Search results for "penetrance"

showing 10 items of 73 documents

Risk Profiles and Penetrance Estimations in Multiple Endocrine Neoplasia Type 2A Caused by Germline RET Mutations Located in Exon 10

2010

Multiple endocrine neoplasia type 2 is characterized by germline mutations in RET. For exon 10, comprehensive molecular and corresponding phenotypic data are scarce. The International RET Exon 10 Consortium, comprising 27 centers from 15 countries, analyzed patients with RET exon 10 mutations for clinical-risk profiles. Presentation, age-dependent penetrance, and stage at presentation of medullary thyroid carcinoma (MTC), pheochromocytoma, and hyperparathyroidism were studied. A total of 340 subjects from 103 families, age 4-86, were registered. There were 21 distinct single nucleotide germline mutations located in codons 609 (45 subjects), 611 (50), 618 (94), and 620 (151). MTC was present…

MalePHEOCHROMOCYTOMAendocrine system diseasesMEDULLARY-THYROID CARCINOMAAdrenal Gland NeoplasmsMultiple Endocrine Neoplasia Type 2aPenetrancemedicine.disease_causePHENOTYPEGermlineExon0302 clinical medicinemedullary thyroid carcinomaMEN2BMEN2AChildGenetics (clinical)GeneticsAged 80 and overMutationHyperparathyroidismLife SciencesExonsMiddle AgedCARRIERSPenetranceCANCERPROPHYLACTIC THYROIDECTOMY3. Good healthgenotype-phenotypeFAMILYMEN2030220 oncology & carcinogenesisChild PreschoolFemaleAdultAdolescent030209 endocrinology & metabolismMultiple endocrine neoplasia type 2BiologyPheochromocytoma03 medical and health sciencesYoung AdultGermline mutationGeneticsmedicineHumansThyroid NeoplasmsCodonGerm-Line MutationAgedNeoplasm StagingProto-Oncogene Proteins c-retCancerHIRSCHSPRUNG-DISEASEPROTOONCOGENEmedicine.diseaseGENECarcinoma NeuroendocrineCancer researchRETHuman Mutation
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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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A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants

2012

Abstract: Background Two recent studies identified a mutation (p.Asp620Asn) in the vacuolar protein sorting 35 gene as a cause for an autosomal dominant form of Parkinson disease. Although additional missense variants were described, their pathogenic role yet remains inconclusive. Methods and results We performed the largest multi-center study to ascertain the frequency and pathogenicity of the reported vacuolar protein sorting 35 gene variants in more than 15,000 individuals worldwide. p.Asp620Asn was detected in 5 familial and 2 sporadic PD cases and not in healthy controls, p.Leu774Met in 6 cases and 1 control, p.Gly51Ser in 3 cases and 2 controls. Overall analyses did not reveal any sig…

MaleParkinson's diseasePopulationVesicular Transport ProteinsLocus (genetics)DiseaseBiologyVPS35 protein humanBioinformaticsgenetics [Vesicular Transport Proteins]genetics [Parkinson Disease]Risk Factorsmedicinemetabolism [Vesicular Transport Proteins]GeneticsMissense mutationVPS35 GeneHumansGenetic epidemiologyGenetic Predisposition to Diseaseddc:6101506Genome-wideeducationGenetics (clinical)Genetic Association StudiesGeneticsVacuolar protein sortingeducation.field_of_studyGenotype-Phenotype CorrelationsParkinson DiseaseComplex traitsmedicine.diseasePenetranceddc:MutationFemaleHuman medicineParkinson-s diseaseJournal of Medical Genetics
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Further delineation of eye manifestations in homozygous 15q13.3 microdeletions including TRPM1: a differential diagnosis of ceroid lipofuscinosis.

2014

The 15q13.3 heterozygous microdeletion is a fairly common microdeletion syndrome with marked clinical variability and incomplete penetrance. The average size of the deletion, which comprises six genes including CHRNA7, is 1.5 Mb. CHRNA7 has been identified as the gene responsible for the neurological phenotype in this microdeletion syndrome. Only seven patients with a homozygous microdeletion that includes at least CHRNA7, and is inherited from both parents have been described in the literature. The aim of this study was to further describe the distinctive eye manifestations from the analysis in the three French patients diagnosed with the classical 1.5 Mb homozygous microdeletion. Patients…

MalePathologymedicine.medical_specialtygenetic structuresalpha7 Nicotinic Acetylcholine ReceptorEncephalopathyTRPM Cation ChannelsChromosome DisordersBiologyBlindnessEyePupilNeuronal Ceroid-LipofuscinosesNight BlindnessSeizuresIntellectual DisabilityRetinal DystrophiesGeneticsmedicineElectroretinographyMyopiaHumansEye AbnormalitiesChildGenetics (clinical)TRPM1Genetic Association StudiesCongenital stationary night blindnessGeneticsChromosomes Human Pair 15DystrophyEye Diseases HereditaryGenetic Diseases X-LinkedOptic NerveMicrodeletion syndromemedicine.diseasePenetranceChild PreschoolFemalesense organsDifferential diagnosisChromosome DeletionAmerican journal of medical genetics. Part A
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Multiple sclerosis in twins from continental Italy and Sardinia: a nationwide study.

2005

Knowledge about the balance between heritable and nonheritable risk in multiple sclerosis (MS) is based on twin studies in high-prevalence areas. In a study that avoided ascertainment limitations and directly compared continental Italy (medium-prevalence) and Sardinia (high-prevalence), we ascertained 216 pairs from 34,549 patients. This gives a twinning rate of 0.62% among MS patients, significantly less than that of the general population. In continental Italy, probandwise concordance was 14.5% (95% confidence interval, 5.1-23.8) for monozygotic and 4.0% (95% confidence interval, 0.8-7.1) for dizygotic twins. Results in Sardinia resemble those in northern populations but in limited number…

MaleQuestionnairesMultiple SclerosisConcordancePopulationTwinsDizygotic twinsDisease causeMultiple Sclerosis Epidemiology TwinsCohort StudiesCohort Studies Disease Susceptibility Female Genetic Predisposition to Disease Humans Italy; epidemiology Male Multiple Sclerosis; epidemiology/genetics Questionnaires Regression Analysis TwinsSurveys and QuestionnairesmedicineHumansGenetic Predisposition to Diseaseeducationeducation.field_of_studyepidemiology/geneticsbusiness.industryMultiple sclerosismedicine.diseasePenetranceTwin studyConfidence intervalNeurologyItalyRegression AnalysisSettore MED/26 - NeurologiaFemaleepidemiologyNeurology (clinical)Disease SusceptibilitybusinessDemography
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Hyperekplexia caused by dominant-negative suppression of glyra1 function.

2007

Hyperekplexia (HE; startle disease; OMIM#149400) is a rare inheritable neurologic disorder characterized by an exaggerated response to sudden stimuli, muscular rigidity, and hyperreflexia, leading to chronic injuries due to unprotected falls. All symptoms are present at birth but gradually decline during the first year of life, although an exaggerated startle response remains during adulthood.1 Dysfunctional inhibitory neurotransmission by glycine (Gly) plays a central role in HE pathogenesis. All patients with HE carry mutations in genes encoding either for α1 (GLYRA1) or β (GLYRB) Gly receptor subunits, presynaptic Gly transporters (SLC6A5), or proteins involved in Gly receptor (GLYR) clu…

Malemedicine.medical_specialtySubunitReflex StartleNonsense mutationCompound heterozygosityGeneReceptors GlycineInternal medicinemedicineMissense mutationHumansGlycine ReceptorHyperekplexiaGlycine receptorNervous System DiseaseGeneticsStartle DiseaseNeuroscience (all)GephyrinbiologyInfantPenetrancePedigreeEndocrinologyHyperekplexiaNON PREVISTO DA NORME REDAZIONALI (“NEUROLOGY”)Codon NonsenseMutationbiology.proteinNeurology (clinical)medicine.symptomNervous System DiseasesCollybistinHuman
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Gut Microbiota Analysis in Postoperative Lynch Syndrome Patients

2019

Lynch syndrome (LS) is a dominantly inherited condition with incomplete penetrance, characterized by high predisposition to colorectal cancer (CRC), endometrial and ovarian cancers, as well as to other tumors. LS is associated with constitutive DNA mismatch repair (MMR) gene defects, and carriers of the same pathogenic variants can show great phenotypic heterogeneity in terms of cancer spectrum. In the last years, human gut microbiota got a foothold among risk factors responsible for the onset and evolution of sporadic CRC, but its possible involvement in the modulation of LS patients’ phenotype still needs to be investigated. In this pilot study, we performed 16S rRNA gene sequencing of ba…

Microbiology (medical)medicine.medical_specialtyfecal biomarkersColorectal cancerlcsh:QR1-502Faecalibacterium prausnitziiGut floraMicrobiologyGastroenterologylcsh:Microbiology16S sequencing03 medical and health sciencesInternal medicinemedicineOriginal Research030304 developmental biology0303 health sciencesfecal microbiotabiology030306 microbiologyGenetic heterogeneityfood and beveragesCancermedicine.diseasebiology.organism_classificationPenetrancedigestive system diseasesLynch syndromeLynch syndromeBacteroides fragilishereditary cancer predispositionFrontiers in Microbiology
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Association of low-penetrance alleles with male breast cancer risk and clinicopathological characteristics: results from a multicenter study in Italy

2013

It is well-known that male breast cancer (MBC) susceptibility is mainly due to high-penetrance BRCA1/2 mutations. Here, we investigated whether common low-penetrance breast cancer (BC) susceptibility alleles may influence MBC risk in Italian population and whether variant alleles may be associated with specific clinicopathological features of MBCs. In the frame of the Italian Multicenter Study on MBC, we genotyped 413 MBCs and 745 age-matched male controls at 9 SNPs annotating known BC susceptibility loci. By multivariate logistic regression models, we found a significant increased MBC risk for 3 SNPs, in particular, with codominant models, for rs2046210/ESR1 (OR = 1.71; 95 % CI: 1.43–2.05;…

OncologyAdultMaleCancer Researchmedicine.medical_specialtyMultivariate analysisSettore MED/06 - Oncologia MedicaClinicopathological characteristicBRCA1/2; Clinicopathological characteristics; ER/PR status; Low-penetrance breast cancer alleles; Male breast cancer; SNPsSingle-nucleotide polymorphismPolymorphism Single NucleotideER/PR statuBreast Neoplasms MaleBreast cancerBRCA1/2Internal medicineGenotypemedicineHumansGenetic Predisposition to DiseaseAlleleReceptor Fibroblast Growth Factor Type 2Low-penetrance breast cancer alleleAllelesAgedAged 80 and overbusiness.industryEstrogen Receptor alphaHigh Mobility Group Proteinsclinicopathological characteristicsMiddle Agedmedicine.diseasePenetranceMale breast cancerer/pr statusOncologyTOX3ItalyReceptors EstrogenMale breast cancerCase-Control StudiesMultivariate AnalysisTrans-Activatorslow-penetrance breast cancer allelesbusinessApoptosis Regulatory ProteinsReceptors Progesteroneclinicopathological characteristics; er/pr status; male breast cancer; brca1/2; snps; low-penetrance breast cancer allelesSNPs
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How Much of Familial Breast Cancer Risk is Currently Explained by the Known Genes?

2012

The need to answer the question “how much of the familial risk is currently explained by the known genes?” has increased ,and although BRCA1 and BRCA2 are considered the two major breast cancer (BC) susceptibility genes, they do not justify the entire percentage of all hereditary BC cases. The current consensus is that other BC predisposing genes could explain at least a portion of the remaining non-mutated familial cases, including not only other high- penetrance BC genes, but also moderate and low-penetrance genes. Considering these three different categories of genes, a gap of risk estimation in breast cancer can be observed. Moreover, different researchers tried to give significance to …

OncologyBreast cancer high-penetrance genes low-moderate penetrance genes.medicine.medical_specialtybusiness.industryInternal medicineObstetrics and GynecologyMedicineFamilial breast cancerbusinessGeneCurrent Women's Health Reviews
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Correction:Cancer risks by gene, age, and gender in 6350 carriers of pathogenic mismatch repair variants: findings from the Prospective Lynch Syndrom…

2020

Lynch syndrome (LS) results from pathogenic variants in the mismatch repair (MMR) genes and is the most common hereditary cancer syndrome, affecting an estimated 1 in 300 individuals. Pathogenic variants in each of the MMR genes path_MLH1, path_MSH2, path_MSH6, and path_PMS2 result in different risks for cancers in organs including the colorectum, endometrium, ovaries, stomach, small bowel, bile duct, pancreas, and upper urinary tract. Accurate estimates of these risks are essential for planning appropriate approaches to the prevention or early diagnosis of cancers but the robustness of previous studies has been limited by factors including retrospective design,1,2 lack of validation in ind…

OncologyMaleColorectal cancer*Lynch syndromePenetranceDNA Mismatch Repair0302 clinical medicineDatabases GeneticMalalties hereditàriesProspective StudiesCàncer*PMS2Genetics (clinical)Mismatch Repair Endonuclease PMS2Cancer0303 health sciencesSex CharacteristicsFactors de risc en les malalties1184 Genetics developmental biology physiologyMLH1Middle Aged16. Peace & justiceLynch syndrome3. Good healthDNA-Binding ProteinsMutS Homolog 2 Proteinsyöpägeenit*MSH2030220 oncology & carcinogenesis*MSH6030211 gastroenterology & hepatologyDNA mismatch repairFemalegeneettiset tekijätMutL Protein Homolog 1Genetic diseasesAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesRisk factors in diseasessuolistosyövätMUTATION CARRIERSMLH1Risk AssessmentArticlesukupuoliAge and gender03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLynchin oireyhtymäGene030304 developmental biologyAgedbusiness.industryEndometrial cancerCorrectionnutritional and metabolic diseasesCancer*MLH1MSH6medicine.diseaseColorectal Neoplasms Hereditary NonpolyposisSurvival Analysisdigestive system diseasesMSH2MSH6Lynch syndromePMS2MSH2Mutation3111 BiomedicineikäbusinessOvarian cancer
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