Search results for "Predisposition"

showing 10 items of 771 documents

Childhood cancer predisposition syndromes-A concise review and recommendations by the Cancer Predisposition Working Group of the Society for Pediatri…

2017

Heritable predisposition is an important cause of cancer in children and adolescents. Although a large number of cancer predisposition genes and their associated syndromes and malignancies have already been described, it appears likely that there are more pediatric cancer patients in whom heritable cancer predisposition syndromes have yet to be recognized. In a consensus meeting in the beginning of 2016, we convened experts in Human Genetics and Pediatric Hematology/Oncology to review the available data, to categorize the large amount of information, and to develop recommendations regarding when a cancer predisposition syndrome should be suspected in a young oncology patient. This review su…

0301 basic medicineHistoryMedizinGene Expression0302 clinical medicineNeoplasm Proteins/geneticsNeoplasmsChildGenetics (clinical)Societies Medicalddc:618HematologyJuvenile myelomonocytic leukemiaCancer predispositionSyndromeFocus Groups21st Century3. Good healthNeoplasm Proteins030220 oncology & carcinogenesisHematologic NeoplasmsGenetic Testing/methodsmedicine.medical_specialtyAdolescentGenetics MedicalGenetic CounselingHistory 21st CenturyMedical/history/instrumentation/methodsFamilial adenomatous polyposis03 medical and health sciencesInternal medicineGeneticsmedicineHumansFocus Groups/methodsGenetic Predisposition to DiseaseGenetic TestingIntensive care medicineGenetic Counseling/ethicsbusiness.industryHematologic Neoplasms/diagnosis/genetics/pathologyCancermedicine.diseasePediatric cancerHuman genetics030104 developmental biologyLi–Fraumeni syndromeNeoplasms/diagnosis/genetics/pathologyMutationMedical/historySocietiesbusinessAmerican journal of medical genetics. Part A
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Role of Immunogenetics in the Outcome of HCMV Infection: Implications for Ageing

2019

The outcome of host-virus interactions is determined by a number of factors, some related to the virus, others to the host, such as environmental factors and genetic factors. Therefore, different individuals vary in their relative susceptibility to infections. Human cytomegalovirus (HCMV) is an important pathogen from a clinical point of view, as it causes significant morbidity and mortality in immunosuppressed or immunosenescent individuals, such as the transplanted patients and the elderly, respectively. It is, therefore, important to understand the mechanisms of virus infection control. In this review, we discuss recent advances in the immunobiology of HCMV-host interactions, with partic…

0301 basic medicineHuman cytomegalovirusAgingCellular immunityvirusesCytomegalovirusReviewlcsh:Chemistry0302 clinical medicineHLA AntigensGenotypeMedicineantibodieslcsh:QH301-705.5SpectroscopyimmunosenescenceImmunity CellularbiologyGeneral MedicineImmunosenescenceGMComputer Science ApplicationsKIRHLAantibodieCytomegalovirus InfectionsHost-Pathogen InteractionsAntibodyGenotypeNKCongenital cytomegalovirus infectionHuman leukocyte antigenelderlyCatalysisVirusInorganic Chemistry03 medical and health sciencesImmunogeneticsAnimalsHumansGenetic Predisposition to DiseasePhysical and Theoretical ChemistryMolecular BiologyHCMVSettore MED/04 - Patologia Generalebusiness.industryOrganic Chemistrymedicine.diseaseImmunity Humoral030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Immunologybiology.proteinbusiness030215 immunology
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Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

2017

International audience; We identified rare coding variants associated with Alzheimer's disease in a three-stage case-control study of 85,133 subjects. In stage 1, we genotyped 34,174 samples using a whole-exome microarray. In stage 2, we tested associated variants (P < 1 × 10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, we used an additional 14,997 samples to test the most significant stage 2 associations (P < 5 × 10-8) using imputed genotypes. We observed three new genome-wide significant nonsynonymous variants associated with Alzheimer's disease: a protective variant in PLCG2 (rs72824905: p.Pro522Arg, P = 5.38 × 10-10, odds ratio (OR) = 0.68…

0301 basic medicineLinkage disequilibrium[SDV]Life Sciences [q-bio]MedizinSequence HomologyGenome-wide association studygenetics [Alzheimer Disease]metabolism [Microglia]Linkage Disequilibrium0302 clinical medicinegenetics [Protein Interaction Maps]genetics [Membrane Glycoproteins]Gene FrequencyImmunologicgenetics [Adaptor Proteins Signal Transducing]Receptorsgenetics [Exome]Odds RatioInnategenetics [Receptors Immunologic]ExomeProtein Interaction Mapsgenetics [Genetic Predisposition to Disease]Receptors ImmunologicABI3 protein humanGeneticsAdaptor Proteins Signal Transducing; Alzheimer Disease; Amino Acid Sequence; Case-Control Studies; Exome; Gene Expression Profiling; Gene Frequency; Genetic Predisposition to Disease; Genotype; Humans; Immunity Innate; Linkage Disequilibrium; Membrane Glycoproteins; Microglia; Odds Ratio; Phospholipase C gamma; Protein Interaction Maps; Receptors Immunologic; Sequence Homology Amino Acid; Polymorphism Single Nucleotide; GeneticsMembrane GlycoproteinsAdaptor ProteinsSingle NucleotideAdaptor Proteins Signal Transducing; Alzheimer Disease; Amino Acid Sequence; Case-Control Studies; Exome; Gene Expression Profiling; Gene Frequency; Genetic Predisposition to Disease; Genotype; Humans; Immunity Innate; Linkage Disequilibrium; Membrane Glycoproteins; Microglia; Odds Ratio; Phospholipase C gamma; Protein Interaction Maps; Receptors Immunologic; Sequence Homology Amino Acid; Polymorphism Single Nucleotide3. Good health[SDV] Life Sciences [q-bio]Amino AcidSettore MED/26 - NEUROLOGIAgenetics [Phospholipase C gamma][SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]MicrogliaAlzheimer's diseaseCommon disease-common variantGenotypeBiologyPolymorphism Single NucleotideArticle03 medical and health sciencesAlzheimer Diseaseddc:570medicineJournal ArticleGeneticsHumansGenetic Predisposition to Disease[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Amino Acid SequencePolymorphismAllele frequencyAdaptor Proteins Signal TransducingTREM2 protein humanSequence Homology Amino AcidTREM2Phospholipase C gammaGene Expression ProfilingCase-control studySignal TransducingImmunitymedicine.diseaseR1Immunity InnateMinor allele frequencygenetics [Immunity Innate]030104 developmental biologyCase-Control StudiesHuman medicine030217 neurology & neurosurgery
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The membrane-bound O-acyltransferase domain-containing 7 variant rs641738 increases inflammation and fibrosis in chronic hepatitis B.

2017

Chronic hepatitis B (CHB) is characterized by hepatic inflammation that promotes progression to cirrhosis and predisposes to the development of hepatocellular carcinoma (HCC). Subtle interindividual genetic variation as well as viral and environmental factors interact to determine disease progression between individuals. Recently, the rs641738 membrane-bound O-acyltransferase domain-containing 7 (MBOAT7) polymorphism was demonstrated to influence histological liver damage in alcoholic liver disease, nonalcoholic fatty liver disease, and hepatitis C, but no data are available for CHB. We evaluated rs641738 influence on disease severity in a cohort of 1,101 patients with CHB. Forty-two patien…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCirrhosisSex FactorSeverity of Illness IndexCohort StudiesGene FrequencyFibrosisNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseAge FactorProspective StudiesChronicMembrane ProteinMultivariate AnalysiAge FactorsHepatitis CSingle NucleotideMiddle AgedHepatitis BPrognosisHepatocellular carcinomaDisease ProgressionFemaleHumanAdultmedicine.medical_specialtyLogistic ModelPrognosiAcyltransferaseLiver CirrhosiAcetyltransferases; Acyltransferases; Adult; Age Factors; Cohort Studies; Confidence Intervals; Disease Progression; Female; Gene Frequency; Genetic Predisposition to Disease; Hepatitis B Chronic; Humans; Liver Cirrhosis; Logistic Models; Male; Membrane Proteins; Middle Aged; Multivariate Analysis; Non-alcoholic Fatty Liver Disease; Polymorphism Single Nucleotide; Prognosis; Prospective Studies; Risk Assessment; Severity of Illness Index; Sex FactorsPolymorphism Single NucleotideRisk Assessment03 medical and health sciencesHepatitis B ChronicSex FactorsSDG 3 - Good Health and Well-beingAcetyltransferasesInternal medicineAcetyltransferasemedicineConfidence IntervalsHumansGenetic Predisposition to DiseasePolymorphismHepatologybusiness.industryMembrane ProteinsHepatologymedicine.diseaseMinor allele frequencyProspective Studie030104 developmental biologyLogistic ModelsImmunologyMultivariate AnalysisCohort StudiebusinessConfidence IntervalAcyltransferasesHepatology (Baltimore, Md.)
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MBOAT7 rs641738 variant and hepatocellular carcinoma in non-cirrhotic individuals

2017

AbstractNonalcoholic fatty liver disease (NAFLD) represents an emerging cause of hepatocellular carcinoma (HCC), especially in non-cirrhotic individuals. The rs641738 C &gt; T MBOAT7/TMC4 variant predisposes to progressive NAFLD, but the impact on hepatic carcinogenesis is unknown. In Italian NAFLD patients, the rs641738 T allele was associated with NAFLD-HCC (OR 1.65, 1.08–2.55; n = 765), particularly in those without advanced fibrosis (p &lt; 0.001). The risk T allele was linked to 3’-UTR variation in MBOAT7 and to reduced MBOAT7 expression in patients without severe fibrosis. The number of PNPLA3, TM6SF2, and MBOAT7 risk variants was associated with NAFLD-HCC independently of clinical fa…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseasePathologyCirrhosisliver diseasesGastroenterology0302 clinical medicineSettore BIO/13 - Biologia ApplicataNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseasefatty liver-disease; cirrhosis; liver cancer; hepatitis C; hepatocellular carcinoma; liver diseases; fibrosis; carcinogenesis; fatty liver; allelesHCCProspective cohort studySettore MED/12 - GastroenterologiaMultidisciplinaryLiver NeoplasmsQRhepatocellular carcinomaSingle NucleotideMiddle Aged3. Good healthItalyfatty liver-diseaseHepatocellular carcinomaCohortMedicine030211 gastroenterology & hepatologyFemalecarcinogenesisAcyltransferases; Adult; Aged; Carcinoma Hepatocellular; Female; Gene Expression Regulation; Genotype; Humans; Italy; Liver Cirrhosis; Liver Neoplasms; Male; Membrane Proteins; Middle Aged; Non-alcoholic Fatty Liver Disease; Polymorphism Single Nucleotide; Risk Factors; Alleles; Genetic Association Studies; Genetic Predisposition to Disease; Genetic VariationAdultmedicine.medical_specialtyCarcinoma HepatocellularGenotypeSciencePolymorphism Single NucleotideArticleliver cancer03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseAllelePolymorphismAllelesGenetic Association Studiesfatty liverAgedSettore MED/06 - ONCOLOGIA MEDICAbusiness.industrycirrhosisfibrosisCarcinomaGenetic VariationMembrane ProteinsHepatocellularmedicine.diseasedigestive system diseases030104 developmental biologyGene Expression Regulationhepatitis CbusinessAcyltransferasesTM6SF2Scientific Reports
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Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation.

2017

Cholestatic liver injury results from impaired bile flow or metabolism and promotes hepatic inflammation and fibrogenesis. Toxic bile acids that accumulate in cholestasis induce apoptosis and contribute to early cholestatic liver injury, which is amplified by accompanying inflammation. The aim of the current study was to evaluate the role of the antiapoptotic caspase 8-homolog cellular FLICE-inhibitory (cFLIP) protein during acute cholestatic liver injury. Transgenic mice exhibiting hepatocyte-specific deletion of cFLIP (cFLIP−/−) were used for in vivo and in vitro analysis of cholestatic liver injury using bile duct ligation (BDL) and the addition of bile acids ex vivo. Loss of cFLIP in h…

0301 basic medicineLiver CirrhosisTime FactorsPhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinInflammationApoptosisp38 Mitogen-Activated Protein KinasesHepatitisBile Acids and Salts03 medical and health sciencesNecrosisCholestasisPhysiology (medical)medicineHepatic Stellate CellsAnimalsASK1Genetic Predisposition to DiseaseLigationCells CulturedTumor Necrosis Factor alpha-Induced Protein 3chemistry.chemical_classificationLiver injuryCommon Bile DuctMice KnockoutReactive oxygen speciesHepatologyBile duct ligationGastroenterologyTranscription Factor RelAmedicine.diseaseOxidative Stress030104 developmental biologyCholedocholithiasisPhenotypechemistryLiverNeutrophil InfiltrationApoptosisFLICE Inhibitory ProteinCancer researchHepatocytesCytokinesmedicine.symptomInflammation MediatorsSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
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Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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Aging-associated genes and let-7 microRNAs: a contribution to myogenic program dysregulation in oculopharyngeal muscular dystrophy

2019

Oculopharyngeal muscular dystrophy (OPMD) is a late-onset muscle disease caused by an abnormal (GCN) triplet expansion within the polyadenylate-binding protein nuclear 1 gene and consequent mRNA pr...

0301 basic medicineMaleAgingOculopharyngealMuscle DevelopmentBiochemistryMyoblasts0302 clinical medicine80 and overMuscular DystrophyHMGB1 ProteinPAX7 Transcription FactorCell DifferentiationdifferentiationMiddle AgedCell biologymedicine.anatomical_structureFemaleMyogeninMitogen-Activated Protein KinasesBiotechnologyDifferentiation regeneration skeletal muscleAdultBiologyInclusion BodyOculopharyngeal muscular dystrophy03 medical and health sciencesmicroRNAGeneticsmedicineHumansGenetic Predisposition to Diseasedifferentiation; regeneration; skeletal muscle; Adult; Aged; Aged 80 and over; Aging; Antigens Neoplasm; Cell Differentiation; Female; Gene Expression Regulation; HMGB1 Protein; Humans; Male; MicroRNAs; Middle Aged; Mitogen-Activated Protein Kinases; Muscle Development; Muscular Dystrophy Oculopharyngeal; Myoblasts; Myogenin; Myositis Inclusion Body; PAX7 Transcription Factor; Genetic Predisposition to Diseaseskeletal muscleAntigensMolecular BiologyGeneAgedMessenger RNAMyositisRegeneration (biology)Skeletal musclemedicine.diseaseMicroRNAs030104 developmental biologyMuscle diseaseGene Expression RegulationregenerationNeoplasm030217 neurology & neurosurgery
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Threshold Effects of Circulating Angiopoietin-Like 3 Levels on Plasma Lipoproteins.

2017

Abstract Context Angiopoietin-like 3 (ANGPTL3) deficiency in plasma due to loss-of-function gene mutations results in familial combined hypobetalipoproteinemia type 2 (FHBL2) in homozygotes. However, the lipid phenotype in heterozygotes is much milder and does not appear to relate directly to ANGPTL3 levels. Furthermore, the low-density lipoprotein (LDL) phenotype in carriers of ANGPTL3 mutations is unexplained. Objective To determine whether reduction below a critical threshold in plasma ANGPTL3 levels is a determinant of lipoprotein metabolism in FHBL2, and to determine whether proprotein convertase subtilisin kexin type 9 (PCSK9) is involved in determining low LDL levels in this conditio…

0301 basic medicineMaleApolipoprotein BEndocrinology Diabetes and MetabolismClinical BiochemistryBiochemistryLipoprotein particlePCSK9Cohort StudiesHypobetalipoproteinemiaschemistry.chemical_compoundEndocrinologyANGPTL3biologyChemistryMiddle AgedPedigreeLipoproteins LDLPhenotypeKexinlipids (amino acids peptides and proteins)FemaleANGPTL3; familial combined hypolipidemia; PCSK9Lipoproteins HDLAdultmedicine.medical_specialtyHeterozygoteBlotting Western03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseClinical Research ArticlesAgedAngiopoietin-Like Protein 3Apolipoproteins BCholesterolPCSK9Biochemistry (medical)medicine.disease030104 developmental biologyEndocrinologyAngiopoietin-like ProteinsLDL receptorMultivariate AnalysisMutationbiology.proteinLinear Modelsfamilial combined hypobetalipoproteinemiaHypobetalipoproteinemiaAngiopoietinsLipoprotein
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Rare Pathogenic Variants Predispose to Hepatocellular Carcinoma in Nonalcoholic Fatty Liver Disease

2019

AbstractNonalcoholic fatty liver disease (NAFLD) is a rising cause of hepatocellular carcinoma (HCC). We examined whether inherited pathogenic variants in candidate genes (n = 181) were enriched in patients with NAFLD-HCC. To this end, we resequenced peripheral blood DNA of 142 NAFLD-HCC, 59 NAFLD with advanced fibrosis, and 50 controls, and considered 404 healthy individuals from 1000 G. Pathogenic variants were defined according to ClinVar, likely pathogenic as rare variants predicted to alter protein activity. In NAFLD-HCC patients, we detected an enrichment in pathogenic (p = 0.024), and likely pathogenic variants (p = 1.9*10−6), particularly in APOB (p = 0.047). APOB variants were asso…

0301 basic medicineMaleCandidate geneApolipoprotein Blcsh:MedicineGastroenterologyLiver diseasechemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseSequestosome-1 ProteinGenetic riskHCClcsh:ScienceMultidisciplinarybiologyLiver NeoplasmsMiddle Aged3. Good healthCholesterolHepatocellular carcinomaApolipoprotein B-100FemaleAged; Apolipoprotein B-100; Carcinoma Hepatocellular; Case-Control Studies; Cholesterol HDL; Female; Genetic Predisposition to Disease; Glial Cell Line-Derived Neurotrophic Factor Receptors; Humans; Liver Neoplasms; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Reproducibility of Results; Risk Factors; Sequestosome-1 Proteinmedicine.medical_specialtyCarcinoma HepatocellularGlial Cell Line-Derived Neurotrophic Factor ReceptorsHDLSettore BIO/18 - GENETICAdigestive systemArticle03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseGeneAgedCholesterolbusiness.industrylcsh:RCarcinomaCholesterol HDLnutritional and metabolic diseasesReproducibility of ResultsHepatocellularmedicine.diseasedigestive system diseases030104 developmental biologychemistryNASH HCCCase-Control Studiesbiology.proteinlcsh:Qgeneticbusiness030217 neurology & neurosurgery
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