Search results for " Pair 19"

showing 8 items of 8 documents

A meta-analysis of Hodgkin lymphoma reveals 19p13.3 TCF3 as a novel susceptibility locus

2014

Contains fulltext : 137763.pdf (Publisher’s version ) (Open Access) Recent genome-wide association studies (GWAS) of Hodgkin lymphoma (HL) have identified associations with genetic variation at both HLA and non-HLA loci; however, much of heritable HL susceptibility remains unexplained. Here we perform a meta-analysis of three HL GWAS totaling 1,816 cases and 7,877 controls followed by replication in an independent set of 1,281 cases and 3,218 controls to find novel risk loci. We identify a novel variant at 19p13.3 associated with HL (rs1860661; odds ratio (OR)=0.81, 95% confidence interval (95% CI)=0.76-0.86, Pcombined=3.5 x 10(-10)), located in intron 2 of TCF3 (also known as E2A), a regul…

AdultMaleAdolescent[SDV]Life Sciences [q-bio]TRANSCRIPTION FACTOR E2AGENETIC-ASSOCIATIONGeneral Physics and AstronomyLocus (genetics)Genome-wide association studyHuman leukocyte antigenBiologyGeneral Biochemistry Genetics and Molecular BiologyArticleDISEASEYoung AdultBasic Helix-Loop-Helix Transcription FactorsHumansTOOLGenetic Predisposition to DiseaseAlleleGENOME-WIDE ASSOCIATIONEPSTEIN-BARR-VIRUSGenetic associationAgedGeneticsAged 80 and overRISKMultidisciplinaryCELL-TYPECase-control studyGenetic VariationGeneral ChemistryOdds ratioGenomicsMiddle AgedALLELESHodgkin DiseaseCANCERMalaltia de HodgkinHodgkin lymphoma (HL)GenòmicaGenetic epidemiologyCase-Control StudiesUrological cancers Radboud Institute for Health Sciences [Radboudumc 15]Hodgkin's diseaseChromosomes Human Pair 19Genome-Wide Association Study
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Apolipoprotein E polymorphism influences not only cerebral senile plaque load but also Alzheimer-type neurofibrillary tangle formation.

1995

Only recently, evidence was provided that apolipoprotein E allele epsilon 4 located on Chromosome 19 is associated with late onset (i.e. senile) sporadic Alzheimer's disease. Histologically, Alzheimer's disease is associated with intraneuronal neurofibrillary changes and extraneuronal A4/beta-amyloid deposition. We set out with a histological staging system which considers the gradual development of Alzheimer's disease-related histological changes over time and correlates highly with the cognitive decline ante mortem. Our analysis revealed that both the mean stage for A4/beta-amyloid deposits and the mean stage for neurofibrillary tangles get significantly shifted upwards in epsilon 4-carri…

Apolipoprotein EPathologymedicine.medical_specialtyGenotypeLate onsetBiologyCentral nervous system diseaseDegenerative diseaseApolipoproteins EAlzheimer DiseasemedicineHumansSenile plaquesCognitive declineAllelesAgedAged 80 and overAmyloid beta-PeptidesPolymorphism GeneticGeneral NeuroscienceAge FactorsBrainNeurofibrillary tangleNeurofibrillary TanglesMiddle Agedmedicine.diseaseRegression AnalysisAlzheimer's diseaseChromosomes Human Pair 19Neuroscience
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Functional impact and evolution of a novel human polymorphic inversion that disrupts a gene and creates a fusion transcript

2015

Despite many years of study into inversions, very little is known about their functional consequences, especially in humans. A common hypothesis is that the selective value of inversions stems in part from their effects on nearby genes, although evidence of this in natural populations is almost nonexistent. Here we present a global analysis of a new 415-kb polymorphic inversion that is among the longest ones found in humans and is the first with clear position effects. This inversion is located in chromosome 19 and has been generated by non-homologous end joining between blocks of transposable elements with low identity. PCR genotyping in 541 individuals from eight different human populatio…

Cancer ResearchDNA End-Joining Repairlcsh:QH426-470GenotypeChromosome inversionPopulationChromosome BreakpointsBiologyChromosome breakpointsGenoma humàPolymorphism Single NucleotideEvolution MolecularChromosome Breakpoints03 medical and health sciences0302 clinical medicinePolymorphism Single nucleotideChromosome 19DNA end-joining repairGeneticsTranscription factorsHumansAlleleeducationMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologyChromosomal inversionGeneticsGene expression regulation0303 health scienceseducation.field_of_studyGenètica de poblacionsHaplotypelcsh:GeneticsDNA transposable elementsGenetics PopulationGene Expression RegulationFusion transcriptChromosome InversionDNA Transposable ElementsChromosomes Human Pair 19030217 neurology & neurosurgeryResearch ArticleTranscription Factors
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Isolated bladder exstrophy associated with a de novo 0.9 Mb microduplication on chromosome 19p13.12

2012

BACKGROUND: The exstrophy-epispadias complex (BEEC) is a urogenital birth defect of varying severity. The causes of the BEEC are likely to be heterogeneous, with individual environmental or genetic risk factors still being largely unknown. In this study, we aimed to identify de novo causative copy number variations (CNVs) that contribute to the BEEC. METHODS: Array-based molecular karyotyping was performed to screen 110 individuals with BEEC. Promising CNVs were tested for de novo occurrence by investigating parental DNAs. Genes located in regions of rearrangements were prioritized through expression analysis in mice to be sequenced in the complete cohort, to identify high-penetrance mutati…

EmbryologyDNA Copy Number VariationsSequence analysisKaryotypeUrinary BladderGene DosageMedizinBiologyGene dosageMicesymbols.namesakeGene DuplicationChromosome DuplicationGene duplicationAnimalsHumansCoding regionCopy-number variationGeneSanger sequencingGeneticsBase SequenceBladder ExstrophySequence Analysis DNAGeneral MedicinePediatrics Perinatology and Child HealthChromosomal regionsymbolsChromosomes Human Pair 19Developmental Biology
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Killer cell immunoglobulin-like receptor genes in Latvian patients with type 1 diabetes mellitus and healthy controls.

2004

T1DM is very common in Sweden and is positively associated with HLA class II genes. Approximately 89% of the newly diagnosed patients carry the high-risk HLA DR4-DQ8 and DR3-DQ2. The remaining 11% develop T1DM without them. This can be due to involvement of other genes and environmental factors. Natural killer (NK) cells of the innate immune system are important in antiviral and antitumor immunity. They are implicated in the etiology of autoimmune T1DM. Human NK cells express killer cell immunoglobulin-like receptors (KIR) that belong to the polymorphic multigene family in chromosome 19q3.4. They modulate NK cell response by interacting with HLA class I. In addition, polymorphic MICA in HLA…

MaleKiller-cell immunoglobulin-like receptorHuman leukocyte antigenBiologyGeneral Biochemistry Genetics and Molecular BiologyHistory and Philosophy of ScienceGene FrequencyReceptors KIRimmune system diseasesPolymorphism (computer science)HumansAlleleReceptors ImmunologicReceptorAllele frequencyAllelesInnate immune systemPolymorphism GeneticGeneral NeuroscienceHistocompatibility Antigens Class Inutritional and metabolic diseasesAcquired immune systemLatviaKiller Cells NaturalDiabetes Mellitus Type 1Gene Expression RegulationCase-Control StudiesReceptors KIR2DL2ImmunologyFemaleChromosomes Human Pair 19Microsatellite RepeatsAnnals of the New York Academy of Sciences
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Prognostic heterogeneity of adult B-cell precursor acute lymphoblastic leukaemia patients with t(1;19)(q23;p13)/TCF3-PBX1 treated with measurable res…

2021

Programa para el Tratamiento de Hemopatias Malignas (PETHEMA) Group (Spanish Society of Hematology, SEHH).

OncologyMalep13)/TCF3-PBX1Neoplasm ResidualOncogene Proteins FusionCytogenetic alterationsmedicine.medical_treatmentDiseaseTranslocation Genetichemic and lymphatic diseasesAntineoplastic Combined Chemotherapy Protocolst(1;19)(q23;p13)/TCF3-PBX1Cumulative incidenceCitogenètica humanaNeoplasm MetastasisLeucèmia limfoblàstica - TractamentHuman cytogeneticsLeukemiaAcute lymphoblastic leukaemiaRemission InductionLeucèmiaDisease ManagementHematologyMiddle AgedPrognosisHaematopoiesismedicine.anatomical_structureTreatment OutcomeChromosomes Human Pair 1TCF3:Other subheadings::Other subheadings::/therapy [Other subheadings]FemaleStem cell:Neoplasms::Neoplasms by Histologic Type::Leukemia::Leukemia Lymphoid::Precursor Cell Lymphoblastic Leukemia-Lymphoma::Precursor B-Cell Lymphoblastic Leukemia-Lymphoma [DISEASES]Adultmedicine.medical_specialtyPronòstic mèdicAdolescentQuimioteràpia combinadaYoung AdultInternal medicinePrecursor B-Cell Lymphoblastic Leukemia-LymphomamedicineAdultsHumansB cell19)(q23Neoplasm Staging:neoplasias::neoplasias por tipo histológico::leucemia::leucemia linfoide::leucemia-linfoma linfoblástico de células precursoras::leucemia-linfoma linfoblástico de células B precursoras [ENFERMEDADES]business.industryacute lymphoblastic leukaemia adults cytogenetic alterations prognosis t(1:Otros calificadores::Otros calificadores::/terapia [Otros calificadores]ImmunotherapyChromosome BandingTransplantationt(1Avaluació de resultats (Assistència sanitària)businessChromosomes Human Pair 19British journal of haematologyReferences
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Linkage analysis and disease models in benign familial infantile seizures: a study of 16 families.

2006

Summary: Purpose: Benign familial infantile seizures (BFIS) is a genetically heterogeneous condition characterized by partial seizures, onset age from 3 to 9 months, and favorable outcome. BFIS loci were identified on chromosomes 19q12-13.1 and 16p12-q12, allelic to infantile convulsions and choreathetosis. The identification of SCN2A mutations in families with only infantile seizures indicated that BFNIS and BFIS may show overlapping clinical features. Infantile seizures also were in a family with familial hemiplegic migraine and mutations in the ATP1A2 gene. We have examined the heterogeneous genetics of BFIS by means of linkage analysis. Methods: Sixteen families were examined. Probands …

ProbandMaleGenetic LinkagePenetranceEpilepsyModelsgeneticsTomographyFamilial hemiplegic migraineGeneticsNeurologic ExaminationBrainChromosome MappingElectroencephalographyPenetranceMagnetic Resonance Imagingstatistics /&/ numerical dataPedigreeX-Ray ComputedNeurologyFemaleHumanmedicine.medical_specialtyBenign NeonatalBrain; pathology/radiography Chromosome Mapping Chromosomes; Human; Pair 16; genetics Chromosomes; Pair 19; genetics Electroencephalography; statistics /&/ numerical data Epilepsy; Benign Neonatal; diagnosis/genetics Family Female Genetic Heterogeneity Genetic Linkage Haplotypes Humans Magnetic Resonance Imaging Male Models; Genetic Mutation; genetics Neurologic Examination Pedigree Penetrance Tomography; X-Ray Computedpathology/radiographyChromosomesGenetic HeterogeneityGeneticGenetic linkageFebrile seizureGenetic modelmedicineHumansFamilyPsychiatryEpilepsyModels GeneticPair 19Genetic heterogeneitybusiness.industryPair 16medicine.diseaseEpilepsy Benign NeonatalHaplotypesMutationNeurology (clinical)Tomography X-Ray ComputedbusinessChromosomes Human Pair 19Chromosomes Human Pair 16diagnosis/genetics
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A girl with an atypical form of ataxia telangiectasia and an additional de novo 3.14Mb microduplication in region 19q12

2011

A 9-year-old girl born to healthy parents showed manifestations suggestive of ataxia telangiectasia (AT), such as short stature, sudden short bouts of horizontal and rotary nystagmus, a weak and dysarthric voice, rolling gait, unstable posture, and atactic movements. She did not show several cardinal features typical of AT such as frequent, severe infections of the respiratory tract. In contrast, she showed symptoms not generally related to AT, including microcephaly, profound motor and mental retardation, small hands and feet, severely and progressively reduced muscle tone with slackly protruding abdomen and undue drooling, excess fat on her upper arms, and severe oligoarthritis. A cranial…

medicine.medical_specialtyMicrocephalyPathologyCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesBiologyShort statureAtaxia Telangiectasia Mutated ProteinsAtaxia TelangiectasiaInternal medicineChromosome DuplicationGene duplicationGeneticsmedicineHumansLymphocytesChildSalivaCerebellar hypoplasiaMetaphaseGenetics (clinical)Mental DisordersTumor Suppressor ProteinsGeneral Medicinemedicine.diseaseDNA-Binding ProteinsEndocrinologyChromosome InversionAtaxia-telangiectasiaChromosomal regionSpeech delayMicrocephalyFemalemedicine.symptomApoptosis Regulatory ProteinsChromosomes Human Pair 19DNA DamageEuropean Journal of Medical Genetics
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