Search results for "missense"

showing 10 items of 303 documents

Functional characterization of protein variants of the human multidrug transporter ABCC2 by a novel targeted expression system in fibrosarcoma cells

2012

The multidrug resistance-associated protein 2 (MRP2/ABCC2) is involved in the efflux of endogenous and xenobiotic substrates, including several anticancer and antiviral drugs. The functional consequences of ABCC2 protein variants remain inconsistent, which may be due to shortcomings of the in vitro assays used. To study systematically the functional consequences of nonsynonymous ABCC2 variants, we used a novel “Screen and Insert” (ScIn) technology to achieve stable and highly reproducible expression of 13 ABCC2 variants in HT1080 cells. Western blotting revealed lower (30–65%) ABCC2 expression for D333G, R1174H, and R1181L as compared with wild type (WT; 100%), whereas the linked variant V1…

Nonsynonymous substitutionFibrosarcomaMutation MissenseATP-binding cassette transporterBiologyCell Line TumorGeneticsHumansGenetics (clinical)GeneticsAsianMultidrug resistance-associated protein 2Endoplasmic reticulumChloraminesWild typeGenetic VariationTetracyclineMolecular biologyMultidrug Resistance-Associated Protein 2Recombinant ProteinsBlack or African AmericanBlotHEK293 CellsGene Expression RegulationHaplotypesHT1080EffluxMultidrug Resistance-Associated ProteinsHuman Mutation
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Clinical, pathologic, and genetic features of massive soft tissue neurofibromas in a Sicilian patient

2008

Abstract CONTEXT: Lipase maturation factor 1 (LMF1) gene is a novel candidate gene in severe hypertriglyceridemia. Lmf1 is involved in the maturation of lipoprotein lipase (LPL) and hepatic lipase in endoplasmic reticulum. To date only one patient with severe hypertriglyceridemia and related disorders was found to be homozygous for a nonsense mutation in LMF1 gene (Y439X). OBJECTIVE: The objective of the study was to investigate LMF1 gene in hypertriglyceridemic patients in whom mutations in LPL, APOC2, and APOA5 genes had been excluded. RESULTS: The resequencing of LMF1 gene led to the discovery of a novel homozygous nonsense mutation in one patient with severe hypertriglyceridemia and rec…

Nonsynonymous substitutionMalecongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyHeterozygoteNeurofibromatosis 1BiopsyDNA Mutational AnalysisMutation MissenseSoft Tissue NeoplasmsDermatologymassive soft tissue neurofibromas NeurofibromatosisBiologymedicine.disease_causeFrameshift mutationExonGenes Neurofibromatosis 1medicineSettore MED/35 - Malattie Cutanee E VenereeMissense mutationHumansNeurofibromatosisFrameshift MutationGeneSicilyGeneticsMutationHeterozygote advantageGeneral MedicineExonsMiddle Agedmedicine.diseasenervous system diseasesGene Expression Regulation NeoplasticButtocks
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germline mutations in women with familial breast cancer and a relative with haematological malignancy

2009

Biallelic inactivation of the ATM gene causes ataxia-telangiectasia (A-T), a complex neurological disease associated with a high risk of leukaemias and lymphomas. Mothers of A-T children, obligate ATM heterozygote mutation carriers, have a breast cancer (BC) relative risk of about 3. The frequency of ATM carriers in BC women with a BC family history has been estimated to be 2.70%. To further our clinical understanding of familial BC and examine whether haematological malignancies are predictive of ATM germline mutation, we estimated the frequency of heterozygote mutation carriers in a series of 122 BC women with a family history of both BC and haematological malignancy and without BRCA1/2 m…

OncologyCancer ResearchLymphomaDNA Mutational AnalysisCell Cycle ProteinsAtaxia Telangiectasia Mutated Proteins0302 clinical medicineBreast cancerGene FrequencyRisk FactorsMissense mutationGenetics0303 health scienceseducation.field_of_studyLeukemiafamilial breast cancerAtaxia–telangiectasiaPedigreeDNA-Binding ProteinsOncology030220 oncology & carcinogenesisMutation (genetic algorithm)EMMAFemaleAdultHeterozygotemedicine.medical_specialtyMolecular Sequence DataPopulationBreast NeoplasmsProtein Serine-Threonine KinasesBiologyRisk Assessment03 medical and health sciencesGermline mutationBreast cancerPredictive Value of TestsInternal medicinemedicineHumansGenetic Predisposition to DiseaseGenetic TestingeducationAllele frequencyGerm-Line Mutation030304 developmental biologyBase SequenceTumor Suppressor ProteinsHeterozygote advantagemedicine.diseaseAtaxia-telangiectasia
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CASP8 SNP D302H (rs1045485) is associated with worse survival in MYCN-amplified neuroblastoma patients

2014

Background Neuroblastoma is a pediatric cancer that exhibits a wide clinical spectrum ranging from spontaneous regression in low-risk patients to fatal disease in high-risk patients. The identification of single nucleotide polymorphisms (SNPs) may help explain the heterogeneity of neuroblastoma and assist in identifying patients at higher risk for poor survival. SNPs in the TP53 pathway are of special importance, as several studies have reported associations between TP53 pathway SNPs and cancer. Of note, less than 2% of neuroblastoma tumors have a TP53 mutation at diagnosis. Patients and Methods We selected 21 of the most frequently studied SNPs in the TP53 pathway and evaluated their assoc…

OncologyGenotyping TechniquesMedizinlcsh:MedicineGenome-wide association studyPROGRESSIONSUSCEPTIBILITYBioinformaticsNeuroblastomaCHEMOSENSITIVITYMedicine and Health SciencesMissense mutationlcsh:ScienceOncogene ProteinsCaspase 8N-Myc Proto-Oncogene ProteinMultidisciplinaryCELL-LINENuclear ProteinsCANCERAPOPTOSISGENOTYPEGene Expression Regulation NeoplasticResearch Articlemedicine.medical_specialtySingle-nucleotide polymorphismBiologyN-Myc Proto-Oncogene ProteinPolymorphism Single NucleotideDisease-Free SurvivalMDM2 SNP309Molecular GeneticsNeuroblastomaInternal medicineCASPASE-8medicineGeneticsCancer GeneticsSNPHumansneoplasmsNeoplasm StagingClinical GeneticsP53lcsh:RGene AmplificationCancerInfantBiology and Life Sciencesmedicine.diseasePediatric cancerGeriatricsGenetics of Diseaselcsh:Q
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Germline loss-of-function variants in the BARD1 gene are associated with early-onset familial breast cancer but not ovarian cancer

2019

Background The role of the BARD1 gene in breast cancer (BC) and ovarian cancer (OC) predisposition remains elusive, as published case-control investigations have revealed controversial results. We aimed to assess the role of deleterious BARD1 germline variants in BC/OC predisposition in a sample of 4920 BRCA1/2-negative female BC/OC index patients of the German Consortium for Hereditary Breast and Ovarian Cancer (GC-HBOC). Methods A total of 4469 female index patients with BC, 451 index patients with OC, and 2767 geographically matched female control individuals were screened for loss-of-function (LoF) mutations and potentially damaging rare missense variants in BARD1. All patients met the …

OncologyGermline0302 clinical medicineLoss of Function MutationSurgical oncologyOdds RatioPrevalenceMissense mutation030212 general & internal medicineAge of Onset10. No inequalityExomeEarly onset breast cancerAged 80 and overOvarian NeoplasmsBARD1 GeneHigh-Throughput Nucleotide SequencingMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens3. Good health030220 oncology & carcinogenesisFemaleTechnology PlatformsResearch ArticleAdultmedicine.medical_specialtyAdolescentUbiquitin-Protein Ligases610Breast Neoplasmslcsh:RC254-282Young Adult03 medical and health sciencesGermline mutationBreast cancerOvarian cancerInternal medicinemedicineBARD1HumansGenetic Predisposition to DiseaseGermline mutationsGenetic Association StudiesGerm-Line MutationAgedbusiness.industryTumor Suppressor ProteinsOdds ratiomedicine.diseaseConfidence intervalBARD1; Early onset breast cancer; Germline mutations; Ovarian cancerOvarian cancerbusiness
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Clinical Impact of GATA2 Mutations in Acute Myeloid Leukemia Patients Harboring CEBPA Mutations: A Study of the AML Study Group (AMLSG)

2013

Abstract Background Based on their association with certain biological and clinical features as well as their prognostic significance, mutations in the CCAAT/enhancer-binding protein-alpha (CEBPA) gene have been included as a provisional entity into the 2008 World Health Organization (WHO) classification of myeloid neoplasms. CEBPA mutations (CEBPAmut) are mainly found in acute myeloid leukemia (AML) with normal cytogenetics, and approximately 60% of the mutated patients (pts) carry biallelic mutations. Several studies showed that in particular pts with double mutant CEBPA (CEBPAdm) have a favorable outcome compared to all others. Recently, mutations in the transcription factor GATA2 were i…

OncologyNPM1medicine.medical_specialtyMyeloidbusiness.industryImmunologyMyeloid leukemiaContext (language use)Cell BiologyHematologyBiochemistryFrameshift mutationmedicine.anatomical_structureInternal medicineCEBPAGenotypemedicineMissense mutationbusinessBlood
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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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C21orf2 is mutated in recessive early-onset retinal dystrophy with macular staphyloma and encodes a protein that localises to the photoreceptor prima…

2015

Background/aim We have noted a phenotype of early-onset retinal dystrophy with macular staphyloma but without high myopia. The aim of this study is to report the underlying genetic mutations and the subcellular localisation of the gene product in the retina. Methods Retrospective case series (2012–2015); immunohistochemical analyses of mammalian retina for in situ protein localisation. Results All three probands were first noted to have decreased vision at 3–6 years old which worsened over time. At ages 39, 37 and 12 years old, all had similar retinal findings: dystrophic changes (retinal pigment epithelium mottling, vessel narrowing), macular staphyloma (despite only mild myopia or high hy…

Pathologygenetic structuresSus scrofaPolymerase Chain ReactionPhotoreceptor cellchemistry.chemical_compoundConsanguinityMiceChildFrameshift MutationGeneticsmedicine.diagnostic_testMagnetic Resonance ImagingSensory SystemsTissue DonorsPedigreemedicine.anatomical_structureFemaleRetinal DystrophiesTomography Optical CoherenceDilatation PathologicAdultmedicine.medical_specialtyBlotting WesternMolecular Sequence DataMutation MissenseGenes RecessiveBiologyRetinaCellular and Molecular NeuroscienceRetinal DystrophiesmedicineElectroretinographyAnimalsHumansAmino Acid SequencePhotoreceptor Connecting CiliumRetrospective StudiesRetinaRetinal pigment epitheliumDystrophyProteinsRetinalmedicine.diseaseeye diseasesOphthalmologyCiliopathyCytoskeletal Proteinschemistrysense organsElectroretinographyThe British journal of ophthalmology
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Novel alpha-galactosidase A mutation in a female with recurrent strokes.

2012

Abstract Anderson–Fabry disease (AFD) is an X-linked inborn error of glycosphingolipid catabolism resulting from the deficient activity of the lysosomal exoglycohydrolase, a-galactosidase A. The complete genomic and cDNA sequences of the human alpha-galactosidase A gene have been determined and to date, several disease-causing alpha-galactosidase A mutations have been identified, including missense mutations, small deletions/insertions, splice mutations, and large gene rearrangements We report a case of a 56-year-old woman with recurrent cryptogenic strokes. Ophthalmological examination revealed whorled opacities of the cornea (cornea verticillata) and dilated tortuous conjunctival vessels.…

Pathologymedicine.medical_specialtyHeterozygoteClinical BiochemistryMolecular Sequence DataMutation MissenseBiologymedicine.disease_causeExonRecurrencemedicineMissense mutationHumansCornea verticillataAmino Acid SequenceGeneMutationBase SequencePoint mutationGeneral MedicineSequence Analysis DNAMiddle Agedmedicine.diseaseFabry diseaseMolecular biologyAngiokeratomaPedigreeStrokealpha-GalactosidaseFabry DiseaseFemalemedicine.symptomClinical biochemistry
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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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