Search results for "breakpoint"

showing 10 items of 70 documents

Deletion mapping on chromosome 10p and definition of a critical region for the second DiGeorge syndrome locus (DGS2)

1998

DiGeorge syndrome (DGS) is a developmental field defect, characterised by absent/hypoplastic thymus and parathyroid, and conotruncal heart defects, with haploinsufficiency loci at 22q (DGS1) and 10p (DGS2). We performed fluorescence in situ hybridisations (FISH) and polymerase chain reaction (PCR) analyses in 12 patients with 10p deletions, nine of them with features of DGS, and in a familial translocation 10p;14q associated with midline defects. The critical DGS2 region is defined by two DGS patients, and maps within a 1 cM interval including D10S547 and D10S585. The other seven DGS patients are hemizygous for both loci. The breakpoint of the reciprocal translocation 10p;14q maps at a dist…

MaleChromosomal translocationLocus (genetics)BiologyPolymerase Chain ReactionTranslocation Geneticlaw.inventionPtosislawDiGeorge syndromeDiGeorge SyndromeGeneticsmedicineHumansDeletion mappingIn Situ HybridizationGenetics (clinical)Polymerase chain reactionCell Line TransformedSequence DeletionGeneticsChromosomes Human Pair 10BreakpointInfant NewbornChromosome MappingInfantmedicine.diseaseFemalemedicine.symptomHaploinsufficiencyEuropean Journal of Human Genetics
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A new case of 2q duplication supports either a locus for orofacial clefting between markers D2S1897 and D2S2023 or a locus for cleft palate only on c…

2005

We report on a pure duplication of the proximal chromosome 2q in a 6.5-year-old boy with V-shaped midline cleft palate and bifid uvula, posteriorly located tongue, and micrognathia (Pierre Robin sequence), celiac disease, failure to thrive, and developmental delay. Cytogenetic and FISH analysis indicated a duplication of chromosome 2q13-q22. In general, pure proximal duplication or triplication of 2q is rare. The clinical features and chromosomal breakpoints of the 10 previously reported patients varied, and no common phenotype or proximal duplication/triplication 2q syndrome could be defined to date. However, based on four previous patients with different orofacial clefts and our case, a l…

MaleDevelopmental DisabilitiesMicrognathismLocus (genetics)BiologyGene mappingTongueGene DuplicationGene duplicationGeneticsmedicineHumansAbnormalities MultipleChildGeneGenetics (clinical)In Situ Hybridization FluorescenceGeneticsChromosome AberrationsBreakpointChromosomeKaryotypeAnatomyChromosome BandingFailure to ThriveCleft PalateCeliac DiseaseUvulaChromosomes Human Pair 2KaryotypingFailure to thrivemedicine.symptomMicrosatellite RepeatsAmerican journal of medical genetics. Part A
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A novel DFNB1 deletion allele supports the existence of a distant cis-regulatory region that controls GJB2 and GJB6 expression

2010

Contains fulltext : 87760_1.pdf (author's version ) (Open Access) Contains fulltext : 87760_2.pdf (Publisher’s version ) (Closed access) Eleven affected members of a large German-American family segregating recessively inherited, congenital, non-syndromic sensorineural hearing loss (SNHL) were found to be homozygous for the common 35delG mutation of GJB2, the gene encoding the gap junction protein Connexin 26. Surprisingly, four additional family members with bilateral profound SNHL carried only a single 35delG mutation. Previously, we demonstrated reduced expression of both GJB2 and GJB6 mRNA from the allele carried in trans with that bearing the 35delG mutation in these four persons. Usin…

MaleGenetics and epigenetic pathways of disease [NCMLS 6][SDV]Life Sciences [q-bio]PenetranceMESH: Base SequenceRegulatory Sequences Nucleic Acidsensorineural hearing lossConnexinsMESH: GenotypeMESH: Hearing Loss Sensorineural/diagnosisMESH: PenetranceGenotypeCopy-number variationGenetics (clinical)Sequence DeletionGeneticsComparative Genomic Hybridization0303 health sciencesMESH: Genetic TestingMESH: Gene Expression Regulation*030305 genetics & heredityPenetranceGJB2PedigreeConnexin 26MESH: Sequence Deletion*MESH: Hearing Loss Sensorineural/geneticsFemaleChromosome DeletionFunctional Neurogenomics [DCN 2]GJB6GenotypeMESH: PedigreeMESH: Chromosome DeletionHearing Loss SensorineuralMolecular Sequence Dataconnexin 26connexin 30DFNB1gene expression regulationGJB2GJB6sensorineural hearing losssequence deletionBiologyMESH: Connexin 30MESH: Connexins/genetics*MESH: Sequence Homology Nucleic AcidArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesMonoallelic MutationGJB6MESH: Connexin 26Sequence Homology Nucleic AcidConnexin 30otorhinolaryngologic diseasesGeneticsHumansGenetic TestingAlleleGeneMESH: Regulatory Sequences Nucleic Acid/genetics*AllelesDFNB1030304 developmental biologyFamily HealthMESH: HumansMESH: Molecular Sequence DataBase SequenceChromosomes Human Pair 13MESH: AllelesBreakpointMESH: MaleMESH: Comparative Genomic HybridizationGene Expression RegulationMESH: Family Healthbiology.proteinHuman medicineMESH: Chromosomes Human Pair 13/geneticsMESH: FemaleClinical Genetics
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Genetic Instability and Intratumoral Heterogeneity in Neuroblastoma with MYCN Amplification Plus 11q Deletion

2013

Background/Aim Genetic analysis in neuroblastoma has identified the profound influence of MYCN amplification and 11q deletion in patients’ prognosis. These two features of high-risk neuroblastoma usually occur as mutually exclusive genetic markers, although in rare cases both are present in the same tumor. The purpose of this study was to characterize the genetic profile of these uncommon neuroblastomas harboring both these high-risk features. Methods We selected 18 neuroblastomas with MNA plus 11q loss detected by FISH. Chromosomal aberrations were analyzed using Multiplex Ligation-dependent Probe Amplification and Single Nucleotide Polymorphism array techniques. Results and Conclusion Thi…

Malelcsh:MedicineMutually exclusive eventsGenetic analysisPediatricsGenetic profileChromosome BreakpointsNeuroblastomaGene duplicationPathologylcsh:ScienceChildGeneticsOncogene ProteinsN-Myc Proto-Oncogene ProteinMultidisciplinaryNuclear ProteinsOncologyChild PreschoolCytogenetic AnalysisMedicineFemaleChromosome DeletionResearch ArticleGenetic MarkersBiologyPolymorphism Single NucleotideCytogeneticsDiagnostic MedicineNeuroblastomamedicineGeneticsCancer GeneticsHumansIn patientGenetic Predisposition to DiseaseneoplasmsBiologyClinical GeneticsChromosomes Human Pair 11lcsh:RGene AmplificationInfantmedicine.diseaseGenetic markerPediatric OncologyMycn amplificationCancer researchlcsh:QBiomarkersGeneral PathologyPLoS ONE
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Disruption of TCBA1 associated with a de novo t(1;6)(q32.2;q22.3) presenting in a child with developmental delay and recurrent infections

2005

A boy with developmental delay, particularly of speech, a distinct face, antineutrophil cytoplasmic antibodies, and recurrent infections was found to have an apparently balanced de novo t(1;6)(q32.3;q22.3) translocation. Fluorescent in situ hybridisation with BAC/PAC clones and long range polymerase chain reaction products assessed in the human genome sequence localised the chromosome 1 breakpoint to a 9.8 kb segment within a hypothetical gene, LOC388735, and the chromosome 6 breakpoint to a 12.8 kb segment in intron 4 of the T-cell lymphoma breakpoint-associated target 1 (TCBA1) gene. Disruption and/or formation of TCBA1 fusion genes in T cell lymphoma and leukaemia cell lines suggests a r…

Malemedicine.medical_specialtyDevelopmental DisabilitiesMolecular Sequence DataShort ReportBiologyInfectionsTranslocation GeneticFusion geneExonMiceMolecular geneticsGeneticsmedicineAnimalsHumansAmino Acid SequenceChildGeneGenetics (clinical)GeneticsGenome HumanGene Expression ProfilingBreakpointChromosome MappingMembrane ProteinsChromosome BreakageExonsNull alleleMolecular biologyGene expression profilingChromosomes Human Pair 1Child PreschoolCytogenetic AnalysisChromosomes Human Pair 6Chromosome breakage
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Characterization of a complex rearrangement involving chromosomes 1, 4 and 8 by fish and array-CGH

2012

Complex chromosomal rearrangements (CCRs) are structural aberrations involving more than two chromosomes with at least three breakpoints. CCRs can be divided into familial and de novo. Balanced CCR are extremely rare in humans and are at high risk of producing unbalanced gametes. Individuals with balanced CCR are usually phenotipically normal but report fertility problems, recurrent miscarriages or congenital anomalies in newborn offsprings as consequence of either meiotic failure or imbalanced chromosomes segregation.We describe the case of an unbalanced CCR involving chromosomes 1, 4 and 8 found in a girl with developmental delay, hexadactilia and microcephaly. The rearrangement, apparent…

MicrocephalyArray-CGHIntellectual disabilityChromosomal rearrangementBiologySettore MED/38 - Pediatria Generale E SpecialisticaFISHMeiosisGeneticsmedicineChromosomes HumanHumansIn Situ Hybridization FluorescenceGene RearrangementGeneticsComparative Genomic HybridizationComplex chromosomal rearrangementBreakpointInfant NewbornInfantChromosomeKaryotypeGeneral Medicinemedicine.diseaseHuman geneticsChromosome BandingSettore MED/03 - Genetica MedicaChromosomes Human Pair 1KaryotypingFish <Actinopterygii>FemaleChromosomes Human Pair 4Chromosomes Human Pair 8Journal of Applied Genetics
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Chromosome 15q BP4-BP5 Deletion in a Girl with Nocturnal Frontal Lobe Epilepsy, Migraine, Circumscribed Hypertrichosis, and Language Impairment

2020

The 15q13.3 microdeletion (microdel15q13.3) syndrome (OMIM 612001) has been reported in healthy subjects as well as in individuals with a wide spectrum of clinical manifestations ranging from mild to severe neurological disorders, including developmental delay/intellectual disability, autism spectrum disorder, schizophrenia, epilepsy, behavioral problems and speech dysfunction. This study explored the link between this genomic rearrangement and nocturnal frontal lobe epilepsy (NFLE), which could improve the clinical interpretation. A clinical and genomic investigation was carried out on an 8-year-girl with a de novo deletion flanking the breakpoints (BPs) 4 and 5 of 15q13.3 detected by arra…

Migraine disorders.HypertrichosisPediatricsmedicine.medical_specialtyfrontal lobe epilepsyCase Report050105 experimental psychology03 medical and health sciencesEpilepsy0302 clinical medicinemigraine disorderslanguage disordersIntellectual disabilityMedicine0501 psychology and cognitive scienceschromosome breakpointsChromosome breakpointbusiness.industry05 social sciencesHypertrichosiLanguage disordermedicine.diseaseMigraine with aurahypertrichosisMigraineAutism spectrum disorderSchizophreniamedicine.symptombusinessLiterature surveychromosome breakpoints; frontal lobe epilepsy; hypertrichosis; language disorders; migraine disorders030217 neurology & neurosurgery
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FISH mapping of the sex-reversal region on human chromosome 9p in two XY females and in primates

2000

Accumulating evidence suggests that haploinsufficiency of a dosage-sensitive gene(s) in human chromosome 9p24.3 is responsible for the failure of testicular development and feminisation in XY patients with monosomy for 9p. We have used molecular cytogenetic methods to characterise the sex-reversing 9p deletions in two XY females. Fluorescence in situ hybridisation (FISH) with YACs from the critical 9p region containing an evolutionarily conserved sex-determining gene, DMRT1, is a very fast and reliable assay for patient screening. Comparative YAC mapping on great ape and Old and New World monkey chromosomes demonstrated that the critical region was moved from an interstitial position on the…

MonosomyX ChromosomeDisorders of Sex DevelopmentChromosome BreakpointsChromosomal translocationBiologyY chromosomePolymerase Chain ReactionTranslocation GeneticY ChromosomeGeneticsmedicineAnimalsHumansChromosomes Artificial YeastIn Situ Hybridization FluorescenceGenetics (clinical)X chromosomeChromosomal inversionGeneticsChromosome MappingChromosomeKaryotypemedicine.diseaseCebidaeKaryotypingFemaleChromosome DeletionChromosomes Human Pair 9Transcription FactorsEuropean Journal of Human Genetics
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Identification of a novel recurrent 1q42.2-1qter deletion in high risk MYCN single copy 11q deleted neuroblastomas

2012

Neuroblastoma is an aggressive embryonal tumor that accounts for similar to 15% of childhood cancer deaths. Hitherto, despite the availability of comprehensive genomic data on DNA copy number changes in neuroblastoma, relatively little is known about the genes driving neuroblastoma tumorigenesis. In this study, high resolution array comparative genome hybridization (CGH) was performed on 188 primary neuroblastoma tumors and 33 neuroblastoma cell lines to search for previously undetected recurrent DNA copy number gains and losses. A new recurrent distal chromosome 1q deletion (del(1)(q42.2qter)) was detected in seven cases. Further analysis of available array CGH datasets revealed 13 additio…

Neuroblastoma/geneticsCancer ResearchProcollagen-Proline DioxygenaseMedizinGene Dosagecomparative genomic hybridizationBiologymedicine.disease_causeGene dosageN-Myc Proto-Oncogene ProteinFumarate HydrataseHypoxia-Inducible Factor-Proline DioxygenasesNeuroblastomaProcollagen-Proline Dioxygenase/geneticsCell Line TumorNeuroblastomamedicineHumansFumarate Hydratase/geneticsGeneOncogene ProteinsGeneticsN-Myc Proto-Oncogene ProteinChromosomes Human Pair 11BreakpointNuclear ProteinsChromosomemedicine.diseaseOncogene Proteins/geneticsNuclear Proteins/geneticsOncologyChromosome DeletionCarcinogenesisComparative genomic hybridization
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Myelodysplastic Syndromes with 20q Deletion: Incidence, Prognostic Value and Impact on Response to Azacitidine of ASXL1 Chromosomal Deletion and Gene…

2020

Introduction : The 20q deletion [del(20q)] is a recurrent chromosomal aberration in myelodysplastic syndromes (MDS) and, as a single abnormality, is associated according to the Revised International Prognostic Scoring System (IPSS-R) with a favorable outcome. However, the breakpoint of del(20q) is very heterogeneous and may cause deletion of the ASXL1 gene (20q11.21). This gene is an important epigenetic regulator of hematopoiesis and its mutations have been associated in MDS with a shorter overall survival (OS) and a lower response to azacitidine (AZA). Aim: To assess the incidence, prognostic value and impact on response to AZA of ASXL1 chromosomal alterations and genetic mutations in MDS…

OncologySanger sequencingmedicine.medical_specialtybusiness.industryMyelodysplastic syndromesImmunologyAzacitidineBreakpointCell BiologyHematologymedicine.diseaseBiochemistryIDH2symbols.namesakeGermline mutationInternational Prognostic Scoring SystemInternal medicinesymbolsMedicinebusinessChromosomal Deletionmedicine.drugBlood
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