Search results for "mutations"

showing 10 items of 205 documents

HSP110 T17 simplifies and improves the microsatellite instability testing in patients with colorectal cancer

2016

IF 5.65; International audience; Background Every colorectal cancer (CRC) patient should be tested for microsatellite instability (MSI, a marker for defective DNA mismatch repair) as a first screen for Lynch syndrome (LS). In this study, we investigated whether it may be possible to improve the detection of MSI in CRC. We examined whether the HT17 DNA repeat (critical for correct splicing of the chaperone HSP110) might constitute a superior marker for diagnosis of the MSI phenotype in patients with CRC compared with the standard panel of markers (pentaplex).Methods The HT17 polymorphism was analysed in germline DNA from 1037 multi-ethnic individuals. We assessed its sensitivity and specific…

0301 basic medicineOncologymedicine.medical_specialtyGenotypeColorectal cancerPopulationMismatch RepairBiologyGuidelinesBioinformaticsDNA Mismatch RepairColon-Cancer03 medical and health sciences0302 clinical medicineMolecular geneticsInternal medicineDiagnostic-TestsGenotypeGeneticsmedicineBiomarkers TumorHumansChemotherapyHSP110 Heat-Shock Proteinseducation[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenotypingneoplasmsGenetics (clinical)Tumorseducation.field_of_studyPentaplex PcrMicrosatellite instabilityDNAmedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisLynch syndromedigestive system diseases3. Good healthMononucleotide Repeats030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics030220 oncology & carcinogenesisDNA mismatch repairMicrosatellite InstabilityLynch-SyndromeColorectal NeoplasmsMutations
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A narrative review of MET inhibitors in non-small cell lung cancer with MET exon 14 skipping mutations

2021

Treatment of advanced non-small cell lung cancer (NSCLC) has radically improved in the last years due to development and clinical approval of highly effective agents including immune checkpoint inhibitors (ICIs) and oncogene-directed therapies. Molecular profiling of lung cancer samples for activated oncogenes, including epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), c-ros oncogene 1 (ROS1) and BRAF, is routinely performed to select the most appropriate up-front treatment. However, the identification of new therapeutic targets remains a high priority. Recently, MET exon 14 skipping mutations have emerged as novel actionable oncogenic alterations in NSCLC, sensiti…

0301 basic medicineOncologymedicine.medical_specialtybiologybusiness.industryCancernon-small cell lung cancer (NSCLC)medicine.disease03 medical and health sciencesExon030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisInternal medicineROS1biology.proteinMET; MET exon 14 skipping mutations; MET-tyrosine kinase inhibitors (TKIs); Non-small cell lung cancer (NSCLC)MedicineAnaplastic lymphoma kinaseEpidermal growth factor receptorbusinessLung cancerTyrosine kinase
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A systematic variant screening in familial cases of congenital heart defects demonstrates the usefulness of molecular genetics in this field

2016

International audience; The etiology of congenital heart defect (CHD) combines environmental and genetic factors. So far, there were studies reporting on the screening of a single gene on unselected CHD or on familial cases selected for specific CHD types. Our goal was to systematically screen a proband of familial cases of CHD on a set of genetic tests to evaluate the prevalence of disease-causing variant identification. A systematic screening of GATA4, NKX2-5, ZIC3 and Multiplex ligation-dependent probe amplification (MLPA) P311 Kit was setup on the proband of 154 families with at least two cases of non-syndromic CHD. Additionally, ELN screening was performed on families with supravalvula…

0301 basic medicineProbandMaleCardiomyopathy22q11.2Disease030204 cardiovascular system & hematologyBioinformatics0302 clinical medicinede-novoEpidemiology3 large registriesGenetics (clinical)zic3 mutationsGeneticsHigh-Throughput Nucleotide Sequencing3. Good healthPedigreeHomeobox Protein Nkx-2.5malformationsFemaleepidemiologyHeart Defects Congenitalmedicine.medical_specialtyGenetic counselingArticle03 medical and health sciences[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyMolecular geneticsGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationGenetic TestingHomeodomain Proteinsdiseasebusiness.industryvariabilityGenetic Variationmedicine.diseaseGATA4 Transcription Factor030104 developmental biologyMutationEtiologycardiovascular defectsbusinessMultiplex Polymerase Chain Reactioncardiomyopathy[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyTranscription Factors
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The ribosome assembly gene network is controlled by the feedback regulation of transcription elongation

2017

Ribosome assembly requires the concerted expression of hundreds of genes, which are transcribed by all three nuclear RNA polymerases. Transcription elongation involves dynamic interactions between RNA polymerases and chromatin. We performed a synthetic lethal screening in Saccharomyces cerevisiae with a conditional allele of SPT6, which encodes one of the factors that facilitates this process. Some of these synthetic mutants corresponded to factors that facilitate pre-rRNA processing and ribosome biogenesis. We found that the in vivo depletion of one of these factors, Arb1, activated transcription elongation in the set of genes involved directly in ribosome assembly. Under these depletion c…

0301 basic medicineRibosomal ProteinsSaccharomyces cerevisiae ProteinsTranscription Elongation GeneticCèl·lulesÀcids nucleicsGene regulatory networkRibosome biogenesisSaccharomyces cerevisiaeBiologyRibosome assembly03 medical and health sciencesRegulació genèticaGeneticsGene Regulatory NetworksHistone ChaperonesRNA Processing Post-TranscriptionalGeneAdenosine TriphosphatasesFeedback PhysiologicalMessenger RNAOrganelle BiogenesisGene regulation Chromatin and EpigeneticsRNAChromatinCell biology030104 developmental biologyRNA RibosomalMutationATP-Binding Cassette TransportersOrganelle biogenesisTranscriptional Elongation FactorsSynthetic Lethal MutationsTranscriptomeRibosomes
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SPEN haploinsufficiency causes a neurodevelopmental disorder overlapping proximal 1p36 deletion syndrome with an episignature of X chromosomes in fem…

2021

Contains fulltext : 231702.pdf (Publisher’s version ) (Closed access) Deletion 1p36 (del1p36) syndrome is the most common human disorder resulting from a terminal autosomal deletion. This condition is molecularly and clinically heterogeneous. Deletions involving two non-overlapping regions, known as the distal (telomeric) and proximal (centromeric) critical regions, are sufficient to cause the majority of the recurrent clinical features, although with different facial features and dysmorphisms. SPEN encodes a transcriptional repressor commonly deleted in proximal del1p36 syndrome and is located centromeric to the proximal 1p36 critical region. Here, we used clinical data from 34 individuals…

0301 basic medicineSHARPMaleobesitygenotype-phenotype correlationsAutism Spectrum DisorderPROTEINChromosome DisordersHaploinsufficiencyRNA-Binding ProteinPHENOTYPE CORRELATIONS1p36; distal 1p36 deletion syndrome; DNA methylome analysis; episignature; genotype-phenotype correlations; neurodevelopmental disorder; obesity; proximal 1p36 deletion syndrome; SPEN; X chromosome; Adolescent; Autism Spectrum Disorder; Child; Child Preschool; Chromosome Deletion; Chromosome Disorders; Chromosomes Human Pair 1; Chromosomes Human X; DNA Methylation; DNA-Binding Proteins; Epigenesis Genetic; Female; Haploinsufficiency; Humans; Intellectual Disability; Male; Neurodevelopmental Disorders; Phenotype; RNA-Binding Proteins; Young AdultEpigenesis GeneticX chromosome0302 clinical medicineNeurodevelopmental disorderNeurodevelopmental DisorderIntellectual disabilityMOLECULAR CHARACTERIZATIONdistal 1p36 deletion syndromeChildGenetics (clinical)X chromosomeGeneticsXDNA methylome analysiRNA-Binding ProteinsSPLIT-ENDSHypotoniaDNA-Binding ProteinsPhenotypeAutism spectrum disorderChromosomes Human Pair 1Child PreschoolDNA methylome analysisMONOSOMY 1P36Pair 1SPENFemalemedicine.symptomChromosome DeletionHaploinsufficiencyRare cancers Radboud Institute for Health Sciences [Radboudumc 9]HumanAdolescentDNA-Binding ProteinBiologygenotype-phenotype correlationChromosomes03 medical and health sciencesYoung AdultGeneticSDG 3 - Good Health and Well-beingReportIntellectual DisabilityREVEALSGeneticsmedicineHumansEpigeneticsPreschoolChromosomes Human XNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]1p361p36 deletion syndromeIDENTIFICATIONMUTATIONSproximal 1p36 deletion syndromeDNA Methylationmedicine.diseaseneurodevelopmental disorderGENEepisignature030104 developmental biologyChromosome DisorderNeurodevelopmental Disorders030217 neurology & neurosurgeryEpigenesis
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The severe phenotype of Diamond-Blackfan anemia is modulated by heat shock protein 70.

2017

International audience; Diamond-Blackfan anemia (DBA) is a rare congenital bone marrow failure syndrome that exhibits an erythroid-specific phenotype. In at least 70% of cases, DBA is related to a haploinsufficient germ line mutation in a ribosomal protein (RP) gene. Additional cases have been associated with mutations in GATA1. We have previously established that the RPL11+/Mut phenotype is more severe than RPS19+/Mut phenotype because of delayed erythroid differentiation and increased apoptosis of RPL11+/Mut erythroid progenitors. The HSP70 protein is known to protect GATA1, the major erythroid transcription factor, from caspase-3 mediated cleavage during normal erythroid differentiation.…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesIdentificationApoptosis-Inducing FactorGata1 MutationsInhibits ApoptosisBiologyHsp7003 medical and health sciencesGermline mutationRed Cells Iron and Erythropoiesishemic and lymphatic diseasesmedicine[ SDV.MHEP.HEM ] Life Sciences [q-bio]/Human health and pathology/HematologyNuclear ImportErythropoiesisDiamond–Blackfan anemiaHuman ErythroblastsBone marrow failure[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyGATA1Hematologymedicine.diseasePhenotypeMolecular biology3. Good healthHsp70030104 developmental biologyRibosomal-ProteinsProtein Gene DeletionsErythropoiesisHaploinsufficiencyBlood advances
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WES/WGS Reporting of Mutations from Cardiovascular "Actionable" Genes in Clinical Practice: A Key Role for UMD Knowledgebases in the Era of Big Datab…

2016

International audience; High-throughput next-generation sequencing such as whole-exome and whole-genome sequencing are being rapidly integrated into clinical practice. The use of these techniques leads to the identification of secondary variants for which decisions about the reporting or not to the patient need to be made. The American College of Medical Genetics and Genomics recently published recommendations for the reporting of these variants in clinical practice for 56 "actionable" genes. Among these, seven are involved in Marfan Syndrome And Related Disorders (MSARD) resulting from mutations of the FBN1, TGFBR1 and 2, ACTA2, SMAD3, MYH11 and MYLK genes. Here, we show that mutations col…

0301 basic medicinemedicine.medical_specialtyKnowledge BasesGenomicsmarfan-syndrome[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics030105 genetics & heredityBiologycomputer.software_genreGenomeExAC03 medical and health sciencesAnnotationincidental findingsGeneticsmedicineHumanspathogenicityGenetic Predisposition to Diseasetgfbr2ExomegenomeESPGenetics (clinical)Exome sequencing[INFO.INFO-BI] Computer Science [cs]/Bioinformatics [q-bio.QM]variantsDatabasethoracic aortic-aneurysmsGenome HumanHigh-Throughput Nucleotide SequencingMYLKGenomicspredictionmutations3. Good healthMarfan syndrome030104 developmental biologydissection[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsCardiovascular DiseasesMutationMedical geneticsIdentification (biology)LSDB[INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM]computerexome
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STABILITY OF A STOCHASTICALLY PERTURBED MODEL OF INTRACELLULAR SINGLE-STRANDED RNA VIRUS REPLICATION

2019

Compared to the replication of double-stranded RNA and DNA viruses, the replication of single-stranded viruses requires the production of a number of intermediate strands that serve as templates for the synthesis of genomic-sense strands. Two theoretical extreme mechanisms for replication for such single-stranded viruses have been proposed; one extreme being represented by the so-called linear stamping machine and the opposite extreme by the exponential growth. Of course, real systems are more complex and examples have been described in which a combination of such extreme mechanisms can also occur: a fraction of the produced progeny resulting from a stamping-machine type of replication that…

92D30 (primary) 34D20 60H10 (secondary)0209 industrial biotechnologyVirus dynamicsDynamical Systems (math.DS)02 engineering and technology03 medical and health scienceschemistry.chemical_compoundMathematical model020901 industrial engineering & automationReplication (statistics)Viral replicationFOS: MathematicsMathematics - Dynamical SystemsViral evolution030304 developmental biologySingle-Stranded RNA51ssRNA virusLyapunov function0303 health sciencesViral mutationsLyapunov methodEcologyApplied MathematicsRNAGeneral MedicineAgricultural and Biological Sciences (miscellaneous)Cell biologyStochastic modelViral replicationchemistryViral evolutionStabilityIntracellularDNAJournal of Biological Systems
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SARS-CoV-2 and its impact on the cardiovascular and digestive systems – The interplay between new virus variants and human cells

2023

Since infection with the novel coronavirus SARS-CoV-2 first emerged in Wuhan, China, in December 2019,the world has been battling the pandemic COVID-19. Patients of all ages and genders are now becoming infected with the new coronavirus variant (Omicron) worldwide, and its subvariants continue to pose a threat to health and life. This article provides a literature review of cardiovascular and gastrointestinal complications resulting from SARS-CoV-2 infection. COVID-19 primarily caused respiratory symptoms, but complications can affect many vital organs. SARS-CoV-2 binds to a human cell receptor (angiotensin-converting enzyme 2 – ACE2) that is predominantly expressed primarily in the heart a…

ACE2 receptor; Cardiovascular and digestive systems; Mutations; Omicron; SARS-CoV-2Structural BiologyGeneticsBiophysicsBiochemistryComputer Science ApplicationsBiotechnologyComputational and Structural Biotechnology Journal
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CLINICAL CHARACTERISTICS AND PLASMA LIPIDS IN SUBJECTS WITH FAMILIAL COMBINED HYPOLIPIDEMIA: A POOLED ANALYSIS

2013

Background. Angiopoietin-like 3 (ANGPTL3) regulates lipoprotein metabolism by modulating extracellular lipases. Loss-of function mutations in ANGPTL3 gene cause familial combined hypolipidemia (FHBL2). The mode of inheritance and hepatic and vascular consequences of FHBL2 have not been fully elucidated. To get further insights on these aspects, we re-evaluated the clinical and the biochemical characteristics of all reported cases of FHBL2. Methods and Results. One hundred fteen FHBL2 individuals carrying 13 different mutations in the ANGPTL3 gene (14 homozygotes, 8 compound heterozygotes and 93 heterozygotes) and 402 controls were considered. Carriers of 2 mutant alleles had undetectable pl…

ANGPTL3 mutations; angiopoietin-like 3; cardiovascular disease; diabetes mellitus; fatty liverSettore MED/09 - Medicina InternaCompound heterozygosityBiochemistryCohort StudiesHypobetalipoproteinemiasEndocrinologyANGPTL3cardiovascular diseaseGenotypeChildLipoproteinclinical characteristicsAged 80 and overbiologydiabetes mellituFatty liverHomozygoteLipoprotein(a)Middle AgedANGPTL3 mutationLipidsCardiovascular Diseasesdiabetes mellitusANGPTL3 Familial combined hypolipidemia LipoproteinAdultmedicine.medical_specialtyHeterozygoteANGPTL3; Familial combined hypolipidemia; clinical characteristicsAdolescentEvinacumabQD415-436Young AdultDiabetes mellitusInternal medicinemedicineHumansANGPTL3 mutationsAlleleFamilial combined hypolipidemiaAgedAngiopoietin-Like Protein 3fatty liverangiopoietin-like 3Cell Biologymedicine.diseaseEndocrinologyAngiopoietin-like ProteinsGene Expression RegulationMutationbiology.proteinPatient-Oriented and Epidemiological ResearchAngiopoietinsLipoproteinLipoprotein(a)
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