Search results for " Heterozygosity"

showing 10 items of 141 documents

Mitochondrial and chromosomal DNA alterations in human chromophobe renal cell carcinomas

1992

Renal cell tumours are characterized by the loss of chromosome 3p and trisomy of 5q segments (common, non-papillary renal cell carcinoma), or by trisomy of chromosomes 7 and 17 and loss of the Y chromosome (papillary renal cell carcinoma), or by random karyotype changes and mitochondrial DNA alterations (renal oncocytoma). We have studied by means of RFLP analysis the genomic and mitochondrial DNA in 11 chromophobe renal cell carcinomas, which have a unique morphology among kidney cancers. We found a loss of the constitutional heterozygosity at chromosomal regions 3p, 5q, 17p, and 17q, a combination of allelic losses that has not been found in other types of renal cell tumours. Three of the…

Pathologymedicine.medical_specialtyMitochondrial DNAChromophobe Renal Cell CarcinomaChromophobe cellBiologyurologic and male genital diseasesDNA MitochondrialChromosomesPathology and Forensic MedicineLoss of heterozygosityRenal cell carcinomamedicineHumansRenal oncocytomaCarcinoma Renal CellChromosome AberrationsKidneyStaining and LabelingPapillary renal cell carcinomasDNA Neoplasmmedicine.diseaseKidney NeoplasmsBlotting Southernmedicine.anatomical_structurePolymorphism Restriction Fragment LengthThe Journal of Pathology
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Identification of a Novel BRCA1 Alteration in Recurrent Melanocytoma Resulting in Increased Proliferation

2020

Abstract Primary meningeal melanocytomas are rare tumors of the central nervous system. Although they are considered benign neoplasms, some reports describe recurrent rates up to 45%. Little is known about their genetic and epigenetic landscape because of their infrequency. Even less has been described about markers with prognostic value. Here we describe a patient who developed a primary meningeal melanocytoma, suffered 3 recurrences in a period of 6 years and died of the tumor. The genetic and epigenetic changes explored confirmed GNAQ mutation as an initiating event. We found an epigenetic alteration of GSTP1, a feature that has recently been described in meningiomas, from the beginning …

Pathologymedicine.medical_specialtyMitotic indexProliferation indexDiseasePathology and Forensic MedicineMeningiomaLoss of heterozygosity03 medical and health sciencesCellular and Molecular NeuroscienceFatal Outcome0302 clinical medicineMeningeal NeoplasmsmedicineHumansEpigeneticsMelanomaCell ProliferationBRCA1 Proteinbusiness.industryGeneral MedicineMiddle Agedmedicine.diseaseGlutathione S-Transferase piNeurology030220 oncology & carcinogenesisMutationGTP-Binding Protein alpha Subunits Gq-G11FemaleNeurology (clinical)Neoplasm Recurrence LocalMelanocytomabusiness030217 neurology & neurosurgeryGNAQJournal of Neuropathology & Experimental Neurology
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Exon deletions of the phenylalanine hydroxylase gene in Italian hyperphenylalaninemics

2009

A consistent finding of many studies describing the spectrum of mutant phenylalanine hydroxylase (PAH) alleles underlying hyperphenylalaninemia is the impossibility of achieving a 100% mutation ascertainment rate using conventional gene-scanning methods. These methods include denaturing gradient gel electrophoresis (DGGE), denaturing high performance liquid chromatography (DHPLC), and direct sequencing. In recent years, it has been shown that a significant proportion of undetermined alleles consist of large deletions overlapping one or more exons. These deletions have been difficult to detect in compound heterozygotes using gene-scanning methods due to a masking effect of the non-deleted al…

Phenylalanine hydroxylasePhenylketonuriasDNA Mutational AnalysisClinical Biochemistrygene dosageCompound heterozygosityBiochemistryGene dosageDenaturing high performance liquid chromatographyExonHyperphenylalaninemiaGene FrequencyPhenylketonuriasmedicineHumansMultiplex ligation-dependent probe amplificationMolecular BiologySequence DeletionGeneticsphenylalanine hydroxylase; phenylketonurias; ligase chain reaction; gene deletion; gene dosagebiologygene deletionReverse Transcriptase Polymerase Chain ReactionPhenylalanine HydroxylaseExonsmedicine.diseaseMolecular biologyItalyDisease Progressionbiology.proteinligase chain reactionMolecular MedicineOriginal ArticleExperimental and Molecular Medicine
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Mutations in MTP gene in abeta- and hypobeta-lipoproteinemia.

2005

Abstract Familial hypobetalipoproteinemia (FHBL) and abetalipoproteinemia (ABL) are inherited disorders of apolipoprotein B (apo B)-containing lipoproteins that result from mutations in apo B and microsomal triglyceride transfer protein (MTP) genes, respectively. Here we report three patients with severe deficiency of plasma low-density lipoprotein (LDL) and apo B. Two of them (probands F.A. and P.E.) had clinical and biochemical phenotype consistent with ABL. Proband F.A. was homozygous for a minute deletion/insertion (c.1228delCCCinsT) in exon 9 of MTP gene predicted to cause a truncated MTP protein of 412 amino acids. Proband P. E. was heterozygous for a mutation in intron 9 (IVS9-1G>A),…

ProbandApolipoprotein EAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BGenotypeDNA Mutational AnalysisGene mutationCompound heterozygosityHypobetalipoproteinemiasApo B genemedicineMissense mutationHumansGene mutationApo E genotypeGeneticsbiologyAbetalipoproteinemia; Hypobetalipoproteinemia; MTP gene; Apo B gene; Gene mutations; Apo E genotypeAbetalipoproteinemiamedicine.diseaseAbetalipoproteinemiaPedigreePhenotypeChild Preschoolbiology.proteinlipids (amino acids peptides and proteins)FemaleHypobetalipoproteinemiaMTP geneCardiology and Cardiovascular MedicineCarrier ProteinsHypobetalipoproteinemia
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Additive effect of mutations in LDLR and PCSK9 genes on the phenotype of familial hypercholesterolemia.

2006

Patients homozygous or Compound heterozygous for LDLR mutations or double heterozygous for LDLR and apo B R3500Q mutation have higher LDL-C levels. more extensive xanthomatosis and more severe premature coronary disease (pCAD) than simple heterozygotes for mutations in either these genes or for missense mutations in PCSK9 gene. It is not known whether combined mutations in LDLR and PKCS9 are associated with such a severe phenotype. We sequenced Apo B and PCSK9 genes in two patients with the clinical diagnosis of homozygous FH who were heterozygous for LDLR gene mutations. Proband Z.P. (LDL-C 13.39 mmol/L and pCAD) was heterozygous for an LDLR mutation (p.E228K) inherited from her father (LD…

ProbandLDLR geneAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemia (FH); Autosomal dominant hypercholesterolemia 3 (ADH3); LDLR gene; PCSK9 gene; Premature coronary artery diseasePremature coronary artery diseaseLDLR PCSK9Mutation MissenseFamilial hypercholesterolemiaCompound heterozygositymedicine.disease_causeHyperlipoproteinemia Type IIFamilial hypercholesterolemia (FH) Autosomal dominant hypercholesterolemia 3 (ADH3) LDLR gene PCSK9 gene Premature coronary artery diseaseFamilial hypercholesterolemia (FH)medicineMissense mutationHumansCells CulturedGeneticsMutationbiologybusiness.industrySerine EndopeptidasesHeterozygote advantageMiddle Agedmedicine.diseaseAutosomal dominant hypercholesterolemia 3 (ADH3)PedigreePhenotypeSettore MED/03 - Genetica MedicaAmino Acid SubstitutionReceptors LDLPCSK9 geneLDL receptorbiology.proteinlipids (amino acids peptides and proteins)FemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessAtherosclerosis
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Lack of phenotypic additive effect of familial defective apolipoprotein B3531 in familial hypercholesterolaemia.

2020

Familial defective apolipoprotein (apo) B (FDB) and familial hypercholesterolaemia (FH) are the two common genetic conditions that cause hypercholesterolaemia. R3531C mutation of the APOB gene is a rare cause of FDB. Individuals with both FDB and FH are rare. A 51-year-old man with hypercholesterolaemia (11.4 mmol/L) and his family were studied. Low-density lipoprotein (LDL) receptor (LDLR) and APOB genes were analysed by direct sequencing. LDL of four subjects were studied in a fibroblast LDL receptor-binding displacement assay. We found a mutation of the LDLR gene (p.Y398X) in the proband and in four other family members: the p.R3531C APOB gene mutation was also found in the proband, his …

ProbandMalemedicine.medical_specialtyApolipoprotein B030204 cardiovascular system & hematologyCompound heterozygosityHyperlipoproteinemia Type II03 medical and health scienceschemistry.chemical_compoundFDB35310302 clinical medicineInternal medicineInternal MedicinemedicineHumans030212 general & internal medicineApolipoproteins Bdouble heterozygotebiologybusiness.industryCholesterolLDL receptornutritional and metabolic diseasesHeterozygote advantageMiddle AgedEndocrinologychemistryItalyReceptors LDLLDL receptorMutation (genetic algorithm)Mutationfamilial hypercholesterolaemiabiology.proteinlipids (amino acids peptides and proteins)businessLipoproteinInternal medicine journalReferences
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A genotype-phenotype correlation in Sicilian patients with GJB2 biallelic mutations

2015

The aim of this work was to study the genotype distribution of Sicilian patients with biallelic GJB2 mutations; to correlate genotype classes and/or specific mutations of GJB2 gene (35delG-non-35delG) with audiologic profiles. A total of 10 different mutations and 11 different genotypes were evidenced in 73 SNHL subjects; 35delG (90.36 % of cases) and IVS1+1 (13.69 %) were the most common mutations found in the cohort with a significant difference in the distribution between North and South Sicily. Audiological evaluation revealed a severe (16/73) to profound (47/73) hearing loss (HL) in 86.13 % of cases without significant difference between the degree of HL and the province of origin of t…

ProbandMalemedicine.medical_specialtyGenotypeHearing lossHearing Loss SensorineuralGJB2 mutations Sensorineural hearing loss Genetic hearing loss · Cx26BiologyDeafnessCompound heterozygositymedicine.disease_causeGastroenterologySeverity of Illness IndexConnexinsCorrelationYoung AdultAudiometryInternal medicineGenotypemedicineHumansChildHearing LossSicilyGenetic Association StudiesGeneticsMutationGeneral Medicinemedicine.diseaseSettore MED/32 - AudiologiaConnexin 26Settore MED/31 - OtorinolaringoiatriaOtorhinolaryngologyChild PreschoolCohortMutationSensorineural hearing lossFemalemedicine.symptom
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Alpha1-antitrypsin heterozygosity plays a positive role in attainment of longevity.

2007

Genes involved in cardiovascular diseases (CVD) play an opposite role in human longevity. The alpha1-antitrypsin (AAT) is a serine-protease inhibitor required for the prevention of proteolytic tissue damage, by neutrophil elastase. The role of AAT in CVD has not been definitively assessed and its effect on longevity has not yet fully been studied. To clarify these points, we have studied the distribution of AAT allele variants in 3 cohorts: 127 young patients affected by acute myocardial infarction (AMI), 255 young controls and 143 centenarians from Sicily. The Z allele frequency was most frequent in centenarians (13.3%), intermediate in healthy young controls (3.1%) and less frequent in AM…

SenescenceAdultMalemedicine.medical_specialtyAgingHeterozygotemedia_common.quotation_subjectPopulationLongevityMyocardial InfarctionBiologyGastroenterologyRisk AssessmentLoss of heterozygosityCohort StudiesGene FrequencyRisk FactorsAAT Serine-protease inhibitor AMI Longevity CentenariansInternal medicineGenotypemedicineHumansGenetic Predisposition to Diseasecardiovascular diseasesAlleleRisk factoreducationAllele frequencySicilymedia_commonSettore MED/04 - Patologia GeneraleGeneticsAged 80 and overeducation.field_of_studyLongevityMiddle AgedSettore MED/11 - Malattie Dell'Apparato CardiovascolareLogistic ModelsCase-Control Studiesalpha 1-AntitrypsinFemaleGeriatrics and GerontologyGerontologyBiogerontology
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Prognostic significance of p16INK4a alterations and 9p21 loss of heterozigosity in locally advanced laryngeal squamous cell carcinoma

2002

The p16INK4a gene, localized within chromosome 9p21, has been identified as a cyclin-dependent kinase inhibitor and may negatively regulate the cell cycle acting as a tumor suppressor. Genetic alterations involving the 9p21 region are common in human cancers. A consecutive series of 64 untreated patients (median of follow up 53 months) undergoing surgical resection for locally advanced laryngeal squamous-cell carcinomas (LSCCs) has been studied prospectively. Our purpose was to investigate p16 alterations (9p21 allelic loss, hypermethylation and point mutations) and their possible association with clinico-pathological data and flow cytometric variables (DNA-ploidy and S-phase fraction (SPF)…

Settore MED/06 - Oncologia MedicaPhysiologyClinical BiochemistryLoss of HeterozygosityBiologyBioinformaticsS PhaseLoss of heterozygosityp16INK4aHumansPoint MutationProspective StudiesLaryngeal NeoplasmsGeneProportional Hazards ModelsUnivariate analysisPloidiesBase SequenceProportional hazards modelGenes p16Point mutationSingle-strand conformation polymorphismDNA NeoplasmCell BiologyDNA MethylationCell cyclePrognosisMultivariate AnalysisDNA methylationCarcinoma Squamous CellCancer researchChromosomes Human Pair 9Journal of Cellular Physiology
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Congenital hypothyroidism caused by new mutations in the thyroid oxidase 2 (THOX2) gene

2006

Summary Objective  Congenital primary hypothyroidism (CH) occurs in one of 4000 births and in 20% of the cases CH is due to a defect in thyroid hormonogenesis. Candidate genes were examined to determine the precise aetiology of suspected dyshormonogenesis in CH. Design  The genes that code for thyroid peroxidase (TPO), pendrin (PDS), sodium iodide symporter (NIS) and thyroid oxidase 2 (THOX2) were sequenced directly from genomic DNA. Patients  Two girls found to have CH in the neonatal screening programme and suspected of having thyroid dyshormonogenesis were investigated to identify their molecular defect. Results  Patient A had a novel heterozygous 1 bp insertion in the THOX2 gene (ins602…

Sodium-iodide symportermedicine.medical_specialtybiologyEndocrinology Diabetes and MetabolismThyroidmedicine.diseaseCompound heterozygosityFrameshift mutationCongenital hypothyroidismEndocrinologyEndocrinologyThyroid dyshormonogenesismedicine.anatomical_structureThyroid peroxidaseInternal medicinemedicinebiology.proteinEuthyroidClinical Endocrinology
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