Search results for " Pair 13"

showing 10 items of 12 documents

Evolution of the human chromosome 13 synteny: Evolutionary rearrangements, plasticity, human disease genes and cancer breakpoints

2020

The history of each human chromosome can be studied through comparative cytogenetic approaches in mammals which permit the identification of human chromosomal homologies and rearrangements between species. Comparative banding, chromosome painting, Bacterial Artificial Chromosome (BAC) mapping and genome data permit researchers to formulate hypotheses about ancestral chromosome forms. Human chromosome 13 has been previously shown to be conserved as a single syntenic element in the Ancestral Primate Karyotype

0106 biological sciences0301 basic medicineChromosomes Artificial Bacteriallcsh:QH426-470PlasticityEvolutionContext (language use)BiologyBAC probeSettore BIO/08 - AntropologiaSynteny010603 evolutionary biology01 natural sciencesGenomeArticleEvolution Molecular03 medical and health sciencesPaintingBAC probesFISHNeoplasmsGeneticsAnimalsHumansPhylogenyGenetics (clinical)Chromosome 13SyntenyGene RearrangementMammalsBacterial artificial chromosomeAutosomeChromosomes Human Pair 13Chromosome MappingChromosomeKaryotypelcsh:Genetics030104 developmental biologyEvolutionary biologyHuman synteny
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Screening of subtelomeric rearrangements in autistic disorder: identification of a partial trisomy of 13q34 in a patient bearing a 13q;21p translocat…

2006

Within the framework of a FISH screening protocol to detect cryptic subtelomeric rearrangements in autistic disorder (AD), a patient bearing three copies of the subtelomeric portion of the q arm of chromosome 13 has been identified. Beside AD, the patient also has severe mental retardation and displays several dysmorphic features. Further FISH analyses revealed that the trisomy was caused by the translocation of a 13q subtelomeric fragment to the acrocentric tip of one chromosome 21 [46,XY.ish der(21) t(13;21) (q34;p13)(D13S1825+)]. Gene dosage experiments carried out with three multiallelic polymorphisms of the subtelomeric region of chromosome 13q showed that the putative length of the tr…

AdultMaleDerivative chromosomeAdolescentGene DosageautismChromosomal translocationTrisomyBiologyGene dosagePolymerase Chain ReactionTranslocation GeneticCellular and Molecular NeurosciencemedicineHumansAutistic DisorderChildGenetics (clinical)In Situ Hybridization FluorescenceChromosome 13GeneticsChromosomes Human Pair 13ChromosomeTelomereSubtelomeremedicine.diseasePsychiatry and Mental healthfrontal bossingFemaleTrisomyChromosome 21American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics
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Clonal evolution in relapsed NPM1-mutated acute myeloid leukemia.

2013

Mutations in the nucleophosmin 1 (NPM1) gene are considered a founder event in the pathogenesis of acute myeloid leukemia (AML). To address the role of clonal evolution in relapsed NPM1-mutated (NPM1mut) AML, we applied high-resolution, genome-wide, single-nucleotide polymorphism array profiling to detect copy number alterations (CNAs) and uniparental disomies (UPDs) and performed comprehensive gene mutation screening in 53 paired bone marrow/peripheral blood samples obtained at diagnosis and relapse. At diagnosis, 15 aberrations (CNAs, n = 10; UPDs, n = 5) were identified in 13 patients (25%), whereas at relapse, 56 genomic alterations (CNAs, n = 46; UPDs, n = 10) were detected in 29 patie…

AdultMaleNPM1MyeloidImmunologyBiologyGene mutationBiochemistrySomatic evolution in cancerPolymorphism Single NucleotideDNA Methyltransferase 3AClonal EvolutionYoung AdultRecurrenceRisk FactorsmedicineHumansDNA (Cytosine-5-)-MethyltransferasesAgedChromosomes Human Pair 13Myeloid leukemiaNuclear ProteinsCell BiologyHematologyMiddle Agedmedicine.diseasePrognosisMinimal residual diseaseDNA FingerprintingLeukemiaETV6Leukemia Myeloid Acutemedicine.anatomical_structureCancer researchFemaleChromosomes Human Pair 9NucleophosminGene DeletionBlood
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Testicular fusocellular rhabdomyosarcoma as a metastasis of elbow sclerosing rhabdomyosarcoma: A clinicopathologic, immunohistochemical and molecular…

2010

Abstract Sclerosing rhabdomyosarcoma (SRMS) is an infrequent variant of rhabdomyosarcoma characterized by extensive intercellular hyaline fibrosis. We report the case of a 37 year-old male with a 9 × 6 cm SRMS on the right elbow. Histologically, the tumor showed an abundant extracellular hyaline matrix with extratumoral vascular emboli and microscopic foci of fusocellular embryonal rhabdomyosarcoma (FRMS) separated by a fibrotic band from the sclerosing areas. One year later the patient presented with a right intratesticular tumor of 1.2 × 0.8 cm, which was reported as pure FRMS. Immunohistochemically, SRMS was positive only for MyoD1 and Vimentin and negative for Myogenin and Desmin. Both …

AdultMalePathologymedicine.medical_specialtyHistologyTime FactorsVimentinCase ReportSoft Tissue NeoplasmsSclerosing rhabdomyosarcomaBiologyTranslocation GeneticPathology and Forensic MedicineMetastasisFatal OutcomeTesticular Neoplasmslcsh:PathologymedicineBiomarkers TumorElbowHumansRhabdomyosarcoma EmbryonalWhole Body ImagingRhabdomyosarcomaHyalineIn Situ Hybridization FluorescenceSclerosisChromosomes Human Pair 13Forkhead Box Protein O1MediastinumForkhead Transcription FactorsGeneral Medicinemedicine.diseasemusculoskeletal systemFibrosisImmunohistochemistrymedicine.anatomical_structureTreatment OutcomeChemotherapy Adjuvantbiology.proteinDesminEmbryonal rhabdomyosarcomaTomography X-Ray ComputedOrchiectomylcsh:RB1-214
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MICRODISSECTION AND DOP-PCR-BASED REVERSE CHROMOSOME PAINTING AS A FAST AND RELIABLE STRATEGY IN THE ANALYSIS OF VARIOUS STRUCTURAL CHROMOSOME ABNORM…

1996

Reverse chromosome painting has become a powerful tool in clinical genetics for the characterization of cytogenetically unclassifiable aberrations. In this report, the application of a sensitive and rapid procedure for the complete and precise identification of four different de novo structural chromosome abnormalities is presented. These chromosome rearrangements include a marker derived from chromosome 3(cen-q11), an interstitial deletion of chromosome 13 [del(13)(q14q22)], an unbalanced translocation [46,XY, -4, +der(4)t(4;8)(p 15.2;p21.1)] leading to Wolf-Hirschhorn syndrome, and a partial inverted duplication in conjunction with a partial deletion of chromosome 5p [46,XX, -5, +der(5)(:…

Cri-du-Chat SyndromeDerivative chromosomeMarker chromosomeChromosomal translocationBiologyPolymerase Chain ReactionTranslocation GeneticChromosome (genetic algorithm)PregnancyPrenatal DiagnosismedicineHumansWolf–Hirschhorn syndromeIn Situ Hybridization FluorescenceGenetics (clinical)Chromosomal inversionChromosome 13Chromosome AberrationsGeneticsChromosomes Human Pair 13DissectionInfant NewbornObstetrics and Gynecologymedicine.diseaseMolecular biologyGenetic TechniquesChromosome 3FemaleChromosomes Human Pair 3Chromosomes Human Pair 4Gene DeletionChromosomes Human Pair 8Prenatal Diagnosis
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De novo 13q deletions in two patients with mild anorectal malformations as part of VATER/VACTERL and VATER/VACTERL-like association and analysis of E…

2013

Item does not contain fulltext Anorectal malformations (ARMs) comprise a broad spectrum of conditions ranging from mild anal anomalies to complex cloacal malformations. In 40-50% of cases, ARM occurs within the context of defined genetic syndromes or complex multiple congenital anomalies, such as VATER/VACTERL (vertebral defects [V], ARMs [A], cardiac defects [C], tracheoesophageal fistula with or without esophageal atresia [TE], renal malformations [R], and limb defects [L]) association. Here, we report the identification of deletions at chromosome 13q using single nucleotide polymorphism-based array analysis in two patients with mild ARM as part of VATER/VACTERL and VATER/VACTERL-like ass…

Heart Defects CongenitalMalemedicine.medical_specialtyCandidate geneLimb Deformities CongenitalTracheoesophageal fistulaSingle-nucleotide polymorphismContext (language use)Chromosome DisordersEphrin-B2BiologyGastroenterologyAnus ImperforateMiceEsophagusInternal medicineGeneticsmedicineAnimalsHumansIn patientGenetics (clinical)Mice KnockoutChromosomes Human Pair 13Infant NewbornChromosomeAnatomymedicine.diseaseAnorectal MalformationsSpineTracheaDisease Models AnimalRadiusHuman Reproduction Renal disorder [NCEBP 12]Evaluation of complex medical interventions [NCEBP 2]AtresiaChild PreschoolMutationMutation testingFemaleChromosome DeletionGenetics and epigenetic pathways of disease Genomic disorders and inherited multi-system disorders [NCMLS 6]American Journal of Medical Genetics. Part A
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A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk

2010

Combined analyses of gene networks and DNA sequence variation can provide new insights into the aetiology of common diseases that may not be apparent from genome-wide association studies alone. Recent advances in rat genomics are facilitating systems-genetics approaches. Here we report the use of integrated genome-wide approaches across seven rat tissues to identify gene networks and the loci underlying their regulation. We defined an interferon regulatory factor 7 (IRF7)-driven inflammatory network (IDIN) enriched for viral response genes, which represents a molecular biomarker for macrophages and which was regulated in multiple tissues by a locus on rat chromosome 15q25. We show that Epst…

Interferon Regulatory Factor-7Quantitative Trait LociGenome-wide association studyLocus (genetics)Single-nucleotide polymorphismBiologyQuantitative trait locusPolymorphism Single NucleotideArticleReceptors G-Protein-Coupled03 medical and health sciences0302 clinical medicineAnimalsHumansGene Regulatory NetworksGenetic Predisposition to DiseaseGene030304 developmental biologyGeneticsInflammation0303 health sciencesMultidisciplinaryBase SequenceChromosomes Human Pair 13MacrophagesChromosomes MammalianImmunity Innate3. Good healthRatsDiabetes Mellitus Type 1Genetic LociOrgan SpecificityVirusesIRF7Trans-acting030217 neurology & neurosurgeryInterferon regulatory factorsGenome-Wide Association Study
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Genetics of retinoblastoma: A study

1997

Abstract We have analyzed 43 families with either familial retinoblastoma (RB) (four kindreds), bilateral sporadic RB (10 individuals), or unilateral sporadic RB (29 individuals). Genetic studies focused on karyotype analysis, loss of heterozygosity of intragenic polymorphisms, and search for point mutations. We have been able to identify the genetic defect underlying the disease in eight cases. Deletions have been found in three patients with sporadic RB, two bilateral in one of which karyotyping had previously detected an interstitial deletion of chromosome 13 affecting (q13–q31) and one unilateral. Five different point mutations were responsible for three cases of bilateral sporadic RB, …

MaleCancer Researchmedicine.medical_specialtyGenetic counselingBiologymedicine.disease_causeLoss of heterozygosityGeneticsmedicineHumansPoint MutationGenes RetinoblastomaMolecular BiologyChromosome 13GeneticsMutationPolymorphism GeneticChromosomes Human Pair 13RetinoblastomaEye NeoplasmsPoint mutationRetinoblastomaCytogeneticsmedicine.diseasePedigreeKaryotypingFemaleCarcinogenesisGene DeletionCancer Genetics and Cytogenetics
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Holoprosencephaly: examples of clinical variability and etiologic heterogeneity.

1990

Clinical variability and causal heterogeneity of holoprosencephaly is discussed in relation to several newborn infants with cyclopia (cases 4,5,6), cebocephaly (cases 2,3), and premaxillary agenesis (case 1). In subjects with holoprosencephaly, the presence of multiple malformations is an indicator of concomitant chromosome aberrations, as in present case 1 (Down syndrome) and case 3 (trisomy 13). Cases 5 and 6 are two monozygotic twins with the same type of cyclopia and alobar holoprosencephaly recognized by prenatal ultrasonography. The diagnostic importance of ultrasonographic, cytogenetic, and pathological studies is pointed out in view of etiologic evaluation, genetic counseling, and p…

MaleDown syndromePediatricsmedicine.medical_specialtyGenetic counselingTrisomyBiologyHoloprosencephalyHoloprosencephalymedicineHumansAbnormalities MultipleMULTIPLE MALFORMATIONSPathologicalGenetics (clinical)Chromosome AberrationsChromosomes Human Pair 13Infant NewbornAnatomyCyclopiamedicine.diseaseFaceCebocephalyFemaleDown SyndromeTrisomyHeadAmerican journal of medical genetics
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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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