Search results for " 11"

showing 10 items of 591 documents

Chromosomal changes in renal oncocytomas Evidence that t(5;11)(q35;q13) may characterize a second subgroup of oncocytomas

1995

Many of the reported oncocytomas have different chromosome abnormalities, indicating that they comprise a cytogenetically heterogenous group of tumors consisting of potentially cytogenetic subgroups. We have performed cytogenetic studies on nine renal oncocytomas. Clonal abnormalities were present in eight tumors. The findings most observed were the loss of the Y chromosome, and abnormalities of chromosomes 1 and 22. We also observed telomeric associations (tas) in two tumors and structural aberrations of chromosomes 9p and 19q, as well as monosomy 10. In two cases we found a similar reciprocal t(5;11)(q35;q13) in two cases. Review of the literature disclosed one other oncocytoma with a t(5…

AdenomaMalecongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchMonosomyPathologymedicine.medical_specialtyChromosomal translocationBiologyurologic and male genital diseasesY chromosomeTranslocation GeneticGeneticsmedicineHumansOncocytomaMolecular BiologyAgedChromosome AberrationsGeneticsChromosome 7 (human)KidneyChromosomes Human Pair 11ChromosomeCancerMiddle Agedmedicine.diseaseKidney Neoplasmsmedicine.anatomical_structureKaryotypingChromosomes Human Pair 5FemaleCancer Genetics and Cytogenetics
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Comparative genetic study of intratumoral heterogenous MYCN amplified neuroblastoma versus aggressive genetic profile neuroblastic tumors.

2016

Intratumoral heterogeneous MYCN amplification (hetMNA) is an unusual event in neuroblastoma with unascertained biological and clinical implications. Diagnosis is based on the detection of MYCN amplification surrounded by non-amplified tumor cells by fluorescence in situ hybridization (FISH). To better define the genetic features of hetMNA tumors, we studied the Spanish cohort of neuroblastic tumors by FISH and single nucleotide polymorphism arrays. We compared hetMNA tumors with homogeneous MNA (homMNA) and nonMNA tumors with 11q deletion (nonMNA w11q-). Of 1091 primary tumors, 28 were hetMNA by FISH. Intratumoral heterogeneity of 1p, 2p, 11q and 17q was closely associated with hetMNA tumor…

Adult0301 basic medicineCancer ResearchCandidate geneAdolescentGene DosageSingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideGene dosageGenetic profileCohort StudiesNeuroblastomaYoung Adult03 medical and health sciences0302 clinical medicineNeuroblastomaGeneticsmedicineHumansChildMolecular BiologyIn Situ Hybridization FluorescenceAgedAged 80 and overOncogene ProteinsGeneticsN-Myc Proto-Oncogene Proteinmedicine.diagnostic_testChromosomes Human Pair 11Nuclear ProteinsChromosomeMiddle Agedmedicine.diseaseNeuroblastic Tumor030104 developmental biologyChromosomes Human Pair 1Child PreschoolChromosomes Human Pair 2030220 oncology & carcinogenesisCancer researchChromosome DeletionChromosomes Human Pair 17Fluorescence in situ hybridization
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Genesis of variant Philadelphia chromosome translocations in chronic myelocytic leukemia.

2003

The Philadelphia (Ph) chromosome is found in more than 90% of chronic myelocytic leukemia (CML) patients. In most cases, it results from the reciprocal t(9;22)(q34;q11), with the ABL proto-oncogene from 9q34 fused to the breakpoint cluster region (BCR) locus on 22q11. In 5%-10% of patients with CML, the Ph chromosome originates from variant translocations, involving various breakpoints in addition to 9q34 and 22q11. In our investigation, three CML cases with complex Ph translocations have been analyzed by G-banding and fluorescence in situ hybridization (FISH). FISH with breakpoint-spanning probes for the BCR and ABL genes revealed information about the genesis of complex Ph translocations.…

AdultGenetic MarkersMaleCancer Researchmedicine.medical_specialtyChromosomes Human Pair 22Chromosomal translocationLocus (genetics)BiologyPhiladelphia chromosomeProto-Oncogene MasTranslocation Genetichemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositiveGeneticsmedicineHumansPhiladelphia ChromosomeMolecular BiologyIn Situ Hybridization FluorescenceGeneticsABLmedicine.diagnostic_testChromosomes Human Pair 11BreakpointCytogeneticsbreakpoint cluster regionGenetic VariationMiddle Agedmedicine.diseaseChromosome BandingKaryotypingFemaleChromosomes Human Pair 9Fluorescence in situ hybridizationCancer genetics and cytogenetics
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Translocations Disrupting PHF21A in the Potocki-Shaffer-Syndrome Region Are Associated with Intellectual Disability and Craniofacial Anomalies

2012

Contains fulltext : 110038.pdf (Publisher’s version ) (Closed access) Potocki-Shaffer syndrome (PSS) is a contiguous gene disorder due to the interstitial deletion of band p11.2 of chromosome 11 and is characterized by multiple exostoses, parietal foramina, intellectual disability (ID), and craniofacial anomalies (CFAs). Despite the identification of individual genes responsible for multiple exostoses and parietal foramina in PSS, the identity of the gene(s) associated with the ID and CFA phenotypes has remained elusive. Through characterization of independent subjects with balanced translocations and supportive comparative deletion mapping of PSS subjects, we have uncovered evidence that t…

AdultMaleAdolescentGenotypePotocki–Shaffer syndromeChromosome DisordersHaploinsufficiencyBiologyHistone DeacetylasesSodium ChannelsTranslocation GeneticArticleChromatin remodelingCraniofacial Abnormalities03 medical and health sciencesSCN3A0302 clinical medicineIntellectual DisabilityNAV1.3 Voltage-Gated Sodium ChannelmedicineTranscriptional regulationGeneticsAnimalsHumansDeletion mappingGenetics(clinical)CraniofacialZebrafishGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesChromosomes Human Pair 11Infant Newbornmedicine.diseaseGenetics and epigenetic pathways of disease DCN MP - Plasticity and memory [NCMLS 6]Child PreschoolHomeoboxFemaleChromosome DeletionHaploinsufficiencyExostoses Multiple Hereditary030217 neurology & neurosurgeryThe American Journal of Human Genetics
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Analysis of translocations that involve theNUP98 gene in patients with 11p15 chromosomal rearrangements

2004

The NUP98 gene has been reported to be fused with at least 15 partner genes in leukemias with 11p15 translocations. We report the results of screening of cases with cytogenetically documented rearrangements of 11p15 and the subsequent identification of involvement of NUP98 and its partner genes. We identified 49 samples from 46 hematology patients with 11p15 (including a few with 11p14) abnormalities, and using fluorescence in situ hybridization (FISH), we found that NUP98 was disrupted in 7 cases. With the use of gene-specific FISH probes, in 6 cases, we identified the partner genes, which were PRRX1 (PMX1; in 2 cases), HOXD13, RAP1GDS1, HOXC13, and TOP1. In the 3 cases for which RNA was a…

AdultMaleCancer Researchmedicine.medical_specialtyAdolescentMolecular Sequence DataChromosomal translocationBiologyTranslocation GeneticComplementary DNAInternal medicineGeneticsmedicineGuanine Nucleotide Exchange FactorsHumansGenetic Predisposition to DiseaseGeneIn Situ Hybridization FluorescenceHomeodomain ProteinsGeneticsNUP98 GeneLeukemiaHematologyBase Sequencemedicine.diagnostic_testChromosomes Human Pair 11BreakpointInfantMolecular biologyNuclear Pore Complex ProteinsDNA Topoisomerases Type IHOXD13Child PreschoolTranscription FactorsFluorescence in situ hybridizationGenes, Chromosomes and Cancer
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An unusual translocation associated with recurrent spontaneous abortions

1989

The authors report a case of 11;17 translocation associated with recurrent spontaneous abortions, and request contact with colleagues who have observed similar cases.

AdultMaleGeneticsAbortion HabitualChromosomes Human Pair 11Chromosomal translocationBiologyMolecular medicineTranslocation GeneticHuman geneticsPregnancyKaryotypingGeneticsHumansFemaleGenetics (clinical)Chromosomes Human Pair 17Human Genetics
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KIAA0556 is a novel ciliary basal body component mutated in Joubert syndrome

2015

Background Joubert syndrome (JBTS) and related disorders are defined by cerebellar malformation (molar tooth sign), together with neurological symptoms of variable expressivity. The ciliary basis of Joubert syndrome related disorders frequently extends the phenotype to tissues such as the eye, kidney, skeleton and craniofacial structures. Results Using autozygome and exome analyses, we identified a null mutation in KIAA0556 in a multiplex consanguineous family with hallmark features of mild Joubert syndrome. Patient-derived fibroblasts displayed reduced ciliogenesis potential and abnormally elongated cilia. Investigation of disease pathophysiology revealed that Kiaa0556-/- null mice possess…

AdultMaleK04F10.2KIAA0556MicrotubuleMicrotubulesRetinaMiceJoubert syndromeCerebellumAnimalsHumansAbnormalities MultipleExomeCiliaEye AbnormalitiesSensory disorders Radboud Institute for Molecular Life Sciences [Radboudumc 12]Caenorhabditis elegansChildCells CulturedAdenosine TriphosphatasesADP-Ribosylation FactorsResearchBrainMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]Kidney Diseases CysticBasal BodiesPedigreeMice Inbred C57BLRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]Basal bodyChild PreschoolMutationFemaleKataninMicrotubule-Associated ProteinsProtein BindingGenome Biology
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Bcl-6 mutation status provides clinically valuable information in early-stage B-cell chronic lymphocytic leukemia

2004

In B-cell chronic lymphocytic leukemia (B-CLL), somatic mutation of IgVH genes defines a subgroup with favorable prognosis, whereas the absence of IgVH mutations is correlated with a worse outcome. Mutations of the BCL-6 gene are also observed in a subset of B-CLL, but the clinical significance of this molecular alteration remains uncertain. We examined the distribution of IgVH and BCL-6 gene mutations in 95 well-characterized patients with Binet stage A B-CLL, and correlated them with clinical, laboratory, cytogenetic findings and disease progression. Mutations of the BCL-6 gene were observed only in cases harboring mutated IgVH. Unexpectedly, coexistence of IgVH and BCL-6 mutations was co…

AdultMaleOncologyCancer Researchmedicine.medical_specialtyChronic lymphocytic leukemiaImmunoglobulin Variable RegionLocus (genetics)BiologyGene mutationDisease-Free SurvivalGermline mutationProto-Oncogene ProteinsInternal medicinemedicineHumansB-cell chronic lymphocytic leukemiaClinical significanceProspective StudiesGeneAgedAged 80 and overHematologyChromosomes Human Pair 11HematologyMiddle AgedPrognosismedicine.diseaseLeukemia Lymphocytic Chronic B-CellDNA-Binding ProteinsOncologyMutationImmunologyProto-Oncogene Proteins c-bcl-6FemaleChromosome DeletionChromosomes Human Pair 17Follow-Up StudiesTranscription FactorsLeukemia
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Somatic loss of an EXT2 gene mutation during malignant progression in a patient with hereditary multiple osteochondromas

2015

Multiple osteochondromas (MO) is an autosomal-dominant skeletal disorder caused by mutations in the exostosin-1 ( EXT1 ) or exostosin-2 ( EXT2 ) genes. In this study, we report the analysis of the mutational status of the EXT2 gene in tumor samples derived from a patient affected by hereditary MO, documenting the somatic loss of the germline mutation in a giant chondrosarcoma and in a rapidly growing osteochondroma. The sequencing of all exons and exon–intron junctions of the EXT1 and EXT2 genes from blood DNA of the proband did not reveal any mutation in the EXT1 gene but did demonstrate the presence of the transition point mutation c.67C > T in the EXT2 gene, determining the introduction …

AdultMaleOsteochondromaCancer ResearchMultiple osteochondromaSettore MED/06 - Oncologia MedicaChondrosarcomaLoss of HeterozygositySettore BIO/11 - Biologia MolecolareBone NeoplasmsGene mutationBiologyN-Acetylglucosaminyltransferasesmedicine.disease_causeGermlineLoss of heterozygosityGermline mutationGeneticChondrosarcoma; Hereditary cancer; Hereditary multiple osteochondromas; Tumor suppressor gene; Molecular Biology; Genetics; Cancer ResearchSkeletal disorderGeneticsmedicineHumansTumor suppressor geneHereditary multiple osteochondromaMolecular BiologyGeneticsMutationChromosomes Human Pair 11DNA Neoplasmmedicine.diseaseHereditary cancerSettore MED/18 - Chirurgia GeneraleSettore MED/03 - Genetica MedicaMutationDisease ProgressionCancer Genetics
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Translocation (11;22) in small cell osteosarcoma

1990

AdultMaleOsteosarcomaCancer Researchmedicine.medical_specialtyLung NeoplasmsChromosomes Human Pair 11Chromosomes Human Pair 22CytogeneticsBone NeoplasmsKaryotypeChromosomal translocationBiologymedicine.diseaseMolecular biologyTranslocation GeneticSmall Cell OsteosarcomaScapulaKaryotypingGeneticsmedicineHumansOsteosarcomaMolecular BiologyCancer Genetics and Cytogenetics
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