Search results for " deletion"

showing 10 items of 361 documents

Contribution of Large Genomic Rearrangements in Italian Lynch Syndrome Patients: Characterization of a Novel Alu-Mediated Deletion

2012

Lynch syndrome is associated with germ-line mutations in the DNA mismatch repair (MMR) genes, mainlyMLH1andMSH2. Most of the mutations reported in these genes to date are point mutations, small deletions, and insertions. Large genomic rearrangements in the MMR genes predisposing to Lynch syndrome also occur, but the frequency varies depending on the population studied on average from 5 to 20%. The aim of this study was to examine the contribution of large rearrangements in theMLH1andMSH2genes in a well-characterised series of 63 unrelated Southern Italian Lynch syndrome patients who were negative for pathogenic point mutations in theMLH1,MSH2, andMSH6genes. We identified a large novel delet…

Malecongenital hereditary and neonatal diseases and abnormalitiesgenomic rearragementArticle SubjectPopulationlcsh:MedicineSettore BIO/11 - Biologia MolecolareBiologyMLH1General Biochemistry Genetics and Molecular Biologynovel Alu-mediated deletionAlu ElementsmedicineHumanseducationneoplasmsAdaptor Proteins Signal TransducingSequence DeletionGene RearrangementGeneticseducation.field_of_studyGeneral Immunology and MicrobiologyPoint mutationlcsh:RNuclear ProteinsLynch syndrome; genomic rearragements; novel Alu-mediated deletionnutritional and metabolic diseasesGeneral MedicineGene rearrangementmedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisMolecular biologyLynch syndromedigestive system diseasesDNA-Binding ProteinsMSH6Settore MED/18 - Chirurgia GeneraleLynch syndromeMutS Homolog 2 ProteinItalyMSH2FemaleDNA mismatch repairMutL Protein Homolog 1Research ArticleBioMed Research International
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2p15-p16.1 microdeletions encompassing and proximal to BCL11A are associated with elevated HbF in addition to neurologic impairment.

2015

Elevated fetal hemoglobin (HbF) ameliorates the clinical severity of hemoglobinopathies such as β-thalassemia and sickle cell anemia. Currently, the only curative approach for individuals under chronic transfusion/chelation support therapy is allogeneic stem cell transplantation. However, recent analyses of heritable variations in HbF levels have provided a new therapeutic target for HbF reactivation: the transcriptional repressor BCL11A. Erythroid-specific BCL11A abrogation is now actively being sought as a therapeutic avenue, but the specific impact of such disruption in humans remains to be determined. Although single nucleotide polymorphisms in BCL11A erythroid regulatory elements have …

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentImmunologyBiologyBiochemistrySettore MED/38 - Pediatria Generale E SpecialisticaRed Cells Iron and ErythropoiesisInternal medicinehemic and lymphatic diseasesFetal hemoglobinmedicineGene silencingHumansChildNervous System DiseaseFetal HemoglobinNuclear ProteinHematologyNuclear ProteinsCell BiologyHematologymedicine.diseasePhenotypeSickle cell anemiaUp-RegulationTransplantationRepressor ProteinsSettore MED/03 - Genetica MedicaChromosomes Human Pair 22p15-p16.1 microdeletions BCL11A HbF neurologicImmunologyFemaleStem cellChromosome DeletionNervous System DiseasesCarrier ProteinHaploinsufficiencyCarrier ProteinsHumanBlood
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Germline deletion of Cetn1 causes infertility in male mice

2013

Centrins are calmodulin-like Ca2+-binding proteins that can be found in all ciliated eukaryotic cells from yeast to mammals. Expressed in male germ cells and photoreceptors, centrin 1 (CETN1) resides in the photoreceptor transition zone and connecting cilium. To identify its function in mammals, we deleted Cetn1 by homologous recombination. Cetn1−/− mice were viable and showed no sign of retina degeneration suggesting that CETN1 is nonessential for photoreceptor ciliogenesis or structural maintenance. Phototransduction components localized normally to the Cetn1−/− photoreceptor outer segments, and loss of CETN1 had no effect on light-induced translocation of transducin to the inner segment.…

Maleendocrine systemLight Signal TransductionCentrioleChromosomal Proteins Non-HistoneSpermiogenesisBiologyMice03 medical and health sciencesRetinal Rod Photoreceptor CellsCiliogenesismedicineAnimalsBasal bodyTransducinSpermatogenesisGerm-Line MutationInfertility MaleCentriolesSequence Deletion030304 developmental biologyMice KnockoutGenetics0303 health sciencesSpermatidCalcium-Binding ProteinsCell Cycle030302 biochemistry & molecular biologyCell DifferentiationCell BiologySpermatidsCell biologyMice Inbred C57BLmedicine.anatomical_structureCentrinFemalesense organsTransducinResearch ArticleVisual phototransductionJournal of Cell Science
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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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Chromosomal rearrangements in childhood acute myeloid leukemia and myelodysplastic syndromes.

1999

Recurrent chromosomal abnormalities present in the malignant cells of children with acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) often correlate closely with specific clinical and biologic characteristics of the disease. Certain unique cytogenetic rearrangements are associated with distinct morphologic leukemic subtypes. These rearrangements should be detectable in most children with AML and MDS with the use of complementary molecular techniques such as fluorescence in situ hybridization (FISH), Southern blotting, and polymerase chain reaction. Apart from the diagnostic assessment, cytogenetic findings sometimes predict clinical outcome and thus also serve as prognostic …

Malemedicine.medical_specialtyAdolescentOncogene Proteins FusionDiseasePatient Care PlanningTranslocation GeneticPolyploidyhemic and lymphatic diseasesBiomarkers TumorMedicineChromosomes HumanHumansChildChromosome Aberrationsmedicine.diagnostic_testbusiness.industryMyelodysplastic syndromesChildhood Acute Myeloid LeukemiaCytogeneticsMyeloid leukemiaInfantNeoplasms Second PrimaryHematologyGene rearrangementOncogenesmedicine.diseasePrognosisFusion proteinOncologyLeukemia MyeloidChild PreschoolMyelodysplastic SyndromesPediatrics Perinatology and Child HealthImmunologyAcute DiseaseCancer researchFemaleChromosome DeletionbusinessFluorescence in situ hybridizationJournal of pediatric hematology/oncology
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Cardiovascular risk factors, angiotensin-converting enzyme gene I/D polymorphism, and left ventricular mass in systemic hypertension.

1999

We investigated the influence of major cardiovascular risk factors (smoking, hypercholesterolemia, diabetes mellitus) on the association between angiotensin-converting enzyme (ACE) gene insertion (I)/deletion (D) polymorphism and echocardiographic left ventricular mass in 225 patients with sustained hypertension, assessed by ambulatory blood pressure monitoring. When the study population was analyzed as a whole, the 3 ACE genotypes did not differ in left ventricular mass (II, 47 g/m2.7; ID, 49 g/m2.7; DD, 51 g/m2.7; p = NS). No difference was found in subjects (n = 135) in whom at least 1 major cardiovascular risk factor was present (II, 51 g/m2.7; ID, 51 g/m2.7; DD: 52 g/m2.7; p = NS). In …

Malemedicine.medical_specialtyAmbulatory blood pressureGenotypeHeart VentriclesPeptidyl-Dipeptidase ALeft ventricular hypertrophyPolymerase Chain ReactionMuscle hypertrophyRisk FactorsInternal medicineDiabetes mellitusmedicineHumansRisk factorAllelesRetrospective StudiesPolymorphism Geneticbiologybusiness.industryAngiotensin-converting enzymeOdds ratioDNABlood Pressure Monitoring AmbulatoryMiddle Agedmedicine.diseasePrognosisEchocardiography DopplerCardiovascular DiseasesHypertensionCardiologybiology.proteinPopulation studyFemaleHypertrophy Left VentricularCardiology and Cardiovascular MedicinebusinessGene DeletionFollow-Up Studies
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Adipocyte cannabinoid CB1 receptor deficiency alleviates high fat diet-induced memory deficit, depressive-like behavior, neuroinflammation and impair…

2019

Abstract Background Obesity is a low-grade inflammation condition that facilitates the development of numerous comorbidities and the dysregulation of brain homeostasis. Additionally, obesity also causes distinct behavioral alterations both in humans and rodents. Here, we investigated the effect of inducible genetic deletion of the cannabinoid type 1 receptor (CB1) in adipocytes (Ati-CB1-KO mice) on obesity-induced memory deficits, depressive-like behavior, neuroinflammation and adult neurogenesis. Methods Behavioral, mRNA expression and immunohistochemical studies were performed in Ati-CB1-KO mice and corresponding wild-type controls under standard and high-fat diet. Results Adipocyte-speci…

Malemedicine.medical_specialtyCannabinoid receptorNeurogenesisEndocrinology Diabetes and Metabolismmedicine.medical_treatmentInflammationDiet High-FatMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineEndocrinologyNeural Stem CellsNeuritisReceptor Cannabinoid CB1AdipocyteInternal medicineAdipocytesmedicineAnimalsBiological PsychiatryNeuroinflammationMice KnockoutMemory DisordersBehavior AnimalDepressionEndocrine and Autonomic Systemsbusiness.industryNeurogenesisBrain030227 psychiatryAdult Stem CellsPsychiatry and Mental healthEndocrinologynervous systemchemistryGliosisOrgan SpecificityCannabinoidmedicine.symptombusinessGene Deletion030217 neurology & neurosurgeryHomeostasisPsychoneuroendocrinology
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14q13.1-21.1 deletion encompassing the HPE8 locus in an adolescent with intellectual disability and bilateral microphthalmia, but without holoprosenc…

2011

Interstitial deletions involving 14q13.1q21.1 are rare. In the literature at least 10 cases involving this region have been described and all patients showed a phenotype within the holoprosencephaly (HPE) spectrum. Previous studies suggested the HPE8 region as a candidate locus for HPE at 14q13. We report an adolescent with a 14q13.1q21.1 deletion encompassing the HPE8 region associated with intellectual disability (ID), bilateral microphthalmia, and coloboma, without cerebral anomalies typical of HPE. Except for ocular defects (i.e., microphthalmia, coloboma) consistent with HPE-type anomalies, the minor facial dysmorphia was not suggestive for HPE and the absence of cerebral anomalies sho…

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesCandidate geneAdolescentID/MCA deletion syndromeLocus (genetics)MicrophthalmiamicroformSettore MED/38 - Pediatria Generale E SpecialisticaHoloprosencephalyIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansMicrophthalmoschromosome 14q deletionIn Situ Hybridization FluorescenceGenetics (clinical)Sequence DeletionChromosomes Human Pair 14GeneticsComparative Genomic HybridizationColobomabiologybusiness.industryNPAS3Faciesmedicine.diseaseeye diseasesDevelopmental disorderPhenotypeholoprosencephalySettore MED/03 - Genetica MedicaGenetic Lociarray-CGHbiology.proteinbusinessAmerican Journal of Medical Genetics Part A
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Rubinstein–Taybi syndrome 2 with cerebellar abnormality and neural tube defect

2019

Rubinstein-Taybi syndrome (RSTS) is a rare dominant disorder with intellectual disability, postnatal growth deficiency, and multiple congenital anomalies. Approximately 50-70% of the patients have a mutation in the CREBBP gene (RSTS1) and 5-10% display an EP300 gene mutation (RSTS2). Craniospinal abnormalities such as microcranium, scoliosis, and lordosis are frequent findings in RSTS1, but malformations of the brain or spinal cord are seen only occasionally. Here, we report on a 3-year-old boy with facial abnormalities of RSTS, broad thumbs and halluces, developmental delay, autistic features, cerebellar underdevelopment, and a neural tube defect. Molecular diagnostic of the CREBBP and EP3…

Malespeech delayHeterozygoteCerebellumGenotypecerebellar abnormalityScoliosisGene mutationPathology and Forensic MedicineCerebellummedicinetethered cordHumansmicrocephalyGenetic TestingNeural Tube DefectsFrameshift MutationEP300Genetic Association StudiesGenetics (clinical)Sequence DeletionRubinstein-Taybi Syndromeautistic behaviorRubinstein–Taybi syndromeNeural tube defectGenome Humanbusiness.industryNeural tubeHigh-Throughput Nucleotide Sequencingstereotypic movementsvesicoureteral refluxOriginal Articleslumbosacral myeloceleExonsGeneral MedicineAnatomymedicine.diseaseSpinal cordCREB-Binding Proteinmedicine.anatomical_structuresyringohydromyeliaChild PreschoolMutationPediatrics Perinatology and Child Healthbroad thumbs and hallucesAnatomybusinessE1A-Associated p300 ProteinClinical Dysmorphology
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Involvement of the long arm of chromosome 9 in medulloblastoma in an adult.

1997

Abstract Medulloblastoma is the most common primitive neuroectodermal tumor (PNET) in children, but is very rare in adults. An isochromosome for the long arms of 17, i(17q), is found in about 30% of pediatric cases. Cytogenetic studies in adults are very scarce; only six cases have been described cytogenetically: three cases had normal karyotype, two were studied partially, and another presented only two clonal structural anomalies: del(9)(q12) and del(11)(q22). We studied the chromosomes from medulloblastoma in a 27-year-old woman and found one hypotetraploid stemline with clonal alterations. In the structural anomalies, chromosomes 3, 9, 12, and i(17q) were involved. Chromosome 9 presente…

MedulloblastomaAdultCancer Researchmedicine.medical_specialtyPathologyAdult MedulloblastomaIsochromosomeCytogeneticsChromosome 9KaryotypeAnatomyBiologymedicine.diseasePrimitive neuroectodermal tumorKaryotypingGeneticsmedicineHumansHistopathologyFemaleChromosome DeletionCerebellar NeoplasmsChromosomes Human Pair 9Molecular BiologyMedulloblastomaCancer genetics and cytogenetics
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