Search results for "MOZ"

showing 10 items of 437 documents

Autosomal-recessive SASH1 variants associated with a new genodermatosis with pigmentation defects, palmoplantar keratoderma and skin carcinoma

2014

SASH1 (SAM and SH3 domain-containing protein 1) is a tumor suppressor gene involved in the tumorigenesis of a spectrum of solid cancers. Heterozygous SASH1 variants are known to cause autosomal-dominant dyschromatosis. Homozygosity mapping and whole-exome sequencing were performed in a consanguineous Moroccan family with two affected siblings presenting an unclassified phenotype associating an abnormal pigmentation pattern (hypo- and hyperpigmented macules of the trunk and face and areas of reticular hypo- and hyperpigmentation of the extremities), alopecia, palmoplantar keratoderma, ungueal dystrophy and recurrent spinocellular carcinoma. We identified a homozygous variant in SASH1 (c.1849…

AdultMaleSkin NeoplasmsDNA Mutational AnalysisMutation MissenseGenes RecessiveConsanguinityBiologyArticleConsanguinityKeratoderma PalmoplantarGeneticsmedicineHumansExomeGenetic Predisposition to DiseaseGenetics (clinical)Pigmentation disorderSkinFamily HealthGeneticsSiblingsTumor Suppressor ProteinsHomozygoteGenodermatosisSequence Analysis DNAFibroblastsmedicine.diseaseDisease gene identificationHyperpigmentationPedigreePalmoplantar keratodermaFemaleSkin cancermedicine.symptomSkin CarcinomaPigmentation DisordersEuropean Journal of Human Genetics
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Outcome of type III Gaucher disease on enzyme replacement therapy: review of 55 cases.

2007

The European Task Force for Neuronopathic Gaucher Disease (NGD) met in 2006 to review its 2001 guidelines. Fifty-five patients from five European countries were reviewed; 29 were male and 26 female. The majority of the patients were homozygous for the L444P mutation. All had been on enzyme replacement therapy (ERT). However, there was considerable variation in the dose of ERT, as well as an uneven distribution of risk factors. Thus, the oldest patients were on the lowest doses, and several had had a total splenectomy, while the youngest patients had a high proportion of compound heterozygosity and were on the highest doses, and very few had had a splenectomy. This heterogeneity rendered ana…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyPediatricsHeterozygoteTime FactorsAdolescentmedicine.medical_treatmentSplenectomyEnzyme TherapyDiseaseCompound heterozygosityCentral nervous system diseaseOlder patientsRisk FactorsGeneticsmedicineTotal splenectomyHumansChildGenetics (clinical)Intelligence TestsChemotherapyGaucher Diseasebusiness.industryHomozygotenutritional and metabolic diseasesEnzyme replacement therapymedicine.diseaseSurgeryTreatment OutcomeChild PreschoolGlucosylceramidaseFemaleNervous System DiseasesbusinessJournal of inherited metabolic disease
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Therapy for Recurrent High-Grade Gliomas: Results of a Prospective Multicenter Study on Health-Related Quality of Life

2017

Objective To assess the impact of therapy on patients' health-related quality of life (HRQoL) in recurrent high-grade glioma (HGG) in an unselected cohort. Methods In this prospective multicenter study, we analyzed European Organization for Research and Treatment of Cancer Quality of Life core questionnaire and European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Brain Neoplasm module questionnaires of 92 patients within 1 year after diagnosis of tumor recurrence of a HGG and respective treatment. We evaluated the influence of re-radiation, second- and third-line chemotherapies, and number of recurrent surgeries on summary scores for functioning, symptoms…

AdultMalemedicine.medical_specialtyBevacizumabAntineoplastic AgentsProcarbazinelaw.inventionCohort StudiesYoung Adult03 medical and health sciences0302 clinical medicineRandomized controlled trialQuality of lifelawSurveys and QuestionnairesInternal medicinemedicineHumansProspective StudiesKarnofsky Performance StatusAgedTemozolomidePerformance statusBrain Neoplasmsbusiness.industryCancerGliomaMiddle Agedmedicine.diseaseEurope030220 oncology & carcinogenesisCohortQuality of LifePhysical therapyFemaleRadiotherapy AdjuvantSurgeryNeurology (clinical)Neoplasm Recurrence Localbusiness030217 neurology & neurosurgerymedicine.drugWorld Neurosurgery
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Treating homozygous familial hypercholesterolemia in a real-world setting: Experiences with lomitapide

2015

Homozygous familial hypercholesterolaemia (HoFH) is a rare genetic disease characterised by markedly elevated plasma levels of low-density lipoprotein-cholesterol (LDL-C). Lomitapide is a microsomal triglyceride transfer protein (MTP) inhibitor approved as an adjunct to other lipid-lowering therapies (LLTs), with or without lipoprotein apheresis (LA), for the treatment of adult HoFH. Diet with <20% calories from fat is required. Due to a varying genetic and phenotypic profile of patients with HoFH, individual patients may respond to therapy differently; therefore examining individual cases in a 'real-world' setting provides valuable information on the effective day-to-day manag…

AdultMalemedicine.medical_specialtyCalorieSettore MED/09 - Medicina InternaEndocrinology Diabetes and MetabolismCase studyFamilial hypercholesterolemiaHomozygous familial hypercholesterolemiaFamilial hypercholesterolemiaDiseaseCompound heterozygosityHyperlipoproteinemia Type IIchemistry.chemical_compoundInternal medicineCase study; Familial hypercholesterolemia; Homozygous familial hypercholesterolemia; Lomitapide; Treatment; Cardiology and Cardiovascular Medicine; Endocrinology Diabetes and Metabolism; Internal Medicine; Nutrition and DieteticsInternal MedicinemedicineHumansAdverse effectNutrition and Dieteticsbusiness.industryAnticholesteremic AgentsHomozygoteCholesterol LDLMiddle Agedmedicine.diseaseLomitapideLomitapideTreatmentClinical trialEndocrinologychemistryBenzimidazolesFemaleSteatosisCardiology and Cardiovascular Medicinebusiness
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Non-classic cystic fibrosis associated with D1152HCFTR mutation

2010

Burgel P-R, Fajac I, Hubert D, Grenet D, Stremler N, Roussey M, Siret D, Languepin J, Mely L, Fanton A, Labbe A, Domblides P, Vic P, Dagorne M, Reynaud-Gaubert M, Counil F, Varaigne F, Bienvenu T, Bellis G, Dusser D. Non-classic cystic fibrosis associated with D1152H CFTR mutation. Background: Limited knowledge exists on phenotypes associated with the D1152H cystic fibrosis transmembrane conductance regulator (CFTR) mutation. Methods: Subjects with a D1152H allele in trans with another CFTR mutation were identified using the French Cystic Fibrosis Registry. Phenotypic characteristics were compared with those of pancreatic insufficient (PI) and pancreatic sufficient (PS) cystic fibrosis (CF)…

AdultMalemedicine.medical_specialtyConsensusPancreatic diseaseAdolescentCystic FibrosisGENETICSmedicine.medical_treatmentCystic Fibrosis Transmembrane Conductance RegulatorCystic fibrosisGastroenterologyMembrane PotentialsCohort StudiesYoung AdultChloridesInterquartile rangeForced Expiratory VolumeInternal medicineCYSTIC_FIBROSISHumansMedicineLung transplantationGenetic Predisposition to DiseaseChildSweatExocrine pancreatic insufficiencyMUTATIONGenetics (clinical)AgedBronchiectasisbiologybusiness.industryHomozygoteMiddle Agedmedicine.diseaseCongenital absence of the vas deferensCystic fibrosis transmembrane conductance regulatorNasal MucosaEndocrinologyAmino Acid SubstitutionChild Preschoolbiology.proteinFemalebusiness
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CC chemokine receptor 5 polymorphism in Italian patients with Beḩet's disease

2012

OBJECTIVE: To evaluate the potential role of CC chemokine receptor 5 (CCR5)Δ32 polymorphism in the susceptibility to and clinical expression of Behcet's disease (BD) in a cohort of Italian patients. METHODS: One hundred and ninety-six consecutive Italian patients satisfying the ISG criteria for BD were followed up for 8 years, and 180 healthy age- and sex-matched blood donors were molecularly genotyped for the CCR5Δ32 polymorphism. A standard microlymphocytotoxicity technique was used to serotype HLA-B51. The patients were subgrouped on the basis of the presence or absence of clinical manifestations. RESULTS: The distribution of the CCR5Δ32 genotype differed between BD patients and controls…

AdultMalemedicine.medical_specialtyHeterozygoteReceptors CCR5Behcet's disease CCR5 polymorphismBehcet's diseaseGastroenterologyRheumatologyGeneticGene FrequencyInternal medicineGenotypeReceptorsMedicineHumansPharmacology (medical)Genetic Predisposition to DiseaseAllelePolymorphismAllele frequencyPolymorphism Geneticbusiness.industryBehcet SyndromeHomozygoteCase-control studyOdds ratiomedicine.diseaseBeḩet's disease; CC chemokine receptor 5 Δ32 olymorphism; Chemokines; Disease manifestations; Adult; Behcet Syndrome; Case-Control Studies; Female; Gene Frequency; Genetic Predisposition to Disease; HLA-B Antigens; Heterozygote; Homozygote; Humans; Italy; Male; Polymorphism Genetic; Receptors CCR5; Rheumatology; Pharmacology (medical)Adult; Behcet Syndrome; Case-Control Studies; Female; Gene Frequency; Genetic Predisposition to Disease; HLA-B Antigens; Heterozygote; Homozygote; Humans; Italy; Male; Polymorphism Genetic; Receptors CCR5ItalyHLA-B AntigensCase-Control StudiesImmunologyCohortFemalebusinessCC chemokine receptorsCCR5
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Clinical experience of lomitapide therapy in patients with homozygous familial hypercholesterolaemia.

2014

The microsomal triglyceride transfer protein (MTP) inhibitor lomitapide is a licenced adjunct to a low-fat diet and other lipid-lowering medication, with or without low-density lipoprotein apheresis, for the treatment of adults with homozygous familial hypercholesterolaemia (HoFH). In a recently published phase 3 study, patients with HoFH received lomitapide in addition to maximally tolerated lipid-lowering therapy. Treatment with lomitapide resulted in a mean approximate 50% reduction in LDL-C levels after 26 weeks compared with baseline levels (p < 0.0001). This decrease in LDL-C was maintained at Weeks 56 and 78 (44% [p < 0.0001] and 38% [p = 0.0001], respectively). This paper offers cli…

AdultMalemedicine.medical_specialtySettore MED/09 - Medicina InternaPhases of clinical researchMicrosomal triglyceride transfer proteinHyperlipoproteinemia Type IIchemistry.chemical_compoundYoung AdultInternal medicineHo-FH lomitapide MTPInternal MedicinemedicineEffective treatmentHumansIn patientAdverse effectbiologymedicine.diagnostic_testbusiness.industryAnticholesteremic AgentsHomozygoteGeneral MedicineCholesterol LDLMiddle AgedLomitapideEndocrinologyApheresisTreatment Outcomechemistrybiology.proteinBenzimidazolesFemaleCardiology and Cardiovascular MedicinebusinessLiver function testsAtherosclerosis. Supplements
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Detection of a germline mutation and somatic homozygous loss of the von Hippel-Lindau tumor-suppressor gene in a family with a de novo mutation

1996

von Hippel-Lindau (VHL) disease is a pleiotropic disorder featuring a variety of malignant and benign tumors of the eye, central nervous system, kidney, and adrenal gland. Recently the VHL gene has been identified in the chromosomal region 3p25-26. Prognosis and successful management of VHL patients and their descendants depend on unambiguous diagnosis. Due to recurrent hemangioblastomas, a29-year-old patient without familial history of VHL disease was diagnosed to be at risk for the disease. Histopathological examination of a small renal mass identified a clear cell tumor with a G1 grading. Genetic characterization of the germline and of the renal tumor was performed. Polymerase chain reac…

AdultMalemedicine.medical_specialtyvon Hippel-Lindau DiseaseTumor suppressor geneDNA Mutational AnalysisMolecular Sequence Dataurologic and male genital diseasesPolymerase Chain ReactionGermlineGermline mutationVon Hippel–Lindau tumor suppressorGeneticsmedicineHumansGenes Tumor SuppressorSpinal Cord NeoplasmsVon Hippel–Lindau diseaseGerm-Line MutationPolymorphism Single-Stranded ConformationalGenetics (clinical)Sequence Deletionbiologymedicine.diagnostic_testHomozygoteCytogeneticsExonsmedicine.diseaseKidney Neoplasmsfemale genital diseases and pregnancy complicationsHemangioblastomaPedigreeKaryotypingChromosomal regionbiology.proteinCancer researchFemaleChromosomes Human Pair 3Chromosome DeletionFluorescence in situ hybridizationHuman Genetics
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Activity and safety of temozolomide in advanced adrenocortical carcinoma patients

2019

Objective Temozolomide has shown a significant anti-proliferative activity on adrenocortical cancer (ACC) cells in vitro. Design On the basis of these results the drug was prescribed as second/third line in advanced metastatic ACC patients in four referral centers in Italy. Methods We retrospectively collected anagraphic, clinical and pathological data of patients with advanced ACC with disease progression to standard chemotherapy plus mitotane who were treated with temozolomide at the dose of 200 mg/m2/die given for 5 consecutive days every 28 days. The primary endpoint was the disease control rate, defined as objective response or disease stabilization after 3 months. Secondary endpoints…

AdultOncologymedicine.medical_specialtytemozolomide adrenocortical carcinomaDisease ResponseSettore MED/06 - Oncologia MedicaEndocrinology Diabetes and Metabolismmedicine.medical_treatment030209 endocrinology & metabolism03 medical and health sciences0302 clinical medicineEndocrinologyStable DiseaseInternal medicineAdrenocortical CarcinomaTemozolomideClinical endpointHumansMedicineAdrenocortical carcinomaMitotaneDNA Modification MethylasesAgedRetrospective StudiesChemotherapyTemozolomidebusiness.industryTumor Suppressor ProteinsRetrospective cohort studyGeneral MedicineMiddle Agedmedicine.diseaseDNA Repair EnzymesEndocrinology030220 oncology & carcinogenesisbusinessmedicine.drug
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VITAMIN K-INDUCED MODIFICATION OF COAGULATION PHENOTYPE IN VKORC1 HOMOZYGOUS DEFICIENCY

2008

Summary.  Background: Combined vitamin K-dependent clotting factor (VKCF) deficiency type 2 (VKCFD2) is a rare bleeding disorder caused by mutated vitamin K 2,3-epoxide reductase complex subunit 1 (VKORC1) gene. Methods and results: An Italian patient with moderate to severe bleeding tendency was genotyped, and found to be homozygous for the unique VKORC1 mutation (Arg98Trp) so far detected in VKCFD2. The activity levels of VKCFs were differentially reduced, and inversely related to the previously estimated affinity of procoagulant factor propeptides for the γ-carboxylase. The normal (factor IX) or reduced antigen levels (other VKCFs) produced a gradient in specific activities. Vitamin K su…

Adultmedicine.medical_specialtycoagulation factor levelsVitamin KProtein SMixed Function OxygenasesTissue factorchemistry.chemical_compoundInternal medicineVitamin K Epoxide ReductasesmedicineVKCFD2HumansFactor IXClotting factorCoagulation factor levels; Thrombin generation; Vitamin K supplementation; VKCFD2; VKORC1 mutation;biologyFactor VIIChemistryFactor XHomozygotevitamin K supplementationHematologyBlood Coagulation DisordersEndocrinologyTreatment OutcomeCoagulationthrombin generationImmunologyMutationbiology.proteinFemaleBlood Coagulation TestsVKCFD2 VKORC1 mutation coagulation factor levels thrombin generation vitamin K supplementationProtein Cmedicine.drugHalf-LifeVKORC1 mutation
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