Search results for " Pair 6"

showing 10 items of 22 documents

Genomic Amplifications and Distal 6q Loss: Novel Markers for Poor Survival in High-risk Neuroblastoma Patients.

2018

Abstract Background Neuroblastoma is characterized by substantial clinical heterogeneity. Despite intensive treatment, the survival rates of high-risk neuroblastoma patients are still disappointingly low. Somatic chromosomal copy number aberrations have been shown to be associated with patient outcome, particularly in low- and intermediate-risk neuroblastoma patients. To improve outcome prediction in high-risk neuroblastoma, we aimed to design a prognostic classification method based on copy number aberrations. Methods In an international collaboration, normalized high-resolution DNA copy number data (arrayCGH and SNP arrays) from 556 high-risk neuroblastomas obtained at diagnosis were coll…

0301 basic medicineOncologyCancer ResearchSomatic cellNeuroblastoma0302 clinical medicineGene duplicationMedicine and Health SciencesHigh risk neuroblastomaN-Myc Proto-Oncogene ProteinABNORMALITIESIntensive treatmentGenomicsArticlesPrognosis3. Good healthOncologyChild Preschool030220 oncology & carcinogenesisChromosomes Human Pair 6Chromosome DeletionINTEGRATIONmedicine.medical_specialtyDNA Copy Number VariationsCLASSIFICATION03 medical and health sciencesAGEInternal medicineNeuroblastomaSTRATIFICATIONClinical heterogeneityBiomarkers TumormedicineHumansGenetic Predisposition to DiseaseCopy number aberrationneoplasmsGenetic Association StudiesNeoplasm StagingACCUMULATIONbusiness.industryOUTCOME PREDICTIONGene AmplificationInfantBiology and Life SciencesDNAmedicine.diseaseDELINEATION030104 developmental biologyCOPY NUMBEROutcome predictionbusiness
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Analysis of Plasminogen Genetic Variants in Multiple Sclerosis Patients.

2016

Multiple sclerosis (MS) is a prevalent neurological disease of complex etiology. Here, we describe the characterization of a multi-incident MS family that nominated a rare missense variant (p.G420D) in plasminogen (PLG) as a putative genetic risk factor for MS. Genotyping of PLG p.G420D (rs139071351) in 2160 MS patients, and 886 controls from Canada, identified 10 additional probands, two sporadic patients and one control with the variant. Segregation in families harboring the rs139071351 variant, identified p.G420D in 26 out of 30 family members diagnosed with MS, 14 unaffected parents, and 12 out of 30 family members not diagnosed with disease. Despite considerably reduced penetrance, lin…

0301 basic medicineProbandMaleGene ExpressionQH426-470multiple sclerosis0302 clinical medicineRisk FactorsGenotypeMissense mutationExomegeneticsguidelinesGenetics (clinical)degradationriskGeneticsLinkagedeficiencyMiddle AgedPenetrance3. Good healthPedigreeplasminogenChromosomes Human Pair 6FemalelinkageAdultGenotype610 Medicine & healthInvestigationsBiologysystemPolymorphism Single Nucleotideblood-brain-barrieractivatorMultiple sclerosisAssociation03 medical and health scienceslamininGenetic linkagemedicineGeneticsHumansAmino Acid Sequenceddc:610Molecular BiologyGenotypingAgeddiseaseSequence Homology Amino AcidMultiple sclerosisCase-control studyassociationPlasminogenmedicine.diseasediagnostic-criteria030104 developmental biologyCase-Control StudiesImmunologySequence Alignment030217 neurology & neurosurgery
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Three de novo losses and one insertion within a pericentric inversion of chromosome 6 in a patient with complete absence of expressive speech and red…

2008

A 32-year-old female patient, observed for 30 years because of a distinctive phenotype consisting of a dysmorphic face non-progressive deficit of motor control, lack of speech development, reduced sensitivity to pain, with a known, complex interstitial deletion 6q14 within a de novo pericentric inversion 6p11.2;q15, was re-examined at the molecular level. Applying the Infinium HumanHap300 BeadChip array and BAC-based FISH we found two new non-contiguous microdeletions in addition to the one detected previously by high resolution G-band analysis. A 360 kb loss in band 6p12.3, containing the genes RHAG, CRISP1, 2, and 3, and PGK2, a 1.15 Mb loss in 6p12.2-p12.1, containing the genes PKHD1, IL…

AdultCell Adhesion Molecules NeuronalSingle-nucleotide polymorphismBiologySpeech DisordersReceptor Cannabinoid CB1GeneticsmedicineHumansGeneGenetics (clinical)Chromosomal inversionChromosome AberrationsFamily HealthGeneticsmedicine.diagnostic_testBrainChromosome MappingChromosomeGeneral MedicinePhenotypeFaceCytogenetic AnalysisRHAGSomatosensory Disordersbiology.proteinChromosomes Human Pair 6FemaleFluorescence in situ hybridizationSNP arrayEuropean Journal of Medical Genetics
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Incomplete penetrance and phenotypic variability of 6q16 deletions including SIM1.

2015

International audience; 6q16 deletions have been described in patients with a Prader-Willi-like (PWS-like) phenotype. Recent studies have shown that certain rare single-minded 1 (SIM1) loss-of-function variants were associated with a high intra-familial risk for obesity with or without features of PWS-like syndrome. Although SIM1 seems to have a key role in the phenotype of patients carrying 6q16 deletions, some data support a contribution of other genes, such as GRIK2, to explain associated behavioural problems. We describe 15 new patients in whom de novo 6q16 deletions were characterised by comparative genomic hybridisation or single-nucleotide polymorphism (SNP) array analysis, including…

AdultMaleAdolescent[SDV]Life Sciences [q-bio]PenetranceBioinformaticsPolymorphism Single NucleotideArticlePregnancyGRIK2Basic Helix-Loop-Helix Transcription FactorsGeneticsHumansSNPObesityChildGeneGenetic Association StudiesGenetics (clinical)GeneticsComparative Genomic Hybridizationbiology[ SDV ] Life Sciences [q-bio]InfantPenetrancePhenotypeRepressor ProteinsChild PreschoolAborted FetusSIM1biology.proteinChromosomes Human Pair 6FemaleHaploinsufficiencyPrader-Willi SyndromeComparative genomic hybridization
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The HTR1B 861GC receptor polymorphism among patients suffering from alcoholism, major depression, anxiety disorders and narcolepsy.

2000

Abstract The HTR1B receptor gene has been linked to antisocial alcoholism in a Finnish population and an American Indian tribe [Lappalainen et al., Arch. Gen. Psychiatry, 55 (1998) 989]. Using a candidate gene approach, we genotyped 209 patients with alcoholism, 108 patients with major depression, 32 patients with panic disorder, 50 patients with generalized anxiety disorder, 58 patients with narcolepsy and 74 healthy volunteers for the HTR1B 861G>C polymorphism. There was a higher frequency of the HTR1B 861G alleles among the alcohol-dependent patients as compared to the control subjects (χ 2 =4.02, d.f.=2, P =0.04). However, the association resulted from higher frequencies of the opposite…

AdultMaleRiskCandidate genemedicine.medical_specialtyGeneralized anxiety disorderGenotypeInternal medicineGermanymedicineHumansPsychiatryTemperamentBiological PsychiatryPsychiatric geneticsAllelesNarcolepsyDepressive Disorder MajorPolymorphism GeneticPanic disorderPanicmedicine.diseaseAnxiety DisordersPsychiatry and Mental healthAlcoholismPhenotypeCase-Control StudiesReceptors SerotoninReceptor Serotonin 5-HT1BAnxietyPanic DisorderChromosomes Human Pair 6Femalemedicine.symptomPsychologyAnxiety disorderNarcolepsyPsychiatry research
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Elusive amines and cluster headache: mutational analysis of trace amine receptor cluster on chromosome 6q23.

2004

Cluster headache (CH) is characterised by unilateral pain and ipsilateral autonomic features. To date, no molecular genetic evidence has been shown for CH. Small pedigrees and low penetrance render the identification of the CH-gene quite difficult. Nonetheless the association of CH and migraine to a new class of amine, namely trace or elusive amines such as tyramine, octopamine and synephrine, has recently been demonstrated. In particular, in comparison to healthy control subjects, all these neurotransmitters have been found to be greatly elevated in CH sufferers in plasma and platelets both in active and remission periods. A cluster of gene-encoding G-protein-coupled receptors that bind an…

Biogenic AminesGenetic LinkageDNA Mutational AnalysisCluster HeadacheDermatologymedicine.disease_causeReceptors G-Protein-Coupledchemistry.chemical_compoundTar (tobacco residue)Genetic linkageReceptors Biogenic AminemedicineHumansReceptorTrace amineMutationGeneral MedicineTyraminePenetrancePsychiatry and Mental healthchemistryBiochemistryMultigene FamilyOctopamine (neurotransmitter)Chromosomes Human Pair 6Neurology (clinical)Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Complex rearrangement of chromosomes 6 and 11 as the sole anomaly in atypical teratoid/rhabdoid tumors of the central nervous system.

2000

Atypical teratoid/rhabdoid tumor of the central nervous system is a rare childhood tumor with a distinct histologic appearance and an aggressive clinical course. Few tumors have been analyzed cytogenetically. The only consistent chromosomal abnormality identified in some of these tumors has been monosomy or deletions of chromosome 22; in others, a normal chromosome 22 was present. The authors report an atypical teratoid/rhabdoid neoplasm of the central nervous system with a novel complex rearrangement affecting chromosomes 6 and 11 as the sole anomaly. The involvement of region 11p15 could be important in the pathogenesis of this entity.

Cancer ResearchMonosomymedicine.medical_specialtyPathologyCentral nervous systemBiologyTranslocation GeneticCentral nervous system diseaseCentral Nervous System NeoplasmsGeneticsmedicineHumansRing ChromosomesChildMolecular BiologyIn Situ Hybridization FluorescenceRhabdoid TumorGeneticsChromosome Aberrationsmedicine.diagnostic_testChromosomes Human Pair 11CytogeneticsTeratomaGene rearrangementmedicine.diseaseTeratoid tumormedicine.anatomical_structureKaryotypingChromosomes Human Pair 6FemaleChromosome 22Fluorescence in situ hybridizationCancer genetics and cytogenetics
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Low frequency of HLA haplotype loss associated with loss of heterozygocity in chromosome region 6p21 in clear renal cell carcinomas.

2004

HLA class I loss or downregulation is a widespread mechanism used by tumor cells to avoid tumor recognition by cytotoxic T lymphocytes favoring tumor immune escape. Multiple molecular mechanisms are responsible for these altered HLA class I tumor phenotypes. It has been described in different epithelial tumors that loss of heterozygosity (LOH) at chromosome region 6p21.3 is a frequent mechanism that leads to HLA haplotype loss, ranging between 40 and 50%, depending on the tumor entity analyzed. Here we have tested the frequency of LOH at 6p21 chromosome region in Renal Cell Carcinomas (RCC) of the clear cell and chromophobe subtype. A low frequency of HLA haplotype loss (6.6%) was found in …

Cancer ResearchPathologymedicine.medical_specialtyLoss of HeterozygosityChromophobe cellHuman leukocyte antigenBiologyurologic and male genital diseasesLoss of heterozygosityAntigens NeoplasmHLA AntigensmedicineCytotoxic T cellHumansneoplasmsCarcinoma Renal CellHaplotypeCytogeneticsKidney NeoplasmsGene Expression Regulation NeoplasticOncologyHaplotypesClear cell carcinomaChromosomes Human Pair 6Clear cellAdenocarcinoma Clear CellMicrosatellite RepeatsInternational journal of cancer
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Evaluation of a susceptibility gene for schizophrenia on chromosome 6p by multipoint affected sib-pair linkage analysis

1995

The influence of genetic factors in schizophrenia has been convincingly demonstrated by family, twin and adoption studies, but the mode of transmission remains uncertain. The reported pattern of recurrence risks suggests a set of interacting loci. Based on prior evidence for linkage on chromosome 6p (K. Kendler, pers. comm.), we have scanned the short arm of chromosome 6 in 54 families for loci predisposing to schizophrenia, using 25 microsatellite markers spanning 60 centiMorgans (cM). Allele sharing identity by descent was examined in affected sib-pairs from these families, followed by multipoint sib-pair linkage analysis. Positive lod scores were obtained over a wide region (D6S470 to D6…

GeneticsModels GeneticGenetic LinkageChromosome MappingChromosomeLocus (genetics)BiologyIdentity by descentNuclear FamilyPedigreeCentimorganGene mappingGenetic linkageSchizophreniaGeneticsHumansMicrosatelliteChromosomes Human Pair 6Lod ScoreNuclear family
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Array-CGH and clinical characterization in a patient with subtelomeric 6p deletion without ocular dysgenesis

2011

Subtelomeric terminal 6p deletion has been recognized as a clinically identifiable syndrome including facial dysmorphism, malformation of the anterior eye chamber, hearing loss, heart defect and developmental delay. Genotype –phenotype correlations of previously published patients have been strongly suggested anterior eye segment anomalies as one of major malformation of the syndrome if the critical 6p25 region containing the FOXC 1 gene. In addition it has been hypothesized the presence in this region of one or more genes involved in hearing loss. We report on a case of terminal 6p deletion in a 47, XYY karyotype. Further characterization of the deletion with array comparative genome hybri…

Heart Defects CongenitalMaleHearing lossDevelopmental DisabilitiesKaryotypeBiologyEyeDysgenesisSettore MED/38 - Pediatria Generale E SpecialisticaChromosome 19GeneticsmedicineHumansarray-CGH.Eye AbnormalitiesGeneGenetics (clinical)Genetic Association StudiesIn Situ Hybridization FluorescenceGeneticsComparative Genomic Hybridizationeye abnormalitieInfantKaryotypeForkhead Transcription Factorshearing loSubtelomereAnterior Eye SegmentSettore MED/03 - Genetica MedicaChromosomes Human Pair 6FOXC1medicine.symptomChromosome Deletionchromosome 6p deletionComparative genomic hybridization
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