documents

Clinical predictors and algorithm for the genetic diagnosis of pheochromocytoma patients.

2009

Abstract Purpose: Six pheochromocytoma susceptibility genes causing distinct syndromes have been identified; approximately one of three of all pheochromocytoma patients carry a predisposing germline mutation. When four major genes (VHL, RET, SDHB, SDHD) are analyzed in a clinical laboratory, costs are ∼$3,400 per patient. The aim of the study is to systematically obtain a robust algorithm to identify who should be genetically tested, and to determine the order in which genes should be tested. Experimental Design: DNA from 989 apparently nonsyndromic patients were scanned for germline mutations in the genes VHL, RET, SDHB, SDHC, and SDHD. Clinical parameters were analyzed as potential predic…

MaleCancer Researchendocrine system diseasesSDHBGenetic Carrier ScreeningAdrenal Gland NeoplasmsPheochromocytomamedicine.disease_causePheochromocytomaParagangliomaGermline mutationMedicineHumansGenetic Predisposition to DiseaseGenetic TestingGeneFamily HealthMutationbusiness.industryGenetic Carrier ScreeningCancerMiddle Agedmedicine.diseaseOncologyHead and Neck NeoplasmsMutationFemaleSDHDbusinessAlgorithmAlgorithmsClinical cancer research : an official journal of the American Association for Cancer Research
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Preconception genome medicine: current state and future perspectives to improve infertility diagnosis and reproductive and health outcomes based on i…

2021

Abstract BACKGROUND Our genetic code is now readable, writable and hackable. The recent escalation of genome-wide sequencing (GS) applications in population diagnostics will not only enable the assessment of risks of transmitting well-defined monogenic disorders at preconceptional stages (i.e. carrier screening), but also facilitate identification of multifactorial genetic predispositions to sub-lethal pathologies, including those affecting reproductive fitness. Through GS, the acquisition and curation of reproductive-related findings will warrant the expansion of genetic assessment to new areas of genomic prediction of reproductive phenotypes, pharmacogenomics and molecular embryology, fur…

MaleInfertilitymedicine.medical_specialtyPopulationReproductive medicineGenome-wide association studyBioinformaticspolygenic medicinegenetic diagnosis03 medical and health sciences0302 clinical medicinePregnancyreproductive geneticsOutcome Assessment Health CaremedicineGenetic predispositionHumanswhole-exome sequencingProspective StudieseducationIVF/ICSI outcomesExome sequencing030304 developmental biologyReproductive healthGenetic testing0303 health scienceseducation.field_of_study030219 obstetrics & reproductive medicinemedicine.diagnostic_testoocyte and embryo genetic defectsbusiness.industryObstetrics and GynecologyGenomicsmedicine.disease3. Good healthReproductive Medicinewhole-genome sequencingInfertilitygenomic sequencingpreconception carrier screeningFemaleinfertilitybusinessGenome-Wide Association StudyHuman Reproduction Update
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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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Gene diagnosis and carrier detection in Hunter syndrome by the iduronate-2-sulphatase cDNA probe.

1992

Hunter disease (McKusick 309900) is an X-chromosomal mucopolysaccharidosis due to deficiency of the lysosomal enzyme iduronate-2-sulphatase (IDS; EC 3.1.6.13). Diagnosis is based on both the typical clinical features of patients and the lack/reduction of IDS activity. Female carriers show no symptoms of the disease. In the past, several different assays were elaborated for measuring enzyme activity in carriers but none of them proved to be suitable for detecting heterozygotes reliably (Zlotogora and Bach 1984)

MaleX ChromosomeMucopolysaccharidosisIduronate SulfataseBiologyGene mappingComplementary DNAGenotypeGeneticsmedicineHumansAlleleChildDeoxyribonucleases Type II Site-SpecificGenetics (clinical)Mucopolysaccharidosis IIGeneticsGenetic Carrier ScreeningHunter syndromeHeterozygote advantagemedicine.diseaseMolecular biologyEnzyme assayPedigreeBlotting Southernbiology.proteinDNA ProbesPolymorphism Restriction Fragment LengthJournal of inherited metabolic disease
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Prenatal diagnosis and carrier detection in mucopolysaccharidosis type II by mutation analysis. A 47,XXY male heterozygous for a missense point mutat…

1994

Identification of iduronate-2-sulphatase (IDS) gene mutations in patients with mucopolysaccharidosis type II (MPS II, Hunter syndrome) allows fast and reliable carrier detection and prenatal diagnosis. We describe here three cases of prenatal diagnosis by direct detection of the gene mutation. In addition to two affected male fetuses from two different families, a 47,XXY fetus carrying both the normal and the mutant allele was diagnosed in a third family. The latter pregnancy was carried to term and the child is obviously not affected by MPS II.

Malemedicine.medical_specialtyHeterozygoteX ChromosomeMucopolysaccharidosisDNA Mutational AnalysisPrenatal diagnosisIduronate SulfataseGene mutationBiologyPregnancyInternal medicinePrenatal DiagnosismedicineMissense mutationHumansPoint MutationMucopolysaccharidosis type IIGenetics (clinical)AllelesSex Chromosome AberrationsMucopolysaccharidosis IIGeneticsPoint mutationGenetic Carrier ScreeningObstetrics and GynecologyHunter syndromeDNAmedicine.diseaseFetal DiseasesEndocrinologyKaryotypingFemaleKlinefelter syndromePrenatal diagnosis
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Duchenne muscular dystrophy and idiopathic hyperCKemia segregating in a family

1995

A 7-month-old boy with gross motor delay and failure to thrive presented with rhabdomyolysis following an acute asthmatic episode. During hospitalization an electrocardiographic conversion to a Wolff-Parkinson-White type 1 (WPW) pattern took place. Duchenne muscular dystrophy (DMD) was suspected based on elevated creatine kinase (CK) serum levels, muscle biopsy, and family history. The diagnosis was confirmed by molecular analysis, which documented a deletion corresponding to cDNA probe 1-2a in the dystrophin gene, in the propositus and in an affected male cousin of his mother. "Idiopathic" hyperCKemia was found in the propositus, his father, and 5 of his relatives. We suggest that the unus…

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesPediatricsmedicine.medical_specialtyDuchenne muscular dystrophyMolecular Sequence DataGene mutationPolymerase Chain ReactionMuscular DystrophiesGenomic ImprintingPrenatal DiagnosisInternal medicinemedicineHumansFamily historyCreatine KinaseGenetics (clinical)X-linked recessive inheritanceDNA PrimersGenes DominantMuscle biopsyBase Sequencebiologymedicine.diagnostic_testGenetic Carrier ScreeningInfantExonsmedicine.diseasePedigreeEndocrinologyMutationFailure to thrivebiology.proteinFemaleCreatine kinasemedicine.symptomDystrophinMetabolism Inborn ErrorsAmerican Journal of Medical Genetics
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Oligosaccharide and Ganglioside Neuraminidase Activities of Mucolipidosis I (Sialidosis) and Mucolipidosis II (I-Cell Disease) Fibroblasts

1979

Fibroblasts cultured from the skin of patients with the genetic diseases mucolipidosis I and mucolipidosis II were found deficient in a neuraminidase specific for both an α23 and and α2 6 type of neuraminosyl linkage of sialyl oligosaccharides. Obligate heterozygotes (parents) showed an intermediate activity in mucolipidosis I, but a normal one in mucolipidosis II. The neuraminidase activity of mucolipidosis I fibroblasts towards gangliosides, measured at pH 4.5 in the presence of Triton X-100, was within the range of normal controls with gangliosides Gm3 and GD3, but somewhat diminished with a bovine brain ganglioside preparation. In mucolipidosis II, neuraminidase activity was markedly de…

NeuraminidaseOligosaccharidesBiochemistryCell LinePolyethylene GlycolsSubstrate SpecificityMucolipidosesGangliosidesmedicineHumansGanglioside GD3SialidosisCells CulturedSkinchemistry.chemical_classificationGangliosidebiologyMucolipidosisGenetic Carrier ScreeningHeterozygote advantageFibroblastsOligosaccharidemedicine.diseaseKineticschemistryBiochemistrybiology.proteinlipids (amino acids peptides and proteins)I-cell diseaseNeuraminidaseEuropean Journal of Biochemistry
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Intron variants of the p53 gene are associated with increased risk for ovarian cancer but not in carriers of BRCA1 or BRCA2 germline mutations

1999

Two biallelic polymorphisms in introns 3 and 6 of the p53 gene were analysed for a possible risk-modifying effect for ovarian cancer. Germline DNA was genotyped from 310 German Caucasian ovarian cancer patients and 364 healthy controls. We also typed 124 affected and 276 unaffected female carriers with known deleterious BRCA1 or BRCA2 germline mutation from high-risk breast-ovarian cancer families. Genotyping was based on PCR and high-resolution gel electrophoresis. German ovarian cancer patients who carried the rare allele of the MspI restriction fragment length polymorphism (RELP) in intron 6 were found to have an overall 1.93-fold increased risk (95% confidence internal (CI) 1.27–2.91) w…

p53AdultCancer Researchendocrine system diseasesAdolescentGenotypeGenes BRCA1BiologypolymorphismGermline mutationRisk FactorsGenotypemedicineTumor Cells CulturedHumansAlleleAllele frequencyGerm-Line MutationAgedGeneticsAged 80 and overBRCA2 ProteinOvarian NeoplasmsGenetic Carrier ScreeningCancerGenetic VariationRegular ArticleMiddle Agedmedicine.diseaseBRCA2 ProteinBRCA1Genes p53BRCA2IntronsNeoplasm Proteinsovarian cancerOncologyCase-Control StudiesCancer researchFemaleRestriction fragment length polymorphismOvarian cancergenetic susceptibilityTranscription FactorsBritish Journal of Cancer
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