Search results for "MUTATION ANALYSIS"

showing 6 items of 6 documents

Prevalence and clinical association of gene mutations through multiplex mutation testing in patients with NSCLC

2017

[EN] Background Reported prevalence of driver gene mutations in non-small-cell lung cancer (NSCLC) is highly variable and clinical correlations are emerging. Using NSCLC biomaterial and clinical data from the European Thoracic Oncology Platform Lungscape iBiobank, we explore the epidemiology of mutations and association to clinicopathologic features and patient outcome (relapse-free survival, time-to-relapse, overall survival). Methods Clinically annotated, resected stage I¿III NSCLC FFPE tissue was assessed for gene mutation using a microfluidics-based multiplex PCR platform. Mutant-allele detection sensitivity is¿>1% for most of the ~150 (13 genes) mutations covered in the multiplex test.…

0301 basic medicineOncologyMaleLung NeoplasmsDNA Mutational AnalysisKRAS MUTATIONSGene mutationmedicine.disease_cause0302 clinical medicinemultiplex mutation analysisCarcinoma Non-Small-Cell LungMultiplex mutation analysisPrevalenceMultiplexAnaplastic Lymphoma KinaseHETEROGENEITYAged 80 and overMutationSmokingHematologyMiddle AgedProto-Oncogene Proteins c-metProgression-Free SurvivalOncology030220 oncology & carcinogenesisAdenocarcinomaFemaleKRASPREDICT SURVIVALAdultmedicine.medical_specialtyEGFRCELL LUNG-CANCERPrognosis molecular stagingprognosis molecular stagingEGFR KRAS PIK3CAVALIDATION03 medical and health sciencesYoung AdultInternal medicineMultiplex polymerase chain reactionmedicineKRASTYROSINE KINASE INHIBITORSHumansProgression-free survivalLung cancerAgedNeoplasm Stagingbusiness.industryMICROBIOLOGIAADENOCARCINOMAAMPLIFICATIONPIK3CAmedicine.disease030104 developmental biologynon-small-cell lung cancerMutationOVEREXPRESSIONbusinessMultiplex Polymerase Chain ReactionNon-small-cell lung cancerAnnals of Oncology
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Six novel mutations of the LDL receptor gene in FH kindred of Sicilian and Paraguayan descent

2006

Familial hypercholesterolemia (FH) is an autosomal dominant inherited disease caused by mutations in the gene coding for the low density lipoprotein receptor (LDL-R). It is characterized by a high concentration of low density lipoprotein (LDL), which frequently gives rise to premature coronary artery disease. We studied the probands of five FH Sicilian families with 'definite' FH and one proband of Paraguayan descent with homozygous FH who has been treated with an effective living-donor liver transplantation. In order to seek the molecular defect in these six families, we used direct sequencing to define the molecular defects of the LDL-R gene responsible for the disease. We described three…

AdultProbandhypercholesterolemia LDL receptor gene mutation analysis direct sequencing splicing living-donor transplantationSettore MED/09 - Medicina InternaDNA Mutational AnalysisDirect sequencingHypercholesterolemiaFamilial hypercholesterolemiaBiologyGene mutationSplicingmedicine.disease_causeFrameshift mutationHyperlipoproteinemia Type IIExonGeneticsmedicineHumansMissense mutationRNA MessengerChildSicilyCells CulturedLiving-donor transplantationLDL receptor geneGeneticsMutationIntronExonsGeneral MedicineMiddle Agedmedicine.diseaseLipidsMolecular biologyPedigreeDirect sequencing; Hypercholesterolemia; LDL receptor gene; Living-donor transplantation; Mutation analysis; SplicingMutation analysisReceptors LDLParaguayChild PreschoolMutationBiological Assay
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Kirsten ras mutations in patients with colorectal cancer: the 'RASCAL II' study

2001

Researchers worldwide with information about the Kirsten ras (Ki-ras) tumour genotype and outcome of patients with colorectal cancer were invited to provide that data in a schematized format for inclusion in a collaborative database called RASCAL (The Kirsten ras in-colorectal-cancer collaborative group). Our results from 2721 such patients have been presented previously and for the first time in any common cancer, showed conclusively that different gene mutations have different impacts on outcome, even when the mutations occur at the same site on the genome. To explore the effect of Ki-ras mutations at different stages of colorectal cancer, more patients were recruited to the database, whi…

MaleOncologyCancer ResearchPathologyMultivariate analysisDatabases FactualSettore MED/06 - Oncologia MedicaColorectal cancerGene mutationmedicine.disease_cause0302 clinical medicineGenotypeColorectal cancer Ki-ras mutationRegistriesAged 80 and over0303 health sciencesMutationValineMiddle Aged3. Good healthKRAS Mutation Analysismedicine.anatomical_structureOncologyPresented by the Kirsten ras in-colorectal-cancer collaborative group030220 oncology & carcinogenesisFemaleColorectal NeoplasmsAdultmedicine.medical_specialtyAdolescentGenotypeoverall survivalMutation MissenseRectumcolorectal cancerDisease-Free Survival03 medical and health sciencesInternal medicinemedicineHumansPoint MutationK-rasCodoncolorectal cancer; K-ras; prognosis; overall survivalAgedNeoplasm StagingProportional Hazards Models030304 developmental biologybusiness.industryCancermedicine.diseaseSurvival AnalysisGenes rasMultivariate Analysisprognosisbusiness
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Mutation analysis of the SPG4 gene in Italian patients with pure and complicated forms of spastic paraplegia

2010

Mutations in the SPG4 gene are the most common causes of hereditary spastic paraplegia (HSP) accounting for up to 40% of autosomal dominant (AD) forms and 12-18% of sporadic cases. The phenotype associated with HSP due to mutations in the SPG4 gene tends to be pure. There is increasing evidence, however, of patients with complicated forms of spastic paraplegia in which SPG4 mutations were identified. A cohort of 38 unrelated Italian patients with spastic paraplegia, of which 24 had a clear dominant inheritance and 14 were apparently sporadic, were screened for mutations in the SPG4 gene.We identified 11 different mutations, six of which were novel (p.Glu143GlyfsX8, p.Tyr415X, p.Asp548Asn, c…

MaleSpastinDNA Mutational AnalysisHereditary spastic paraplegiaEXON DELETIONSGene mutationmedicine.disease_causeSpastinFAMILIESCohort StudiesExonGenotypeSpasticMutation frequencyChild3' Untranslated RegionsChromatography High Pressure LiquidAdenosine TriphosphatasesGeneticsMutationHereditary spastic paraplegia SPG4Reverse Transcriptase Polymerase Chain ReactionMutation analysiExonsMiddle AgedMLPAPhenotypeMutation analysisItalyNeurologySettore MED/26 - NeurologiaFemaleAdultAdolescentGenotypeHereditary spastic paraplegia3 ' UTR3′ UTRMutation MissenseFREQUENTSPG4CLASSIFICATIONYoung AdultmedicineHumansAgedParaplegiaSPECTRUMbusiness.industrymedicine.diseaseNeurology (clinical)businessCOLLECTIONEXPRESSION ANALYSISGene Deletion
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Analysis of the RET, GDNF, EDN3, and EDNRB genes in patients with intestinal neuronal dysplasia and Hirschsprung disease

2001

BACKGROUNDHirschsprung disease (HSCR) is a frequent congenital disorder with an incidence of 1 in 5000 live births, characterised by the absence of parasympathetic intramural ganglion cells in the hindgut resulting in intestinal obstruction in neonates and severe constipation in infants and adults. Intestinal neuronal dysplasia (IND) shares clinical features with HSCR but the submucosal parasympathetic plexus is affected. IND has been proposed as one of the most frequent causes of chronic constipation and is often associated with HSCR.METHODSWe examined 29 patients diagnosed with sporadic HSCR, 20 patients with IND, and 12 patients with mixed HSCR/IND for mutations in the coding regions of …

Pathologymedicine.medical_specialtyGlial Cell Line-Derived Neurotrophic Factor ReceptorsHirschsprung diseaseMUTATION ANALYSISNerve Tissue ProteinsTYROSINE KINASEEDNRBArticleExonGermline mutationProto-Oncogene ProteinsNEUROTROPHIC FACTOR GDNFmedicineGlial cell line-derived neurotrophic factorDrosophila ProteinsHumansGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorsAlleleintestinal neuronal dysplasiaAllelesPolymorphism Single-Stranded ConformationalIntestinal neuronal dysplasiabiologyReceptors EndothelinSHAH-WAARDENBURG SYNDROMEProto-Oncogene Proteins c-retENDOTHELIN-B-RECEPTORMULTIGENIC INHERITANCEGastroenterologyReceptor Protein-Tyrosine KinasesSequence Analysis DNAGERMLINE MUTATIONSbiochemical phenomena metabolism and nutritionPROTOONCOGENEmedicine.diseasePHENOTYPIC-EXPRESSIONGDNFPedigreeProto-Oncogene Proteins c-retDysplasiaCase-Control StudiesMutationbiology.proteinLIGANDRETCongenital disorderEDN3
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Rho GTPases in human breast tumours: expression and mutation analyses and correlation with clinical parameters

2002

In the present study, we addressed the question of a putative relevance of Rho proteins in tumour progression by analysing their expression on protein and mRNA level in breast tumours. We show that the level of RhoA, RhoB, Rac1 and Cdc42 protein is largely enhanced in all tumour samples analysed (n=15) as compared to normal tissues originating from the same individual. The same is true for 32P-ADP-ribosylation of Rho proteins which is catalysed by Clostridium botulinum exoenzyme C3. Also the amount of Rho-GDI and ERK2 as well as the level of overall 32P-GTP binding acvitity was tumour-specific elevated, yet to a lower extent than Rho proteins. Although the amount of Rho proteins was enhance…

rac1 GTP-Binding Proteinrho GTP-Binding ProteinsCancer ResearchRHOAProliferation indexRHOBBlotting WesternDNA Mutational AnalysisRhoCGene ExpressionBreast NeoplasmsRAC1breast tumoursCDC42Polymerase Chain ReactionRho GTPasesRhoB GTP-Binding ProteinHumansBreastRNA Messengercdc42 GTP-Binding ProteinrhoB GTP-Binding Proteinmutation analysisADP Ribose TransferasesMitogen-Activated Protein Kinase 1biologyGenetics and GenomicsMolecular biologyOncologyCdc42 GTP-Binding ProteinMutationtumour progressionDisease Progressionbiology.proteinFemaleGuanosine TriphosphaterhoA GTP-Binding ProteinBritish Journal of Cancer
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