Search results for "gene mutations"

showing 10 items of 10 documents

Identification of a novel mutation of MTP gene in a patient with abetalipoproteinemia.

2011

Abetalipoproteinemia (ABL), or Bassen-Kornzweig syndrome, is a rare autosomal recessive disorder of lipoprotein metabolism, characterized by fat malabsorption, hypocholesterolemia retinitis pigmentosa, progressive neuropathy and acanthocytosis from early infancy. We describe the clinical and molecular characterization of a 6-month-old infant born of consanguineous, apparently healthy parents from Iran. The patient was hospitalized because of failure to thrive, greasy stool and vomiting. The patient's serum lipid profile, the clinical phenotype and the duodenal histology suggested the clinical diagnosis of ABL. The MTP gene analysis by direct sequencing revealed a novel homozygous mutation (…

medicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaDuodenumSpecialties of internal medicineInternal medicineRetinitis pigmentosamedicineHumansgeneticsFamily HealthMTP gene mutations.ABLHepatologymedicine.diagnostic_testApoB-containing lipoproteins.business.industryAbetalipoproteinemiaInfantAbetalipoproteinemia.Heterozygote advantageGeneral Medicinemedicine.diseaseLipidsAbetalipoproteinemiaFat malabsorptionHypocholesterolemiaEndocrinologyPhenotypeRC581-951Failure to thriveFemaleHypocholesterolemia.medicine.symptomLipid profilebusinessCarrier Proteins
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Trouble always comes in threes: three mutations for three auto inflammatory genes in a child and in his father

2014

The coexistence of mutations in more than one gene, linked to Autoinflammatory Diesases, can confuse and make difficult the diagnosis and management of these patients, especially in childhood, when the clinical history is still brief.

Pediatricsmedicine.medical_specialtyauto inflammatory geneBioinformaticsSettore MED/38 - Pediatria Generale E SpecialisticaRheumatologyClinical historyInternal medicinemedicineImmunology and AllergyPediatrics Perinatology and Child HealthGeneInflammatory genesHeterozygous mutationgene mutationsbusiness.industryMultiple sclerosisfood and beveragesmedicine.diseaseRheumatologyPharyngitisCanakinumabPediatrics Perinatology and Child HealthPoster Presentationmedicine.symptombusinessmedicine.drug
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Analysis of thiamine transporter genes in sporadic beriberi

2014

Abstract Objective Thiamine or vitamin B 1 deficiency diminishes thiamine-dependent enzymatic activity, alters mitochondrial function, impairs oxidative metabolism, and causes selective neuronal death. We analyzed for the first time, the role of all known mutations within three specific thiamine carrier genes, SLC19 A2, SLC19 A3 , and SLC25 A19 , in a patient with atrophic beriberi, a multiorgan nutritional disease caused by thiamine deficiency. Methods A 44-year-old male alcoholic patient from Morocco developed massive bilateral leg edema, a subacute sensorimotor neuropathy, and incontinence. Despite normal vitamin B 1 serum levels, his clinical picture was rapidly reverted by high-dose in…

AdultMalemedicine.medical_specialtySLC19 A- SLC25 A19SLC19 AEndocrinology Diabetes and MetabolismGene mutationBeriberimedicine.disease_causeMitochondrial Membrane Transport Proteinslaw.inventionBeriberilawInternal medicineGenotypemedicineThiamine transporterObjective: Thiamine or vitamin B1 deficiency diminishes thiamine-dependent enzymatic activity alters mitochondrial function impairs oxidative metabolism and causes selective neuronal death. We analyzed for the first time the role of all known mutations within three specific thiamine carrier genes SLC19 A2 SLC19 A3 and SLC25 A19 in a patient with atrophic beriberi a multiorgan nutritional disease caused by thiamine deficiency. Methods: A 44-year-old male alcoholic patient from Morocco developed massive bilateral leg edema a subacute sensorimotor neuropathy and incontinence. Despite normal vitamin B1 serum levels his clinical picture was rapidly reverted by high-dose intramuscular thiamine treatment suggesting a possible genetic resistance. We used polymerase chain reaction followed by amplicon sequencing to study all the known thiamine-related gene mutations identified within the Human Gene Mutation Database. Results: Thirty-seven mutations were tested: 29 in SLC19 A2 6 in SLC19 A3 and 2 in SLC25 A19. Mutational analyses showed a wild-type genotype for all sequences investigated. Conclusion: This is the first genetic study in beriberi disease. We did not detect any known mutation in any of the three genes in a sporadic dry beriberi patient. We cannot exclude a role for other known or unknown mutations in the same genes or in other thiamine-associated genes in the occurrence of this nutritional neuropathy.HumansThiamineGenePolymerase chain reactionGeneticsMutationNutrition and DieteticsbiologyMembrane Transport ProteinsThiamine Deficiencymedicine.diseaseAlcoholismEndocrinologyMutationbiology.proteinThiamineMutations
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Autoimmune polyendocrine syndrome type 1: an Italian survey on 158 patients

2021

Abstract Background Autoimmune Polyglandular Syndrome type 1 (APS-1) is a rare recessive inherited disease, caused by AutoImmune Regulator (AIRE) gene mutations and characterized by three major manifestations: chronic mucocutaneous candidiasis (CMC), chronic hypoparathyroidism (CH) and Addison’s disease (AD). Methods Autoimmune conditions and associated autoantibodies (Abs) were analyzed in 158 Italian patients (103 females and 55 males; F/M 1.9/1) at the onset and during a follow-up of 23.7 ± 15.1 years. AIRE mutations were determined. Results The prevalence of APS-1 was 2.6 cases/million (range 0.5–17 in different regions). At the onset 93% of patients presented with one or more component…

MaleTranscription FactorEndocrinology Diabetes and MetabolismAutoimmune hepatitisGene mutationGastroenterologyChronic mucocutaneous candidiasisEndocrinologyAddison DiseaseAutoimmune Polyglandular Syndrome type 1 (APS-1)PrevalenceMedicineChronic mucocutaneous candidiasisPolyendocrinopathies AutoimmuneCandidiasis Chronic MucocutaneouAddison’s disease AIRE gene mutations Autoimmune Polyglandular Syndrome type 1 (APS-1) Autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED) Chronic hypoparathyroidism Chronic mucocutaneous candidiasis Interferon autoantibodiesCandidiasis Chronic MucocutaneousAIRE gene mutations; Addison’s disease; autoimmune polyglandular syndrome type 1 (APS-1); autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED); chronic hypoparathyroidism; chronic mucocutaneous candidiasis; interferon autoantibodiesAutoimmune regulatorAutoantibodieItalyInterferon autoantibodieAddison's diseaseInterferon Type IOriginal ArticleFemaleChronic hypoparathyroidismHumanAdultmedicine.medical_specialtyAutoimmune GastritisHypoparathyroidismAddison’s diseaseAIRE gene mutationsInternal medicineInterferon autoantibodiesHumansMortalityAutoantibodiesAddison’s disease; AIRE gene mutations; Autoimmune Polyglandular Syndrome type 1 (APS-1); Autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED); Chronic hypoparathyroidism; Chronic mucocutaneous candidiasis; Interferon autoantibodiesbusiness.industryChronic mucocutaneous candidiasiAIRE gene mutationAutoantibodymedicine.diseaseAutoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED)Interferon autoantibodies.Autoimmune polyendocrine syndrome type 1MutationbusinessTranscription Factors
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Myelodysplastic syndromes with 20q deletion: incidence, prognostic value and impact on response to azacitidine of ASXL1 chromosomal deletion and gene…

2021

In myelodysplastic syndromes (MDS), the 20q deletion [del(20q)] may cause deletion of the ASXL1 gene. We studied 153 patients with MDS and del(20q) to assess the incidence, prognostic value and impact on response to azacitidine (AZA) of ASXL1 chromosomal alterations and genetic mutations. Additionally, in vitro assay of the response to AZA in HAP1 (HAP1(WT)) and HAP1 ASXL1 knockout (HAP1(KN)) cells was performed. ASXL1 chromosomal alterations were detected in 44 patients (28 center dot 5%): 34 patients (22%) with a gene deletion (ASXL1(DEL)) and 10 patients (6 center dot 5%) with additional gene copies. ASXL1(DEL) was associated with a lower platelet count. The most frequently mutated genes…

MaleOncologyAntimetabolites Antineoplasticazacitidinemedicine.medical_specialtyAzacitidineASXL1Gene mutationInternal medicinemedicineHumansGeneChromosomal DeletionAged20q deletiongene mutationsAged 80 and overbusiness.industryIncidenceMyelodysplastic syndromesIncidence (epidemiology)Hazard ratioHematologyMiddle AgedPrognosismedicine.diseasemyelodysplastic syndromesConfidence intervalRepressor ProteinsMyelodysplastic SyndromesMutationAzacitidineFemaleChromosome Deletionbusinessmedicine.drugBritish Journal of Haematology
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Novel mutations of CETP gene in Italian subjects with hyeralphalipoproteinemia

2009

Abstract Cholesteryl ester transfer protein (CETP) is a plasma glycoprotein that catalyses the transfer of cholesteryl esters from HDL to the other plasma lipoproteins. Genetic deficiency of CETP is one of the known causes of elevation of plasma HDL-C (primary hyperalphalipoproteinemia, HALP). We sequenced CETP gene in a group of 24 Italian subjects with primary HALP (HDL-C>80 mg/dl) suspected to have CETP deficiency. Two unrelated subjects both coming from the same geographical district, were found to be heterozygous for a nucleotide substitution in exon 6 (c.544C>T) and another subject was found to be heterozygous for a C>T transition in exon 9 (c.802C>T). Both mutations introduce a prema…

MaleHyperlipoproteinemiasMessengerDNA Mutational Analysismedicine.disease_causeExonFamilial hyperalphalipoproteinemiaChlorocebus aethiopsCETP activity; CETP gene mutations; Familial hyperalphalipoproteinemia; HDL size; Adolescent; Adult; Aged; Animals; Biomarkers; COS Cells; Cercopithecus aethiops; Cholesterol Ester Transfer Proteins; Cholesterol HDL; DNA Mutational Analysis; European Continental Ancestry Group; Female; Humans; Hyperlipoproteinemias; Italy; Male; Middle Aged; Phenotype; RNA Messenger; Transfection; Up-Regulation; Young Adult; Mutation; Cardiology and Cardiovascular MedicineGeneticsMutationTransition (genetics)biologyCETP activityMiddle AgedUp-RegulationCholesterolPhenotypeItalyCOS CellsRNA splicingFemaleFamilial hyperalphalipoproteinemia; CETP gene mutations; CETP activity; HDL sizelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAdultHDLAdolescentEuropean Continental Ancestry GroupSocio-culturaleHDL sizeTransfectionWhite PeopleCercopithecus aethiopsYoung AdultCETP gene mutationsCholesterylester transfer proteinmedicineAnimalsHumansRNA MessengerGeneAgedCholesterol HDLIntroncetpCholesterol Ester Transfer Proteinscarbohydrates (lipids)biology.proteinRNAmutationBiomarkersMinigene
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Nonsense-mediated decay mechanism is a possible modifying factor of clinical outcome in nonsense cd39 beta thalassemia genotype

2012

Nonsense-mediated mRNA decay (NMD) is a surveillance system to prevent the synthesis of non-functional proteins. In β-thalassemia, NMD may have a role in clinical outcome. An example of premature translation stop codons appearing for the first time is the β-globin cd39 mutation; when homozygous, this results in a severe phenotype. The aim of this study was to determine whether the homozygous nonsense cd39 may have a milder phenotype in comparison with IVS1,nt110/cd39 genotype. Genotypes have been identified from a cohort of 568 patients affected by β-thalassemia. These genotypes were compared with those found in 577 affected fetuses detected among 2292 prenatal diagnoses. The…

Pediatricsmedicine.medical_specialtymedia_common.quotation_subjectNonsense-mediated decayNonsenseBeta thalassemiaBiologynonsense-mediated mRNA decay; beta-thalassemia; clinical outcame; beta-globin gene mutationsmedicine.diseaseGastroenterologynonsense-mediated mRNA decay beta-thalassemia beta-globin gene mutationsnonsense-mediated mRNA decay beta-thalassemia clinical outcame beta-globin gene mutations.Internal medicineGenotypemedicineDiseases of the blood and blood-forming organsRC633-647.5media_commonThalassemia Reports
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Determination of somatic oncogenic mutations linked to target-based therapies using MassARRAY technology

2016

Somatic mutation analysis represents a useful tool in selecting personalized therapy. The aim of our study was to determine the presence of common genetic events affecting actionable oncogenes using a MassARRAY technology in patients with advanced solid tumors who were potential candidates for target-based therapies. The analysis of 238 mutations across 19 oncogenes was performed in 197 formalin-fixed paraffin-embedded samples of different tumors using the OncoCarta Panel v1.0 (Sequenom Hamburg, Germany). Of the 197 specimens, 97 (49.2%) presented at least one mutation. Forty-nine different oncogenic mutations in 16 genes were detected. Mutations in KRAS and PIK3CA were detected in 40/97 (4…

AdultMale0301 basic medicineOncologymedicine.medical_specialtyColorectal cancersomatic oncogene mutationsDNA Mutational Analysismedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationNeoplasmsInternal medicineHumansMedicineoncocartaPrecision MedicineGeneAgedAged 80 and overGeneticsMutationbusiness.industryHigh-Throughput Nucleotide Sequencingpersonalized medicineMiddle AgedPrecision medicinemedicine.diseaseClinical trial030104 developmental biologyOncologySpectrometry Mass Matrix-Assisted Laser Desorption-Ionization030220 oncology & carcinogenesisFemalePersonalized medicineKRASbusinessResearch PaperOncotarget
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Refractory Acne and 21-Hydroxylase Deficiency in a Selected Group of Female Patients.

2009

<i>Background:</i> Excessive androgen production, suspected in women when acne is accompanied by hirsutism and menstrual irregularities, may be due to congenital adrenal hyperplasia. This inherited disorder of cortisol biosynthesis is caused in more than 90–95% of all cases by 21-hydroxylase deficiency (21-OHD). The steroid 21-hydroxylase gene <i>(CYP21)</i> has a high degree of variability. <i>Objective:</i> This study was conducted to evaluate <i>CYP21 </i>gene mutations in a selected group of women with papulopustular and comedonal acne refractory to treatment, irregular menses and hirsutism. <i>Methods:</i> 30 out of 61 women e…

Adultmedicine.medical_specialtyAdolescentDrug ResistancePhysiologyDermatologyAdrenocorticotropic hormoneYoung AdultSettore MED/38 - Pediatria Generale E SpecialisticaPapulopustularInternal medicineAcne VulgarismedicineHumansPoint MutationCongenital adrenal hyperplasiaGenetic TestingRefractory acne Excessive androgen production Non-classical 21-hydroxylase deficiency CYP21 gene mutations.AcnehirsutismAdrenal Hyperplasia Congenitalmedicine.diagnostic_testbiologybusiness.industry17-alpha-HydroxyprogesteroneACTH stimulation test21-Hydroxylasemedicine.diseasePolycystic ovaryEndocrinologybiology.proteinFemaleSteroid 21-HydroxylaseHyperandrogenismbusinessPolycystic Ovary Syndrome
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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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