Search results for "copy number"

showing 10 items of 77 documents

Hereditary prostate cancer – Primetime for genetic testing?

2019

Prostate cancer (PCa) remains the most common cancer in men. The proportion of all PCa attributable to high-risk hereditary factors has been estimated to 5-15%. Recent landmark discoveries in PCa genetics led to the identification of germline mutations/alterations (eg. BRCA1, BRCA2, ATM or HOXB13), single nucleotide polymorphisms or copy number variations associated with PCa incidence and progression. However, offering germline testing to men with an assumed hereditary component is currently controversial. In the present review article, we provide an overview about the epidemiology and the genetic basis of PCa predisposition and critically discuss the significance and consequence in the cli…

0301 basic medicineMaleGenetic testingDNA Copy Number VariationsGenome-wide association studySingle-nucleotide polymorphismDiseaseBioinformaticsPolymorphism Single Nucleotide03 medical and health sciencesProstate cancer0302 clinical medicineGermline mutationMedicineHumansRadiology Nuclear Medicine and imagingGenetic Predisposition to DiseaseCopy-number variationGenetic TestingPrecision MedicineGenetic testingBRCA2 ProteinHomeodomain ProteinsClinical Trials as TopicProstate cancermedicine.diagnostic_testbusiness.industryBRCA1 ProteinCancerProstatic NeoplasmsPrecision oncologyGeneral Medicinemedicine.diseaseCheckpoint Kinase 2030104 developmental biologyHereditaryOncology030220 oncology & carcinogenesisMutationbusiness
researchProduct

DNA methylation changes and somatic mutations as tumorigenic events in Lynch syndrome-associated adenomas retaining mismatch repair protein expression

2018

Background: DNA mismatch repair (MMR) defects are a major factor in colorectal tumorigenesis in Lynch syndrome (LS) and 15% of sporadic cases. Some adenomas from carriers of inherited MMR gene mutations have intact MMR protein expression implying other mechanisms accelerating tumorigenesis. We determined roles of DNA methylation changes and somatic mutations in cancer-associated genes as tumorigenic events in LS-associated colorectal adenomas with intact MMR. Methods: We investigated 122 archival colorectal specimens of normal mucosae, adenomas and carcinomas from 57 LS patients. MMR-deficient (MMR-D, n 49) and MMR-proficient (MMR-P, n 18) adenomas were of particular interest and were inter…

0301 basic medicineMaleResearch paperMICROSATELLITE INSTABILITYHYPOMETHYLATIONDNA mismatch repairPHENOTYPEmedicine.disease_causeEpigenesis Genetic0302 clinical medicineCOLORECTAL ADENOMASCDKN2APromoter Regions Geneticcolorectal adenomaDNA methylationLINE-1 methylationTumor suppressorGeneral MedicineMethylationMiddle AgedCANCERTUMORSLynch syndromeDNA-metylaatio3. Good healthDEFICIENCY030220 oncology & carcinogenesisDNA methylationsyöpätauditFemaleColorectal adenomaAdultcongenital hereditary and neonatal diseases and abnormalitiesAdenomatumor suppressorsuolistosyövätColorectal adenomaBiologycomplex mixturesGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesBRAF MUTATIONmedicineHumansLynchin oireyhtymäAgedTumor Suppressor ProteinsMicrosatellite instabilityDNAUNE-1 methylationta3122medicine.diseaseGENEColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasestumorigenesisCOPY NUMBER030104 developmental biologyLynch syndromeLong Interspersed Nucleotide Elements3121 General medicine internal medicine and other clinical medicineMutationTumorigenesisCancer research3111 BiomedicineTumotigenesismutationCarcinogenesisEBioMedicine
researchProduct

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
researchProduct

Detection of MET Alterations Using Cell Free DNA and Circulating Tumor Cells from Cancer Patients

2020

MET alterations may provide a potential biomarker to evaluate patients who will benefit from treatment with MET inhibitors. Therefore, the purpose of the present study is to investigate the utility of a liquid biopsy-based strategy to assess MET alterations in cancer patients. We analyzed MET amplification in circulating free DNA (cfDNA) from 174 patients with cancer and 49 healthy controls and demonstrated the accuracy of the analysis to detect its alteration in patients. Importantly, a significant correlation between cfDNA concentration and MET copy number (CN) in cancer patients (r = 0.57, p &lt

0301 basic medicineOncologyMale<i>MET</i> copy numbermedicine.medical_treatmentproteínas protooncogénicas c-metdosificación génicahumanosresistencia a medicamentosDrug ResistanceGene Dosagecirculating free DNA (cfDNA)<i>MET</i> amplificationTargeted therapyTargeted therapy0302 clinical medicineCirculating tumor cellestudios prospectivosNeoplasmsantineoplásicosProspective Studieslcsh:QH301-705.5Circulating tumor cells (CTCs)neoplasiasGeneral MedicineProto-Oncogene Proteins c-mettargeted therapyNeoplastic Cells CirculatingErbB ReceptorsCell-free fetal DNA030220 oncology & carcinogenesisinhibidores de proteína cinasasBiomarker (medicine)FemaleMET protein expressionCell-Free Nucleic AcidsMET amplificationmedicine.medical_specialtycirculating tumor cells (CTCs)estudios de casos y controlesMet amplificationCirculating free DNA (cfDNA)Antineoplastic AgentsArticle03 medical and health sciencesInternal medicinemedicineBiomarkers TumorHumansLiquid biopsyProtein Kinase InhibitorsRetrospective Studiesbusiness.industryHead and neck cancerestudios retrospectivosLiquid BiopsyCancermedicine.disease030104 developmental biologylcsh:Biology (General)Drug Resistance NeoplasmCase-Control StudiesMET copy numberbusinessCells
researchProduct

Next‐generation sequencing reveals the mutational landscape of clinically diagnosed Usher syndrome: copy number variations, phenocopies, a predominan…

2017

Background Combined retinal degeneration and sensorineural hearing impairment is mostly due to autosomal recessive Usher syndrome (USH1: congenital deafness, early retinitis pigmentosa (RP); USH2: progressive hearing impairment, RP). Methods Sanger sequencing and NGS of 112 genes (Usher syndrome, nonsyndromic deafness, overlapping conditions), MLPA, and array-CGH were conducted in 138 patients clinically diagnosed with Usher syndrome. Results A molecular diagnosis was achieved in 97% of both USH1 and USH2 patients, with biallelic mutations in 97% (USH1) and 90% (USH2), respectively. Quantitative readout reliably detected CNVs (confirmed by MLPA or array-CGH), qualifying targeted NGS as one …

0301 basic medicineUsher syndromeNonsense mutationnext‐generation sequencingBiologyGene mutationBioinformatics03 medical and health sciencessymbols.namesakeRetinitis pigmentosaGeneticsmedicineotorhinolaryngologic diseasesMultiplex ligation-dependent probe amplificationNonsyndromic deafnessMolecular BiologyGenetics (clinical)Sanger sequencingGeneticsHeimler syndromeCopy number variationPoint mutationOriginal Articlesmedicine.diseaseeye diseases030104 developmental biologysymbolsphenocopiestranslational read‐throughOriginal ArticleUsher syndromeMolecular Genetics & Genomic Medicine
researchProduct

T-Cell Lymphoma Clonality by Copy Number Variation Analysis of T-Cell Receptor Genes

2021

Simple Summary T-cells defend the human body from pathogenic invasion via specific recognition by T-cell receptors (TCRs). The TCR genes undergo recombination (rearrangement) in a myriad of possible ways to generate different TCRs that can recognize a wide diversity of foreign antigens. However, in patients with T-cell lymphoma (TCL), a particular T-cell becomes malignant and proliferates, resulting in a population of genetically identical cells with same TCR rearrangement pattern. To help diagnose patients with TCL, a polymerase chain reaction (PCR)-based assay is currently used to determine if neoplastic cells in patient samples are of T-cell origin and bear identical (monoclonal) TCR rea…

0301 basic medicineclone (Java method)Cancer ResearchclonalityBiologylcsh:RC254-282Article03 medical and health sciences0302 clinical medicinemedicineT-cell lymphomaT-cell receptorCopy-number variationcopy number variation analysisGeneWhole genome sequencingwhole genome sequencingT-cell receptorlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseMolecular biology030104 developmental biologyOncology030220 oncology & carcinogenesisT-Cell Receptor GeneMonoclonalT-cell lymphomaClonality Copy number variation analysis T-cell lymphoma T-cell receptor Whole genome sequencingCancers
researchProduct

Genetic and Epigenetic Factors of Takotsubo Syndrome: A Systematic Review

2021

Takotsubo syndrome (TTS), recognized as stress’s cardiomyopathy, or as left ventricular apical balloon syndrome in recent years, is a rare pathology, described for the first time by Japanese researchers in 1990. TTS is characterized by an interindividual heterogeneity in onset and progression, and by strong predominance in postmenopausal women. The clear causes of these TTS features are uncertain, given the limited understanding of this intriguing syndrome until now. However, the increasing frequency of TTS cases in recent years, and particularly correlated to the SARS-CoV-2 pandemic, leads us to the imperative necessity both of a complete knowledge of TTS pathophysiology for identifying bi…

2019-20 coronavirus outbreakTTS managementCoronavirus disease 2019 (COVID-19)DNA Copy Number VariationsQH301-705.5Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Heart VentriclesReviewBioinformaticsPolymorphism Single NucleotideCatalysisEpigenesis GeneticInorganic ChemistryGenetic Heterogeneitysystematic reviewTakotsubo CardiomyopathyMedicineHumansGenetic Predisposition to DiseaseEpigeneticsTakotsubo cardiomyopathy (TTS)Biology (General)Physical and Theoretical ChemistryMedical History TakingQD1-999Molecular BiologySpectroscopyTakotsubo syndromePostmenopausal womenbusiness.industryGenetic heterogeneitySARS-CoV-2Organic ChemistrybiomarkersCOVID-19General Medicinespecific and effective treatmentsgenetic and epigenetic factorsComputer Science ApplicationsChemistrySettore MED/03Genetic LociIdentification (biology)businessInternational Journal of Molecular Sciences
researchProduct

Whole genome paired-end sequencing elucidates functional and phenotypic consequences of balanced chromosomal rearrangement in patients with developme…

2019

BackgroundBalanced chromosomal rearrangements associated with abnormal phenotype are rare events, but may be challenging for genetic counselling, since molecular characterisation of breakpoints is not performed routinely. We used next-generation sequencing to characterise breakpoints of balanced chromosomal rearrangements at the molecular level in patients with intellectual disability and/or congenital anomalies.MethodsBreakpoints were characterised by a paired-end low depth whole genome sequencing (WGS) strategy and validated by Sanger sequencing. Expression study of disrupted and neighbouring genes was performed by RT-qPCR from blood or lymphoblastoid cell line RNA.ResultsAmong the 55 pat…

AdultMale0301 basic medicineCandidate geneAdolescentDNA Copy Number VariationsDevelopmental Disabilities030105 genetics & heredityGenomeTranslocation GeneticStructural variationChromosome BreakpointsStructure-Activity RelationshipYoung Adult03 medical and health sciencessymbols.namesakeposition effectGeneticsHumansChildGeneGenetic Association StudiesGenetics (clinical)Paired-end tagComputingMilieux_MISCELLANEOUSchromosomal rearrangementsChromosome AberrationsGene RearrangementWhole genome sequencingGeneticsSanger sequencingwhole genome sequencingbiologystructural variationInfantNFIXPhenotype030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsintellectual disabilityChild Preschoolbiology.proteinsymbolsFemaleBiomarkers
researchProduct

Mutation spectrum and clinical investigation of achromatopsia patients with mutations in the GNAT2 gene

2019

Achromatopsia (ACHM) is a hereditary cone photoreceptor disorder characterized by the inability to discriminate colors, nystagmus, photophobia, and low-visual acuity. Six genes have been associated with this rare autosomal recessively inherited disease, including the GNAT2 gene encoding the catalytic α-subunit of the G-protein transducin which is expressed in the cone photoreceptor outer segment. Out of a cohort of 1,116 independent families diagnosed with a primary clinical diagnosis of ACHM, we identified 23 patients with ACHM from 19 independent families with likely causative mutations in GNAT2, representing 1.7% of our large ACHM cohort. In total 22 different potentially disease-causing…

AdultMaleAchromatopsiagenetic structuresAdolescentChild preschoolDNA Copy Number VariationsColor Vision DefectsBiologymedicine.disease_causeHeterotrimeric GTP-Binding Proteins/genetics03 medical and health sciencesExonGene duplicationGeneticsmedicineHumansGenetic Predisposition to DiseaseCopy-number variationColor Vision Defects/geneticsChildGenetics (clinical)030304 developmental biologyAgedGenetics0303 health sciencesGNAT2MutationSettore MED/30 - Malattie Apparato Visivo030305 genetics & heredityBreakpointInfantSequence Analysis DNAExonsMiddle Agedmedicine.diseaseHeterotrimeric GTP-Binding ProteinsPhotoreceptor outer segmenteye diseasesPedigreeSettore BIO/18 - GeneticaSequence Analysis DNA/methodsyoung adultFemalesense organsachromatopsia copy number variations GNAT2 mutations transducinmutation
researchProduct

1q gain and CDT2 overexpression underlie an aggressive and highly proliferative form of Ewing sarcoma

2012

12 páginas, 6 figuras, 1 tabla.-- et al.

AdultMaleCancer ResearchCandidate geneAdolescentDNA Copy Number VariationsUbiquitin-Protein Ligasesclinical outcomeBone NeoplasmsSarcoma EwingBiologyBioinformaticsPolymorphism Single NucleotideTranscriptomeIn vivoCell Line TumorGeneticsmedicineHumansChildMolecular BiologymicroarraysAgedCell ProliferationAged 80 and overCell CycleComputational BiologyInfantNuclear ProteinsMiddle Agedmedicine.disease1q GainIn vitroChromosomes Human Pair 1Child PreschoolCancer researchImmunohistochemistryFemaleCDT2SarcomaDNA microarrayEwing sarcomaComparative genomic hybridization
researchProduct