Search results for "Genomic Hybridization"

showing 10 items of 95 documents

Performance comparison of two whole genome amplification techniques in frame of multifactor preimplantation genetic testing

2018

Purpose To compare multiple displacement amplification and OmniPlex whole genome amplification technique performance during array comparative genome hybridization (aCGH), Sanger sequencing, SNaPshot and fragment size analysis downstream applications in frame of multifactor embryo preimplantation genetic testing. Methods Preclinical workup included linked short tandem repeat (STR) marker selection and primer design for loci of interest. It was followed by a family haplotyping, after which an in vitro fertilization preimplantation genetic testing (IVF-PGT) cycle was carried out. A total of 62 embryos were retrieved from nine couples with a confirmed single gene disorder being transmitted in t…

0301 basic medicineMalePregnancy RateFertilization in VitroBiology03 medical and health sciencessymbols.namesake0302 clinical medicinePregnancymedicineGeneticsSingle Embryo TransferHumansGenetic TestingAlleleGenetics (clinical)Preimplantation DiagnosisGenetic testingGeneticsWhole Genome AmplificationSanger sequencingComparative Genomic Hybridization030219 obstetrics & reproductive medicinePreimplantation genetic testingSingle gene disordermedicine.diagnostic_testTripeptidyl-Peptidase 1HaplotypeMultiple displacement amplificationObstetrics and GynecologyGeneral MedicineAneuploidyHuman geneticsWhole genome amplification030104 developmental biologyBlastocystReproductive MedicineEmbryosymbolsMicrosatelliteFemaleNucleic Acid Amplification TechniquesDevelopmental BiologyJournal of Assisted Reproduction and Genetics
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NF1 microdeletion syndrome: case report of two new patients

2019

Abstract Background 17q11.2 microdeletions, which include the neurofibromatosis type 1 (NF1) gene region, are responsible for the NF1 microdeletion syndrome, observed in 4.2% of all NF1 patients. Large deletions of the NF1 gene and its flanking regions are associated with a more severe NF1 phenotype than the NF1 general population. Case presentation We hereby describe the clinical and molecular features of two girls (aged 2 and 4 years, respectively), with non-mosaic atypical deletions. Patient 1 showed fifteen café-au-lait spots and axillary freckling, as well as a Lisch nodule in the left eye, strabismus, high-arched palate, malocclusion, severe kyphoscoliosis, bilateral calcaneovalgus fo…

0301 basic medicinePathologymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesGenotype-phenotype correlationNeurofibromatosesLisch noduleContiguous gene syndromePopulationCase ReportContiguous gene syndromeChromosomesCraniofacial Abnormalities03 medical and health sciences0302 clinical medicineAtypical deletionIntellectual DisabilitymedicineHumansMultiplex ligation-dependent probe amplificationNeurofibromatosiseducationChildPreschoolNeurofibromatoseseducation.field_of_studybusiness.industryLearning DisabilitiesPair 17lcsh:RJ1-570Axillary frecklinglcsh:Pediatricsmedicine.diseaseeye diseasesMLPA030104 developmental biologyNF1 geneChild PreschoolFemalemedicine.symptomChromosome DeletionbusinessAtypical deletion; Contiguous gene syndrome; Genotype-phenotype correlation; MLPA; NF1 gene; Child Preschool; Chromosome Deletion; Chromosomes Human Pair 17; Craniofacial Abnormalities; Female; Humans; Intellectual Disability; Learning Disabilities; Neurofibromatoses030217 neurology & neurosurgeryChromosomes Human Pair 17Comparative genomic hybridizationHumanItalian Journal of Pediatrics
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Jacobsen syndrome and neonatal bleeding: report on two unrelated patients

2021

Abstract Introduction In 1973, Petrea Jacobsen described the first patient showing dysmorphic features, developmental delay and congenital heart disease (atrial and ventricular septal defect) associated to a 11q deletion, inherited from the father. Since then, more than 200 patients have been reported, and the chromosomal critical region responsible for this contiguous gene disorder has been identified. Patients’ presentation We report on two unrelated newborns observed in Italy affected by Jacobsen syndrome (JBS, also known as 11q23 deletion). Both patients presented prenatal and postnatal bleeding, growth and developmental delay, craniofacial dysmorphisms, multiple congenital anomalies, a…

0301 basic medicinePediatricsmedicine.medical_specialtyGenotype-phenotype correlationHeart diseaseGenetic counselingCase ReportIn situ hybridization030105 genetics & heredityPediatricsRJ1-57003 medical and health sciences0302 clinical medicineaCGHJBSmedicineHumansJacobsen Distal 11q Deletion SyndromeJacobsen syndromeCraniofacialGenetic Association StudiesCerebral Hemorrhage11q23 deletionbusiness.industryInfant NewbornEarly diagnosimedicine.diseaseEarly diagnosisPancytopeniaThrombocytopeniaItalyFemalePresentation (obstetrics)business030217 neurology & neurosurgeryComparative genomic hybridizationItalian Journal of Pediatrics
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Paternal uniparental disomy chromosome 14-like syndrome due a maternal de novo 160 kb deletion at the 14q32.2 region not encompassing the IG- and the…

2015

The human chromosome 14q32 carries a cluster of imprinted genes which include the paternally expressed genes (PEGs) DLK1 and RTL1, as well as the maternally expressed genes (MEGs) MEG3, RTL1as, and MEG8. PEGs and MEGs expression at the 14q32.2-imprinted region are regulated by two differentially methylated regions (DMRs): the IG-DMR and the MEG3-DMR, which are respectively methylated on the paternal and unmethylated on the maternal chromosome 14 in most cells. Genetic and epigenetic abnormalities affecting these imprinted gene clusters result in two different phenotypes currently known as maternal upd(14) syndrome and paternal upd(14) syndrome. However, only few patients carrying a maternal…

14q32.2 imprinted regionGenotypeBiologyPregnancy ProteinsMEG3-DMRGenomic ImprintingPaternal uniparental disomy chromosome 14 [upd(14)pat]GeneticsmedicineHumans14q32.2 maternal deletionEpigenetics"coat-hanger" rib signGeneGenetics (clinical)Sequence DeletionGeneticsMEG3Chromosomes Human Pair 14Comparative Genomic HybridizationIG-DMRMEG3 geneCalcium-Binding ProteinsInfant NewbornChromosomeMembrane ProteinsSyndromeDNA MethylationUniparental Disomymedicine.diseasePrognosisPhenotypeMolecular biologyUniparental disomyDifferentially methylated regionsPhenotypeSkeletal dysplasiaIntercellular Signaling Peptides and ProteinsFemaleRNA Long NoncodingRTL1as geneGenomic imprintingAmerican journal of medical genetics. Part A
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Integrated CGH/WES Analyses Advance Understanding of Aggressive Neuroblastoma Evolution: A Case Study

2021

Neuroblastoma (NB) is the most common extra-cranial malignancy in preschool children. To portray the genetic landscape of an overly aggressive NB leading to a rapid clinical progression of the disease, tumor DNA collected pre- and post-treatment has been analyzed. Array comparative genomic hybridization (aCGH), whole-exome sequencing (WES), and pharmacogenetics approaches, respectively, have identified relevant copy number alterations (CNAs), single nucleotide variants (SNVs), and polymorphisms (SNPs) that were then combined into an integrated analysis. Spontaneously formed 3D tumoroids obtained from the recurrent mass have also been characterized. The results prove the power of combining C…

3D tumoroids; Array CGH; Clonal evolution; Neuroblastoma; Pharmacogenetics; Recurrent tumor; Single nucleotide variants; Whole exome sequencing; Child Preschool; Disease Progression; Drug Resistance Neoplasm; Fatal Outcome; Humans; Immunophenotyping; Neuroblastoma; Polymorphism Single Nucleotide; Comparative Genomic Hybridization; Whole Exome SequencingQH301-705.5Drug Resistanceclonal evolutionCase Report3D tumoroidsSingle-nucleotide polymorphismDiseaseComputational biologyBiologyMalignancyPolymorphism Single NucleotideSomatic evolution in cancerImmunophenotypingwhole exome sequencingNeuroblastomaFatal OutcomeNeuroblastomaExome SequencingmedicineHumansarray CGHrecurrent tumorPolymorphismBiology (General)ChildPreschoolExome sequencingTumorsComparative Genomic HybridizationSingle NucleotideGeneral Medicinemedicine.diseaseSingle nucleotide variantsDrug Resistance NeoplasmPharmacogeneticsChild PreschoolDisease ProgressionFarmacogenèticaNeoplasmPharmacogeneticsComparative genomic hybridization
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False positive rate of an arrayCGH platform for single-cell preimplantation genetic screening and subsequent clinical application on day-3

2013

In this work, false positive rate of an arrayCGH platform for its use in day-3 single-blastomere analysis was calculated. For this purpose, 38 embryos diagnosed as abnormal on day-3 by FISH were re-biopsied on day-4. Single-cell day-4 arrayCGH diagnosis was then performed. A successful amplification was obtained in 97.4 % (37/38) of the day-4 cells analysed by arrayCGH. Day-3 FISH and day-4 arrayCGH diagnosis were concordant in 35/37 cases. The two discordant embryos were spread and all the cells from each embryo were re-analysed by FISH on day 5. The same error rate (2.7 %) for day-3 FISH and day-4 arrayCGH was obtained when comparing day-5 FISH re-analysis. After this pre-clinical phase, …

AdultBlastomeresmedicine.medical_specialtyTime FactorsPregnancy RateBiopsyConcordanceClinical pregnancyBiologySensitivity and SpecificityMiscarriagePregnancyarrayCGHDay-5 FISH re-analysisGeneticsmedicineChromosomes HumanHumansFalse Positive ReactionsEmbryo ImplantationGenetic TestingProspective StudiesIn Situ Hybridization FluorescenceGenetics (clinical)CryopreservationGynecologyComparative Genomic HybridizationReproducibility of ResultsObstetrics and GynecologyGeneral MedicineAneuploidyEmbryo Transfermedicine.diseaseBlastocystReproductive MedicineBlastomere biopsyBlastomere biopsyFish <Actinopterygii>Day-3 PGSFemaleFalse positive rateDevelopmental Biology
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Molecular characterization of 39 de novo sSMC: contribution to prognosis and genetic counselling, a prospective study.

2012

Small supernumerary marker chromosomes (sSMCs) are structurally abnormal chromosomes that cannot be characterized by karyotype. In many prenatal cases of de novo sSMC, the outcome of pregnancy is difficult to predict because the euchromatin content is unclear. This study aimed to determine the presence or absence of euchromatin material of 39 de novo prenatally ascertained sSMC by array-comparative genomic hybridization (array-CGH) or single nucleotide polymorphism (SNP) array. Cases were prospectively ascertained from the study of 65,000 prenatal samples [0.060%; 95% confidence interval (CI), 0.042-0.082]. Array-CGH showed that 22 markers were derived from non-acrocentric markers (56.4%) a…

AdultGenetic MarkersRiskEuchromatinKaryotypeContext (language use)Prenatal diagnosisSingle-nucleotide polymorphismGenetic CounselingBiologyPolymorphism Single NucleotideYoung AdultPregnancyPrenatal DiagnosisGeneticsmedicineSNPHumansGenetic Predisposition to DiseaseProspective StudiesGenetics (clinical)Genetic Association StudiesIn Situ Hybridization FluorescenceGeneticsChromosome AberrationsComparative Genomic Hybridizationmedicine.diagnostic_testKaryotypeMiddle AgedPrognosisMolecular biologyFemaleFranceSwitzerlandSNP arrayFluorescence in situ hybridizationGenome-Wide Association StudyClinical genetics
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Search for a gene responsible for Floating-Harbor syndrome on chromosome 12q15q21.1.

2012

International audience; Floating-Harbor syndrome (FHS) is characterized by characteristic facial dysmorphism, short stature with delayed bone age, and expressive language delay. To date, the gene(s) responsible for FHS is (are) unknown and the diagnosis is only made on the basis of the clinical phenotype. The majority of cases appeared to be sporadic but rare cases following autosomal dominant inheritance have been reported. We identified a 4.7 Mb de novo 12q15-q21.1 microdeletion in a patient with FHS and intellectual deficiency. Pangenomic 244K array-CGH performed in a series of 12 patients with FHS failed to identify overlapping deletions. We hypothesized that FHS is caused by haploinsuf…

AdultHeart Septal Defects VentricularMaleCandidate geneFloating Harbor syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsHaploinsufficiencyBiologyBioinformaticsShort statureCraniofacial Abnormalities03 medical and health sciences12q15q21.1 microdeletion[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to Disease[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyChild[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Growth Disorders030304 developmental biologySequence DeletionPhenocopyGenetics0303 health sciencesComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsChromosomes Human Pair 12Genetic heterogeneity030305 genetics & heredityChromosomeHigh-Throughput Nucleotide Sequencinghigh-throughput sequencingmedicine.disease3. Good healthPhenotypeFloating–Harbor syndromeChild PreschoolMutation (genetic algorithm)Femalemedicine.symptomHaploinsufficiency[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Incomplete penetrance and phenotypic variability of 6q16 deletions including SIM1.

2015

International audience; 6q16 deletions have been described in patients with a Prader-Willi-like (PWS-like) phenotype. Recent studies have shown that certain rare single-minded 1 (SIM1) loss-of-function variants were associated with a high intra-familial risk for obesity with or without features of PWS-like syndrome. Although SIM1 seems to have a key role in the phenotype of patients carrying 6q16 deletions, some data support a contribution of other genes, such as GRIK2, to explain associated behavioural problems. We describe 15 new patients in whom de novo 6q16 deletions were characterised by comparative genomic hybridisation or single-nucleotide polymorphism (SNP) array analysis, including…

AdultMaleAdolescent[SDV]Life Sciences [q-bio]PenetranceBioinformaticsPolymorphism Single NucleotideArticlePregnancyGRIK2Basic Helix-Loop-Helix Transcription FactorsGeneticsHumansSNPObesityChildGeneGenetic Association StudiesGenetics (clinical)GeneticsComparative Genomic Hybridizationbiology[ SDV ] Life Sciences [q-bio]InfantPenetrancePhenotypeRepressor ProteinsChild PreschoolAborted FetusSIM1biology.proteinChromosomes Human Pair 6FemaleHaploinsufficiencyPrader-Willi SyndromeComparative genomic hybridization
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1q gain and CDT2 overexpression underlie an aggressive and highly proliferative form of Ewing sarcoma

2012

12 páginas, 6 figuras, 1 tabla.-- et al.

AdultMaleCancer ResearchCandidate geneAdolescentDNA Copy Number VariationsUbiquitin-Protein Ligasesclinical outcomeBone NeoplasmsSarcoma EwingBiologyBioinformaticsPolymorphism Single NucleotideTranscriptomeIn vivoCell Line TumorGeneticsmedicineHumansChildMolecular BiologymicroarraysAgedCell ProliferationAged 80 and overCell CycleComputational BiologyInfantNuclear ProteinsMiddle Agedmedicine.disease1q GainIn vitroChromosomes Human Pair 1Child PreschoolCancer researchImmunohistochemistryFemaleCDT2SarcomaDNA microarrayEwing sarcomaComparative genomic hybridization
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