Search results for " Gene Expression Regulation"

showing 10 items of 70 documents

Castration-Induced Downregulation of SPARC in Stromal Cells Drives Neuroendocrine Differentiation of Prostate Cancer.

2021

Abstract Fatal neuroendocrine differentiation (NED) of castration-resistant prostate cancer is a recurrent mechanism of resistance to androgen deprivation therapies (ADT) and antiandrogen receptor pathway inhibitors (ARPI) in patients. The design of effective therapies for neuroendocrine prostate cancer (NEPC) is complicated by limited knowledge of the molecular mechanisms governing NED. The paucity of acquired genomic alterations and the deregulation of epigenetic and transcription factors suggest a potential contribution from the microenvironment. In this context, whether ADT/ARPI induces stromal cells to release NED-promoting molecules and the underlying molecular networks are unestablis…

MaleCancer ResearchStromal cellAnimals Biomarkers Tumor Cell Differentiation Cell Line Tumor Coculture Techniques Endoplasmic Reticulum Chaperone BiP Epigenesis Genetic Gene Expression Regulation Neoplastic Humans Male Mice Mice Inbred C57BL Neuroendocrine Cells Osteonectin Prostatic Neoplasms Stromal Cells Transgenes Tumor Microenvironment Down-RegulationDown-RegulationContext (language use)Settore MED/08 - Anatomia PatologicaNeuroendocrine differentiationEpigenesis GeneticProstate cancerMiceStromaDownregulation and upregulationNeuroendocrine CellsCell Line TumormedicineBiomarkers TumorTumor MicroenvironmentSettore MED/05 - Patologia ClinicaAnimalsHumansOsteonectinEpigeneticsTransgenesEndoplasmic Reticulum Chaperone BiPbusiness.industryMatricellular proteinProstatic NeoplasmsCell Differentiationmedicine.diseaseCoculture TechniquesGene Expression Regulation NeoplasticMice Inbred C57BLOncologyCancer researchStromal CellsbusinessCancer research
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A novel DFNB1 deletion allele supports the existence of a distant cis-regulatory region that controls GJB2 and GJB6 expression

2010

Contains fulltext : 87760_1.pdf (author's version ) (Open Access) Contains fulltext : 87760_2.pdf (Publisher’s version ) (Closed access) Eleven affected members of a large German-American family segregating recessively inherited, congenital, non-syndromic sensorineural hearing loss (SNHL) were found to be homozygous for the common 35delG mutation of GJB2, the gene encoding the gap junction protein Connexin 26. Surprisingly, four additional family members with bilateral profound SNHL carried only a single 35delG mutation. Previously, we demonstrated reduced expression of both GJB2 and GJB6 mRNA from the allele carried in trans with that bearing the 35delG mutation in these four persons. Usin…

MaleGenetics and epigenetic pathways of disease [NCMLS 6][SDV]Life Sciences [q-bio]PenetranceMESH: Base SequenceRegulatory Sequences Nucleic Acidsensorineural hearing lossConnexinsMESH: GenotypeMESH: Hearing Loss Sensorineural/diagnosisMESH: PenetranceGenotypeCopy-number variationGenetics (clinical)Sequence DeletionGeneticsComparative Genomic Hybridization0303 health sciencesMESH: Genetic TestingMESH: Gene Expression Regulation*030305 genetics & heredityPenetranceGJB2PedigreeConnexin 26MESH: Sequence Deletion*MESH: Hearing Loss Sensorineural/geneticsFemaleChromosome DeletionFunctional Neurogenomics [DCN 2]GJB6GenotypeMESH: PedigreeMESH: Chromosome DeletionHearing Loss SensorineuralMolecular Sequence Dataconnexin 26connexin 30DFNB1gene expression regulationGJB2GJB6sensorineural hearing losssequence deletionBiologyMESH: Connexin 30MESH: Connexins/genetics*MESH: Sequence Homology Nucleic AcidArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesMonoallelic MutationGJB6MESH: Connexin 26Sequence Homology Nucleic AcidConnexin 30otorhinolaryngologic diseasesGeneticsHumansGenetic TestingAlleleGeneMESH: Regulatory Sequences Nucleic Acid/genetics*AllelesDFNB1030304 developmental biologyFamily HealthMESH: HumansMESH: Molecular Sequence DataBase SequenceChromosomes Human Pair 13MESH: AllelesBreakpointMESH: MaleMESH: Comparative Genomic HybridizationGene Expression RegulationMESH: Family Healthbiology.proteinHuman medicineMESH: Chromosomes Human Pair 13/geneticsMESH: FemaleClinical Genetics
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Modeling human osteosarcoma in mice through 3AB‐OS cancer stem cell xenografts

2012

Osteosarcoma is the second leading cause of cancer-related death for children and young adults. In this study, we have subcutaneously injected—with and without matrigel—athymic mice (Fox1nu/nu) with human osteosarcoma 3AB-OS pluripotent cancer stem cells (CSCs), which we previously isolated from human osteosarcoma MG63 cells. Engrafted 3AB-OS cells were highly tumorigenic and matrigel greatly accelerated both tumor engraftment and growth rate. 3AB-OS CSC xenografts lacked crucial regulators of beta-catenin levels (E-cadherin, APC, and GSK-3beta), and crucial factors to restrain proliferation, resulting therefore in a strong proliferation potential. During the first weeks of engraftment 3AB-…

MaleIntegrin beta ChainsXENOGRAFTNudeAnimals; Bone Neoplasms; Collagen; Drug Combinations; Focal Adhesion Kinase 1; Gene Expression Regulation Neoplastic; Humans; Injections Subcutaneous; Integrin beta Chains; Laminin; Male; Mice; Mice Nude; Neoplasm Transplantation; Neoplastic Stem Cells; Osteosarcoma; Pluripotent Stem Cells; Proteoglycans; Proto-Oncogene Proteins c-akt; Signal Transduction; Transplantation Heterologous; Tumor Markers Biological3AB-OS CSCSBiochemistryMiceInduced pluripotent stem cellTumor MarkersOsteosarcomaHeterologousSubcutaneousXIAPGene Expression Regulation NeoplasticDrug CombinationsANIMAL MODELSNeoplastic Stem CellsOsteosarcomaProteoglycansCollagenMATRIGELSignal TransductionPluripotent Stem CellsInjections SubcutaneousTransplantation HeterologousMice NudeBone NeoplasmsBiologyInjectionsCyclin D2Cancer stem cellBiomarkers TumormedicineAnimalsHumansMolecular BiologyProtein kinase BNeoplasticTransplantationMatrigelMesenchymal stem cellCell BiologyBiologicalmedicine.disease3AB-OS CSCS; OSTEOSARCOMA; XENOGRAFT; MATRIGEL; ANIMAL MODELSGene Expression RegulationFocal Adhesion Kinase 1ImmunologyCancer researchLamininProto-Oncogene Proteins c-aktNeoplasm TransplantationJournal of Cellular Biochemistry
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A role for the peroxisomal 3-ketoacyl-CoA thiolase B enzyme in the control of PPARα-mediated upregulation of SREBP-2 target genes in the liver.: ThB …

2011

International audience; Peroxisomal 3-ketoacyl-CoA thiolase B (Thb) catalyzes the final step in the peroxisomal β-oxidation of straight-chain acyl-CoAs and is under the transcription control of the nuclear hormone receptor PPARα. PPARα binds to and is activated by the synthetic compound Wy14,643 (Wy). Here, we show that the magnitude of Wy-mediated induction of peroxisomal β-oxidation of radiolabeled (1-(14)C) palmitate was significantly reduced in mice deficient for Thb. In contrast, mitochondrial β-oxidation was unaltered in Thb(-/-) mice. Given that Wy-treatment induced Acox1 and MFP-1/-2 activity at a similar level in both genotypes, we concluded that the thiolase step alone was respons…

MaleMESH: HepatomegalyPalmitatesMESH : PyrimidinesMESH : Gene DeletionBiochemistryelement-binding proteinsMESH : Acetyl-CoA C-AcyltransferaseMiceMESH: Up-RegulationMESH: AnimalsMESH : Up-RegulationMESH: Lipid Metabolism0303 health sciencesMESH : Gene Expression RegulationThiolase030302 biochemistry & molecular biologyGeneral MedicineMESH : HepatomegalyUp-Regulationzellweger-syndromePeroxisome ProliferatorsMESH: Peroxisome ProliferatorsHepatomegalySterol Regulatory Element Binding Protein 2peroxisomal 3-ketoacyl-CoA thiolase BMESH: Mitochondria3-oxoacyl-coa thiolaseLathosterolfatty-acid oxidationrat-liverMESH: Sterol Regulatory Element Binding Protein 203 medical and health sciencesMESH : Sterol Regulatory Element Binding Protein 2HumansPPAR alphaMESH : Peroxisome Proliferators[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyPPARaVLAGMESH : Oxidation-ReductionFatty Acid Oxidation.MESH: HumansCholesterolMESH : HumanscholesterolLipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinchemistryMESH: PyrimidinesCholesterol; Micro-array analysis; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα and SREBP-2; Wy14643Fatty Acid OxidationGene DeletionMESH: LiverMESH: Oxidation-ReductionMESH: Signal TransductionMESH: Mice KnockoutVoeding Metabolisme en Genomicachemistry.chemical_compoundMESH: CholesterolMESH : Lipid MetabolismWy14MESH : PalmitatesMESH: PPAR alphaMESH : CholesterolMice Knockoutneuronal migration643PeroxisomeAcetyl-CoA C-AcyltransferaseMESH: Gene Expression RegulationMetabolism and GenomicsMitochondriaLiverBiochemistryMicro-array analysisMetabolisme en GenomicaACOX1Nutrition Metabolism and GenomicsMESH : MitochondriaOxidation-ReductionSignal Transductionacyl-coa oxidasecholesterol-synthesisMESH : MaleMESH : PPAR alphaPeroxisome ProliferationPPARα and SREBP-2Biologybeta-oxidationVoedingproliferator-activated receptorsMESH : MicePeroxisomesAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Mice030304 developmental biologySCP2NutritionMESH : Signal TransductionMESH : LiverMESH: PalmitatesMESH: MalePyrimidinesMESH: Acetyl-CoA C-AcyltransferaseGene Expression RegulationMESH: Gene DeletionMESH : Mice KnockoutMESH : AnimalsMESH : Peroxisomes
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The Genome of the Sea Urchin Strongylocentrotus purpuratus

2006

We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus , a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.

MaleMESH: Signal TransductionMESH: Sequence Analysis DNAMESH : Transcription FactorsMESH : Calcification PhysiologicGenomeMESH : Proteins0302 clinical medicineMESH : Embryonic DevelopmentMESH: Gene Expression Regulation DevelopmentalInnateMESH: Embryonic DevelopmentDevelopmentalNervous System Physiological PhenomenaMESH: AnimalsMESH: Proteins[SDV.BDD]Life Sciences [q-bio]/Development BiologyComplement ActivationComputingMilieux_MISCELLANEOUSMESH: Evolution MolecularMESH : Strongylocentrotus purpuratusGenetics0303 health sciencesMESH: Nervous System Physiological PhenomenaMultidisciplinaryGenomebiologyMedicine (all)MESH: Immunologic FactorsGene Expression Regulation DevelopmentalGenome projectMESH: Transcription FactorsMESH : Immunity InnateMESH : Complement ActivationMESH: GenesBacterial artificial chromosome (BAC)DeuterostomesStrongylocentrotus purpuratusVertebrate innovationsEchinodermMESH : Nervous System Physiological Phenomenaembryonic structuresMESH: Cell Adhesion MoleculesMESH : GenesMESH: Immunity InnateSequence AnalysisSignal TransductionMESH: Computational BiologyGenome evolutionMESH: Complement ActivationSequence analysisEvolutionMESH: Strongylocentrotus purpuratusMESH : MaleEmbryonic DevelopmentMESH : Immunologic FactorsArticleMESH: Calcification PhysiologicCalcificationMESH : Cell Adhesion MoleculesEvolution Molecular03 medical and health sciencesCalcification PhysiologicAnimalsImmunologic FactorsMESH: Genome[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Evolution MolecularPhysiologicGeneStrongylocentrotus purpuratus[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionBacterial artificial chromosomeImmunityMolecularComputational BiologyProteinsAnimals; Calcification Physiologic; Cell Adhesion Molecules; Complement Activation; Computational Biology; Embryonic Development; Evolution Molecular; Gene Expression Regulation Developmental; Genes; Immunity Innate; Immunologic Factors; Male; Nervous System Physiological Phenomena; Proteins; Signal Transduction; Strongylocentrotus purpuratus; Transcription Factors; Genome; Sequence Analysis DNA; Medicine (all); MultidisciplinaryDNASequence Analysis DNAbiology.organism_classificationStrongylocentrotus purpuratusImmunity InnateMESH: MaleGene Expression RegulationGenesMESH : AnimalsMESH : Gene Expression Regulation DevelopmentalMESH : GenomeCell Adhesion Molecules030217 neurology & neurosurgeryMESH : Computational BiologyTranscription FactorsMESH : Sequence Analysis DNA
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Rare variants in the genetic background modulate cognitive and developmental phenotypes in individuals carrying disease-associated variants

2019

Purpose: To assess the contribution of rare variants in the genetic background toward variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive variants. Methods: We analyzed quantitative clinical information, exome sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated variants. Results: The number of rare likely deleterious variants in functionally intolerant genes (“other hits”) correlated with expression of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in autism probands carrying gene-disruptive variants (n=184, p=0.03) compared with thei…

MaleParents0301 basic medicineProbandNeuronalGenetic Carrier Screening16p11.2 deletion030105 genetics & heredityCognitionFamily historyNeural Cell Adhesion MoleculesGenetics (clinical)Exome sequencingSequence DeletionGeneticsGenetic Carrier ScreeningPhenotypePenetrancePedigreePhenotypeAutistic Disorder/genetics; Autistic Disorder/physiopathology; Cell Adhesion Molecules Neuronal/genetics; Chromosomes Human Pair 16/genetics; Cognition/physiology; DNA Copy Number Variations/genetics; Female; Gene Expression Regulation/genetics; Genetic Background; Genetic Carrier Screening; Humans; Male; Methyltransferases/genetics; Nerve Tissue Proteins/genetics; Parents; Pedigree; Phenotype; Proteins/genetics; Sequence Deletion/genetics; Siblings; 16p11.2 deletion; CNV; autism; modifier; phenotypic variabilityFemaleGenetic BackgroundHumanDNA Copy Number VariationsCell Adhesion Molecules NeuronalCNVautismNerve Tissue ProteinsBiologyChromosomesArticle03 medical and health sciencesmental disordersmedicineHumansAutistic DisorderBiologyGenemodifierPair 16SiblingsCalcium-Binding ProteinsProteinsMethyltransferasesmedicine.disease16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Genetics (clinical)Cytoskeletal Proteins030104 developmental biologyGene Expression Regulation[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutismphenotypic variabilityHuman medicine16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Autistic Disorder; Cell Adhesion Molecules Neuronal; Chromosomes Human Pair 16; Cognition; DNA Copy Number Variations; Female; Gene Expression Regulation; Genetic Background; Humans; Male; Methyltransferases; Nerve Tissue Proteins; Parents; Pedigree; Phenotype; Proteins; Sequence Deletion; Siblings; Genetic Carrier ScreeningCell Adhesion MoleculesChromosomes Human Pair 16Transcription FactorsGenetics in Medicine
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Genome-wide DNA profiling of marginal zone lymphomas identifies subtype-specific lesions with an impact on the clinical outcome

2011

Abstract Marginal zone B-cell lymphomas (MZLs) have been divided into 3 distinct subtypes (extranodal MZLs of mucosa-associated lymphoid tissue [MALT] type, nodal MZLs, and splenic MZLs). Nevertheless, the relationship between the subtypes is still unclear. We performed a comprehensive analysis of genomic DNA copy number changes in a very large series of MZL cases with the aim of addressing this question. Samples from 218 MZL patients (25 nodal, 57 MALT, 134 splenic, and 2 not better specified MZLs) were analyzed with the Affymetrix Human Mapping 250K SNP arrays, and the data combined with matched gene expression in 33 of 218 cases. MALT lymphoma presented significantly more frequently gain…

MalePathologyLymphomaMarginal ZoneBiochemistryExtranodal Diseaseclassification/genetics/pathologyhemic and lymphatic diseases80 and overgeneticsAged 80 and overComparative Genomic HybridizationGenomeMALT lymphomaHematologySingle NucleotideMiddle AgedMarginal zonePrognosisGene Expression Regulation NeoplasticAdult Aged Aged; 80 and over Chromosome Aberrations Comparative Genomic Hybridization DNA Fingerprinting Female Gene Expression Profiling Gene Expression Regulation; Neoplastic Genome; Human Humans Lymphoma; B-Cell; Marginal Zone; classification/genetics/pathology Male Middle Aged Polymorphism; Single Nucleotide; genetics Prognosis Splenic Neoplasms; classification/genetics/pathology Young AdultFemaleHumanAdultmedicine.medical_specialtyGenome-wide DNA profilingImmunologyBiologyPolymorphism Single NucleotideYoung AdultGenome-wide DNA profiling; marginal zone lymphomas; clinical outcome.medicineSNPHumansSplenic marginal zone lymphomaPolymorphismAgedChromosome AberrationsNeoplasticGenome HumanSplenic Marginal Zone Lymphoma; GenomicGene Expression ProfilingSplenic NeoplasmsB-CellLymphoma B-Cell Marginal ZoneCell Biologyclinical outcome.medicine.diseasemarginal zone lymphomaDNA FingerprintingLymphomaGene expression profilingGene Expression RegulationComparative genomic hybridization
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MiR-133 Modulates the β1Adrenergic Receptor Transduction Cascade.

2014

Rationale : The sympathetic nervous system plays a fundamental role in the regulation of myocardial function. During chronic pressure overload, overactivation of the sympathetic nervous system induces the release of catecholamines, which activate β-adrenergic receptors in cardiomyocytes and lead to increased heart rate and cardiac contractility. However, chronic stimulation of β-adrenergic receptors leads to impaired cardiac function, and β-blockers are widely used as therapeutic agents for the treatment of cardiac disease. MicroRNA-133 (miR-133) is highly expressed in the myocardium and is involved in controlling cardiac function through regulation of messenger RNA translation/stability. …

MalePhysiologyMessengerheart failureApoptosiscardiomyocytesInbred C57BLSecond Messenger SystemsTransgenicRats Sprague-DawleyBeta-1 adrenergic receptorMiceGenes ReporterReceptorsCyclic AMPGuanine Nucleotide Exchange FactorsMyocytes CardiacAlpha-1D adrenergic receptor3' Untranslated RegionsCells CulturedCulturedbiologyChemistryadrenergic beta-1 receptor antagonists; cardiac; cyclic AMP; heart failure; microRNAs; myocytes; 3' Untranslated Regions; Adenylyl Cyclases; Animals; Apoptosis; Cells Cultured; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Disease Progression; Gene Expression Regulation; Genes Reporter; Guanine Nucleotide Exchange Factors; Male; Metoprolol; Mice; Mice Inbred C57BL; Mice Transgenic; MicroRNAs; Myocardium; Myocytes Cardiac; RNA Messenger; Rats; Rats Sprague-Dawley; Receptors Adrenergic beta-1; Recombinant Fusion Proteins; Second Messenger Systems; Physiology; Cardiology and Cardiovascular Medicine; Medicine (all)Medicine (all)Cell biologyAdrenergicadrenergic beta-1 receptor antagonistsDisease ProgressionCARDIAC HYPERTROPHYSignal transductionCardiology and Cardiovascular MedicineAdenylyl CyclasesMetoprololmedicine.medical_specialtyAdrenergic receptorcardiacCellsRecombinant Fusion ProteinsMice Transgenicbeta-1Alpha-1B adrenergic receptorInternal medicinecAMPmedicineAnimalsRNA MessengerReporterPressure overloadalpha and beta adrenoceptorsMyocytesMyocardiumBeta adrenergic receptor kinaseCyclic AMP-Dependent Protein KinasesAlpha-1A adrenergic receptorRatsMice Inbred C57BLMicroRNAsEndocrinologyGenesGene Expression Regulationbiology.proteinRNASprague-DawleyReceptors Adrenergic beta-1MicroRNAs; alpha and beta adrenoceptors; cardiomyocytes; CARDIAC HYPERTROPHY; cAMP
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Expression and differential localization of xenobiotic transporters in the rat olfactory neuro-epithelium.

2011

International audience; Transporters, such as multidrug resistance P-glycoproteins (MDR), multidrug resistance-related proteins (MRP) and organic anion transporters (OATs), are involved in xenobiotic metabolism, particularly the cellular uptake or efflux of xenobiotics (and endobiotics) or their metabolites. The olfactory epithelium is exposed to both inhaled xenobiotics and those coming from systemic circulation. This tissue has been described as a pathway for xenobiotics to the brain via olfactory perineural space. Thereby, olfactory transporters and xenobiotic metabolizing enzymes, dedicated to the inactivation and the elimination of xenobiotics, have been involved in the toxicological p…

Male[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionMESH : Multidrug Resistance-Associated Proteinsp glycoproteinATP-binding cassette transporterMESH : HepatocytesReceptors OdorantMESH : P-GlycoproteinMESH: HepatocytesMESH : Lymphatic Vessels0302 clinical medicineMESH : Protein Transportugt2a1MESH: SmellMESH: Receptors OdorantMESH: AnimalsReceptorxenobiotic metabolizingmucosa0303 health sciencesMESH : Gene Expression RegulationMESH : RatsGeneral NeuroscienceMESH : OdorsMESH: Gene Expression RegulationSmellProtein Transportmedicine.anatomical_structureBiochemistryLivertransporterbarrierEffluxMultidrug Resistance-Associated ProteinsMESH: Multidrug Resistance-Associated ProteinsMESH: XenobioticsMESH: Protein TransportMESH: P-GlycoproteinMESH: RatsMESH: Lymphatic VesselsMESH : Maleodorant clearancebrainMESH : XenobioticsxenobioticBiologysystemMESH : Rats WistarOlfactory Receptor NeuronsXenobiotics03 medical and health sciencesbulbOlfactory Mucosamultidrug resistanceMESH : Receptors OdorantmedicineAnimalsATP Binding Cassette Transporter Subfamily B Member 1Rats WistardetoxificationMESH: Olfactory Mucosa030304 developmental biologyLymphatic VesselsMESH : Olfactory MucosaMESH: OdorsMESH : LiverTransporterMESH: Rats WistarMESH: Olfactory Receptor NeuronsEpitheliumMESH: MaleOlfactory bulbRatsenzymeGene Expression RegulationOdorantsHepatocytesMESH : SmellMESH : Olfactory Receptor NeuronsMESH : Animalsolfactory epitheliumOlfactory epitheliumperireceptor event[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgeryDrug metabolismMESH: Liver
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Micro-RNA in pancreatic adenocarcinoma: Predictive/prognostic biomarkers or therapeutic targets?

2015

Pancreatic ductal adenocarcinoma (PDAC) is a tumor with a poor prognosis, short overall survival and few chemotherapeutic choices. MicroRNAs (miRNAs) are non-coding, single-stranded RNAs of around 22 nucleotides involved in the pathogenic mechanisms of carcinogenesis and metastasis. They have been studied in many tumors in order to identify potential diagnostic, prognostic or therapeutic targets. In the current literature, many studies have analyzed the role of miRNAs in PDAC. In fact, the absence of appropriate biomarkers, the difficultly of early detection of this tumor, and the lack of effective chemotherapy in patients with unresectable disease have focused attention on miRNAs as new, i…

Maleendocrine system diseasesPrognosiSettore MED/06 - Oncologia MedicaMice NudeReviewDiseaseAdenocarcinomaMalignancymedicine.disease_causeMetastasisMicemicroRNABiomarkers TumorCarcinomamedicineAnimalsHumansmiRNAbiomarkers; miRNAs; pancreatic adenocarcinoma; prognosis; therapyAnimalbusiness.industryPancreatic NeoplasmbiomarkersMicroRNABiomarkerPrognosismedicine.diseasePhenotypedigestive system diseasesPancreatic NeoplasmsGene Expression Regulation NeoplasticMicroRNAsPhenotypeBiomarkers; miRNAs; Pancreatic adenocarcinoma; Prognosis; Therapy; Adenocarcinoma; Animals; Biomarkers Tumor; Carcinoma Pancreatic Ductal; Female; Gene Expression Regulation Neoplastic; Humans; Male; Mice; Mice Nude; MicroRNAs; Pancreatic Neoplasms; Phenotype; Prognosis; OncologyOncologymiRNAsImmunologyCancer researchAdenocarcinomaFemaleTherapybusinessCarcinogenesisPancreatic adenocarcinomaCarcinoma Pancreatic DuctalHuman
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