Search results for "Mutational analysis"

showing 10 items of 245 documents

Novel P53 mutations detected by FAMA in colorectal cancers

2006

Background The aim of the study was to identify p53 gene mutations by FAMA (fluorescence-assisted mismatch analysis) in colorectal cancers. Patients and methods Analytical scanning of the p53 gene (exons 5–9) was performed in colon cancer samples from 44 consecutive patients by FAMA. FAMA is a semiautomatic scanning approach based on the chemical cleavage of the mismatch in fluorescently labeled heteroduplex DNA, obtained from the combination of a normal and a mutated allele. FAMA has already shown optimal levels of diagnostic accuracy and sensitivity in detecting gene mutations (nucleotide substitutions, insertions/deletions) both at the germline and somatic level. The peculiar feature of …

Oncologymedicine.medical_specialtyMutantDNA Mutational AnalysisMutation MissenseGene mutationmedicine.disease_causeExonInternal medicinemedicineMissense mutationHumansKey words: colon cancer p53 mutations FAMAAlleleGeneMutationbusiness.industryHematologyDNA NeoplasmExonsGenes p53Molecular biologyOncologybusinessColorectal NeoplasmsHeteroduplex
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Functional categories of TP53 mutation in colorectal cancer: results of an International Collaborative Study.

2006

Item does not contain fulltext BACKGROUND: Loss of TP53 function through gene mutation is a critical event in the development and progression of many tumour types including colorectal cancer (CRC). In vitro studies have found considerable heterogeneity amongst different TP53 mutants in terms of their transactivating abilities. The aim of this work was to evaluate whether TP53 mutations classified as functionally inactive (< or=20% of wildtype transactivation ability) had different prognostic and predictive values in CRC compared with mutations that retained significant activity. MATERIALS AND METHODS: TP53 mutations within a large, international database of CRC (n = 3583) were classified ac…

Oncologyp53MaleNutrition and Diseasebinding domainsLymphovascular invasionColorectal cancerDNA Mutational AnalysisAetiology screening and detection [ONCOL 5]Gene mutationmedicine.disease_causeTransactivationVoeding en ZiekteAntineoplastic Combined Chemotherapy ProtocolsDeterminants in Health and Disease [EBP 1]transcriptional activityMutationHematologyExonsMiddle AgedSurvival RateOncologyAdenocarcinomaFemaleColorectal Neoplasmsmedicine.medical_specialtyAdenocarcinomachemotherapy colorectal cancer mutation prognosis TP53 transactivational abilityMolecular epidemiology [NCEBP 1]Breast cancerTranslational research [ONCOL 3]Interventional oncology [UMCN 1.5]Internal medicinemedicineHumansNeoplasm InvasivenessSurvival rateneoplasmsbreast-cancerVLAGAgedNeoplasm StagingHereditary cancer and cancer-related syndromes [ONCOL 1]business.industryInternational Agenciesmedicine.diseaseImmunologyMutationTumor Suppressor Protein p53businessFollow-Up Studies
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The cytoplasmic PASC domain of the sensor kinase DcuS of Escherichia coli : role in signal transduction, dimer formation, and DctA interaction

2013

The cytoplasmic PAS(C) domain of the fumarate responsive sensor kinase DcuS of Escherichia coli links the transmembrane to the kinase domain. PAS(C) is also required for interaction with the transporter DctA serving as a cosensor of DcuS. Earlier studies suggested that PAS(C) functions as a hinge and transmits the signal to the kinase. Reorganizing the PAS(C) dimer interaction and, independently, removal of DctA, converts DcuS to the constitutive ON state (active without fumarate stimulation). ON mutants were categorized with respect to these two biophysical interactions and the functional state of DcuS: type I-ON mutations grossly reorganize the homodimer, and decrease interaction with Dct…

PAS domainDicarboxylic Acid TransportersModels MolecularfumarateProtein ConformationEscherichia coli ProteinsDNA Mutational AnalysisDctAModels Biological570 Life sciencessignal transduction.Escherichia coliProtein Interaction Domains and MotifsProtein MultimerizationDcuS sensor kinaseProtein KinasesOriginal ResearchSignal Transduction570 Biowissenschaften
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Identification of novel mutations in the ABCA12 gene, c.1857delA and c.5653–5655delTAT, causing harlequin ichthyosis

2013

Abstract Harlequin ichthyosis (HI) is a severe autosomal recessive developmental disorder of the skin that is frequently but not always fatal in the first few days of life. In HI, mutations in both ABCA12 gene alleles must have a severe impact on protein function and most mutations are truncating. The presence of at least one nontruncating mutation (predicting a residual protein function) usually causes a less severe congenital ichthyosis (lamellar ichthyosis or congenital ichthyosiform erythroderma). Here we report on a girl with severe HI diagnosed by prenatal ultrasound at 33 5/7 week gestation. Ultrasound findings included ectropion, eclabium, deformed nose, hands and feet, joint contra…

Pathologymedicine.medical_specialtyCongenital ichthyosiform erythrodermaDNA Mutational AnalysisBiologyModels BiologicalPolymorphism Single NucleotideUltrasonography PrenatalExonFatal OutcomePregnancyCongenital ichthyosisGeneticsmedicineHumansABCA12Sequence DeletionGeneticsInfant NewbornEctropionGeneral MedicineLamellar ichthyosisHarlequin Ichthyosismedicine.diseaseEclabiumbiology.proteinATP-Binding Cassette TransportersFemalemedicine.symptomIchthyosis LamellarGene
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Acquired IFNγ resistance impairs anti-tumor immunity and gives rise to T-cell-resistant melanoma lesions

2016

Melanoma treatment has been revolutionized by antibody-based immunotherapies. IFNγ secretion by CD8+ T cells is critical for therapy efficacy having anti-proliferative and pro-apoptotic effects on tumour cells. Our study demonstrates a genetic evolution of IFNγ resistance in different melanoma patient models. Chromosomal alterations and subsequent inactivating mutations in genes of the IFNγ signalling cascade, most often JAK1 or JAK2, protect melanoma cells from anti-tumour IFNγ activity. JAK1/2 mutants further evolve into T-cell-resistant HLA class I-negative lesions with genes involved in antigen presentation silenced and no longer inducible by IFNγ. Allelic JAK1/2 losses predisposing to …

Patient-Specific Modeling0301 basic medicineSkin NeoplasmsBiopsyT-LymphocytesDNA Mutational AnalysisDatasets as TopicGeneral Physics and AstronomyAntineoplastic Agents ImmunologicalMutation RatePrecision MedicineMelanomaSkinAntigen PresentationMultidisciplinarybiologyMelanomaQfood and beverages3. Good healthTreatment Outcomemedicine.anatomical_structureImmunotherapyAntibodySignal TransductionScienceT cellAntigen presentationHuman leukocyte antigenArticleGeneral Biochemistry Genetics and Molecular BiologyInterferon-gamma03 medical and health sciencesAntigenAntigens NeoplasmCell Line TumormedicineHumansWhole Genome SequencingHistocompatibility Antigens Class IJanus Kinase 1General ChemistryJanus Kinase 2medicine.disease030104 developmental biologyImmunoeditingDrug Resistance NeoplasmMutationImmunologybiology.proteinTumor EscapeCD8Nature Communications
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Late infantile neuronal ceroid lipofuscinosis: Quantitative description of the clinical course in patients withCLN2 mutations

2002

We examined 26 individuals with clinical and electron microscopic signs of late infantile neuronal ceroid lipofuscinosis (LINCL). In 22 cases, we found both pathogenic alleles. Sixteen patients exclusively carried either one or a combination of the two common mutations R208X and IVS5-1G > C. In the remaining cases, four missense mutations could be detected, of which R127Q, N286S, and T353P represent novel, previously not described alleles. A clinical performance score was developed by rating motor, visual, and verbal functions and the incidence of cerebral seizures in 3-month intervals during the course of the disease. A Total Disability Score was derived by summing up the single scores for…

Pediatricsmedicine.medical_specialtyDNA Mutational AnalysisCerliponase alfaDiseaseNeurological disorderAminopeptidasesSeverity of Illness IndexNeuronal Ceroid-LipofuscinosesSeizuresEndopeptidasesSeverity of illnessmedicineMissense mutationDipeptidyl-Peptidases and Tripeptidyl-PeptidasesVision OcularGenetics (clinical)Tripeptidyl-Peptidase 1business.industryDNAmedicine.diseaseTripeptidyl peptidase INeuronal Ceroid Lipofuscinosis Type 2MutationNeuronal ceroid lipofuscinosisSerine ProteasesbusinessPsychomotor PerformancePeptide HydrolasesAmerican Journal of Medical Genetics
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Molecular Basis Of Mild Hyperphenylalaninaemia In Turkey

2000

Öz bulunamadı.

Phenylalanine hydroxylaseGenotypeTurkeyPhenylalanineDNA Mutational AnalysisMEDLINEHyperphenylalaninemiaGene FrequencyPhenylketonuriasGenotypeDNA Mutational AnalysisGeneticsmedicineHumansChildAllele frequencyGenetics (clinical)Geneticsbiologybusiness.industryInfantPhenylalanine Hydroxylasemedicine.diseasePhenotypeHuman geneticsPhenotypeChild Preschoolbiology.proteinbusiness
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Exon deletions of the phenylalanine hydroxylase gene in Italian hyperphenylalaninemics

2009

A consistent finding of many studies describing the spectrum of mutant phenylalanine hydroxylase (PAH) alleles underlying hyperphenylalaninemia is the impossibility of achieving a 100% mutation ascertainment rate using conventional gene-scanning methods. These methods include denaturing gradient gel electrophoresis (DGGE), denaturing high performance liquid chromatography (DHPLC), and direct sequencing. In recent years, it has been shown that a significant proportion of undetermined alleles consist of large deletions overlapping one or more exons. These deletions have been difficult to detect in compound heterozygotes using gene-scanning methods due to a masking effect of the non-deleted al…

Phenylalanine hydroxylasePhenylketonuriasDNA Mutational AnalysisClinical Biochemistrygene dosageCompound heterozygosityBiochemistryGene dosageDenaturing high performance liquid chromatographyExonHyperphenylalaninemiaGene FrequencyPhenylketonuriasmedicineHumansMultiplex ligation-dependent probe amplificationMolecular BiologySequence DeletionGeneticsphenylalanine hydroxylase; phenylketonurias; ligase chain reaction; gene deletion; gene dosagebiologygene deletionReverse Transcriptase Polymerase Chain ReactionPhenylalanine HydroxylaseExonsmedicine.diseaseMolecular biologyItalyDisease Progressionbiology.proteinligase chain reactionMolecular MedicineOriginal ArticleExperimental and Molecular Medicine
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Single amino acids in the lumenal loop domain influence the stability of the major light-harvesting chlorophyll a/b complex.

2004

The major light-harvesting complex of photosystem II (LHCIIb) is one of the most abundant integral membrane proteins. It greatly enhances the efficiency of photosynthesis in green plants by binding a large number of accessory pigments that absorb light energy and conduct it toward the photosynthetic reaction centers. Most of these pigments are associated with the three transmembrane and one amphiphilic alpha helices of the protein. Less is known about the significance of the loop domains connecting the alpha helices for pigment binding. Therefore, we randomly exchanged single amino acids in the lumenal loop domain of the bacterially expressed apoprotein Lhcb1 and then reconstituted the muta…

Photosynthetic reaction centreProtein FoldingPhotosystem IIPigment bindingDNA Mutational AnalysisLight-Harvesting Protein ComplexesPeasPhotosystem II Protein ComplexBiologyBiochemistryTransmembrane proteinProtein Structure SecondaryProtein Structure TertiaryB vitaminsBiochemistryAmino Acid SubstitutionMutant proteinMutagenesis Site-DirectedPoint MutationAmino AcidsIntegral membrane proteinAccessory pigmentGene LibraryPlant ProteinsBiochemistry
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Homozygous familial hypobetalipoproteinemia: two novel mutations in the splicing sites of apolipoprotein B gene and review of the literature.

2015

Objective: Familial hypobetalipoproteinemia (FHBL) is autosomal codominant disorder of lipoprotein metabolism characterized by low plasma levels of total cholesterol (TC), low-density lipoproteincholesterol (LDL-C) and apolipoprotein B (apoB) below the 5 th percentile of the distribution in the population. Patients with the clinical diagnosis of homozygous FHBL (Ho-FHBL) are extremely rare and few patients have been characterized at the molecular level. Here we report the medical history and the molecular characterization of one paediatric patient with clinical features of Ho-FHBL. Methods: A one month old infant with failure to thrive, severe hypocholesterolemia and acanthocytosis was clin…

ProbandAdultMaleAcanthocytosiSettore MED/09 - Medicina InternaApolipoprotein BPopulationDNA Mutational AnalysisBiologyHypobetalipoproteinemiasExonHumanseducationGeneGeneticseducation.field_of_studyHomozygoteIntronInfantCholesterol LDLAbetalipoproteinemiaIntronsAlternative SplicingHomozygous familial hypobetalipoproteinemiaCholesterolRNA splicingApolipoprotein B-100Mutationbiology.proteinlipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineApolipoprotein BMinigeneAtherosclerosis
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