Search results for "Ligation-dependent"

showing 10 items of 28 documents

High prevalence of BRCA1 deletions in BRCAPRO-positive patients with high carrier probability.

2007

Mutation screening of the BRCA1 and BRCA2 genes in probands with familial breast/ovarian cancer has been greatly improved by the multiplex ligation-dependent probe amplification (MLPA) assay able to evidence gene rearrangements not detectable by standard screening methods. However, no criteria for selection of cases to be submitted to the MLPA test have been reported yet. We used the BRCAPro software for the selection of familial breast/ovarian cancer probands investigated with the MLPA approach after negative BRCA1/2 conventional mutation screening. One hundred and seventy-seven probands were investigated for germline BRCA1/2 mutations after assessment of genetic risk using BRCAPro. Proban…

AdultMaleOncologyProbandcongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyendocrine system diseasesBreast NeoplasmsGermlineBreast Neoplasms MaleGermline mutationBreast cancerRisk FactorsInternal medicinePrevalenceHumansMedicineGenetic Predisposition to DiseaseMultiplexMultiplex ligation-dependent probe amplificationskin and connective tissue diseasesAgedSequence DeletionOvarian NeoplasmsGeneticsBRCA1 Proteinbusiness.industryGenetic Carrier ScreeningProstatic NeoplasmsHematologyMiddle Agedmedicine.diseaseBRCA1 BRCA2 BRCAPro breast cancer MLPA ovarian cancerPedigreeOncologyMutation (genetic algorithm)FemalebusinessOvarian cancerSoftware
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De novo 15q21.1q21.2 deletion identified through FBN1 MLPA and refined by 244K array-CGH in a female teenager with incomplete Marfan syndrome

2010

International audience; Interstitial deletions involving the 15q21.1 band are very rare. Only 4 of these cases have been studied using molecular cytogenetic techniques in order to confirm the deletion of the whole FBN1 gene. The presence of clinical features of the Marfan syndrome (MFS) spectrum associated with mental retardation has been described in only 2/4 patients. Here we report on a 16-year-old female referred for suspicion of MFS (positive thumb and wrist sign, scoliosis, joint hyperlaxity, high-arched palate with dental crowding, dysmorphism, mitral insufficiency with dystrophic valve, striae). She had therefore 3 minor criteria according to the Ghent nosology. She also had speech …

AdultMalemusculoskeletal diseasesProbandMarfan syndromecongenital hereditary and neonatal diseases and abnormalitiesAdolescent[SDV]Life Sciences [q-bio]Fibrillin-1BiologyFibrillinsBioinformaticsPolymerase Chain ReactionMarfan SyndromeLoss of heterozygosity03 medical and health sciencesTransforming Growth Factor betaIntellectual DisabilityGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationAlleleChildGeneIn Situ Hybridization FluorescenceGenetics (clinical)Oligonucleotide Array Sequence AnalysisSequence Deletion030304 developmental biologyGeneticsChromosomes Human Pair 15Comparative Genomic Hybridization0303 health sciencesMicrofilament Proteins030305 genetics & heredityGeneral Medicinemedicine.diseasePedigree3. Good healthPhenotypeMutationMicrosatelliteFemaleDNA ProbesHaploinsufficiencyMicrosatellite RepeatsEuropean Journal of Medical Genetics
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Abstract 5379: Recurrent inactivation of PARD3, a polarity-related gene, in squamous cell carcinomas of the lung.

2013

Abstract In spite of the recent advances in cancer genomics, the genetics underlying the development of lung squamous cell carcinomas (SCC) is still poorly understood. Here, we investigated the contribution of the cell polarity-related gene, PARD3, to lung SCC carcinogenesis. First, we tested for PARD3 alterations in lung cancer cell lines from various histopathological types. The analysis confirmed an intragenic deletion at the H157 cells and unveiled biallelic mutations in another cell line. Both cell lines are SCCs, which circumscribed PARD3 alterations to this lung cancer type. Next, we extended the genetic screening, which included the determination of mutations and of intragenic delet…

Cancer ResearchPathologymedicine.medical_specialtyCell growthCellWild typeCancerBiologymedicine.diseasemedicine.disease_causemedicine.anatomical_structureOncologymedicineCancer researchMultiplex ligation-dependent probe amplificationLung cancerCarcinogenesisGeneCancer Research
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Neuroblastoma with MYCN amplification plus 11q deletion: immunohistochemical expression of angiogenic factors

2010

Neuroblastoma (NB) is an extra-cranial solid neoplasm in childhood. Genetic markers as MYCN amplification (MNA) and deletion of 11q (11q ) are considered factors with an adverse prognosis. Usually, an inverse relationship between MNA and 11q is found. Approximately 13% of the MNA cases present with 11q . These cases show a dramatic decline in survival rates. Hypoxia-inducible factor-2a (HIF-2a) protein expression has been described as an indicator of poor outcome, has been correlated with an aggressive phenotype in NB, and serves as a marker for stem cell-like phenotypes. Additionally, HIF-2a positive cells strongly express vascular endothelial growth factor (VEGF) and, as such, could be in…

Cancer Researchmedicine.diagnostic_testCancerBiologymedicine.diseaseVascular endothelial growth factorchemistry.chemical_compoundchemistryGenetic markerNeuroblastomaGene duplicationGeneticsCancer researchmedicineImmunohistochemistryMultiplex ligation-dependent probe amplificationMolecular BiologyFluorescence in situ hybridizationCancer Genetics and Cytogenetics
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Influence of segmental chromosome abnormalities on survival in children over the age of 12 months with unresectable localised peripheral neuroblastic…

2014

Background: The prognostic impact of segmental chromosome alterations (SCAs) in children older than 1 year, diagnosed with localised unresectable neuroblastoma (NB) without MYCN amplification enrolled in the European Unresectable Neuroblastoma (EUNB) protocol is still to be clarified, while, for other group of patients, the presence of SCAs is associated with poor prognosis. Methods: To understand the role of SCAs we performed multilocus/pangenomic analysis of 98 tumour samples from patients enrolled in the EUNB protocol. Results: Age at diagnosis was categorised into two groups using 18 months as the age cutoff. Significant difference in the presence of SCAs was seen in tumours of patients…

Cancer Researchmedicine.medical_specialtyPathologyMYCN AmplificationKaplan-Meier EstimateunresectableGastroenterologyDisease-Free Survivalsegmental chromosome alterationsNeuroblastomaneuroblastomaDDX1FISHaCGHOlder patientsPeripheral Nervous System NeoplasmsInternal medicineNeuroblastomaMYCNmedicineHumansMultiplex ligation-dependent probe amplificationGainChromosome AberrationsOncogene ProteinsComparative Genomic HybridizationN-Myc Proto-Oncogene Proteinbusiness.industrySignificant differenceGene AmplificationSegmental Chromosome abnormalitiesInfantNuclear ProteinsChromosomePrognosislocalisedmedicine.diseaseDoenças GenéticasMLPA3. Good healthPeripheralOncologyMycn amplificationClinical StudyHistopathologybusinessBritish Journal of Cancer
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Are the new genetic tools for diagnosis of Wilson disease helpful in clinical practice?

2020

Summary The diagnosis of Wilson disease is not always easy. For many patients, a combination of tests reflecting disturbed copper metabolism may be needed. Testing for ATP7B variants has become part of the routine diagnostic approach. The methods of genetic testing include analysis of the 21 coding exons and intronic flanking sequences, in which exons with recurrent variants would be prioritised depending on the mutation frequency in the local population. If sequencing the entire ATP7B gene cannot identify 2 variants and the suspicion for Wilson disease is high, after reviewing the clinical data, WES (whole-exome sequencing) or WGS (whole-genome sequencing) could be applied. A workflow base…

DiseaseReviewIndian childhood cirrhosisBioinformaticsDNA sequencingWES whole-exome sequencingPFIC progressive familial intrahepatic cholestasisInternal MedicinemedicineImmunology and AllergyMultiplex ligation-dependent probe amplificationWGS whole-genome sequencingExome sequencingGenetic testingWilson diseaseWhole genome sequencingWhole-genome sequencingHepatologymedicine.diagnostic_testMEDNIK syndromebusiness.industryCopper metabolismGastroenterologyMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseICC Indian childhood cirrhosisNGS next-generation sequencingDMR differentially methylated regionsWhole-exome sequencingNext-generation sequencingbusinessICT idiopathic or primary copper toxicosisCDG congenital disorders of glycosylationGenetic diseasesJHEP Reports
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Broad spectrum of Fabry disease manifestation in an extended Spanish family with a new deletion in the GLA gene

2012

Background. Fabry disease (FD) is an X-linked inherited disease based on the absence or reduction of lysosomal-galactosidase (Gla) activity. The enzymatic defect results in progressive impairment of cerebrovascular, renal and cardiac function. Normally, female heterozygote mutation carriers are less strongly affected than male hemizygotes aggravating disease diagnosis. Method. Close examination of the patients by renal biopsy, echo- and electrocardiography and MRI. Blood work and subsequent DNA analysis were carried out utilizing approved protocols for PCR and Sequencing. MLPA analysis was done to unveil deletions within the GLA gene locus. Quantitative detection of Glycolipids in patient p…

Fabry diseaseTransplantationPathologymedicine.medical_specialtybusiness.industryOriginal ContributionsGenetic disorderLocus (genetics)Heterozygote advantageOriginal Articleslyso-Gb3multiple sclerosismedicine.diseaseBioinformaticsrenal involvementFabry diseaseExonNephrologyMedicineBiomarker (medicine)Multiplex ligation-dependent probe amplificationbusinessX-linked recessive inheritanceClinical Kidney Journal
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Microduplications At 22q11.21 are Associated with Classic Bladder Exstrophy

2010

Purpose Classic exstrophy of the bladder (CBE) is part of the exstrophy-epispadias complex (EEC), a spectrum of urogenital anomalies in which part or all of the distal urinary tract fails to close. Familial occurrence has been observed, and previous studies have suggested an underlying multifactorial mode of inheritance. To date, no causative genetic or non-genetic factor has been unequivocally identified in humans. The present study aimed to identify microaberrations characterized by loss or gain of genomic material that contribute to the EEC at a genome-wide level. Material and Methods Molecular karyotyping, utilizing 549,839 single nucleotide polymorphisms (SNPs) with an average spacing …

Geneticsbusiness.industryUrologySingle-nucleotide polymorphismKaryotypemedicine.diseasePenetranceBladder exstrophyDiGeorge syndromePediatrics Perinatology and Child HealthGene duplicationChromosomal regionMedicineMultiplex ligation-dependent probe amplificationbusinessJournal of Pediatric Urology
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Multiplex ligation-dependent probe amplification detection of an unknown large deletion of the CREB-binding protein gene in a patient with Rubinstein…

2013

Rubinstein-Taybi syndrome is a rare autosomal dominant congenital disorder characterized by postnatal growth retardation, psychomotor developmental delay, skeletal anomalies, peculiar facial morphology, and tumorigenesis. Mutations in the gene encoding the cAMP response element-binding protein (CREB, also known as CREBBP or CBP) on chromosome 16p13.3 have been identified. In addition, some patients with low intelligence quotients and autistic features bear large deletions. Based on these observations, we used multiplex ligation-dependent probe amplification to search for large deletions affecting the CREBBP gene in a Rubinstein-Taybi syndrome patient. We identified a novel heterozygote dele…

HeterozygoteCREBExonSettore BIO/13 - Biologia ApplicataGeneticsmedicineHumansMultiplexMultiplex ligation-dependent probe amplificationGenetic TestingCREB-binding proteinMolecular BiologyGeneGeneticsRubinstein-Taybi SyndromeRubinstein–Taybi syndromebiologyMultiplex ligation-dependent probe amplification Comparative multiplex dosage analysis CREB-binding protein Rubinstein-Taybi syndromeHeterozygote advantageGeneral Medicinemedicine.diseaseMolecular biologyCREB-Binding ProteinChild Preschoolbiology.proteinFemaleMultiplex Polymerase Chain ReactionGene Deletion
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Novel deletion of the E3A ubiquitin protein ligase gene detected by multiplex ligation-dependent probe amplification in a patient with Angelman syndr…

2010

Angelman syndrome (AS) is a severe neurobehavioural disorder caused by failure of expression of the maternal copy of the imprinted domain located on 15q11-q13. There are different mechanisms leading to AS: maternal microdeletion, uniparental disomy, defects in a putative imprinting centre, mutations of the E3 ubiquitin protein ligase (UBE3A) gene. However, some of suspected cases of AS are still scored negative to all the latter mutations. Recently, it has been shown that a proportion of negative cases bear large deletions overlapping one or more exons of the UBE3A gene. These deletions are difficult to detect by conventional gene-scanning methods due to the masking effect by the non-delete…

Malecongenital hereditary and neonatal diseases and abnormalitiesClinical Biochemistrygene dosageBiochemistryGene dosageExonSettore BIO/13 - Biologia ApplicataAngelman syndromemedicineUBE3AHumansMultiplexGenetic TestingMultiplex ligation-dependent probe amplificationChildMolecular BiologyGeneticsbiologyubiquitin-protein ligasesgenetic association studiemedicine.diseaseMolecular biologyUniparental disomyUbiquitin ligaseAngelman syndromebiology.proteinMolecular MedicineOriginal ArticleFemaleGene Deletion
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