Search results for "Mutational analysis"

showing 10 items of 245 documents

Cathepsin C gene: First compound heterozygous patient with Papillon-Lefèvre syndrome and a novel symptomless mutation.

2001

Papillon-Lefevre syndrome (PLS) has recently been shown to be caused by mutations in the cathepsin C gene resulting in periodontal disease and palmoplantar keratosis. Thirteen different homozygous mutations have been characterised in PLS patients of different ethnic origin. In the present paper, a PLS patient is described who carries two novel mutations (706G>T and 872G>A) in the paternal and maternal chromosomes, respectively. This is the first compound patient described so far. In addition, a novel symptomless mutation (458C>T) in the cathepsin C gene is described in three homozygous individuals. Thus, not all mutations should be considered as a cause of disease, whether case studies or g…

MaleHeterozygoteHaim–Munk syndromeDNA Mutational AnalysisMolecular Sequence DataMutation MissensePapillon–Lefèvre syndromeBiologyCompound heterozygositymedicine.disease_causePapillon-Lefevre DiseaseCathepsin CCathepsin CPapillon-Lefevre DiseaseGene FrequencyGeneticsmedicineHumansAlleleAllele frequencyAllelesGenetics (clinical)Family HealthGeneticsMutationDNAmedicine.diseaseMutationFemale
researchProduct

Hydrops, fetal pleural effusions and chylothorax in three patients with CBL mutations.

2014

Fetal hydrops, fetal pleural effusions, hydrothorax, and chylothorax, may be associated with various genetic disorders, in particular with the Noonan, cardio-facio-cutaneous and Costello syndromes. These syndromes, collectively called RASopathies, are caused by mutations in the RAS/MAPK pathway, which is known to play a major role in lymphangiogenesis. Recently, germline mutations in the Casitas B-cell lymphoma (CBL) gene were reported in 25 patients and of these, 20 had juvenile myelomonocytic leukemia (JMML). The disorder was named "CBL syndrome" or "Noonan syndrome-like disorder with or without juvenile myelomonocytic leukemia" (NSLL). To date, prenatal abnormalities have not been report…

MaleHeterozygoteHydrops FetalisDNA Mutational AnalysisRASopathyChylothoraxGermline mutationhemic and lymphatic diseasesHydrops fetalisGeneticsmedicineHumansProto-Oncogene Proteins c-cblGenetics (clinical)FetusJuvenile myelomonocytic leukemiabusiness.industryChylothoraxFaciesInfantmedicine.diseaseLymphomaPleural EffusionPhenotypeChild PreschoolImmunologyMutationHydrothoraxFemaleRNA Splice SitesbusinessAmerican journal of medical genetics. Part A
researchProduct

Frontotemporal dementia: the post-tau era.

2006

As scientists have begun to decipher the molecular genetic bases of hereditary frontotemporal dementia (FTD), it has become clear that the biology of these human neurodegenerative diseases has a complexity not previously suspected. FTD has been found to be linked to several chromosomal loci including those in chromosome 9, chromosome 17, and chromosome 3. The article by Guyant-Marechal et al. in this issue of Neurology reports the clinical, pathologic, and molecular characteristics of a form of FTD associated with inclusion body myopathy and Paget disease of the bone observed in members of two families and expands our knowledge on genetically determined FTD.1 The disorder is associated with…

MaleHeterozygoteMultiple Organ FailureDNA Mutational AnalysisChromosome 9Cell Cycle ProteinsChromosome Disorderstau ProteinsBiologyRisk AssessmentMyositis Inclusion BodyExonRisk FactorsValosin Containing ProteinmedicinePrevalenceHumansGenetic Predisposition to DiseaseGeneRetrospective StudiesGeneticsAdenosine TriphosphatasesIncidenceChromosomeSyndromeMiddle Agedmedicine.diseaseOsteitis DeformansPhenotypePedigreeChromosome 17 (human)Chromosome 3MutationDementiaFemaleNeurology (clinical)FranceFrontotemporal dementiaNeurology
researchProduct

Compound heterozygosity in the SPG4 gene causes hereditary spastic paraplegia

2008

The SPG4 gene is frequently mutated in autosomal dominant form of hereditary spastic paraplegia (HSP). We report that the compound heterozygous sequence variants S44L, a known polymorphism, and c.1687G>A, a novel mutation in SPG4 cause a severe form of HSP in a patient. The family members carrying solely c.1687G>A mutation are asymptomatic for HSP. The reverse transcriptase-polymerase chain reaction (RT-PCR) analysis revealed that the c.1687G>A mutation is a splice site mutation and causes skipping of the exon 15 of spastin. Furthermore, quantification of RT-PCR products by sequencing and quantification of allele-specific expression by pyrosequencing assay revealed that c.1687G>A is a leaky…

MaleHeterozygoteSpastinHereditary spastic paraplegiaDNA Mutational AnalysisMolecular Sequence DataMutantIntracellular SpaceBiologyCompound heterozygositySpastinPolymorphism Single NucleotideWhite PeopleLoss of heterozygosity03 medical and health sciencesExon0302 clinical medicineGermanyGeneticsmedicineHumansRNA MessengerAllelesGenetics (clinical)030304 developmental biologyAdenosine TriphosphatasesRegulation of gene expressionGenetics0303 health sciencesSplice site mutationBase SequenceSpastic Paraplegia HereditaryComputational BiologyExonsmedicine.diseasePedigreeProtein TransportAmino Acid SubstitutionGene Expression RegulationMutationFemaleRNA Splice Sites030217 neurology & neurosurgeryHeLa CellsClinical Genetics
researchProduct

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
researchProduct

Mutant K-ras2 in serum

2003

Mutant tumour derived DNA has been detected in the sera of colorectal cancer patients. We investigated if mutant serum KRAS2 was detectable preoperatively in a large group of patients with colorectal neoplasia. A prospective study of 94 patients who underwent putative curative resection for colorectal carcinoma (CRC) was performed to ascertain if serum mutant KRAS2 could be used postoperatively as a disease marker.Preoperative sera from 78 patients were analysed (group A). Sera from 94 patients were obtained three monthly for up to three years during the postoperative period (group B). Codon 12 and 13 KRAS2 mutations were analysed in matched tumour and serum samples.In the preoperative grou…

MaleLetterColorectal cancervirusesMutantDNA Mutational AnalysisBioinformaticsProto-Oncogene Proteins p21(ras)03 medical and health sciencesCollaborative group0302 clinical medicineProto-Oncogene ProteinsMedicineHumansRas2neoplasmsGene030304 developmental biologyAged0303 health sciencesbusiness.industryPoint mutationGastroenterologyDNA NeoplasmMiddle Agedmedicine.diseasePrognosis3. Good healthProto-Oncogene Proteins p21(ras)Molecular analysisCarcinoembryonic AntigenEpidemiologic Studies030220 oncology & carcinogenesisCancer researchras ProteinsFemaleNeoplasm Recurrence LocalbusinessColorectal NeoplasmsBiomarkers
researchProduct

Molecular surveillance of pandemic influenza A(H1N1) viruses circulating in Italy from May 2009 to February 2010: association between haemagglutinin …

2010

Haemagglutinin sequences of pandemic influenza A(H1N1) viruses circulating in Italy were examined, focusing on amino acid changes at position 222 because of its suggested pathogenic relevance. Among 169 patients, the D222G substitution was detected in three of 52 (5.8%) severe cases and in one of 117 (0.9%) mild cases, whereas the D222E mutation was more frequent and evenly distributed in mild (31.6%) and severe cases (38.4%). A cluster of D222E viruses among school children confirms reported human-to-human transmission of viruses mutated at amino acid position 222.

MaleMolecular surveillance; Pandemic influenza A(H1N1); Haemagglutinin mutations; Italy from May 2009 to February 2010pandemic influenzasurveillance of pandemic influenza A(H1N1); Molecular surveillance; pandemic influenzaEpidemiologyvirusesHaemagglutinin mutationssurveillance of pandemic influenza A(H1N1)Settore MED/42 - Igiene Generale E Applicatamedicine.disease_causeSeverity of Illness IndexInfluenza A Virus H1N1 SubtypePandemic influenza A(H1N1)PandemicInfluenza A VirusA(H1N1)ChildMutationReverse Transcriptase Polymerase Chain ReactionTransmission (medicine)Adolescent; Adult; Age Distribution; Aged; Amino Acid Substitution; Child; Child Preschool; Female; Hemagglutinins; Humans; Infant; Influenza A Virus H1N1 Subtype; Influenza Human; Italy; Male; Middle Aged; Mutation; Population Surveillance; Reverse Transcriptase Polymerase Chain Reaction; Severity of Illness Index; Sex Distribution; Young Adult; PandemicsMiddle AgedItaly from May 2009 to February 2010Molecular surveillance; pandemic influenza; A(H1N1); Italy; haemagglutinin mutationsHemagglutininsMolecular surveillanceItalyChild PreschoolPopulation SurveillanceFemaleHumanAdultAdolescentBiologyDisease clusterDisease courseYoung AdultAge DistributionVirologyInfluenza HumanmedicineHumansH1N1 SubtypeSex DistributionPreschoolhaemagglutinin mutationsPandemicsAgedMolecular epidemiologyPublic Health Environmental and Occupational HealthPandemic influenzaInfantVirologyInfluenzaMutational analysisAmino Acid SubstitutionMutationEurosurveillance
researchProduct

Elevated serum triiodothyronine and intellectual and motor disability with paroxysmal dyskinesia caused by a monocarboxylate transporter 8 gene mutat…

2008

Monocarboxylate transporter 8 (MCT8 or SLC16A2) is important for the neuronal uptake of triiodothyronine (T3) in its function as a specific and active transporter of thyroid hormones across the cell membrane, thus being essential for human brain development. We report on a German male with Allan-Herndon-Dudley syndrome presenting with severe intellectual and motor disability, paroxysmal dyskinesia combined with truncal muscular hypotonia, and peripheral muscular hypertonia at his current age of 9 years. Additionally, the patient has a lesion in the left putamen region revealed by magnetic resonance imaging and elevated serum T3 levels. The male appeared to have a hemizygous mutation (R271H)…

MaleMonocarboxylic Acid Transportersmedicine.medical_specialtyDevelopmental DisabilitiesDNA Mutational AnalysisEnzyme-Linked Immunosorbent AssayGene mutationArginineLesionDevelopmental NeuroscienceChoreaInternal medicineIntellectual DisabilitymedicineHumansHistidineChildMonocarboxylate transporterAllan–Herndon–Dudley syndromeTriiodothyroninebiologyMuscular hypotoniaSymportersParoxysmal dyskinesiamedicine.diseaseMagnetic Resonance ImagingEndocrinologyPediatrics Perinatology and Child HealthMutationbiology.proteinHypertoniaTriiodothyronineNeurology (clinical)medicine.symptomDevelopmental medicine and child neurology
researchProduct

Actin-related myopathy without any missense mutation in the ACTA1 gene.

2004

Actinopathies are defined by missense mutations in the ACTA1 gene coding for sarcomeric actin, of which some 70 families have, so far, been identified. Often, but not always, muscle fibers carry large patches of actin filaments. Many such patients also have nemaline myopathy, qualifying actinopathies as a subgroup of nemaline myopathies. This article concerns a then newborn, now 21/2-year-old boy, the first and single child of nonconsanguineous parents, who was born floppy, requiring immediate postnatal assisted ventilation. A quadriceps muscle biopsy revealed large patches of thin myofilaments reacting at light and electron microscopic levels with antibodies against actin but only a few s…

MaleMyofilamentBiopsyDNA Mutational AnalysisMutation MissenseGene mutationBiologymedicine.disease_cause03 medical and health sciences0302 clinical medicineNemaline myopathyMuscular Diseases030225 pediatricsmedicineMissense mutationHumansPoint MutationMyopathyMuscle SkeletalActinMutationInfantmedicine.diseaseMolecular biologyCongenital myopathyActinsPediatrics Perinatology and Child HealthNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryJournal of child neurology
researchProduct

The TP53 colorectal cancer international collaborative study on the prognostic and predictive significance of p53 mutation: influence of tumor site, …

2005

Purpose The aims of the TP53 Colorectal Cancer (CRC) International Collaborative Study were to evaluate the possible associations between specific TP53 mutations and tumor site, and to evaluate the prognostic and predictive significance of these mutations in different site, stage, and treatment subgroups. Patients and Methods A total of 3,583 CRC patients from 25 different research groups in 17 countries were recruited to the study. Patients were divided into three groups according to site of the primary tumor. TP53 mutational analyses spanned exons 4 to 8. Results TP53 mutations were found in 34% of the proximal colon tumors and in 45% of the distal colon and rectal tumors. They were assoc…

MaleOncologyCancer Researchmedicine.medical_specialtyPathologyRECTAL-CARCINOMATumor suppressor geneColorectal cancerLymphovascular invasionMICROSATELLITE INSTABILITYCELL LUNG-CANCERDNA Mutational AnalysisALLELIC LOSSDUKES STAGE-BMOLECULAR MARKERSInternal medicineAntineoplastic Combined Chemotherapy ProtocolsHumansMedicineGenetic Predisposition to DiseaseNeoplasm InvasivenessStage (cooking)neoplasmsSurvival rateAgedNeoplasm Stagingbusiness.industryCOLON-CANCERMicrosatellite instabilityZINC-BINDING DOMAINExonsMiddle AgedWILD-TYPE P53medicine.diseaseAdenocarcinoma MucinousPrimary tumorSurvival RateOncologyChemotherapy AdjuvantMutationAdenocarcinomaFemaleZINC-BINDING DOMAIN; CELL LUNG-CANCER; DUKES STAGE-B; WILD-TYPE P53; GENETIC PATHWAYS; COLON-CANCER; MICROSATELLITE INSTABILITY; MOLECULAR MARKERS; RECTAL-CARCINOMA; ALLELIC LOSSGENETIC PATHWAYSTumor Suppressor Protein p53Colorectal NeoplasmsbusinessFollow-Up Studies
researchProduct