Search results for "duplication"

showing 10 items of 216 documents

A New Mutation of the p53 Gene in Human Neuroblastoma, Not Correlated with N-myc Amplification

1999

N-myc gene amplification and/or loss of heterozygosity of chromosome 1 (LOH lp) are important criteria for prognosis and progression in human neuroblastoma (NB). Despite the high incidence of alterations of the p53 gene in human cancers, very few p53 mutations have been reported in NB. The objective of our study was to search for p53 mutations in NB and their correlation with N-myc amplification and clinical or pathologic parameters. We analyzed 14 selected cases of NB from the Spanish Protocol N-II-92. We found a missense mutation in codon 248 CGG to GGG (Arg/Gly) in one case of stage 4 NB with no N-myc amplification. Our results confirm the low incidence of p53 gene mutation in neuroblas…

0301 basic medicineChromosomeBiologyGene mutationmedicine.diseaseMolecular biologyPathology and Forensic MedicineLoss of heterozygosity03 medical and health sciences030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisNeuroblastomaGene duplicationmedicineCancer researchMissense mutationSurgeryAnatomyGeneN-MycInternational Journal of Surgical Pathology
researchProduct

Diversification of spatiotemporal expression and copy number variation of the echinoid hbox12/pmar1/micro1 multigene family

2017

Changes occurring during evolution in the cis-regulatory landscapes of individual members of multigene families might impart diversification in their spatiotemporal expression and function. The archetypal member of the echinoid hbox12/pmar1/micro1 family is hbox12-a, a homeobox-containing gene expressed exclusively by dorsal blastomeres, where it governs the dorsal/ventral gene regulatory network during embryogenesis of the sea urchin Paracentrotus lividus. Here we describe the inventory of the hbox12/pmar1/micro1 genes in P. lividus, highlighting that gene copy number variation occurs across individual sea urchins of the same species. We show that the various hbox12/pmar1/micro1 genes grou…

0301 basic medicineEvolutionary GeneticsEmbryologyGene regulatory networklcsh:MedicineGene ExpressionMedicine (all); Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Database and Informatics MethodsGene duplicationGene Regulatory NetworksCopy-number variationlcsh:ScienceSea urchinPhylogenyMultidisciplinarybiologyPhylogenetic treeMedicine (all)Genes HomeoboxGene Expression Regulation DevelopmentalAnimal ModelsGenomicsExperimental Organism SystemsMultigene FamilySequence AnalysisResearch ArticleEchinodermsDNA Copy Number VariationsBioinformaticsDNA transcriptionZoologySettore BIO/11 - Biologia MolecolareResearch and Analysis MethodsParacentrotus lividus03 medical and health sciencesSequence Motif Analysisbiology.animalGeneticsGene familyAnimalsGeneEvolutionary BiologyBiochemistry Genetics and Molecular Biology (all)lcsh:REmbryosOrganismsBiology and Life SciencesComputational Biologybiology.organism_classificationGenome AnalysisGenomic LibrariesInvertebrates030104 developmental biologyAgricultural and Biological Sciences (all)Evolutionary biologySea Urchinslcsh:QSequence AlignmentDevelopmental Biology
researchProduct

Q-nexus: a comprehensive and efficient analysis pipeline designed for ChIP-nexus

2016

Background: ChIP-nexus, an extension of the ChIP-exo protocol, can be used to map the borders of protein-bound DNA sequences at nucleotide resolution, requires less input DNA and enables selective PCR duplicate removal using random barcodes. However, the use of random barcodes requires additional preprocessing of the mapping data, which complicates the computational analysis. To date, only a very limited number of software packages are available for the analysis of ChIP-exo data, which have not yet been systematically tested and compared on ChIP-nexus data. Results: Here, we present a comprehensive software package for ChIP-nexus data that exploits the random barcodes for selective removal …

0301 basic medicineFOS: Computer and information sciencesDuplication ratesChromatin ImmunoprecipitationBioinformaticsPipeline (computing)610Biologycomputer.software_genre600 Technik Medizin angewandte Wissenschaften::610 Medizin und Gesundheit03 medical and health sciencesSoftwareChIP-nexusGeneticsPreprocessorNucleotide MotifsLibrary complexityChIP-exoGeneticsProtocol (science)Binding Sitesbusiness.industryfungiComputational BiologyHigh-Throughput Nucleotide SequencingReproducibility of ResultsChipChromatin immunoprecipitationData mappingDNA-Binding ProteinsAlgorithm030104 developmental biologyChIP-exoData miningbusinessPeak callingcomputerAlgorithmsSoftwareProtein BindingTranscription FactorsResearch ArticleBiotechnologyBMC Genomics
researchProduct

Xq28 duplication includingMECP2in six unreported affected females: what can we learn for diagnosis and genetic counselling?

2017

Duplication of the Xq28 region, involving MECP2 (dupMECP2), has been primarily described in males with severe developmental delay, spasticity, epilepsy, stereotyped movements and recurrent infections. Carrier mothers are usually asymptomatic with an extremely skewed X chromosome inactivation (XCI) pattern. We report a series of six novel symptomatic females carrying a de novo interstitial dupMECP2, and review the 14 symptomatic females reported to date, with the aim to further delineate their phenotype and give clues for genetic counselling. One patient was adopted and among the other 19 patients, seven (37%) had inherited their duplication from their mother, including three mildly (XCI: 70…

0301 basic medicineGeneticsPediatricsmedicine.medical_specialtyGenetic counselingMECP2 duplication syndrome030105 genetics & heredityBiologymedicine.diseaseX-inactivation3. Good healthXq2803 medical and health sciencesEpilepsy0302 clinical medicineGene duplicationGeneticsmedicineAsymptomatic carrierSkewed X-inactivation030217 neurology & neurosurgeryGenetics (clinical)Clinical Genetics
researchProduct

A Novel Role for CSRP1 in a Lebanese Family with Congenital Cardiac Defects

2017

Despite an obvious role for consanguinity in congenital heart disease (CHD), most studies fail to document a monogenic model of inheritance except for few cases. We hereby describe a first-degree cousins consanguineous Lebanese family with 7 conceived children: 2 died in utero of unknown causes, 3 have CHD, and 4 have polydactyly. The aim of the study is to unveil the genetic variant(s) causing these phenotypes using next generation sequencing (NGS) technology. Targeted exome sequencing identified a heterozygous duplication in CSRP1 which leads to a potential frameshift mutation at position 154 of the protein. This mutation is inherited from the father, and segregates only with the CHD phen…

0301 basic medicineGeneticsPolydactylylcsh:QH426-470ConsanguinityBiologypolydactylymedicine.diseasecongenital heart diseaseFrameshift mutation03 medical and health scienceslcsh:Genetics030104 developmental biologyTRPS1Gene duplicationMutation (genetic algorithm)medicineGeneticsMolecular MedicineMissense mutationExomeGenetics (clinical)Exome sequencingOriginal ResearchCSRP1Frontiers in Genetics
researchProduct

Evolutionary impact of copy number variation rates.

2017

[Objective]: Copy number variation is now recognized as one of the major sources of genetic variation among individuals in natural populations of any species. However, the relevance of these unexpected observations goes beyond diagnosing high diversity. [Results]: Here, it is argued that the molecular rates of copy number variation, mainly the deletion rate upon variation, determine the evolutionary road of the genome regarding size. Genetic drift will govern this process only if the efective population size is lower than the inverse of the deletion rate. Otherwise, natural selection will do.

0301 basic medicineGenome sizeDNA Copy Number VariationsGene duplicationPopulation geneticsPopulation geneticslcsh:MedicineBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesEffective population sizeGenetic driftGenetic variationAnimalsHumansCopy-number variationlcsh:Science (General)Genome sizelcsh:QH301-705.5GeneticsNatural selectionlcsh:RGenetic DriftBirth–death processGeneral MedicineBiological EvolutionResearch Note030104 developmental biologyGenetics Populationlcsh:Biology (General)Evolutionary biologyNeutral theory of molecular evolutionNeutral evolutionlcsh:Q1-390BMC research notes
researchProduct

Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
researchProduct

Large national series of patients with Xq28 duplication involving MECP2: Delineation of brain MRI abnormalities in 30 affected patients.

2016

International audience; Xq28 duplications encompassing MECP2 have been described in male patients with a severe neurodevelopmental disorder associated with hypotonia and spasticity, severe learning disability, stereotyped movements, and recurrent pulmonary infections. We report on standardized brain magnetic resonance imaging (MRI) data of 30 affected patients carrying an Xq28 duplication involving MECP2 of various sizes (228 kb to 11.7 Mb). The aim of this study was to seek recurrent malformations and attempt to determine whether variations in imaging features could be explained by differences in the size of the duplications. We showed that 93% of patients had brain MRI abnormalities such …

0301 basic medicineMalePathologyMethyl-CpG-Binding Protein 2[SDV]Life Sciences [q-bio]030105 genetics & heredityCorpus callosumLateral ventricles0302 clinical medicineGene DuplicationIKBKGFLNAChildGenetics (clinical)GeneticsBrain Diseasesmedicine.diagnostic_testMiddle AgedPrognosisMagnetic Resonance ImagingHypotonia3. Good healthPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structurePhenotypeXq28 duplicationChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentGenotypeBiologygenotype-phenotype correlationWhite matter03 medical and health sciencesYoung AdultGeneticsmedicineHumansGenetic Association StudiesChromosomes Human X[ SDV ] Life Sciences [q-bio]Infant NewbornInfantMagnetic resonance imagingHyperintensitynervous system diseasesMental Retardation X-LinkedMECP2 gene030217 neurology & neurosurgeryAmerican journal of medical genetics. Part A
researchProduct

Expanding the phenotype of reciprocal 1q21.1 deletions and duplications: a case series

2017

Abstract Background Recurrent reciprocal 1q21.1 deletions and duplications have been associated with variable phenotypes. Phenotypic features described in association with 1q21.1 microdeletions include developmental delay, craniofacial dysmorphism and congenital anomalies. The 1q21.1 reciprocal duplication has been associated with macrocephaly or relative macrocephaly, frontal bossing, hypertelorism, developmental delay, intellectual disability and autism spectrum disorder. Methods Our study describes seven patients, who were referred to us for developmental delay/intellectual disability, dysmorphic features and, in some cases, congenital anomalies, in whom we identified 1q21.1 CNVs by arra…

0301 basic medicineMalePediatricsmedicine.medical_specialtyArray-CGHDevelopmental delayTrigonocephaly03 medical and health sciencesFrontal BossingPregnancyPrenatal DiagnosisGene duplicationIntellectual disabilityMedicineHumansAbnormalities MultipleMegalencephalyHypertelorismChild1q21.1 deletionGeneticsbusiness.industryResearchMacrocephalylcsh:RJ1-570Infantlcsh:Pediatricsmedicine.diseaseMegalencephalyDysmorphism030104 developmental biologyPhenotypeAutism spectrum disorderChromosomes Human Pair 1Female1q21.1 duplicationmedicine.symptomChromosome DeletionbusinessItalian Journal of Pediatrics
researchProduct

Analysis of DNA Polymerases Reveals Specific Genes Expansion in Leishmania and Trypanosoma spp.

2020

Leishmaniasis and trypanosomiasis are largely neglected diseases prevailing in tropical and subtropical conditions. These are an arthropod-borne zoonosis that affects humans and some animals and is caused by infection with protozoan of the genera Leishmania and Trypanosoma, respectively. These parasites present high genomic plasticity and are able to adapt themselves to adverse conditions like the attack of host cells or toxicity induced by drug exposure. Different mechanisms allow these adapting responses induced by stress, such as mutation, chromosomal rearrangements, establishment of mosaic ploidies, and gene expansion. Here we describe how a subset of genes encoding for DNA polymerases …

0301 basic medicineMicrobiology (medical)TrypanosomaDNA polymeraseDNA repairgene amplification030106 microbiologyImmunologylcsh:QR1-502DNA repairtrypanosomatidsDNA-Directed DNA Polymerasemedicine.disease_causeMicrobiologylcsh:Microbiology03 medical and health sciencesDNA polymerasesCellular and Infection MicrobiologyTrypanosomiasisGene duplicationTrypanosomatidamedicineAnimalsHumanstranslesion synthesisGeneLeishmaniasisGeneticsLeishmaniaMutationbiologyLeishmaniabiology.organism_classification030104 developmental biologyInfectious DiseasesPerspectivebiology.proteinTrypanosomagenome stabilityFrontiers in Cellular and Infection Microbiology
researchProduct