Search results for "muta"

showing 10 items of 6895 documents

Molecular diagnosis of PIK3CA-related overgrowth spectrum (PROS) in 162 patients and recommendations for genetic testing.

2017

Postzygotic activating mutations of PIK3CA cause a wide range of mosaic disorders collectively referred to as PIK3CA-related overgrowth spectrum (PROS). We describe the diagnostic yield and characteristics of PIK3CA sequencing in PROS. We performed ultradeep next-generation sequencing (NGS) of PIK3CA in various tissues from 162 patients referred to our clinical laboratory and assessed diagnostic yield by phenotype and tissue tested. We identified disease-causing mutations in 66.7% (108/162) of patients, with mutant allele levels as low as 1%. The diagnostic rate was higher (74%) in syndromic than in isolated cases (35.5%; P = 9.03 × 10−5). We identified 40 different mutations and found stro…

0301 basic medicineAdultMalePathologymedicine.medical_specialtyAdolescentGenotypeClass I Phosphatidylinositol 3-KinasesPrenatal diagnosisBioinformaticsmedicine.disease_causeDNA sequencing03 medical and health sciencesYoung Adult0302 clinical medicinePrenatal DiagnosisGenotypemedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleChildGenetics (clinical)AllelesGenetic Association StudiesGrowth DisordersGenetic testingMutationmedicine.diagnostic_testbusiness.industryMosaicismInfant NewbornDisease ManagementHigh-Throughput Nucleotide SequencingInfantSequence Analysis DNAPhenotype030104 developmental biologyPhenotypeAmino Acid SubstitutionChild PreschoolMutationAllelic heterogeneityFemalebusiness030217 neurology & neurosurgeryGenetics in medicine : official journal of the American College of Medical Genetics
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The Amount of Melanin Influences p16 Loss in Spitzoid Melanocytic Lesions: Correlation With CDKN2A Status by FISH and MLPA.

2019

AIMS The risk assessment of spitzoid lesions is one of the most difficult challenges in dermatopathology practice. In this regard, the loss of p16 expression and the homozygous deletion of CDKN2A, have been pointed in the literature as reliable indicators of high risk. However, these findings are poorly reproducible, and the molecular bases underlying the loss of p16 expression remain unclear. We aimed to identify the underlying events causing loss of CDKN2A/p16 in spitzoid tumors. MATERIALS AND METHODS We evaluated the immunohistochemical expression of p16, and the presence of CDKN2A genetic alterations detected through fluorescence in situ hybridization (FISH) and multiplex ligation-depen…

0301 basic medicineAdultMalePathologymedicine.medical_specialtyHistologySkin NeoplasmsPathology and Forensic MedicineMelanin03 medical and health sciencesYoung Adult0302 clinical medicineCDKN2ANevus Epithelioid and Spindle CellmedicineBiomarkers TumorNevusHumansMultiplex ligation-dependent probe amplificationneoplasmsMelanomaCyclin-Dependent Kinase Inhibitor p16In Situ Hybridization FluorescenceMelaninsmedicine.diagnostic_testbusiness.industryMelanomamedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticMedical Laboratory Technology030104 developmental biology030220 oncology & carcinogenesisMutationImmunohistochemistryMelanocytesFemaleDermatopathologybusinessMultiplex Polymerase Chain ReactionFluorescence in situ hybridizationApplied immunohistochemistrymolecular morphology : AIMM
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The largest caucasian kindred with dentatorubral-pallidoluysian atrophy: A founder mutation in italy

2019

BACKGROUND: Dentatorubral-pallidoluysian atrophy is a hereditary neurodegenerative disease prevalently reported in Japan but rare in Caucasians. The objective of this study was to reconstruct the pedigree of Italian dentatorubral-pallidoluysian atrophy familial cases describing their clinical features. METHODS: We investigated 6 apparently unrelated dentatorubral-pallidoluysian atrophy families comprising a total of 51 affected individuals: 13 patients were clinically examined, and for 38 patients clinical data were collected from clinical sources. The dentatorubral-pallidoluysian atrophy diagnosis was genetically confirmed in 18 patients. Genealogical data from historical archives were ana…

0301 basic medicineAdultMalePediatricsmedicine.medical_specialtyAdolescentDiseaseNeuropsychological TestsWhite People03 medical and health sciencesEpilepsyYoung Adult0302 clinical medicineAtrophyTrinucleotide Repeatsdentatorubral-pallidoluysian atrophymedicineHumansFamilyATN1 geneChildFounder mutationAgedDentatorubral-pallidoluysian atrophyEpilepsybusiness.industrygenealogical methodMiddle Agedmedicine.diseaseMyoclonic Epilepsies ProgressivePedigree030104 developmental biologyfounder effectNeurologyCerebellar cognitive affective syndromeItalycerebellar cognitive-affective syndromeMutationFemaleNeurology (clinical)business030217 neurology & neurosurgeryFounder effect
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Altered chemotactic response to CXCL12 in patients carrying GATA2 mutations.

2015

Abstract GATA2 deficiency—formerly described as MonoMAC syndrome; dendritic cells, monocytes, B cells, and natural killer cell deficiency; familial myelodysplastic syndrome/acute myeloid leukemia; or Emberger syndrome—encompasses a range of hematologic and nonhematologic anomalies, mainly characterized by monocytopenia, B lymphopenia, natural killer cell cytopenia, neutropenia, immunodeficiency, and a high risk of developing acute myeloid leukemia. Herein, we present 7 patients with GATA2 deficiency recruited into the French Severe Chronic Neutropenia Registry, which enrolls patients with all kinds of congenital neutropenia. We performed extended immunophenotyping of their whole blood lymph…

0301 basic medicineAdultMaleReceptors CXCR4AdolescentLymphocyteT-LymphocytesImmunologyMonocytopeniaBiologyNatural killer cell03 medical and health sciencesYoung AdultImmunophenotypinghemic and lymphatic diseasesmedicineImmunology and AllergyHumansLymphocyte CountCongenital NeutropeniaChildAgedCytopeniaB-LymphocytesGATA2 DeficiencyTraditional medicineChemotaxisCell MembraneMyeloid leukemiaCell Biologymedicine.diseaseCD56 AntigenChemokine CXCL12GATA2 Transcription FactorKiller Cells Natural030104 developmental biologymedicine.anatomical_structureImmunologyMutationFemaleJournal of leukocyte biology
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Systemic redox biomarkers and their relationship to prognostic risk markers in autosomal dominant polycystic kidney disease and IgA nephropathy.

2017

Abstract Background Oxidative stress is evident from an early stage in chronic kidney disease (CKD). Therefore, we investigated redox biomarkers in polycystic kidney disease (ADPKD) and IgA nephropathy (IGAN). Methods This is a case-control study with three groups: ADPKD (n = 54), IGAN (n = 58) and healthy controls (n = 86). The major plasma aminothiols with their redox species were examined: homocysteine (Hcy), cysteinglycine (CG), cysteine (Cys) and glutathione (GSH). The redox ratio was the ratio of reduced free and oxidized aminothiols in plasma. We investigated malonedialdehyde (MDA) and advanced oxidation protein products (AOPP), and ten single nucleotide polymorphisms of antioxidant …

0301 basic medicineAdultMaleRiskmedicine.medical_specialtyHomocysteineClinical Biochemistry030232 urology & nephrologyAutosomal dominant polycystic kidney diseaseurologic and male genital diseasesmedicine.disease_causePolymorphism Single NucleotideNephropathy03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinePolycystic kidney diseaseMedicineHumansHomocysteineGenetic Association StudiesProteinuriabusiness.industrySuperoxide DismutaseGlomerulonephritis IGAGeneral MedicineDipeptidesMiddle Agedmedicine.diseasePolycystic Kidney Autosomal DominantPrognosisOxidative Stress030104 developmental biologyEndocrinologychemistryAdvanced Oxidation Protein ProductsCase-Control StudiesDisease ProgressionFemaleGene polymorphismLipid Peroxidationmedicine.symptombusinessOxidoreductasesOxidation-ReductionOxidative stressBiomarkersKidney diseaseClinical biochemistry
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Sperm DNA fragmentation: An early and reliable marker of air pollution.

2017

Environmental factors could have a key role in the continuous and remarkable decline of sperm quality observed in the last decades. This study compared the seminal parameters and sperm DFI in men living in areas with different levels of air pollution. Results demonstrate that both steel plants workers and patients living in a high polluted area show a mean percentage of sperm DNA fragmentation above 30%, highlighting a clear sperm damage. In this work, two different techniques were used to measure sperm DNA damage in patients’ groups, finding in both cases a high sperm DFI in patients living in polluted areas. We candidate sperm DNA fragmentation as a valuable early marker of the presence…

0301 basic medicineAdultMaleendocrine systemHealth Toxicology and MutagenesisAir pollutionDNA FragmentationBiologymedicine.disease_causeToxicologyAndrology03 medical and health sciences0302 clinical medicineAir PollutionmedicineHumansIn patientSettore BIO/06 - Anatomia Comparata E Citologiareproductive and urinary physiologySperm motilityTUNELPharmacologyAir Pollutants030219 obstetrics & reproductive medicineurogenital systemSperm dnaApoptosiGeneral MedicineEnvironmental exposureEnvironmental ExposureSpermSpermatozoaSCD030104 developmental biologyEnvironmental healthItalySteelSperm MotilityDNA fragmentationParticulate MatterReproductive capacityEnvironmental toxicology and pharmacology
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Treatment for hereditary angioedema with normal C1-INH and specific mutations in the F12 gene (HAE-FXII).

2016

Hereditary angioedema with normal C1 esterase inhibitor and mutations in the F12 gene (HAE-FXII) is associated with skin swellings, abdominal pain attacks, and the risk of asphyxiation due to upper airway obstruction. It occurs nearly exclusively in women. We report our experience treating HAE-FXII with discontinuation of potential trigger factors and drug therapies. The study included 72 patients with HAE-FXII. Potential triggers included estrogen-containing oral contraceptives (eOC), hormonal replacement therapy, or angiotensin-converting enzyme inhibitors. Drug treatment comprised plasma-derived C1 inhibitor (pdC1-INH) for acute swelling attacks and progestins, tranexamic acid, and danaz…

0301 basic medicineAdultMalemedicine.medical_specialtyExacerbationAdolescentImmunologyAngiotensin-Converting Enzyme InhibitorsGastroenterologyChemopreventionC1-inhibitorHereditary Angioedema Type III03 medical and health sciencesYoung Adult0302 clinical medicineRisk FactorsInternal medicinemedicineImmunology and AllergyHumansHereditary Angioedema Type IIIChildAgedDanazolbiologybusiness.industryEstrogensMiddle Agedmedicine.diseaseSurgeryDiscontinuation030104 developmental biologyTreatment Outcome030228 respiratory systemQuinaprilHereditary angioedemaFactor XIIMutationbiology.proteinDisease ProgressionFemalebusinessComplement C1 Inhibitor ProteinTranexamic acidBiomarkersmedicine.drugAllergy
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Impact of somatic mutations in myelodysplastic patients with isolated partial or total loss of chromosome 7

2020

Monosomy 7 [-7] and/or partial loss of chromosome 7 [del(7q)] are associated with poor and intermediate prognosis, respectively, in myelodysplastic syndromes (MDS), but somatic mutations may also play a key complementary role. We analyzed the impact on the outcomes of deep targeted mutational screening in 280 MDS patients with -7/del(7q) as isolated cytogenetic abnormality (86 with del(7q) and 194 with -7). Patients with del(7q) or -7 had similar demographic and disease-related characteristics. Somatic mutations were detected in 79% (93/117) of patients (82% in -7 and 73% in del(7q) group). Median number of mutations per patient was 2 (range 0-8). There was no difference in mutation frequen…

0301 basic medicineAdultMalemyelodysplastic syndromes chromosome abnormalities prognosisCancer Researchmedicine.medical_specialtyAdolescentSomatic cellTp53 mutationGastroenterology03 medical and health sciences0302 clinical medicinePartial lossCytogenetic AbnormalityInternal medicineAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansMutation frequencyAgedChromosome 7 (human)Aged 80 and overbusiness.industryMyelodysplastic syndromesHematologyMiddle Agedmedicine.diseasePrognosisSurvival AnalysisMutational analysis030104 developmental biologyOncology030220 oncology & carcinogenesisMyelodysplastic SyndromesMutationFemaleChromosome DeletionbusinessChromosomes Human Pair 7
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Molecular and clinical studies in five index cases with novel mutations in the GLA gene

2016

Fabry disease is a metabolic and lysosomal storage disorder caused by the functional defect of the α-galactosidase A enzyme; this defect is due to mutations in the GLA gene, that is composed of seven exons and is located on the long arm of the X-chromosome (Xq21–22). The enzymatic deficit is responsible for the accumulation of glycosphingolipids in lysosomes of different cellular types, mainly in those ones of vascular endothelium. It consequently causes a cellular and microvascular dysfunction. In this paper, we described five novel mutations in the GLA gene, related to absent enzymatic activity and typical manifestations of Fabry disease. We identified three mutations (c.846_847delTC, p.E…

0301 basic medicineAdultMalep.R227Pnovel moutationAdolescentc.639 + 5G > TMutation MissenseBiologyLeft ventricular hypertrophy03 medical and health sciencesExonYoung Adult0302 clinical medicineSettore BIO/13 - Biologia ApplicataGeneticsmedicinefabry; novel moutationMissense mutationAlpha-galactosidase AHumansPoint MutationCornea verticillataGenetic Predisposition to DiseaseChildfabryGLA genec.846_847delTCGeneticsAlpha-galactosidasePoint mutationFabry disease; Alpha-galactosidase A; c.846_847delTC; p.E341X; p.C382X; p.R227P; c.639 + 5G > Tp.E341XGeneral MedicineMiddle Agedmedicine.diseaseMolecular biologyFabry diseaseStop codon030104 developmental biologyp.C382Xalpha-Galactosidasebiology.proteinFabry DiseaseFemalemedicine.symptom030217 neurology & neurosurgery
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Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

2020

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin i…

0301 basic medicineAdvanced glycation end product (AGE)AMP-activated protein kinase (AMPK)endocrine system diseasesglycerol 3-phosphate dehydrogenase (GPD)Clinical Biochemistrytype 1 diabetes (T1D)Type 2 diabetesmTORC1Review Articleelectron transport chain (ETC)PharmacologyMitochondrionmedicine.disease_causeBiochemistry0302 clinical medicineLeukocytesCREB-binding protein (CBP)inner mitochondrial membrane (IMM)lcsh:QH301-705.5lcsh:R5-920cAMP response element-binding (CREB)glucagon-like peptide 1 (GLP-1)type 2 diabetes (T2D)Type 2 diabetesMetforminMetforminMitochondriamedicine.anatomical_structurereactive nitrogen species (RNS)reactive oxygen species (ROS)sirtuin (SIRT)medicine.symptomlcsh:Medicine (General)cardiovascular diseases (CVD)medicine.drugEndotheliumnitric oxide synthase (NOS)polycystic ovary syndrome (PCOS)Pathophysiologyinsulin resistance (IR)superoxide dismutase (SOD)03 medical and health sciencesglycated haemoglobin (HbA1c)medicineorganic cation transporter (OCT)HumansEndotheliumintercellular adhesion molecule-1 (ICAM-1)business.industryoxidative phosphorylation (OXPHOS)Organic Chemistryperoxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)AMPKmedicine.diseaseAtherosclerosisvascular cell adhesion molecule-1 (VCAM-1)Treatment030104 developmental biologylcsh:Biology (General)Mechanism of actionDiabetes Mellitus Type 2Oxidative stressbusinessinsulin receptor substrate (IRS)030217 neurology & neurosurgeryOxidative stress
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