Search results for "Duplication"

showing 10 items of 216 documents

Amplification of ETS2 oncogene in acute nonlymphoblastic leukemia with t(6;21;18).

1992

Cytogenetic and molecular studies in a case of acute nonlymphoblastic leukemia (ANLL) are reported in this paper. Bone marrow blasts carried a hypodiploid karyotype with a complex t(6;18;21)(6qter----6p21::21q22----21qter;18qter ----18p11::6p22----6pter; 21pter----21q22::6p21----6p22::18p11----18pte r) and other numerical and structural changes. We studied the organization and the expression of the ETS2 gene which is located on chromosome 21 in order to investigate its possible involvement in the disease. DNA analysis showed a 20-fold amplification of ETS2 sequences; an increase of 3- to 4-fold in the mRNAs level compared to normal was shown by Northern hybridization.

MaleCancer ResearchChromosomes Human Pair 21Chromosomal translocationBiologyTranslocation GeneticProto-Oncogene Protein c-ets-2Proto-Oncogene ProteinsGene duplicationGeneticsmedicineHumansNorthern blotMolecular BiologySouthern blotAgedChromosome AberrationsOncogeneGene AmplificationKaryotypeProtein-Tyrosine KinasesBlotting NorthernMolecular biologyDNA-Binding ProteinsRepressor ProteinsBlotting SouthernLeukemia Myeloid Acutemedicine.anatomical_structureCancer researchTrans-ActivatorsChromosomes Human Pair 6Bone marrowChromosome 21Chromosomes Human Pair 18Transcription FactorsCancer genetics and cytogenetics
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Cytogenetic and molecular findings related to rhabdomyosarcoma. An analysis of seven cases.

2003

Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma in childhood. Histologically, it is subdivided histologically into two main subtypes: alveolar (ARMS) and embryonal (ERMS). ARMS is characterized by t(2;13)(q35;q14) or its variant t(1;13)(p36;q14), which fuse PAX3 and PAX7, respectively, with FKHR to produce chimeric genes. ERMS is frequently associated with loss of heterozygosity of 11p15.5. We investigated seven RMS (three ARMS and four ERMS) by means of cytogenetic, fluorescence in situ hybridization, and molecular analyses, including the study of the main genes implicated in the G1- to S-phase cell cycle transition, and correlated these studies with pathologic findings and c…

MaleCancer ResearchPAX3Genes mycLocus (genetics)Chimeric geneBiologyLoss of heterozygosityGene duplicationRhabdomyosarcomaGeneticsmedicineHumansPaired Box Transcription FactorsRhabdomyosarcomaChildMolecular BiologyPAX3 Transcription FactorIn Situ Hybridization FluorescenceChromosome AberrationsHomeodomain Proteinsmedicine.diagnostic_testForkhead Box Protein O1Hybridization probePAX7 Transcription FactorForkhead Transcription Factorsmedicine.diseaseMolecular biologyDNA-Binding ProteinsChild PreschoolFemaleFluorescence in situ hybridizationTranscription FactorsCancer genetics and cytogenetics
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Deregulation of the G1 to S-phase cell cycle checkpoint is involved in the pathogenesis of human osteosarcoma.

2004

Osteosarcoma (OS) displays complex karyotypes with numerical changes as well as structural abnormalities suggesting that several oncogenes and tumor suppressor genes may be implicated in the biology of OS. The aim of our study was to investigate the possible implication of the molecular alterations of the G1 to S-phase checkpoint genes in the pathogenesis of OS. We analyzed samples from 29 patients and found molecular alterations of the RB and TP53 genes in 6 (21%) and 3 (10%) cases, respectively. Homozygous deletion of the INK4A/ARF locus and methylation of INK4A was detected in 3 (10%) and 2 (7%) cases, respectively. CDK4 and MDM2 co-amplification was observed in 1 case (3%). Cyclin D3 is…

MaleCell cycle checkpointAdolescentLocus (genetics)Bone NeoplasmsBiologyPathology and Forensic MedicineS PhasePathogenesisGene duplicationmedicineHumansCHEK1Cyclin D3ChildMolecular BiologyAgedOsteosarcomaReverse Transcriptase Polymerase Chain ReactionCell CycleAge FactorsG1 PhaseGene AmplificationCell BiologyG2-M DNA damage checkpointMiddle Agedmedicine.diseaseGenes cdcHistory 16th CenturyCancer researchOsteosarcomaFemaleChromosomes Human Pair 9Diagnostic molecular pathology : the American journal of surgical pathology, part B
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Mantle-cell lymphoma genotypes identified with CGH to BAC microarrays define a leukemic subgroup of disease and predict patient outcome

2005

To identify recurrent genomic changes in mantle cell lymphoma (MCL), we used high-resolution comparative genomic hybridization (CGH) to bacterial artificial chromosome (BAC) microarrays in 68 patients and 9 MCL-derived cell lines. Array CGH defined an MCL genomic signature distinct from other B-cell lymphomas, including deletions of 1p21 and 11q22.3-ATM gene with coincident 10p12-BMI1 gene amplification and 10p14 deletion, along with a previously unidentified loss within 9q21-q22. Specific genomic alterations were associated with different subgroups of disease. Notably, 11 patients with leukemic MCL showed a different genomic profile than nodal cases, including 8p21.3 deletion at tumor necr…

MaleChromosomes Artificial BacterialGenotypeImmunologyLocus (genetics)Lymphoma Mantle-CellBiologyBiochemistryGene duplicationmedicineHumansAgedOligonucleotide Array Sequence AnalysisSequence DeletionAged 80 and overGeneticsLeukemiaGene Expression ProfilingGenomic signatureGenomicsCell BiologyHematologyMiddle Agedmedicine.diseaseLymphomaSurvival RateGene expression profilingTreatment OutcomeGenomic ProfileCancer researchFemaleMantle cell lymphomaComparative genomic hybridizationBlood
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The first case of myoclonic epilepsy in a child with a de novo 22q11.2 microduplication

2011

Chromosome 22, particularly the q11.2 sub-band, has long been recognized as responsible for multiple congenital anomaly disorders. In particular, its susceptibility to subtle microdeletions or, more rarely, microduplications has been attributed to the presence of several low-copy repeats spanning the region as mediators of nonallelic homologous recombination that result in 22q11.2 rearrangements. While recent data suggest that the frequency of 22q11.2 microduplications could be approximately half of all deletions, now only 50 unrelated cases have been reported thus far. However, it is reasonable to suppose that microduplications of 22q11.2 may be largely undetected as a result of a less-dis…

MaleChromosomes Human Pair 22Non-allelic homologous recombinationEpilepsies MyoclonicMultiple congenital anomalyBiologyRAB36 genemyoclonic epilepsySettore MED/38 - Pediatria Generale E SpecialisticaChromosome DuplicationGene duplicationClinical heterogeneityGeneticsmedicineHumansChildIn Situ Hybridization FluorescenceGenetics (clinical)GeneticsComparative Genomic HybridizationFaciesmedicine.diseaseMild learning difficultiesdevelopmental delayPhenotypeSettore MED/03 - Genetica MedicaChild PreschoolMyoclonic epilepsynonallelic homologous recombinationChromosome 2222q11.2 microduplicationComparative genomic hybridizationAmerican Journal of Medical Genetics Part A
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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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Delineation of a new chromosome 20q11.2 duplication syndrome including the ASXL1 gene.

2013

We report on three males with de novo overlapping 7.5, 9.8, and 10 Mb duplication of chromosome 20q11.2. Together with another patient previously published in the literature with overlapping 20q11 microduplication, we show that such patients display common clinical features including metopic ridging/trigonocephaly, developmental delay, epicanthal folds, and short hands. The duplication comprised the ASXL1 gene, in which de novo heterozygous nonsense or truncating mutations have recently been reported in patients with Borhing-Opitz syndrome. Because of craniofacial features in common with Borhing-Opitz syndrome, in particular metopic ridging/trigonocephaly, we suggest that duplication of ASX…

MaleHeterozygotemedia_common.quotation_subjectDevelopmental DisabilitiesNonsenseChromosomes Human Pair 20TrigonocephalyTrisomyBiologymedicine.disease_causeCraniosynostosesPregnancyIntellectual DisabilityGene duplicationGeneticsmedicineHumansCraniofacialChildGenetics (clinical)media_commonGeneticsMutationMosaicismChromosomeInfantHeterozygote advantageSyndromemedicine.diseasePhenotypeRepressor ProteinsChild PreschoolMutationFemaleHand Deformities CongenitalAmerican journal of medical genetics. Part A
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MALT1 is deregulated by both chromosomal translocation and amplification in B-cell non-Hodgkin lymphoma

2003

The MALT1 gene was identified through its involvement in t(11;18)(q21;q21), seen in 30% of cases of mucosa-associated lymphoid tissue (MALT) lymphoma. Here, we show that deregulated MALT1 expression may occur in B-cell non-Hodgkin lymphoma (B-NHL) of various histologic subtypes either through translocation to the immunoglobulin heavy chain (IGH) locus or by genomic amplification. First, 2 cases, one case of MALT lymphoma and another of aggressive marginal zone lymphoma (MZL) with t(14;18)(q32;q21), cytogenetically identical to the translocation involving BCL2, were shown by fluorescence in situ hybridization (FISH) to involve MALT1, which lies about 5 Mb centromeric of BCL2. Molecular cloni…

MaleLymphoma B-CellImmunologyBiologyBiochemistryTranslocation Geneticimmune system diseaseshemic and lymphatic diseasesGene duplicationmedicineHumansRNA NeoplasmAgedChromosomes Human Pair 14medicine.diagnostic_testGene Expression ProfilingGene AmplificationMALT lymphomaLymphoma B-Cell Marginal ZoneCell BiologyHematologyMiddle Agedmedicine.diseaseMolecular biologyGenes bcl-2Neoplasm ProteinsGene Expression Regulation NeoplasticGene expression profilingMALT1Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinCaspasesB-Cell Non-Hodgkin LymphomaImmunoglobulin heavy chainFemaleChromosomes Human Pair 18Comparative genomic hybridizationFluorescence in situ hybridizationBlood
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SNPs array karyotyping reveals a novel recurrent 20p13 amplification in primary myelofibrosis.

2011

The molecular pathogenesis of primary mielofibrosis (PMF) is still largely unknown. Recently, single-nucleotide polymorphism arrays (SNP-A) allowed for genome-wide profiling of copy-number alterations and acquired uniparental disomy (aUPD) at high-resolution. In this study we analyzed 20 PMF patients using the Genome-Wide Human SNP Array 6.0 in order to identify novel recurrent genomic abnormalities. We observed a complex karyotype in all cases, detecting all the previously reported lesions (del(5q), del(20q), del(13q), +8, aUPD at 9p24 and abnormalities on chromosome 1). In addition, we identified several novel cryptic lesions. In particular, we found a recurrent alteration involving cytob…

MaleMicroarraysMIELOFIBROSISChromosomes Human Pair 20Loss of Heterozygositylcsh:MedicineLoss of heterozygosityCohort StudiesHematologic Cancers and Related DisordersGene duplicationTaq Polymeraselcsh:ScienceOligonucleotide Array Sequence AnalysisMultidisciplinaryMYELOFIBROSIS; SNPKaryotypeGenomicsHematologyUniparental disomyMedicineFemaleImmunohistochemical AnalysisSNP arrayResearch ArticleTest Evaluationmedicine.medical_specialtyDNA Copy Number VariationsImmunologySNPLocus (genetics)Single-nucleotide polymorphismReceptors Cell SurfaceBiologyPolymorphism Single NucleotideDiagnostic MedicinemedicineGeneticsHumansBiologyAgedEvolutionary BiologyMyeloproliferative DisordersPopulation Biologylcsh:RCytogeneticsGene AmplificationComputational BiologyDNAUniparental Disomymedicine.diseaseMolecular biologyMYELOFIBROSISPrimary MyelofibrosisKaryotypingGenetic PolymorphismImmunologic TechniquesClinical Immunologylcsh:QPopulation GeneticsPLoS ONE
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Acute onset of esophageal duplication cyst in adult. Case report.

2009

Esophageal duplication (ED) cyst is unusual congenital disorder of the foregut, accounting for 10% to 15% of duplications of all foregut cysts. We report a case of esophageal duplication with acute clinical presentation, treated successfully with surgical resection.46-year-old man with acute dysphagia and gastroesophageal reflux of 2 weeks duration, showed submucosal bulging mass in the posterior wall of the middle third of oesophagus, fluid-filled cystic structure, dyshomogeneous, low-attenuation mass with smooth borders compatible with an hemorrhagic esophageal duplication cyst. With the suspect of acute presentation of a complicated esophageal cyst, the patient underwent surgery by right…

MaleMiddle AgedEsophageal DiseasesRadiographyEsophageal duplication cyst thoracic surgeryEsophagusThoracotomyEsophagoplastyAcute DiseaseGastroesophageal RefluxHumansEsophageal CystAge of OnsetDeglutition DisordersGastrointestinal Hemorrhage
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