Search results for "Mutational analysis"

showing 10 items of 245 documents

Absence of mutation at the GAP-related domain of the neurofibromatosis type 1 gene in sporadic neurofibrosarcomas and other bone and soft tissue sarc…

1995

The NF1 gene encodes neurofibromin, a GTPase-activating protein containing a GAP-related domain (NF1-GRD) that is capable of downregulating ras by stimulating ras intrinsic GTPase activity. We tested 44 sarcomas, nine of which corresponded to sporadic neurofibrosarcomas, for mutations at the NF1-GRD by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) technique, finding no mutation in every sample tested. We suggest that inactivation of the NF1-GRD by gene mutation seems not to be an important event in the tumorigenesis of sarcomas.

congenital hereditary and neonatal diseases and abnormalitiesCancer ResearchNeurofibromatosis 1DNA Mutational AnalysisBone NeoplasmsSoft Tissue NeoplasmsGTPaseBiologyGene mutationmedicine.disease_causePolymerase Chain ReactionGeneticsmedicineHumansneoplasmsMolecular BiologyGenePolymorphism Single-Stranded ConformationalGeneticsMutationNeurofibromin 1ProteinsSarcomaSingle-strand conformation polymorphismmedicine.diseaseNeurofibromin 1eye diseasesnervous system diseasesNeurofibrosarcomaCancer researchbiology.proteinSarcomaCarcinogenesisCancer Genetics and Cytogenetics
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EZH2 mutations are frequent and represent an early event in follicular lymphoma

2013

Gain of function mutations in the H3K27 methyltransferase EZH2 represent a promising therapeutic target in germinal center lymphomas. In this study, we assessed the frequency and distribution of EZH2 mutations in a large cohort of patients with follicular lymphoma (FL) (n = 366) and performed a longitudinal analysis of mutation during the disease progression from FL to transformed FL (tFL) (n = 33). Mutations were detected at 3 recurrent mutation hot spots (Y646, A682, and A692) in 27% of FL cases with variant allele frequencies (VAF) ranging from 2% to 61%. By comparing VAF of EZH2 with other mutation targets (CREBBP, MLL2, TNFRSF14, and MEF2B), we were able to distinguish patients harbori…

endocrine systemTime FactorsMethyltransferasemedicine.medical_treatmentDNA Mutational AnalysisImmunologyFollicular lymphomaKaplan-Meier Estimatemacromolecular substancesBiologymedicine.disease_causeBiochemistryTargeted therapyCohort StudiesGene Frequencyhemic and lymphatic diseasesBiomarkers TumormedicineHumansEnhancer of Zeste Homolog 2 ProteinLymphoma FollicularAllele frequencyMutationLymphoid NeoplasiaMEF2 Transcription FactorsGene Expression ProfilingEZH2Polycomb Repressive Complex 2Germinal centerCell BiologyHematologymedicine.diseaseCREB-Binding ProteinLymphomaMutationDisease ProgressionCancer researchReceptors Tumor Necrosis Factor Member 14Blood
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Mutation Analysis of LMX1B Gene in Nail-Patella Syndrome Patients

1998

SummaryNail-patella syndrome (NPS), a pleiotropic disorder exhibiting autosomal dominant inheritance, has been studied for >100 years. Recent evidence shows that NPS is the result of mutations in the LIM-homeodomain gene LMX1B. To determine whether specific LMX1B mutations are associated with different aspects of the NPS phenotype, we screened a cohort of 41 NPS families for LMX1B mutations. A total of 25 mutations were identified in 37 families. The nature of the mutations supports the hypothesis that NPS is the result of haploinsufficiency for LMX1B. There was no evidence of correlation between aspects of the NPS phenotype and specific mutations.

inorganic chemicalsGenotype-phenotype correlationDNA Mutational AnalysisLIM-Homeodomain ProteinsHomeodomainHaploinsufficiencyHeteroduplex AnalysisBiologymedicine.disease_causeGenetic determinismNail patellaNail-Patella SyndromeGenotypemental disordersmedicineGeneticsAnimalsHumansInsulinGenetics(clinical)Promoter Regions GeneticGeneGenetics (clinical)health care economics and organizationsNail patella syndromeGenes DominantGeneticsFamily HealthHomeodomain ProteinsMutationLMX1B.technology industry and agricultureDNArespiratory systemmedicine.diseasePhenotypeRatsPhenotypeMutationCancer researchMutation testingHaploinsufficiencyResearch ArticleTranscription FactorsThe American Journal of Human Genetics
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A classical phenotype of Anderson-Fabry disease in a female patient with intronic mutations of the GLA gene: a case report

2012

Abstract Background Fabry disease (FD) is a hereditary metabolic disorder caused by the partial or total inactivation of a lysosomal hydrolase, the enzyme α-galactosidase A (GLA). This inactivation is responsible for the storage of undegraded glycosphingolipids in the lysosomes with subsequent cellular and microvascular dysfunction. The incidence of disease is estimated at 1:40,000 in the general population, although neonatal screening initiatives have found an unexpectedly high prevalence of genetic alterations, up to 1:3,100, in newborns in Italy, and have identified a surprisingly high frequency of newborn males with genetic alterations (about 1:1,500) in Taiwan. Case presentation We des…

lcsh:Diseases of the circulatory (Cardiovascular) systemPathologyα-galactosidase AAnderson-Fabry mutationBiopsyDNA Mutational AnalysisCase Reportmedicine.disease_causeGlobotriaosylceramide0302 clinical medicineSettore BIO/13 - Biologia ApplicataPromoter Regions Genetic0303 health sciencesMutationeducation.field_of_studymedicine.diagnostic_testbiologyMetabolic disorderMagnetic Resonance Imaging3. Good healthPhenotypeCardiovascular DiseasesDisease ProgressionFemaleKidney DiseasesRenal biopsyCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtyPopulation03 medical and health sciencesPredictive Value of TestsBiopsymedicineHumansHigh resolution meltingGenetic Predisposition to Diseaseeducation030304 developmental biologyFabry diseaseAlpha-galactosidasebusiness.industrymedicine.diseaseFabry diseaseIntronslcsh:RC666-701alpha-GalactosidaseMutationGLAbiology.proteinbusiness030217 neurology & neurosurgeryKidney disease
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Secondary reduction in calpain 3 expression in patients with limb girdle muscular dystrophy type 2B and Miyoshi myopathy (primary dysferlinopathies).

2000

Made available in DSpace on 2016-10-10T03:52:18Z (GMT). No. of bitstreams: 5 Secondary reduction in calpain 3 expression in patients with limb girdle muscular dystrophy type 2B and Miyoshi myopathy.pdf: 167085 bytes, checksum: b445ec059ea2d0f06bd4fa913354872a (MD5) license_url: 52 bytes, checksum: 2f32edb9c19a57e928372a33fd08dba5 (MD5) license_text: 24259 bytes, checksum: f1f24f769b03eb8f9cd3f53c1090841c (MD5) license_rdf: 24658 bytes, checksum: 9d3847733d3c0b59c7c89a1d40d3d240 (MD5) license.txt: 1887 bytes, checksum: 445d1980f282ec865917de35a4c622f6 (MD5) Previous issue date: 2000 Dysferlin is the protein product of the gene (DYSF) that is defective in patients with limb girdle muscular dy…

medicine.medical_specialtyDysferlinopathyDNA Mutational AnalysisMuscle ProteinsMuscular DystrophiesWestern blottingDysferlinMuscular DiseasesLamininInternal medicinemedicineMissense mutationCalpain 3HumansMuscular dystrophyDysferlinGenetics (clinical)Geneticsbiologybusiness.industryCalpainMembrane ProteinsCalpainmedicine.diseaseMuscular dystrophyLaminin alpha 2EndocrinologyMuscle proteinsNeurologyPediatrics Perinatology and Child Healthbiology.proteinNeurology (clinical)LamininbusinessMerosinLimb-girdle muscular dystrophyNeuromuscular disorders : NMD
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Microarray-based mutation analysis of 183 Spanish families with Usher syndrome.

2010

PURPOSE. The purpose of this study was to test the ability of the genotyping microarray for Usher syndrome (USH) to identify the mutations responsible for the disease in a cohort of 183 patients with USH. METHODS. DNA from 183 patients with Usher syndrome from the Spanish population was analyzed using a genotyping microarray containing 429 previously identified disease-associated variants in eight USH genes. Mutations detected by the array were confirmed by direct sequencing. Haplotype analysis was also performed in families carrying common Spanish mutations. RESULTS. The genotyping microarray identified 43 different variants, divided into 32 disease causative and 11 probably non-pathologic…

medicine.medical_specialtyGenotypeMicroarrayUsher syndromeDNA Mutational AnalysisCadherin Related ProteinsCell Cycle ProteinsNerve Tissue ProteinsMyosinsBiologymedicine.disease_causePolymerase Chain ReactionReceptors G-Protein-CoupledMolecular geneticsGenotypemedicineotorhinolaryngologic diseasesHumansGenotypingAllelesAdaptor Proteins Signal TransducingOligonucleotide Array Sequence AnalysisGeneticsExtracellular Matrix ProteinsMutationGene Expression ProfilingHaplotypeMembrane ProteinsCadherinsmedicine.diseaseGene expression profilingCytoskeletal ProteinsSpainMyosin VIIaMutationUsher Syndromes
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Specific mutations of the RET proto-oncogene are related to disease phenotype in MEN 2A and FMTC.

1994

We have analysed 118 families with inherited medullary thyroid carcinoma (MTC) for mutations of the RET proto-oncogene. These included cases of multiple endocrine neoplasia types 2A (MEN 2A) and 2B (MEN 2B) and familial MTC (FMTC). Mutations at one of 5 cysteines in the extracellular domain were found in 97% of patients with MEN 2A and 86% with FMTC but not in MEN 2B patients or normal controls. 84% of the MEN2A mutations affected codon 634. MEN 2A patients with a Cys634 to Arg substitution had a greater risk of developing parathyroid disease than those with other codon 634 mutations. Our data show a strong correlation between disease phenotype and the nature and position of the RET mutatio…

medicine.medical_specialtyendocrine system diseasesOncogene RETDNA Mutational AnalysisMolecular Sequence DataMultiple endocrine neoplasia type 2RET proto-oncogeneBiologymedicine.disease_causeProto-Oncogene MasInternal medicineProto-Oncogene ProteinsProto-OncogenesGeneticsmedicineDrosophila ProteinsHumansPoint MutationThyroid NeoplasmsMultiple endocrine neoplasiaDNA PrimersMutationBase SequencePoint mutationMultiple Endocrine NeoplasiaProto-Oncogene Proteins c-retReceptor Protein-Tyrosine KinasesExonsmedicine.diseasePhenotypeEndocrinologyPhenotypeProto-Oncogene Proteins c-retCarcinoma MedullaryCancer researchNature genetics
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Amplicon-based high-throughput pooled sequencing identifies mutations in CYP7B1 and SPG7 in sporadic spastic paraplegia patients

2011

Hereditary spastic paraplegia (HSP) is a neurodegenerative disorder defined clinically by progressive lower limb spasticity and weakness. HSP is a genetically highly heterogeneous condition with at least 46 gene loci identified so far, involving X-linked, autosomal recessive (AR) and autosomal dominant inheritance. For correct diagnosis, molecular testing is essential because clinical parameters by themselves are not reliable to differentiate HSP forms. The purpose of this study was to establish amplicon-based high-throughput genotyping for AR-HSP. A sample of 187 index cases with apparently sporadic or recessive spastic paraplegia were analyzed by applying an array-based amplification stra…

methods [High-Throughput Nucleotide Sequencing]GenotypeHereditary spastic paraplegiaDNA Mutational AnalysisMolecular Sequence DataSPG7 protein humanCytochrome P450 Family 7diagnosis [Paraplegia]Biologymedicine.disease_causegenetics [Paraplegia]Cohort Studiesgenetics [Metalloendopeptidases]03 medical and health sciences0302 clinical medicineGenetic variationGenotypeGeneticsmedicineHumansddc:610Genetic TestingGenotypingGenetics (clinical)CYP7B1 protein human030304 developmental biologyGenetic testingParaplegiaGenetics0303 health sciencesMutationBase SequenceParapleginmedicine.diagnostic_testgenetics [Steroid Hydroxylases]Genetic VariationHigh-Throughput Nucleotide SequencingMetalloendopeptidasesmethods [DNA Mutational Analysis]Ampliconmedicine.diseasegenetics [Genetic Variation]3. Good healthMutationSteroid HydroxylasesATPases Associated with Diverse Cellular Activities030217 neurology & neurosurgeryClinical Genetics
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Does δ-sarcoglycan-associated autosomal-dominant cardiomyopathy exist?

2009

In this study we clinically and genetically characterize a consanguineous family with a homozygous novel missense mutation in the delta-sarcoglycan gene and a second delta-sarcoglycan mutation that has previously been reported to cause severe autosomal-dominant dilated cardiomyopathy. We identified a novel missense mutation in exon 6 (p.A131P) of the delta-sarcoglycan gene, which in a homozygous state leads to the clinical picture of a limb girdle muscular dystrophy. In four heterozygous carriers for the mutation, aged 3-64 years, a second sequence variant in exon 6 (p.S151A) of the delta-sarcoglycan gene was detected on the other allele. This second missense change had previously been repo…

musculoskeletal diseasesAdultCardiomyopathy DilatedMalemedicine.medical_specialtyAdolescentBiopsyDNA Mutational AnalysisCardiomyopathyMutation MissenseCompound heterozygosityArticleExonConsanguinityElectrocardiographyYoung AdultInternal medicineSarcoglycansGeneticsMedicineMissense mutationHumansMuscular dystrophyChildGenetics (clinical)Genes DominantGeneticsFamily Healthbusiness.industryMusclesMyocardiumDilated cardiomyopathyMiddle Agedmedicine.diseasePedigreeEndocrinologyEchocardiographyChild PreschoolMutation (genetic algorithm)FemalebusinessLimb-girdle muscular dystrophy
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Abnormalities in alpha-dystroglycan expression in MDC1C and LGMD2I muscular dystrophies

2004

We recently identified mutations in the fukutin related protein (FKRP) gene in patients with congenital muscular dystrophy type 1C (MDC1C) and limb girdle muscular dystrophy type 2I (LGMD2I). The sarcolemma of these patients typically displays an immunocytochemical reduction of alpha-dystroglycan. In this report we extend these observations and report a clear correlation between the residual expression of alpha-dystroglycan and the phenotype. Three broad categories were identified. Patients at the severe end of the clinical spectrum (MDC1C) were compound heterozygote between a null allele and a missense mutation or carried two missense mutations and displayed a profound depletion of alpha-d…

musculoskeletal diseasesAdultPathologymedicine.medical_specialtyNonsense mutationBlotting WesternDNA Mutational AnalysisMedizinCompound heterozygosityPolymerase Chain ReactionMuscular DystrophiesPathology and Forensic MedicineFetusDystroglycanmedicineMissense mutationHumansPentosyltransferasesMuscular dystrophyChildDystroglycansMuscle SkeletalGeneticsFukutin-related proteinMembrane GlycoproteinsbiologyProteinsmedicine.diseasemusculoskeletal systemImmunohistochemistryCytoskeletal ProteinsPhenotypeMutationbiology.proteinCongenital muscular dystrophyLimb-girdle muscular dystrophyRegular Articles
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