Search results for "MUTATION"

showing 10 items of 2830 documents

Janus kinase (JAK) 2 V617F mutation as the cause of primary thrombocythemia in acromegaly with severe visceromegaly and divergence between growth hor…

2012

OBJECTIVE: An increased prevalence of hematological abnormalities is reported in acromegaly, but to date no reports about the presence of the Janus Kinase (JAK) 2 mutation in acromegalic patients have been described. DESIGN: We report the complex clinical presentation of the unique case, never described, of acromegaly due to GH-secreting pituitary adenoma associated with JAK2 V617F mutation. RESULTS: The patient shows primary thrombocythemia and myelofibrosis, due to JAK2 V617F mutation, severe visceromegaly and a peculiar clinical course of the disease characterized by discrepant values of GH and IGF-1 during somatostatin analog (SA) treatment despite a significant reduction in pituitary a…

Malemedicine.medical_specialtyTime FactorsEndocrinology Diabetes and MetabolismGrowth hormone receptorAcromegaly HGH IGF-1GastroenterologySettore MED/13 - EndocrinologiaCohort StudiesEndocrinologyPituitary adenomahemic and lymphatic diseasesInternal medicineAcromegalymedicineAnimalsHumansPituitary NeoplasmsInsulin-Like Growth Factor IRadiometryMyelofibrosisAgedJanus kinase 2biologyHuman Growth HormonePlatelet Countbusiness.industryJanus Kinase 2medicine.diseaseAcromegaly Growth hormone Insulin-like growth factor-1 Janus kinase 2 Growth hormone receptorEndocrinologyAcromegalyMutationPegvisomantbiology.proteinJanus kinasebusinessVisceromegalyFollow-Up StudiesThrombocythemia Essentialmedicine.drug
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Association of cathepsin B gene polymorphisms with tropical calcific pancreatitis

2006

Background and aims: Tropical calcific pancreatitis (TCP) is a type of chronic pancreatitis unique to countries in the tropics. Mutations in pancreatic secretory trypsin inhibitor (SPINK1) rather than cationic trypsinogen (PRSS1) explain the disease in only 50% of TCP patients. As cathepsin B (CTSB) is known to activate cationic trypsinogen, we attempted to understand the role of CTSB mutations in TCP. Evidence of epistatic interaction was investigated with the previously associated N34S SPINK1 allele, a variant considered to be a modifier rather than a true susceptibility allele. Subjects and methods: We sequenced the coding region of CTSB gene in 51 TCP patients and 25 controls and furthe…

Malemedicine.medical_specialtyTrypsinogenSingle-nucleotide polymorphismBiologyPolymerase Chain ReactionGastroenterologyCathepsin BCathepsin Bchemistry.chemical_compoundGene FrequencyPancreatitis ChronicInternal medicinemedicineHumansGenetic Predisposition to DiseaseTrypsinogen activationAlleleAllele frequencyGeneticsPolymorphism GeneticHaplotypeGastroenterologyCase-control studyCalcinosisHaplotypesPancreatitischemistryCase-Control StudiesMutationAcute DiseaseFemaleGut
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Mild phenotypes in a series of patients with Opitz GBBB syndrome with MID1 mutations

2004

Contains fulltext : 48815.pdf (Publisher’s version ) (Closed access) Opitz syndrome (OS; MIM 145410 and MIM 300000) is a congenital midline malformation syndrome characterized by hypertelorism, hypospadias, cleft lip/palate, laryngotracheoesophageal (LTE) abnormalities, imperforate anus, developmental delay, and cardiac defects. The X-linked form (XLOS) is caused by mutations in the MID1 gene, which encodes a microtubule-associated RBCC protein. In this study, phenotypic manifestations of patients with and without MID1 mutations were compared to determine genotype-phenotype correlations. We detected 10 novel mutations, 5 in familial cases, 2 in sporadic cases, and 3 in families for whom it …

Malemedicine.medical_specialtyUbiquitin-Protein LigasesBiologymedicine.disease_causeGastroenterologyG/BBB SYNDROMEFAMILIESGenomic disorders and inherited multi-system disorders [IGMD 3]Genotype-phenotype distinctionInternal medicineGeneticsmedicineHumansHypertelorismGeneGenetics (clinical)GeneticsFamily HealthX-linked Opitz syndromeMutationMID1Nuclear ProteinsGenetic Diseases X-LinkedExonsOpitz G/BBB Syndromemedicine.diseasePhenotypeGENEPedigreeSmith-Lemli-Opitz SyndromePhenotypeGenetic defects of metabolism [UMCN 5.1]HypospadiasMutationMicrotubule ProteinsFemalephenotypic variabilityXP22medicine.symptomImperforate anusFunctional Neurogenomics [DCN 2]BBBTranscription FactorsAmerican Journal of Medical Genetics. Part A
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Four new cases of congenital secondary hypothyroidism due to a splice site mutation in the thyrotropin-beta gene: Phenotypic variability and founder …

2004

WOS: 000223072400081 PubMed ID: 15292359 Isolated TSH deficiency is a rare cause of congenital hypothyroidism. We here report four children from two consanguineous Turkish families with isolated TSH deficiency. Affected children who were screened at newborn age had an unremarkable TSH result and a low serum TSH level at diagnosis. Age at diagnosis and clinical phenotype were variable. All affected children carried an identical homozygous splice site mutation (IVS2 + 5 Gdouble right arrowA) in the TSHbeta gene. This mutation leads to skipping of exon 2 and a loss of the translational start codon without ability to produce a TSH-like protein. However, using specific monoclonal antibodies, we …

Malemedicine.medical_specialtyendocrine systemGuanineendocrine system diseasesEndocrinology Diabetes and MetabolismClinical BiochemistryThyrotropinLocus (genetics)Thyrotropin beta SubunitBiologyBiochemistryExonEndocrinologyHypothyroidismInternal medicinemedicineCongenital HypothyroidismHumansChildGeneGenotypingGeneticsSplice site mutationAdenineBiochemistry (medical)HaplotypeHomozygoteInfant NewbornInfantmedicine.diseaseFounder EffectIntronsCongenital hypothyroidismPedigreeEndocrinologyPhenotypeHaplotypesChild PreschoolMutationFemalehormones hormone substitutes and hormone antagonistsFounder effect
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ISDR pattern and evolution in patients with chronic hepatitis C treated with standard or Peg-IFN plus ribavirin

2003

The aim of the study was to characterize the interferon sensitivity determining region (ISDR) mutation pattern and its changes at 4 weeks of treatment in a population of patients infected with hepatitis C virus (HCV) genotype 1b receiving standard or PEG-IFN plus ribavirin (RBV), to find possible early correlates of therapy outcome.Forty-five patients with chronic hepatitis due to HCV 1b were treated by PEG-IFN-α2b (n=23) or IFN-α2b (n=22) plus RBV 1000–1200 mg/day. They were classified 24 weeks after stopping therapy as sustained responders (SR), relapsers (REL) or non-responders (NR). Sixteen patients were SR, 12 REL and 17 NR. ISDR mutations were evaluated by direct sequencing at baselin…

Malemedicine.medical_treatmentHepacivirusHepacivirusViral Nonstructural Proteinsmedicine.disease_causePolyethylene GlycolPolyethylene GlycolsCohort Studieschemistry.chemical_compoundInterferonMedicinePharmacology (medical)education.field_of_studybiologyRecombinant ProteinMiddle AgedRecombinant ProteinsTreatment OutcomeInfectious DiseasesDrug Therapy CombinationFemaleHumanmedicine.drugGenotypeHepatitis C virusMolecular Sequence DataPopulationInterferon alpha-2Antiviral AgentsVirusFlaviviridaeRibavirinHumansAmino Acid SequenceeducationAntiviral AgentPharmacologyChemotherapyHepacivirubusiness.industryRibavirinInterferon-alphaHepatitis C Chronicbiology.organism_classificationVirologychemistryMutationCohort StudiebusinessSequence Alignment
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UNC-52/perlecan affects gonadal leader cell migrations in C. elegans hermaphrodites through alterations in growth factor signaling.

2003

0012-1606 doi: DOI: 10.1016/S0012-1606(03)00014-9; The unc-52 gene of Claenorhabditis elegans encodes a homologue of the basement membrane heparan sulfate proteoglycan perlecan. Viable alleles reduce the abundance of UNC-52 in late larval stages and increase the frequency of distal tip cell (DTC) migration defects caused by mutations disrupting the UNC-6/netrin guidance system. These unc-52 alleles do not cause circumferential DTC migration defects in an otherwise wild-type genetic background. The effects of unc-52 mutations on DTC migrations are distinct from effects on myofilament organization and can be partially suppressed by mutations in several genes encoding growth factor-like molecu…

Malemedicine.medical_treatmentOrganogenesisCellDisorders of Sex DevelopmentReceptor-Like Protein Tyrosine PhosphatasesFibroblast growth factorAnimals Genetically ModifiedCell MovementNetrinGrowth SubstancesGenes HelminthGeneticsMusclesCell migrationsWnt signaling pathwayHelminth Proteinsmedicine.anatomical_structurePhenotypeLarvaC. elegansFemaleNetrinsProteoglycansSignal transductionSignal TransductionUNC-52Nerve Tissue ProteinsReceptors Cell SurfacePerlecanmacromolecular substancesBiologymedicineAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsGonadsGeneMolecular BiologyGrowth factorfungiMembrane ProteinsCell BiologyPerlecanReceptors Fibroblast Growth Factornervous systemMutationbiology.proteinProtein Tyrosine PhosphatasesDevelopmental BiologyDevelopmental biology
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Overlapping phenotypes between SHORT and Noonan syndromes in patients with PTPN11 pathogenic variants

2020

Overlapping syndromes such as Noonan, Cardio-Facio-Cutaneous, Noonan syndrome (NS) with multiple lentigines and Costello syndromes are genetically heterogeneous conditions sharing a dysregulation of the RAS/mitogen-activated protein kinase (MAPK) pathway and are known collectively as the RASopathies. PTPN11 was the first disease-causing gene identified in NS and remains the more prevalent. We report seven patients from three families presenting heterozygous missense variants in PTPN11 probably responsible for a disease phenotype distinct from the classical Noonan syndrome. The clinical presentation and common features of these seven cases overlap with the SHORT syndrome. The latter is the c…

Malemusculoskeletal diseases0301 basic medicineMAPK/ERK pathwaycongenital hereditary and neonatal diseases and abnormalitiesMAP Kinase Signaling SystemProtein Tyrosine Phosphatase Non-Receptor Type 11030105 genetics & heredityBiologyGene productPhosphatidylinositol 3-Kinases03 medical and health sciencesMetabolic DiseasesGeneticsmedicineHumansMissense mutationskin and connective tissue diseasesProtein kinase BGrowth DisordersGenetics (clinical)GeneticsGenetic heterogeneityNoonan SyndromeGenetic Variationmedicine.diseasePTPN11NephrocalcinosisPhenotype030104 developmental biologySHORT syndromeHypercalcemiaNoonan syndromeFemaleMitogen-Activated Protein KinasesSignal TransductionClinical Genetics
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A new heterozygous mutation (D196N) in the Gs alpha gene as a cause for pseudohypoparathyroidism type IA in a boy who had gallstones

2011

Background Pseudohypoparathyroidism (PHP) is characterized by hypocalcemia and hyperphosphatemia in association with an increased secretion of parathyroid hormone (PTH) due to decreased target tissue responsiveness to PTH. Patients with PHP type Ia are not only resistant to PTH, but also to other hormones that bind to receptors coupled to stimulatory G protein (Gsalpha). PHP Ia and Albright hereditary osteodystrophy (AHO) are caused by a reduced activity of the Gsalpha protein. Heterozygous inactivating Gs alpha (GNAS) gene mutations have been identified in these patients. Methods We studied a boy with PHP Ia. During follow-up the patient developed elevated liver enzyme serum levels and abd…

Malemusculoskeletal diseasesHeterozygotemedicine.medical_specialtyErythrocytesFoot Deformities CongenitalEndocrinology Diabetes and MetabolismMutation MissenseParathyroid hormoneGallstonesGene mutationHyperphosphatemiaEndocrinologyInternal medicineChromograninsGTP-Binding Protein alpha Subunits GsGNAS complex locusHumansMedicineMissense mutationnatural sciencesAmino Acid SequenceChildConserved SequencePseudohypoparathyroidismBase SequenceSequence Homology Amino Acidbiologybusiness.industryDNAExonsGallstonesmedicine.diseasePedigreeCholesterolEndocrinologyAmino Acid SubstitutionPseudohypoparathyroidismPediatrics Perinatology and Child Healthbiology.proteinbusinessHand Deformities CongenitalHormoneJournal of Pediatric Endocrinology and Metabolism
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Q289P mutation in the FGFR2 gene: first report in a patient with type 1 Pfeiffer syndrome.

2008

When normal development and growth of the calvarial sutures is disrupted, craniosynostosis (premature calvarial suture fusion) may result. Classical craniosynostosis syndromes are autosomal dominant traits and include Apert, Pfeiffer, Crouzon, Jackson-Weiss, and Saethre-Chotzen syndromes. In these conditions, there is premature fusion of skull bones leading to an abnormal head shape, ocular hypertelorism with proptosis, and midface hypoplasia. It is known that mutations in the fibroblast growth factor receptors 1, 2, and 3 cause craniosynostosis. We report on a child with a clinically diagnosed Pfeiffer syndrome that shows the missense point mutation Q289P in exon 8 of the FGFR2 gene. This …

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyCraniosynostosisSettore MED/38 - Pediatria Generale E SpecialisticaHumansPoint MutationMedicineMissense mutationReceptor Fibroblast Growth Factor Type 2HypertelorismGeneticsFibrous jointbusiness.industryFibroblast growth factor receptor 2Craniofacial DysostosisInfantDysostosisExonsAcrocephalosyndactyliamedicine.diseaseSkullPhenotypemedicine.anatomical_structurePfeiffer - Crouzon - Apert - Craniosynostosis - Finger and toes abnormalities - Fibroblast growth factor receptorPediatrics Perinatology and Child HealthPfeiffer syndromeFemalemedicine.symptombusiness
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Duchenne muscular dystrophy and idiopathic hyperCKemia segregating in a family

1995

A 7-month-old boy with gross motor delay and failure to thrive presented with rhabdomyolysis following an acute asthmatic episode. During hospitalization an electrocardiographic conversion to a Wolff-Parkinson-White type 1 (WPW) pattern took place. Duchenne muscular dystrophy (DMD) was suspected based on elevated creatine kinase (CK) serum levels, muscle biopsy, and family history. The diagnosis was confirmed by molecular analysis, which documented a deletion corresponding to cDNA probe 1-2a in the dystrophin gene, in the propositus and in an affected male cousin of his mother. "Idiopathic" hyperCKemia was found in the propositus, his father, and 5 of his relatives. We suggest that the unus…

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesPediatricsmedicine.medical_specialtyDuchenne muscular dystrophyMolecular Sequence DataGene mutationPolymerase Chain ReactionMuscular DystrophiesGenomic ImprintingPrenatal DiagnosisInternal medicinemedicineHumansFamily historyCreatine KinaseGenetics (clinical)X-linked recessive inheritanceDNA PrimersGenes DominantMuscle biopsyBase Sequencebiologymedicine.diagnostic_testGenetic Carrier ScreeningInfantExonsmedicine.diseasePedigreeEndocrinologyMutationFailure to thrivebiology.proteinFemaleCreatine kinasemedicine.symptomDystrophinMetabolism Inborn ErrorsAmerican Journal of Medical Genetics
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