Search results for "ML"

showing 10 items of 1465 documents

Somatic copy number alterations are associated with EGFR amplification and shortened survival in patients with primary glioblastoma.

2019

Glioblastoma (GBM) is the most common malignant primary tumor of the central nervous system. With no effective therapy, the prognosis for patients is terrible poor. It is highly heterogeneous and EGFR amplification is its most frequent molecular alteration. In this light, we aimed to examine the genetic heterogeneity of GBM and to correlate it with the clinical characteristics of the patients. For that purpose, we analyzed the status of EGFR and the somatic copy number alterations (CNAs) of a set of tumor suppressor genes and oncogenes. Thus, we found GBMs with high level of EGFR amplification, low level and with no EGFR amplification. Highly amplified tumors showed histological features of…

0301 basic medicineMaleCancer ResearchBiopsyL-amp GB EGFR-low amplified glioblastomamedicine.disease_causewt wildtypeMYBPC3 myosin-binding protein C0302 clinical medicineHIC1 hypermethylated in cancer 1Gene duplicationIn Situ Hybridization FluorescenceIDH2 isocitrate dehydrogenase 2MutationRB-pat RB signaling pathwayEGFRvIII epidermal growth factor receptor variant number IIIPAH phenylalanine hydroxylaseGBM glioblastoma IDH-wildtype (glioblastoma multiforme primary glioblastoma).ANOVA ANalysis Of VArianceN-amp GB EGFR-no amplified glioblastomaMiddle AgedCDKN2A cyclin-dependent kinase inhibitor 2Alcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumorImmunohistochemistryH-amp GB EGFR-high amplified glioblastomaErbB ReceptorsTKR-pat tyrosine-kinase receptors signaling pathway030220 oncology & carcinogenesisDisease ProgressionCDK6 cyclin-dependent kinase 6CDH1 Cadherin 1FemaleCREM cAMP response element modulatorIHC immunohistochemistryAdultOriginal articleDNA Copy Number VariationsCDKN1B cyclin-dependent kinase inhibitor 1BBiologyRARB retinoic acid receptor betaCNS central nervous systemlcsh:RC254-282IDH1 isocitrate dehydrogenase 1BCL2 B-cell cll/ lymphoma 2CNAs copy number algerationsWHO World Health Organization03 medical and health sciencesYoung Adultp53-pat p53 signaling pathwaymedicineBiomarkers TumorTMA tissue microarrayPTENHumansProtein kinase BPI3K/AKT/mTOR pathwaySurvival analysisAgedGenetic heterogeneityGene AmplificationGFAP glial fibrillary acidic proteinMLPA multiplex ligation-dependent probe amplificationmedicine.diseaseFISH fluorescence in situ hibridizationSurvival AnalysisCDKN2B cyclin-dependent kinase inhibitor 2BPTEN phosphatase and tensin homologEGFR epidermal growth factor receptorCNV-load load of copy number variations030104 developmental biologyMutationPARK2 parkinCancer researchbiology.proteinTCGA The Cancer Genome AtlasLARGE1 acetylglucosaminyltransferase-like protein 1GlioblastomaCHD7 Chromodomain Helicase DNA Binding Protein 7DAPI 4′6-diamidino-2-phenylindoleNeoplasia (New York, N.Y.)
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Exome-wide somatic mutation characterization of small bowel adenocarcinoma

2018

Small bowel adenocarcinoma (SBA) is an aggressive disease with limited treatment options. Despite previous studies, its molecular genetic background has remained somewhat elusive. To comprehensively characterize the mutational landscape of this tumor type, and to identify possible targets of treatment, we conducted the first large exome sequencing study on a population-based set of SBA samples from all three small bowel segments. Archival tissue from 106 primary tumors with appropriate clinical information were available for exome sequencing from a patient series consisting of a majority of confirmed SBA cases diagnosed in Finland between the years 2003–2011. Paired-end exome sequencing was…

0301 basic medicineMaleCancer ResearchMICROSATELLITE INSTABILITYColorectal canceroncogenesReceptor ErbB-2medicine.disease_causeCOLORECTAL-CANCERACTIVATIONCohort Studies0302 clinical medicineAnimal CellsAdenocarcinomasMedicine and Health SciencesExomeFrameshift MutationExomeGenetics (clinical)Exome sequencingAged 80 and overSMALL-INTESTINEeducation.field_of_study1184 Genetics developmental biology physiologyCELIAC-DISEASENonsense MutationMiddle Aged3. Good healthsyöpägeenitOncology030220 oncology & carcinogenesissyöpätauditFemaleSIGNALING PATHWAYKRASCellular TypesResearch ArticleAdultProto-Oncogene Proteins B-raflcsh:QH426-470SEQUENCING DATAImmune CellsNonsense mutationPopulationImmunologyAntigen-Presenting CellsComputational biologysuolistosyövätBiologyAdenocarcinomata3111CarcinomasFrameshift mutation03 medical and health sciencesGermline mutationQUALITY-CONTROLGenetiikka kehitysbiologia fysiologia - Genetics developmental biology physiologySyöpätaudit - CancersIntestinal NeoplasmsmedicineGeneticsPoint MutationHumanseducationMolecular BiologyEcology Evolution Behavior and SystematicsAgedColorectal CancerBiology and Life SciencesCancers and Neoplasmscancerous diseasesCell Biologymedicine.diseaseta3122mutationsCOMPREHENSIVE MOLECULAR CHARACTERIZATIONlcsh:Genetics030104 developmental biologyMutationSomatic Mutationbowel cancer3111 BiomedicinemutaatiotHIGH-RESOLUTIONPLoS Genetics
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Antibiotic resistance and population structure of cystic fibrosis Pseudomonas aeruginosa isolates from a Spanish multi-centre study

2017

The first Spanish multi-centre study on the microbiology of cystic fibrosis (CF) was conducted from 2013 to 2014. The study involved 24 CF units from 17 hospitals, and recruited 341 patients. The aim of this study was to characterise Pseudomonas aeruginosa isolates, 79 of which were recovered from 75 (22%) patients. The study determined the population structure, antibiotic susceptibility profile and genetic background of the strains. Fifty-five percent of the isolates were multi-drug-resistant, and 16% were extensively drug-resistant. Defective mutS and mutL genes were observed in mutator isolates (15.2%). Considerable genetic diversity was observed by pulsed-field gel electrophoresis (70 p…

0301 basic medicineMaleCystic FibrosisAntibiotic resistanceArray tubeMulti-locus sequence typing (MLST)medicine.disease_causeGenotypePharmacology (medical)ChildGeneticseducation.field_of_studyMolecular EpidemiologyVirulencePseucforrumus aeruginosaGeneral MedicineMiddle AgedMutS DNA Mismatch-Binding ProteinElectrophoresis Gel Pulsed-FieldInfectious DiseasesChild PreschoolPseudomonas aeruginosaFemalemedicine.drugMicrobiology (medical)AdultAdolescentGenotype030106 microbiologyPopulationVirulenceBiologyCystic fibrosisMicrobiology03 medical and health sciencesYoung AdultAntibiotic resistanceDrug Resistance BacterialmedicineHumansPseudomonas InfectionsTypingeducationGenetic diversityPseudomonas aeruginosaGenetic VariationMutL ProteinsSpainColistinMultilocus Sequence Typing
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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
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Expanding the Phenotype Associated with NAA10-Related N-Terminal Acetylation Deficiency

2016

International audience; N-terminal acetylation is a common protein modification in eukaryotes associated with numerous cellular processes. Inherited mutations in NAA10, encoding the catalytic subunit of the major N-terminal acetylation complex NatA have been associated with diverse, syndromic X-linked recessive disorders, whereas de novo missense mutations have been reported in one male and one female individual with severe intellectual disability but otherwise unspecific phenotypes. Thus, the full genetic and clinical spectrum of NAA10 deficiency is yet to be delineated. We identified three different novel and one known missense mutation in NAA10, de novo in 11 females, and due to maternal…

0301 basic medicineMaleModels MolecularMicrocephalyMutation MissenseBiologyGermlineKEY WORDS: NAA1003 medical and health sciencesGermline mutationGenes X-LinkedIntellectual disabilityGeneticsmedicineMissense mutationHumansGenetic Predisposition to DiseaseN-Terminal Acetyltransferase EGenetics (clinical)Genetic Association StudiesGerm-Line MutationN-Terminal Acetyltransferase AResearch ArticlesGeneticsX-linked[SDV.GEN]Life Sciences [q-bio]/GeneticsRegional Council of BurgundyMosaicismN-terminal acetylationAcetylationmedicine.diseasePhenotypePedigreeOgden SyndromeX‐linked030104 developmental biologyNAA10intellectual disabilityN‐terminal acetylationContract grant sponsors: Dijon University HospitalFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsNAA15Research ArticleHuman Mutation
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A possible role of FANCM mutations in male breast cancer susceptibility: Results from a multicenter study in Italy

2018

Abstract Introduction Breast cancer (BC) in men is a rare disease, whose etiology appears to be associated with genetic factors. Inherited mutations in BRCA1/2 genes account for about 10–15% of all cases. FANCM, functionally linked to BRCA1/2, has been suggested as a novel BC susceptibility gene. Our aim was to test if FANCM germline mutations could further explain male BC (MBC) susceptibility. Methods We screened the entire coding region of FANCM in 286 MBCs by a multi-gene panel analysis, and compared these data with available whole exome sequencing data from 415 men used as population controls. Moreover, we genotyped the two most frequent FANCM mutations (c.5101C>T and c.5791C>T) in 506 …

0301 basic medicineMaleMutation rateSettore MED/06 - Oncologia MedicaDNA Helicasemedicine.disease_causeBRCA1/2; Breast cancer susceptibility; FANCM; Germline mutations; Male breast cancer; Adult; Aged; Aged 80 and over; Biomarkers Tumor; Breast Neoplasms Male; Case-Control Studies; DNA Helicases; Genetic Predisposition to Disease; Genotype; Germ-Line Mutation; Humans; Italy; Male; Middle Aged; Risk Factors; Whole Genome Sequencing; Young Adult; Surgery0302 clinical medicineFANCMRisk Factorshemic and lymphatic diseasesGermline mutationGenotypeBRCA1/2; Breast cancer susceptibility; FANCM; Germline mutations; Male breast cancer; SurgeryFANCMMutation frequencyGeneticsAged 80 and overeducation.field_of_studyMutationGeneral MedicineMiddle AgedItaly030220 oncology & carcinogenesisMale breast cancerCase-Control StudieHumanAdultcongenital hereditary and neonatal diseases and abnormalitiesGenotypePopulationBreast Neoplasms Male03 medical and health sciencesYoung AdultGermline mutationBRCA1/2medicineBiomarkers TumorHumansGenetic Predisposition to DiseaseeducationGermline mutationsGerm-Line MutationAgedBreast cancer susceptibilityWhole Genome Sequencingbusiness.industryRisk FactorDNA Helicasesnutritional and metabolic diseasesmedicine.diseaseMale breast cancer030104 developmental biologyCase-Control StudiesSurgerybusiness
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Pathogenic DDX3X Mutations Impair RNA Metabolism and Neurogenesis during Fetal Cortical Development.

2020

Summary De novo germline mutations in the RNA helicase DDX3X account for 1%–3% of unexplained intellectual disability (ID) cases in females and are associated with autism, brain malformations, and epilepsy. Yet, the developmental and molecular mechanisms by which DDX3X mutations impair brain function are unknown. Here, we use human and mouse genetics and cell biological and biochemical approaches to elucidate mechanisms by which pathogenic DDX3X variants disrupt brain development. We report the largest clinical cohort to date with DDX3X mutations (n = 107), demonstrating a striking correlation between recurrent dominant missense mutations, polymicrogyria, and the most severe clinical outcom…

0301 basic medicineMaleNeurogenesisMutation MissenseBiologyPathogenesisDEAD-box RNA Helicases03 medical and health sciencesMice0302 clinical medicineGermline mutationStress granuleCell Line TumorPolymicrogyriamedicineMissense mutationAnimalsHumansCells CulturedGeneticsCerebral CortexGeneral NeuroscienceNeurogenesismedicine.diseaseRNA Helicase AMice Inbred C57BL030104 developmental biologyNeurodevelopmental DisordersRNAFemaleDDX3X030217 neurology & neurosurgeryNeuron
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Facial cutaneo-mucosal venous malformations can develop independently of mutation of TEK gene but may be associated with excessive expression of Src…

2017

International audience; We aimed to search for mutations in the germline and somatic DNA of the TEK gene and to analyze the expression level of Src and phospho- Src (p-Src) in tumor and healthy tissues from patients with facial cutaneo-mucosal venous malformations (VMCM). Eligible patients from twelve families and thirty healthy controls were recruited respectively at the Departments of Stomatology and Oral Surgery, and Transfusion Medicine of Tlemcen University Medical Centre. Immunoblot analyses of Src and p-Src were performed after direct DNA sequencing. No somatic or germline mutations were found in all the 23 exons and their 5' and 3' intronic flanking regions, except for one case in w…

0301 basic medicineMaleSomatic cellVascular MalformationsCutaneo-mucosal venous malformationsTyrosine Kinase Tie2Bioinformaticsmedicine.disease_causeGermlineMetastasisp-SrcExonPharmacology Toxicology and Pharmaceutics(all)General Pharmacology Toxicology and PharmaceuticsPhosphorylationCancerMedicine(all)MutationBrief ReportGeneral MedicineReceptor TIE-2[SDV.BDD.MOR] Life Sciences [q-bio]/Development Biology/Morphogenesis3. Good healthsrc-Family Kinases[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]FemaleProto-oncogene tyrosine-protein kinase SrcReceptorSrc[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]AdolescentDirect sequencingContext (language use)BiologyVegfGeneral Biochemistry Genetics and Molecular BiologyPermeability03 medical and health sciencesGermline mutationTEK gene[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN][ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansAmino Acid SequenceGeneMucous MembraneCell-Lines[ SDV ] Life Sciences [q-bio]Base SequenceBiochemistry Genetics and Molecular Biology(all)[SDV.BDD.MOR]Life Sciences [q-bio]/Development Biology/MorphogenesisGermline and somatic DNA030104 developmental biologyFaceMutationCancer researchSkin AbnormalitiesAngiogenesisPathwayJournal of negative results in biomedicine
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Total colonic aganglionosis and cleft palate in a newborn with Janus-cysteine 618 mutation of RET proto-oncogene: a case report.

2020

Abstract Background Hirschsprung disease, the most important congenital colonic dysmotility in children results from neural crest migration, differentiation, proliferation, or apoptosis defects where the rearranged during transfection (RET)-Protooncogene pathway has a central role. Although palatal and retinal anomalies in the context of chromosomopathies and some mono−/oligogenic syndromes are reported associated with Hirschsprung disease the role of inactivating RET mutations in these cases is not clarified. Case presentation We report on a dysmorphic newborn with cleft palate and palatal synechia, who showed intestinal obstruction after 24 h of life. Transient ileostomy and surgical biop…

0301 basic medicineMalecongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyCongenital digestive system abnormalitieNeurocristopathyCase ReportContext (language use)RET proto-oncogenemedicine.disease_causeProto-Oncogene MasCongenital digestive system abnormalities03 medical and health sciences0302 clinical medicineGermline mutationCase-reportmedicineCarcinomaHumansCysteineHirschsprung DiseaseTotal colonic aganglionosisLoss functionGerm-Line MutationJanus KinasesNeurocristopathyMutationbusiness.industryProto-Oncogene Proteins c-retlcsh:RJ1-570Infant Newbornlcsh:Pediatricsmedicine.diseaseCleft Palate030104 developmental biologyItaly030220 oncology & carcinogenesisREarranged during TransfectionbusinessItalian journal of pediatrics
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When Three Isn't a Crowd: A Digyny Concept for Treatment-Resistant, Near-Triploid Human Cancers.

2019

Near-triploid human tumors are frequently resistant to radio/chemotherapy through mechanisms that are unclear. We recently reported a tight association of male tumor triploidy with XXY karyotypes based on a meta-analysis of 15 tumor cohorts extracted from the Mitelman database. Here we provide a conceptual framework of the digyny-like origin of this karyotype based on the germline features of malignant tumors and adaptive capacity of digyny, which supports survival in adverse conditions. Studying how the recombinatorial reproduction via diploidy can be executed in primary cancer samples and HeLa cells after DNA damage, we report the first evidence that diploid and triploid cell sub-populati…

0301 basic medicineMalelcsh:QH426-470DNA repairKaryotypeSpindle ApparatusDigynyBiologyGenomeGermline03 medical and health sciencesnear-triploid cancer0302 clinical medicineMeiosisNeoplasmsGeneticsTumor Cells Culturedtumor blastomeresHumansGeneGenetics (clinical)GeneticsChromosomes Human XChromosomes Human YModels Geneticfungifood and beverageschemoresistancereprogrammingKaryotypeConcept Papertripolar mitosisTriploidyradioresistancelcsh:GeneticsMeiosis030104 developmental biologyGerm Cellspedogamy030220 oncology & carcinogenesisNeoplastic Stem Cellspolynuclear cancer cellsPloidyHeLa CellsdigynyGenes
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