Search results for "Molecular Genetics"

showing 10 items of 81 documents

Comprehensive exploration of the effects of miRNA SNPs on monocyte gene expression.

2012

We aimed to assess whether pri-miRNA SNPs (miSNPs) could influence monocyte gene expression, either through marginal association or by interacting with polymorphisms located in 3'UTR regions (3utrSNPs). We then conducted a genome-wide search for marginal miSNPs effects and pairwise miSNPs × 3utrSNPs interactions in a sample of 1,467 individuals for which genome-wide monocyte expression and genotype data were available. Statistical associations that survived multiple testing correction were tested for replication in an independent sample of 758 individuals with both monocyte gene expression and genotype data. In both studies, the hsa-mir-1279 rs1463335 was found to modulate in cis the expres…

MaleGene Expressionlcsh:MedicineGenome-wide association studyCoronary Artery DiseaseLinkage DisequilibriumMonocytes0302 clinical medicineGene expressionGenotypelcsh:Science3' Untranslated RegionsOligonucleotide Array Sequence AnalysisGenetics0303 health sciencesMultidisciplinaryGenomicsMiddle Aged3. Good healthFemaleRNA InterferenceEpigeneticsResearch ArticleAdultmedicine.medical_specialtyImmune CellsImmunologyLocus (genetics)Single-nucleotide polymorphismBiologyPolymorphism Single Nucleotide03 medical and health sciencesMolecular geneticsmedicineGeneticsHumansGeneBiology030304 developmental biologyAgedPopulation BiologyHaplotypelcsh:RComputational BiologyMicroRNAsCase-Control StudiesLeukocytes MononuclearLinear ModelsGenetic Polymorphismlcsh:QTranscriptomeGenome Expression Analysis030217 neurology & neurosurgeryPopulation GeneticsGenome-Wide Association StudyPLoS ONE
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Transforming RNA-Seq Data to Improve the Performance of Prognostic Gene Signatures

2014

Gene expression measurements have successfully been used for building prognostic signatures, i.e for identifying a short list of important genes that can predict patient outcome. Mostly microarray measurements have been considered, and there is little advice available for building multivariable risk prediction models from RNA-Seq data. We specifically consider penalized regression techniques, such as the lasso and componentwise boosting, which can simultaneously consider all measurements and provide both, multivariable regression models for prediction and automated variable selection. However, they might be affected by the typical skewness, mean-variance-dependency or extreme values of RNA-…

MaleGene Expressionlcsh:Medicinecomputer.software_genreBioinformaticslcsh:ScienceExtreme value theoryMultidisciplinaryMultivariable calculusStatisticsRegression analysisGenomicsPrognosisKidney NeoplasmsNeoplasm ProteinsLeukemia Myeloid AcuteMedicineProbability distributionFemaleSequence AnalysisAlgorithmsResearch ArticleStatistical DistributionsRiskBoosting (machine learning)Clinical Research DesignFeature selectionBiostatisticsBiologyMachine learningMolecular GeneticsGenome Analysis ToolsCovariateHumansStatistical MethodsGene PredictionBiologyCarcinoma Renal CellProbabilityClinical GeneticsSequence Analysis RNAbusiness.industrylcsh:RPersonalized MedicineModelingComputational BiologyProbability TheorySurvival AnalysisSkewnessMultivariate AnalysisRNAlcsh:QArtificial intelligenceGenome Expression AnalysisTranscriptomebusinesscomputerMathematicsPLoS ONE
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Phenotypic and biochemical analysis of an international cohort of individuals with variants in NAA10 and NAA15.

2019

Abstract N-alpha-acetylation is one of the most common co-translational protein modifications in humans and is essential for normal cell function. NAA10 encodes for the enzyme NAA10, which is the catalytic subunit in the N-terminal acetyltransferase A (NatA) complex. The auxiliary and regulatory subunits of the NatA complex are NAA15 and Huntington-interacting protein (HYPK), respectively. Through a genotype-first approach with exome sequencing, we identified and phenotypically characterized 30 individuals from 30 unrelated families with 17 different de novo or inherited, dominantly acting missense variants in NAA10 or NAA15. Clinical features of affected individuals include variable levels…

MaleModels Molecular0301 basic medicineProtein ConformationMicrophthalmia0302 clinical medicineEnzyme StabilityMissense mutationN-Terminal Acetyltransferase EChildN-Terminal Acetyltransferase AExome sequencingGenetics (clinical)GeneticsbiologyGeneral MedicinePhenotypeRecombinant ProteinsChemistryPhenotypeChild PreschoolHMG-CoA reductaseCohortFemaleGeneral ArticleCorrigendumAdultNatA complexmedicine.medical_specialtyAdolescentGenotypeFrameshift mutationStructure-Activity RelationshipYoung Adult03 medical and health sciencesMolecular geneticsGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleBiologyMolecular BiologyAllelesGenetic Association StudiesComputational BiologyFaciesGenetic VariationInfantmedicine.diseaseEnzyme ActivationLenz microphthalmia syndrome030104 developmental biologyGenetic LociMutationbiology.proteinHuman medicineBiomarkers030217 neurology & neurosurgeryNAA15Human molecular genetics
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Role of Kras Status in Patients with Metastatic Colorectal Cancer Receiving First-Line Chemotherapy plus Bevacizumab: A TTD Group Cooperative Study

2012

Background: In the MACRO study, patients with metastatic colorectal cancer (mCRC) were randomised to first-line treatment with 6 cycles of capecitabine and oxaliplatin (XELOX) plus bevacizumab followed by either single-agent bevacizumab or XELOX plus bevacizumab until disease progression. An additional retrospective analysis was performed to define the prognostic value of tumour KRAS status on progression-free survival (PFS), overall survival (OS) and response rates. Methodology/Principal Findings: KRAS data (tumour KRAS status and type of mutation) were collected by questionnaire from participating centres that performed KRAS analyses. These data were then cross-referenced with efficacy da…

MaleOncologyOrganoplatinum Compoundsendocrine system diseasesEpidemiologyColorectal cancer:Named Groups::Persons::Age Groups::Adult::Middle Aged [Medical Subject Headings]DeoxycytidineMetastasis:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]Antineoplastic Combined Chemotherapy ProtocolsPathologyMedicineNeoplasm Metastasisgeneslcsh:Sciencemediana edad:Analytical Diagnostic and Therapeutic Techniques and Equipment::Therapeutics::Clinical Protocols::Antineoplastic Protocols::Antineoplastic Combined Chemotherapy Protocols [Medical Subject Headings]Aged 80 and overanciano:Chemicals and Drugs::Organic Chemicals::Organometallic Compounds::Organoplatinum Compounds [Medical Subject Headings]Cancer Risk FactorsClinical Pharmacologyprotocolos de quimioterapia antineoplásica combinadaColon AdenocarcinomaPronósticoCombination chemotherapyadultoPrognosisBevacizumabOxaliplatinpronósticoOncologyMedicineOncology Agentsmedicine.medical_specialty:Phenomena and Processes::Genetic Phenomena::Genetic Variation::Mutation [Medical Subject Headings]FluorouraciloBevacizumab:Chemicals and Drugs::Heterocyclic Compounds::Heterocyclic Compounds 1-Ring::Pyrimidines::Pyrimidine Nucleosides::Cytidine::Deoxycytidine [Medical Subject Headings]:Check Tags::Male [Medical Subject Headings]Molecular GeneticsCapecitabine:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Blood Proteins::Immunoproteins::Immunoglobulins::Antibodies::Antibodies Monoclonal::Antibodies Monoclonal Humanized [Medical Subject Headings]Gastrointestinal TumorsGenetics:Named Groups::Persons::Age Groups::Adult [Medical Subject Headings]HumansClinical TrialsBiologyneoplasmsCapecitabineAgedlcsh:R:Diseases::Neoplasms::Neoplasms by Site::Digestive System Neoplasms::Gastrointestinal Neoplasms::Intestinal Neoplasms::Colorectal Neoplasms [Medical Subject Headings]:Phenomena and Processes::Genetic Phenomena::Genetic Structures::Genome::Genome Components::Genes::Genes Neoplasm::Oncogenes::Proto-Oncogenes::Genes ras [Medical Subject Headings]medicine.diseasedigestive system diseasesOxaliplatin:Check Tags::Female [Medical Subject Headings]PharmacogeneticsMutationlcsh:QfluorouraciloMultivariate analysisDesoxicitidinahumanosCancer Treatment:Named Groups::Persons::Age Groups::Adult::Aged::Aged 80 and over [Medical Subject Headings]lcsh:Medicinemedicine.disease_causeNeoplasias colorrectalesSurgical oncologyBasic Cancer Research:Chemicals and Drugs::Heterocyclic Compounds::Heterocyclic Compounds 1-Ring::Pyrimidines::Pyrimidinones::Uracil::Fluorouracil [Medical Subject Headings]Clinical Trials (Cancer Treatment)metástasis neoplásicaMetástasis neoplásicaMultidisciplinaryMiddle AgedGenetic EpidemiologyProtocolos de quimioterapia antineoplásica combinadaFemaleAntiangiogenesis TherapyFluorouracilKRASColorectal NeoplasmsResearch Articlemedicine.drugAdultDrugs and DevicesClinical Pathologyneoplasias colorrectalesClinical Research DesignGenetic Causes of CancerAntibodies Monoclonal HumanizedAntibodiesRectal CancerAntibody TherapyDiagnostic MedicineInternal medicine:Diseases::Neoplasms::Neoplastic Processes::Neoplasm Metastasis [Medical Subject Headings]:Named Groups::Persons::Age Groups::Adult::Aged [Medical Subject Headings]mutaciónClinical GeneticsMutaciónbusiness.industryPharmacoepidemiologyCancers and NeoplasmsHuman GeneticsChemotherapy and Drug TreatmentdesoxicitidinaGenes rasanticuerposGenetics of Diseasebusinesscompuestos organoplatinoPLoS ONE
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CCR5 Proinflammatory Allele in Prostate Cancer Risk

2009

Prostate cancer (PCa) is the most common malignant neoplasm in older men in Western countries. The number of affected older men is increasing. Therefore, strategies for prevention of prostate cancer are crucial. To this purpose it is essential to know the mechanisms involved in development and progression of this malignancy. Recently, an increasing body of genetic and epidemiological studies proposed new hypotheses for prostate carcinogenesis. It has been suggested that genetic factors as well as exposure to environmental factors such as infectious agents, dietary carcinogens, and hormonal imbalances participate in PCa development. Besides, chronic inflammation plays a key role in PCa. Taki…

MaleOncologyProstate Cancer Inflammation CCR5delta32 deletionmedicine.medical_specialtyReceptors CCR5Pilot ProjectsInflammationBiologyMalignancyGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineProstate cancerHistory and Philosophy of ScienceProstateInternal medicineMolecular geneticsEpidemiologymedicineHumansAlleleAllelesAgedSettore MED/04 - Patologia GeneraleAged 80 and overGeneral NeuroscienceProstatic Neoplasmsmedicine.diseasemedicine.anatomical_structureImmunologyInflammation Mediatorsmedicine.symptomAnnals of the New York Academy of Sciences
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Pregnane X receptor and yin yang 1 contribute to the differential tissue expression and induction of CYP3A5 and CYP3A4.

2012

The hepato-intestinal induction of the detoxifying enzymes CYP3A4 and CYP3A5 by the xenosensing pregnane X receptor (PXR) constitutes a key adaptive response to oral drugs and dietary xenobiotics. In contrast to CYP3A4, CYP3A5 is additionally expressed in several, mostly steroidogenic organs, which creates potential for induction-driven disturbances of the steroid homeostasis. Using cell lines and mice transgenic for a CYP3A5 promoter we demonstrate that the CYP3A5 expression in these organs is non-inducible and independent from PXR. Instead, it is enabled by the loss of a suppressing yin yang 1 (YY1)-binding site from the CYP3A5 promoter which occurred in haplorrhine primates. This YY1 sit…

MaleReceptors SteroidDrugs and DevicesMolecular Sequence Datalcsh:MedicineSequence HomologyMice TransgenicBiologyModels BiologicalMolecular GeneticsMiceDogsGene expressionMolecular Cell BiologyGeneticsAnimalsCytochrome P-450 CYP3AHumansTissue DistributionEvolutionary SystematicsPharmacokineticsEnzyme inducerBinding sitelcsh:ScienceBiologyCYP3A5 GeneCells CulturedPhylogenyYY1 Transcription FactorPregnane X receptorEvolutionary BiologyMultidisciplinaryCYP3A4Base SequenceYY1lcsh:RPregnane X ReceptorComputational BiologyPromoterMolecular biologyOrganismal EvolutionMice Inbred C57BLNephrologyEnzyme Inductionbiology.proteinMedicinelcsh:QFemaleResearch ArticlePloS one
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Convergent sets of data from in vivo and in vitro methods point to an active role of Hsp60 in chronic obstructive pulmonary disease pathogenesis.

2011

BackgroundIt is increasingly clear that some heat shock proteins (Hsps) play a role in inflammation. Here, we report results showing participation of Hsp60 in the pathogenesis of chronic obstructive pulmonary diseases (COPD), as indicated by data from both in vivo and in vitro analyses.Methods and resultsBronchial biopsies from patients with stable COPD, smoker controls with normal lung function, and non-smoker controls were studied. We quantified by immunohistochemistry levels of Hsp10, Hsp27, Hsp40, Hsp60, Hsp70, Hsp90, and HSF-1, along with levels of inflammatory markers. Hsp10, Hsp40, and Hsp60 were increased during progression of disease. We found also a positive correlation between th…

MaleSTRESSPulmonologyChronic Obstructive Pulmonary DiseasesNeutrophilsBiopsyGene ExpressionCD8-Positive T-Lymphocytesmedicine.disease_causeBiochemistryEpitheliumPulmonary function testingPathogenesisACTIVATIONPulmonary Disease Chronic ObstructiveMolecular Cell BiologyLungCOPDMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionCOPD Hsp60QRCOPD heat shock proteins inflammationMiddle AgedImmunohistochemistrymedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMedicineFemalemedicine.symptomInflammation MediatorsSPINAL-CORDResearch ArticleEXPRESSIONanimal structuresCOPD; heat shock proteins; inflammationScienceImmunologyMolecular Sequence DataInflammationBronchichemical and pharmacologic phenomenaHEAT-SHOCK-PROTEIN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS ACUTE LUNG INJURY SPINAL-CORD CELL-DEATH KAPPA-B HEAT-SHOCK-PROTEIN-60 STRESS EXPRESSION ACTIVATIONKAPPA-BBiologyHEAT-SHOCK-PROTEINMicrobiologycomplex mixturesCell LineACUTE LUNG INJURYMolecular GeneticsIn vivoStress PhysiologicalHeat shock proteinmedicineGeneticsHumansCOPDRNA MessengerBiologyAgedLungMucous MembraneBase SequenceSettore BIO/16 - Anatomia UmanaMacrophagesfungiImmunityTranscription Factor RelAProteinsComputational BiologyChaperonin 60medicine.diseaseChaperone Proteinsrespiratory tract diseasesGene Expression RegulationCELL-DEATHHEAT-SHOCK-PROTEIN-60inflammationImmunologyheat shock proteinsClinical ImmunologyOxidative stressBiomarkers
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17beta-hydroxysteroid dehydrogenase-3 deficiency: a rare endocrine cause of male-to-female sex reversal.

2006

Deficiency of 17beta-hydroxysteroid dehydrogenase type 3 (17beta-HSD3), due to mutations in the gene encoding the enzyme, results in a rare autosomal recessive form of male-to-female sex reversal. Mutated genes encode an abnormal enzyme with absent or reduced ability to convert Delta4-androstenedione to testosterone in the testis. Affected individuals are genetically males who developed internal male Wolffian structures but female external genitalia. Such individuals are usually raised as females and diagnosis is made at puberty, when they show virilization. Correct diagnosis is mandatory to optimize treatment and follow-up. In the present paper we report the clinical history, endocrine eva…

Malemedicine.medical_specialty17-Hydroxysteroid DehydrogenasesEndocrinology Diabetes and MetabolismDisorders of Sex Development17beta-hydroxysteroid dehydrogenaseBiologyEndocrine System Diseaseschemistry.chemical_compoundEndocrinologyMolecular geneticsInternal medicinemedicineEndocrine systemHumansGeneTestosteroneVirilizationObstetrics and GynecologySex reversalmedicine.diseaseEndocrinologychemistryChild PreschoolAndrogensAndrogen insensitivity syndromeFemalemedicine.symptomGynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology
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Disruption of TCBA1 associated with a de novo t(1;6)(q32.2;q22.3) presenting in a child with developmental delay and recurrent infections

2005

A boy with developmental delay, particularly of speech, a distinct face, antineutrophil cytoplasmic antibodies, and recurrent infections was found to have an apparently balanced de novo t(1;6)(q32.3;q22.3) translocation. Fluorescent in situ hybridisation with BAC/PAC clones and long range polymerase chain reaction products assessed in the human genome sequence localised the chromosome 1 breakpoint to a 9.8 kb segment within a hypothetical gene, LOC388735, and the chromosome 6 breakpoint to a 12.8 kb segment in intron 4 of the T-cell lymphoma breakpoint-associated target 1 (TCBA1) gene. Disruption and/or formation of TCBA1 fusion genes in T cell lymphoma and leukaemia cell lines suggests a r…

Malemedicine.medical_specialtyDevelopmental DisabilitiesMolecular Sequence DataShort ReportBiologyInfectionsTranslocation GeneticFusion geneExonMiceMolecular geneticsGeneticsmedicineAnimalsHumansAmino Acid SequenceChildGeneGenetics (clinical)GeneticsGenome HumanGene Expression ProfilingBreakpointChromosome MappingMembrane ProteinsChromosome BreakageExonsNull alleleMolecular biologyGene expression profilingChromosomes Human Pair 1Child PreschoolCytogenetic AnalysisChromosomes Human Pair 6Chromosome breakage
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A new type of autosomal recessive spondyloepiphyseal dysplasia tarda

2004

Repeated occurrence of a hitherto unrecognized form of spondyloepiphyseal dysplasia tarda (SED tarda) has been studied in two independent families. Because parental consanguinity was also present in one family, autosomal recessive inheritance is proposed. The onset was in late childhood. The slowly evolving disorder shared several features of the already known types of SED tarda. The radiographic abnormalities were limited to the spine and proximal femora. The patients' hands were normal. The entity described is set apart not only from the X-linked and autosomal-dominant forms of SED tarda but also from the already delineated autosomal recessive types by significant clinical and radiographi…

Malemusculoskeletal diseasesSpondyloepiphyseal dysplasiaSpondyloepiphyseal dysplasia tardamedicine.medical_specialtyAdolescentGenes RecessiveBiologyOsteochondrodysplasiasGenetic linkageMolecular geneticsGenotypemedicineHumansChildGenetics (clinical)Family HealthGeneticsSpondyloepimetaphyseal dysplasiaFemur Headmedicine.diseaseOsteochondrodysplasiaSpineRadiographyParental consanguinityFemaleEpiphysesAmerican Journal of Medical Genetics
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