Search results for "Gene Deletion"

showing 10 items of 159 documents

Non-pheochromocytoma (PCC)/paraganglioma (PGL) tumors in patients with succinate dehydrogenase-related PCC-PGL syndromes: a clinicopathological and m…

2014

ObjectiveAlthough the succinate dehydrogenase (SDH)-related tumor spectrum has been recently expanded, there are only rare reports of non-pheochromocytoma/paraganglioma tumors in SDHx-mutated patients. Therefore, questions still remain unresolved concerning the aforementioned tumors with regard to their pathogenesis, clinicopathological phenotype, and even causal relatedness to SDHx mutations. Absence of SDHB expression in tumors derived from tissues susceptible to SDH deficiency is not fully elucidated.Design and methodsThree unrelated SDHD patients, two with pituitary adenoma (PA) and one with papillary thyroid carcinoma (PTC), and three SDHB patients affected by renal cell carcinomas (RC…

AdenomaAdultMalemedicine.medical_specialtyPathologySDHBEndocrinology Diabetes and MetabolismSDHALoss of HeterozygosityBiologyPheochromocytomaLoss of heterozygosityEndocrinologyParagangliomaInternal medicinemedicineHumansPituitary NeoplasmsThyroid NeoplasmsCarcinoma Renal CellGerm-Line MutationCarcinomaGeneral MedicineExonsMiddle Agedmedicine.diseaseNeuroblastic TumorCarcinoma Papillary3. Good healthNeoplasm ProteinsSuccinate DehydrogenaseEndocrinologyThyroid Cancer PapillaryMutationFemaleSDHDClear cellGene DeletionEuropean Journal of Endocrinology
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Congenital primary hypothyroidism with subsequent adenomatous goiter in a Turkish patient caused by a homozygous 10-bp deletion in the thyroid peroxi…

2006

Summary Objective  Congenital primary hypothyroidism occurs in 1 of 4000 births. Whereas the majority of the cases are due to developmental defects of the thyroid gland, 20% carry a defect in thyroid hormonogenesis. We report a Turkish boy who had goitrous hypothyroidism due to a mutation in the thyroid peroxidase (TPO) gene. Design  The TPO gene was sequenced directly from genomic DNA and cDNA which was transcribed from three RNA samples harvested from different parts of the patient's excised thyroid gland. Patient  The boy was thyroidectomized because of continuing growth of his thyroid gland and development of multiple nodes suspected of malignancy by ultrasound examination. Histopatholo…

AdenomaMaleThyroid Hormonesendocrine systemmedicine.medical_specialtyPathologyGoiterAdolescentTurkeyendocrine system diseasesEndocrinology Diabetes and Metabolismmedicine.medical_treatmentThyroid Function TestsBiologyIodide PeroxidaseThyroid function testsFrameshift mutationConsanguinityEndocrinologyThyroid peroxidaseInternal medicineCongenital HypothyroidismmedicineHumansIntracellular partmedicine.diagnostic_testHomozygoteThyroidThyroidectomyPrimary hypothyroidismmedicine.diseasePedigreeThyroxinemedicine.anatomical_structureEndocrinologyThyroidectomybiology.proteinGene DeletionGoiter NodularClinical Endocrinology
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Molecular analysis of the 9p21 locus and p53 genes in Ewing family tumors.

2001

The EWS-ETS rearrangements, and their respective fusion gene products, are specifically associated with histopathologically Ewing family tumors (EFT). These translocations are implicated in generating malignant transformation of EFT, but the presence of additional genetic alterations must be considered in the pathogenesis of such tumors. We analyzed 26 samples (biopsies and/or nude mice xenotransplants) collected from 19 patients with an EFT to determine whether molecular and cytogenetic alterations of the G(1)/S checkpoint genes are implicated in the pathogenesis of EFT. We found inactivating p53 mutations in three (16%) cases, which correlated with a loss of p21(WAF1/Cip1) expression and …

AdultCyclin-Dependent Kinase Inhibitor p21MaleMonosomyTumor suppressor geneAdolescentTransplantation HeterologousGene ExpressionChromosome 9Locus (genetics)Sarcoma EwingBiologymedicine.disease_causePathology and Forensic MedicineFusion geneMiceCyclinsProto-Oncogene ProteinsmedicineAnimalsHumansPoint MutationCyclin D1ChildMolecular BiologyGeneGene AmplificationChromosome MappingCyclin-Dependent Kinase 4Nuclear ProteinsProto-Oncogene Proteins c-mdm2Cell BiologyDNA Methylationmedicine.diseaseGenes p53Survival AnalysisCyclin-Dependent KinasesChromosome 17 (human)Child PreschoolCancer researchFemaleCarcinogenesisChromosomes Human Pair 9Gene DeletionNeoplasm TransplantationLaboratory investigation; a journal of technical methods and pathology
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Does angiotensin-converting enzyme gene polymorphism affect blood pressure? Findings after 6 years of follow-up in healthy subjects.

2003

Background: There has been an increase in research into the association between angiotensin-converting enzyme (ACE) gene deletion polymorphism and cardiovascular disease, with conflicting results. The present prospective long-term study was conducted to evaluate whether the DD genotype could also be associated with a higher prevalence of hypertension in healthy subjects, over 6 years of follow-up. Methods: Population: 684 healthy volunteers (aged, 25–55 years): normotensive and free of cardiovascular diseases, with acceptable echocardiographic window. All subjects had to have a normal electrocardiogram (ECG) and echocardiogram (ECHO) at entry. Study protocol: All subjects underwent a comple…

AdultMaleACE-I/D gene polymorphismmedicine.medical_specialtyTime FactorsGenotypePopulationBlood PressurePeptidyl-Dipeptidase AReference ValuesInternal medicineMedicineHumansProspective StudiesFamily historyeducationeducation.field_of_studyPolymorphism Geneticbiologybusiness.industryIncidence (epidemiology)IncidenceAngiotensin-converting enzymeVenous bloodMiddle Agedmedicine.diseaseMutagenesis InsertionalEndocrinologyBlood pressureHeart failureHypertensionbiology.proteinFemaleGene polymorphismCardiology and Cardiovascular MedicinebusinessHealthy subjectGene DeletionFollow-Up StudiesEuropean journal of heart failure
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Molecular analysis of Gaucher disease: distribution of eight mutations and the complete gene deletion in 27 patients from Germany

1997

Gaucher disease is the most common lysosomal storage disease with a high prevalence in the Ashkenazi Jewish population but it is also present in other populations. The presence of eight mutations (1226G, 1448C, IVS2+1. 84GG, 1504T, 1604T, 1342C and 1297T) and the complete deletion of the beta-glucocerebrosidase gene was investigated in 25 unrelated non-Jewish patients with Gaucher's disease in Germany. In the Jewish population, three of these mutations account for more than 90% of all mutated alleles. In addition, relatives of two patients were included in our study. Restriction fragment length polymorphism analysis and sequencing of PCR products obtained from DNA of peripheral blood leukoc…

AdultMaleAdolescentGenotypePopulationBiologymedicine.disease_causeCompound heterozygosityFrameshift mutationGermanyGenotypeGeneticsmedicineHumansAlleleChildeducationGeneAllelesGenetics (clinical)GeneticsMutationeducation.field_of_studyGaucher DiseaseMiddle AgedPhenotypeChild PreschoolMutationFemaleRestriction fragment length polymorphismGene DeletionPolymorphism Restriction Fragment LengthHuman Genetics
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C4, BF, C3 Allele Distribution and Complement Activity in Healthy Aged People and Centenarians

1999

The aim of this study was to examine the complement system and the distribution of some human leukocyte antigen (HLA) class III alleles (C4, BF) in healthy aged people (77 centenarians and 89 elderly subjects). We have also studied the alleles of C3, a complement component genetically unrelated to HLA, the immunochemical levels of C4 and C3 and serum functional hemolytic activity for classical (CH50) and alternative (AP50) complement pathway. The levels of C3 and C4 and the CH50 and AP50 were found to be within the normal range. The frequencies of C3, BF, and C4A alleles were similar in the cohorts that have been studied. For C4B null allele (C4BQ0) a trend toward an increase in the older c…

AdultMaleAgingComplement Pathway AlternativeHuman leukocyte antigenBiologyComplement Hemolytic Activity AssayHemolysisComplement factor BCohort StudiesHLA AntigensHumansComplement Pathway ClassicalAlleleComplement ActivationAllelesAgedAged 80 and overPolymorphism GeneticC4AComplement C4Complement C3DNAMiddle AgedNull alleleComplement systemImmunologyCohortFemaleGeriatrics and GerontologyGene DeletionComplement Factor BThe Journals of Gerontology Series A: Biological Sciences and Medical Sciences
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PAI-1 plasma levels in a general population without clinical evidence of atherosclerosis: relation to environmental and genetic determinants.

1998

Abstract —Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion ( I )/deletion ( D ) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels we…

AdultMaleAgingmedicine.medical_specialtyAlcohol DrinkingGenotypePopulationPeptidyl-Dipeptidase ABody Mass Indexchemistry.chemical_compoundInsulin resistanceGene FrequencyInternal medicinePlasminogen Activator Inhibitor 1Blood plasmaGenotypemedicineHumanseducationAllele frequencyTriglyceridesAgedSex Characteristicseducation.field_of_studyPolymorphism GeneticbiologySmokingAngiotensin-converting enzymeMiddle Agedmedicine.diseaseCholesterolEndocrinologychemistryPlasminogen activator inhibitor-1Hypertensionbiology.proteinFemaleCardiology and Cardiovascular MedicineBody mass indexGene Deletion
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C4A deficiency and nonresponse to hepatitis B vaccination

2002

Hepatitis B vaccination failure has been linked to the presence of certain human leukocyte antigen class II alleles. However, the functional background of these associations has remained unclear. Complement component C 4 is encoded within the major histocompatibility complex and is essential for classical pathway activation.Healthy individuals (n=4269) were vaccinated in a prospective trial with Engerix B. Nonresponse was classified as anti-HBs10 U/l after the last vaccination. Seventy-three nonresponders (NR) (1.7%) were identified. For comparison 53 responders (R) (anti-HBs10 IU/l) were drawn randomly from the same cohort. C4 allotyping was carried out by high-voltage agarose gel electrop…

AdultMaleBiologyMajor histocompatibility complexClassical complement pathwaySeroepidemiologic StudiesHumansHepatitis B VaccinesProspective StudiesTreatment FailureHepatitis B AntibodiesSouthern blotGel electrophoresisB-LymphocytesHepatologyHaplotypeComplement C4aHLA-DR AntigensMiddle AgedHepatitis BVirologyComplement systemLogistic ModelsHaplotypesAgarose gel electrophoresisImmunologybiology.proteinFemaleVaccine failureGene DeletionHLA-DRB1 ChainsJournal of Hepatology
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Oligophrenin 1 mutations frequently cause X-linked mental retardation with cerebellar hypoplasia

2005

Background: Mutations of oligophrenin 1, one of the first genes identified in nonspecific X-linked mental retardation (MRX), have been described in patients with moderate to severe cognitive impairment and predominant cerebellar hypoplasia, in the vermis. Objective: To further delineate the phenotypic and mutational spectrum of the syndrome, by screening oligophrenin 1 in two cohorts of male patients with mental retardation (MR) with or without known posterior fossa anomalies. Methods: Clinical examination, cognitive testing, MRI studies, and mutational analysis (denaturing gradient gel electrophoresis and direct sequencing) on blood lymphocytes were performed in 213 unrelated affected indi…

AdultMaleCerebellumAdolescentGenotypeDNA Mutational AnalysisNonsense mutationNervous System Malformationsmedicine.disease_causeCohort StudiesExonCerebellar DiseasesCerebellummedicineHumansGenetic TestingChildCerebellar hypoplasiaGeneticsMutationSplice site mutationGTPase-Activating ProteinsNuclear Proteinsmedicine.diseaseMagnetic Resonance ImagingHypoplasiaPedigreeDevelopmental disorderAlternative SplicingCytoskeletal ProteinsPhenotypemedicine.anatomical_structureFacial AsymmetryCodon NonsenseChild PreschoolMutationMental Retardation X-LinkedRNA Splice SitesNeurology (clinical)PsychologyGene DeletionNeurology
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Clinical and molecular genetic spectrum of autosomal dominant Emery-Dreifuss muscular dystrophy due to mutations of the lamin A/C gene.

2000

Emery-Dreifuss muscular dystrophy (EDMD) is characterized by early contractures of the elbows and Achilles tendons, slowly progressive muscle wasting and weakness, and life-threatening cardiomyopathy with conduction blocks. We recently identified LMNA encoding two nuclear envelope proteins, lamins A and C, to be implicated in the autosomal dominant form of EDMD. Here, we report on the variability of the phenotype and spectrum of LMNA mutations in 53 autosomal dominant EDMD patients (36 members of 6 families and 17 sporadic cases). Twelve of the 53 patients showed cardiac involvement exclusively, although the remaining 41 all showed muscle weakness and contractures. We were able to identify …

AdultMaleContractureAdolescentGenotypeBiopsyNonsense mutationDNA Mutational AnalysisEmerinMutation MissenseLaminopathyBiologyLMNACardiovascular Physiological PhenomenamedicineMissense mutationHumansEmery–Dreifuss muscular dystrophyMuscular dystrophyAge of OnsetChildCreatine KinasePhysical ExaminationMuscle contractureAgedGenes DominantGeneticsMuscle WeaknessMyocardiumNuclear ProteinsHeartMiddle Agedmedicine.diseaseLamin Type ALaminsMuscular Dystrophy Emery-DreifussPedigreeMuscular AtrophyPhenotypeNeurologyDisease ProgressionFemaleNeurology (clinical)Gene DeletionAnnals of neurology
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