Search results for "Genetic Mutation"

showing 10 items of 14 documents

Epigenetic and Genetic Contributions to Adaptation in Chlamydomonas

2017

Epigenetic modifications, such as DNA methylation or histone modifications, can be transmitted between cellular or organismal generations. However, there are no experiments measuring their role in adaptation, so here we use experimental evolution to investigate how epigenetic variation can contribute to adaptation. We manipulated DNA methylation and histone acetylation in the unicellular green alga Chlamydomonas reinhardtii both genetically and chemically to change the amount of epigenetic variation generated or transmitted in adapting populations in three different environments (salt stress, phosphate starvation, and high CO2) for two hundred asexual generations. We find that reducing the …

0106 biological sciences0301 basic medicinehiilidioksidiEpigenomicsAdaptation Biological01 natural sciencestolerance (physical)Epigenesis GeneticEpigenomicssietokyky2. Zero hungerGeneticsExperimental evolutionepigeneettinen periytyminenSalt Tolerancegreen algaeAdaptation PhysiologicalHistoneDNA methylationepigenetic inheritancephosphate starvationBiologyEnvironment010603 evolutionary biologysuolapitoisuus03 medical and health sciencesviherlevätGenetic variationGeneticsEpigeneticssalt contentexperimental evolutionravinnepitoisuusMolecular BiologyGeneEcology Evolution Behavior and Systematicssalt tolerancefosfaatitta1183ChlamydomonasGenetic Variationadaptive walkcarbon dioxideDNA Methylation030104 developmental biologyepigenetic mutationMutationbiology.proteinta1181methylationAdaptationDirected Molecular EvolutionChlamydomonas reinhardtii
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Apert Syndrome With FGFR2 758 C > G Mutation: A Chinese Case Report

2018

Background: Apert syndrome is considered as one of the most common craniosynostosis syndromes with a prevalence of 1 in 65,000 individuals, and has a close relationship with point mutations in FGFR2 gene.Case report: Here, we described a Apert syndrome case, who was referred to genetic consultation in our hospital with the symptom of craniosynostosis and syndactyly of the hands and feet. Craniosynostosis, midfacial retrusion, steep wide forehead, larger head circumference, marked depression of the nasal bridge, short and wide nose and proptosis could be found obviously, apart from these, ears were mildly low compared with normal children and there was no cleft lip and palate. Mutation was i…

0301 basic medicinemusculoskeletal diseasesPediatricsmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNasal bridgelcsh:QH426-470Case ReportApert syndromeCraniosynostosis03 medical and health sciencesExonsymbols.namesake0302 clinical medicineGeneticsmedicineSyndactylyGenetics (clinical)NoseSanger sequencingbusiness.industryPoint mutationmedicine.diseaseexons sequencingcraniosynostosislcsh:Genetics030104 developmental biologymedicine.anatomical_structureFGFR2genetic mutationsymbolsMolecular Medicinebusiness030217 neurology & neurosurgeryApert syndromeFrontiers in Genetics
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Blastic plasmacytoid dendritic cell neoplasm: genomics mark epigenetic dysregulation as a primary therapeutic target

2018

Blastic Plasmacytoid Dendritic Cell Neoplasm is a rare and aggressive hematological malignancy currently lacking an effective therapy. To possibly identify genetic alterations useful for a new treatment design, we analyzed by whole-exome sequencing fourteen Blastic Plasmacytoid Dendritic Cell Neoplasm patients and the patient-derived CAL-1 cell line. The functional enrichment analysis of mutational data reported the epigenetic regulatory program as the most significantly undermined (P<.0001). In particular, twenty-five epigenetic-modifiers were found mutated (e.g., ASXL1, TET2, SUZ12, ARID1A, PHF2, CHD8); ASXL1 was the most frequently affected (28.6% of cases). To evaluate the impact of …

Acute Myeloid LeukemiaBlastic plasmacytoid dendritic cell neoplasm epigenetic mutationsSkin NeoplasmsAzacitidineDecitabinePlasmacytoid dendritic cellGene mutationBiologyDecitabineBPDCNArticleEpigenesis Genetic03 medical and health sciences0302 clinical medicineHistone methylation5’-Azacytidine; Acute Myeloid Leukemia; BPDCN; Decitabine; WESmedicineHumansEpigeneticsExome sequencingRegulation of gene expressionMyeloproliferative DisordersDendritic CellsGenomicsHematology5 -AzacytidineMyeloid Neoplasms5’-AzacytidineCancer researchWES030215 immunologymedicine.drugHaematologica
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Molecular characterization of congenital myasthenic syndromes in Spain.

2017

Congenital myasthenic syndromes (CMS) are a heterogeneous group of genetic disorders, all of which impair neuromuscular transmission. Epidemiological data and frequencies of gene mutations are scarce in the literature. Here we describe the molecular genetic and clinical findings of sixty-four genetically confirmed CMS patients from Spain. Thirty-six mutations in the CHRNE, RAPSN, COLQ, GFPT1, DOK7, CHRNG, GMPPB, CHAT, CHRNA1, and CHRNB1 genes were identified in our patients, with five of them not reported so far.. These data provide an overview on the relative frequencies of the different CMS subtypes in a large Spanish population. CHRNE mutations are the most common cause of CMS in Spain, …

AdultMale0301 basic medicineSlow-channel syndromeAdolescentNeuromuscular transmissionGMPPBGene mutationCOLQCongenital myasthenic syndromeYoung Adult03 medical and health sciences0302 clinical medicineDOK7COLQmedicineHumansCHRNECHRNEGeneGenetics (clinical)health care economics and organizationsMyasthenic Syndromes CongenitalGeneticsbiologyRAPSNMiddle AgedCongenital myasthenic syndromemedicine.diseasePhenotype3. Good healthGenetic mutationsRAPSN030104 developmental biologyGFPT1NeurologySpainPediatrics Perinatology and Child Healthbiology.proteinFemaleNeurology (clinical)030217 neurology & neurosurgery
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On the power and the systematic biases of the detection of chromosomal inversions by paired-end genome sequencing

2013

One of the most used techniques to study structural variation at a genome level is paired-end mapping (PEM). PEM has the advantage of being able to detect balanced events, such as inversions and translocations. However, inversions are still quite difficult to predict reliably, especially from high-throughput sequencing data. We simulated realistic PEM experiments with different combinations of read and library fragment lengths, including sequencing errors and meaningful base-qualities, to quantify and track down the origin of false positives and negatives along sequencing, mapping, and downstream analysis. We show that PEM is very appropriate to detect a wide range of inversions, even with …

Evolutionary GeneticsChromosome Structure and Functionlcsh:MedicineComputational biologyBiologyGenomeDNA sequencingStructural variation03 medical and health sciences0302 clinical medicineGenetic MutationGeneticsFalse positive paradoxHumansComputer SimulationFalse Positive ReactionsGenomic libraryGenome Sequencinglcsh:ScienceBiologyGenome EvolutionFalse Negative Reactions030304 developmental biologyChromosomal inversionSegmental duplicationGeneticsEvolutionary Biology0303 health sciencesMultidisciplinaryChromosome Biologylcsh:RBreakpointMutation TypesComputational BiologyChromosome MappingGenomic EvolutionGenomicsSequence Analysis DNAComparative GenomicsChromosomes Human Pair 1Chromosome Inversionlcsh:QStructural GenomicsSequence AnalysisAlgorithms030217 neurology & neurosurgeryResearch Article
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Confidence-based Somatic Mutation Evaluation and Prioritization

2012

Next generation sequencing (NGS) has enabled high throughput discovery of somatic mutations. Detection depends on experimental design, lab platforms, parameters and analysis algorithms. However, NGS-based somatic mutation detection is prone to erroneous calls, with reported validation rates near 54% and congruence between algorithms less than 50%. Here, we developed an algorithm to assign a single statistic, a false discovery rate (FDR), to each somatic mutation identified by NGS. This FDR confidence value accurately discriminates true mutations from erroneous calls. Using sequencing data generated from triplicate exome profiling of C57BL/6 mice and B16-F10 melanoma cells, we used the exist…

False discovery rateSequence analysisSomatic cellQH301-705.5Low ConfidenceDNA Mutational AnalysisBiologySensitivity and SpecificityDNA sequencing03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineGermline mutationGenetic MutationGeneticsAnimalsExomeFalse Positive ReactionsGenome SequencingBiology (General)Molecular BiologyExomeBiologyMelanomaEcology Evolution Behavior and SystematicsHealth aging / healthy living Cardiovascular diseases [IGMD 5]030304 developmental biologyGenetics0303 health sciencesEcologyReceiver operating characteristicComputational BiologyReproducibility of ResultsGenomicsDNA NeoplasmSequence Analysis DNAMice Inbred C57BLComputational Theory and Mathematics030220 oncology & carcinogenesisModeling and SimulationMutationArtifactsResearch Article
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Cell of origin markers identify different prognostic subgroups of lung adenocarcinoma

2018

Strong prognostic markers able to stratify lung adenocarcinoma (ADC) patients are lacking. We evaluated whether a six-immunohistochemical markers panel (TTF1, SP-A, Napsin A, MUC5AC, CDX2 and CK5), defining the putative neoplastic “cell of origin,” allows to identify prognostic subgroups among lung ADC. We screened a large cohort of ADC specimens (2003–2013) from Torino Institutional Repository identifying: (i) marker positivity by immunohistochemistry, (ii) main morphological appearance by light microscopy, (iii) presence of “hotspot” mutations of candidate genes by Sequenom technology. To evaluate possible predictors of survival and time to recurrence, uni- and multivariable-adjusted comp…

Lung adenocarcinomaMorphologyAdultMale0301 basic medicineOncologyBiomarkers; Genetic mutations; Immunohistochemistry; Lung adenocarcinoma; Morphology; Survival analysisPathologymedicine.medical_specialtyCandidate geneCell of originsix-immunohistochemical markers panel (TTF1 SP-A Napsin A MUC5AC CDX2 and CK5)Adenocarcinoma of LungKaplan-Meier Estimategenetic mutationsGene mutationBiologymedicine.disease_causeadenocarcinoma (ADC)survival analysisPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineInternal medicinemorphologyBiomarkers TumormedicineHumansCDX2Survival analysisAgedbiomarkers; genetic mutations; immunohistochemistry; lung adenocarcinoma; morphology; survival analysisbiomarkersSurvival analysisMiddle Agedrespiratory systemPrognosislung adenocarcinomamedicine.diseaseImmunohistochemistryGenetic mutations030104 developmental biology030220 oncology & carcinogenesisimmunohistochemistryAdenocarcinomaImmunohistochemistryFemaleKRASBiomarkersHuman Pathology
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Functional Inactivation of the Genome-Wide Association Study Obesity Gene Neuronal Growth Regulator 1 in Mice Causes a Body Mass Phenotype

2012

To date, genome-wide association studies (GWAS) have identified at least 32 novel loci for obesity and body mass-related traits. However, the causal genetic variant and molecular mechanisms of specific susceptibility genes in relation to obesity are yet to be fully confirmed and characterised. Here, we examined whether the candidate gene NEGR1 encoding the neuronal growth regulator 1, also termed neurotractin or Kilon, accounts for the obesity association. To characterise the function of NEGR1 for body weight control in vivo, we generated two novel mutant mouse lines, including a constitutive NEGR1-deficient mouse line as well as an ENU-mutagenised line carrying a loss-of-function mutation …

MaleCandidate geneMutantlcsh:MedicineGenome-wide association studymedicine.disease_causeEndoplasmic ReticulumEatingGene Knockout TechniquesMice0302 clinical medicineEndocrinologylcsh:ScienceObesity; NEGR1; GWAS; body weight control2. Zero hungerGenetics0303 health sciencesMutationMultidisciplinaryNeuronal growth regulator 1GenomicsPhenotypePhenotypeMedicineFemaleFunction and Dysfunction of the Nervous SystemResearch ArticleGenotypeHypothalamusNerve Tissue ProteinsBiologyMotor ActivityDiet High-FatCell Line03 medical and health sciencesGenetic MutationGenome Analysis ToolsmedicineGeneticsGenome-Wide Association StudiesCell AdhesionNeuritesAnimalsHumansObesityGene SilencingGeneBiologyAlleles030304 developmental biologyNutritionlcsh:RBody WeightMembrane ProteinsHuman GeneticsNeuroendocrinologyBody HeightMetabolic DisordersGenetics of DiseaseLean body masslcsh:QEnergy Metabolism030217 neurology & neurosurgeryGenome-Wide Association StudyPLoS ONE
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Exploring by whole exome sequencing patients with initial diagnosis of Rubinstein-Taybi syndrome: the interconnections of epigenetic machinery disord…

2019

Rubinstein–Taybi syndrome (RSTS) is an autosomal-dominant neurodevelopmental disease affecting 1:125,000 newborns characterized by intellectual disability, growth retardation, facial dysmorphisms and skeletal abnormalities. RSTS is caused by mutations in genes encoding for writers of the epigenetic machinery: CREBBP (~ 60%) or its homologous EP300 (~ 10%). No causative mutation is identified in up to 30% of patients. We performed whole-exome sequencing (WES) on eight RSTS-like individuals who had normal high-resolution array CGH testing and were CREBBP- and EP300-mutation -negative, to identify the molecular cause. In four cases, we identified putatively causal variants in three genes (ASXL…

MaleGenetic Association StudieCompound heterozygosityWhole Exome SequencingArticleEpigenesis Genetic03 medical and health scienceswhole exome sequencing Rubinstein–Taybi syndrome epigenetic mutationsExome SequencingGeneticsmedicineHumansEpigeneticsEP300ChildGenetics (clinical)Exome sequencingGenetic Association Studies030304 developmental biologyGeneticsRubinstein-Taybi Syndrome0303 health sciencesComparative Genomic HybridizationbiologyRubinstein–Taybi syndrome030305 genetics & heredityInfant NewbornFaciesInfantmedicine.diseaseFacieCREB-Binding ProteinHuman geneticsRSTSKMT2APhenotypeChild PreschoolMutationbiology.proteinNeurodegenerative disordersFemaleHaploinsufficiencyE1A-Associated p300 ProteinHumanHuman genetics
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Recapitulating thyroid cancer histotypes through engineering embryonic stem cells

2023

AbstractThyroid carcinoma (TC) is the most common malignancy of endocrine organs. The cell subpopulation in the lineage hierarchy that serves as cell of origin for the different TC histotypes is unknown. Human embryonic stem cells (hESCs) with appropriate in vitro stimulation undergo sequential differentiation into thyroid progenitor cells (TPCs-day 22), which maturate into thyrocytes (day 30). Here, we create follicular cell-derived TCs of all the different histotypes based on specific genomic alterations delivered by CRISPR-Cas9 in hESC-derived TPCs. Specifically, TPCs harboring BRAFV600E or NRASQ61R mutations generate papillary or follicular TC, respectively, whereas addition of TP53R248…

MultidisciplinaryGeneral Physics and AstronomyGeneral ChemistryGeneral Biochemistry Genetics and Molecular BiologyThyroid cancer thyroid progenitor cells genetic mutation model CD44 TIMP1 KISS1 KISS1R.
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