Search results for "Oncology"

showing 10 items of 10554 documents

DNA Hypomethylation and Histone Variant macroH2A1 Synergistically Attenuate Chemotherapy-Induced Senescence to Promote Hepatocellular Carcinoma Progr…

2016

Abstract Aging is a major risk factor for progression of liver diseases to hepatocellular carcinoma (HCC). Cellular senescence contributes to age-related tissue dysfunction, but the epigenetic basis underlying drug-induced senescence remains unclear. macroH2A1, a variant of histone H2A, is a marker of senescence-associated heterochromatic foci that synergizes with DNA methylation to silence tumor-suppressor genes in human fibroblasts. In this study, we investigated the relationship between macroH2A1 splice variants, macroH2A1.1 and macroH2A1.2, and liver carcinogenesis. We found that protein levels of both macroH2A1 isoforms were increased in the livers of very elderly rodents and humans, a…

0301 basic medicineEpigenomicsCHROMATINCancer ResearchLIVERCancer Research; OncologyGene ExpressionSECRETORY PHENOTYPEHCV CORE PROTEINHistonesCell MovementProtein IsoformsCellular SenescenceEpigenomicsAged 80 and overMice KnockoutbiologyLiver NeoplasmsMETHYLATIONHep G2 CellsCANCERChromatinHistoneOncologyDNA methylationAzacitidineDisease ProgressionCell agingSTEM-CELLSSenescenceAdultEXPRESSIONCarcinoma HepatocellularArticle5-AZA-2'-DEOXYCYTIDINE03 medical and health sciencesCell Line TumorAnimalsHumansEpigeneticsCell ProliferationDNA Methylationbeta-GalactosidaseMolecular biologyMice Inbred C57BLMICE030104 developmental biologybiology.proteinCancer researchDNA hypomethylation
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Genome wide DNA methylation profiling identifies specific epigenetic features in high-risk cutaneous squamous cell carcinoma

2019

ABSTRACTCutaneous squamous cell carcinoma (cSCC) is the second most common skin cancer. Although most cSCCs have good prognosis, a subgroup of high-risk cSCC has a higher frequency of recurrence and mortality. Therefore, the identification of molecular risk factors associated with this aggressive subtype is of major interest. In this work we carried out a global-scale approach to investigate the DNA-methylation profile in patients at different stages, from premalignant actinic keratosis to low-risk invasive and high-risk non-metastatic and metastatic cSCC. The results showed massive non-sequential changes in DNA-methylome and identified a minimal methylation signature that discriminates bet…

0301 basic medicineEpigenomicsMaleSkin NeoplasmsDiseaseBiochemistryActinic KeratosisGenomeEpigenesis Genetic0302 clinical medicineRisk FactorsMedicine and Health SciencesSkin TumorsAged 80 and overMultidisciplinaryDNA methylationQRSquamous Cell CarcinomasMethylationMiddle AgedPrognosisChromatinNucleic acidsGene Expression Regulation NeoplasticKeratosis ActinicOncology030220 oncology & carcinogenesisDNA methylationCarcinoma Squamous CellDisease ProgressionMedicineEpigeneticsFemaleDNA modificationChromatin modificationResearch ArticleChromosome biologyCell biologyCutaneous squamous cell carcinomaKeratosisScienceDermatologyBiologyCarcinomas03 medical and health sciencesDiagnostic MedicineCarcinomaGeneticsCancer Detection and DiagnosismedicineHumansEpigeneticsAgedNeoplasm StagingTreatment GuidelinesHealth Care PolicyBiology and life sciencesActinic keratosisCancers and NeoplasmsDNAmedicine.diseaseDNA FingerprintingDna methylation profilingHealth Care030104 developmental biologyCancer researchGene expressionNeoplasm Recurrence LocalSkin cancerGenome-Wide Association Study
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Intrasinusoidal HHV8-EBV–Positive Large B-Cell Lymphoma With Features of Germinotropic Lymphoproliferative Disorder

2020

Germinotropic lymphoproliferative disorder (GLPD) is a poorly characterized lymphoproliferative entity, recently included in the World Health Organization classification of hematolymphoid neoplasms. The histological pattern of this disease comprises monotypic plasmablasts that involve the germinal centers of the lymphoid follicles (germinotrophism), forming confluent aggregates positive for both human herpes virus type 8 (HHV8) and Epstein-Barr virus. Currently, after 17 years of its first description, only 18 cases have been reported. In this article, we describe a case of a GLPD presenting in an immunocompetent 79-year-old woman with localized axillary lymphadenopathy, showing a prominen…

0301 basic medicineEpstein-Barr Virus InfectionsHerpesvirus 4 HumanPathologymedicine.medical_specialtyLymphoma B-Cellmedicine.disease_causePathology and Forensic Medicine03 medical and health sciences0302 clinical medicinemedicineAxillary LymphadenopathyHumansB-cell lymphomaAnaplastic large-cell lymphomaAgedbusiness.industryGerminal centerHerpesviridae Infectionsmedicine.diseaseEpstein–Barr virusLymphoproliferative DisordersLymphoma030104 developmental biologyPleomorphism (cytology)030220 oncology & carcinogenesisHerpesvirus 8 HumanFemaleSurgeryLymph NodesAnatomyDifferential diagnosisbusinessInternational Journal of Surgical Pathology
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7-Keto-Cholesterol and Cholestan-3beta, 5alpha, 6beta-Triol Induce Eryptosis through Distinct Pathways Leading to NADPH Oxidase and Nitric Oxide Synt…

2019

Background/aims We showed that patho-physiological concentrations of either 7-keto-cholesterol (7-KC), or cholestane-3beta, 5alpha, 6beta-triol (TRIOL) caused the eryptotic death of human red blood cells (RBC), strictly dependent on the early production of reactive oxygen species (ROS). The goal of the current study was to assess the contribution of the erythrocyte ROS-generating enzymes, NADPH oxidase (RBC-NOX), nitric oxide synthase (RBC-NOS) and xanthine oxido-reductase (XOR) to the oxysterol-dependent eryptosis and pertinent activation pathways. Methods Phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, reactive oxygen/nitrogen species (RONS) and nitri…

0301 basic medicineErythrocytesPhysiologyEryptosisNADPH Oxidaselcsh:PhysiologyMethemoglobinHemoglobinsPhosphatidylinositol 3-Kinaseschemistry.chemical_compound0302 clinical medicinelcsh:QD415-436RBC-NOS activationKetocholesterolsHemechemistry.chemical_classificationNADPH oxidaselcsh:QP1-981biologyrac GTP-Binding ProteinsCholestanolErythrocyteNitric oxide synthaseRac GTP-Binding ProteinsRBC-NOX activationToxic oxysterolBiochemistry030220 oncology & carcinogenesisOxidation-ReductionHumanSignal Transductioncirculatory and respiratory physiologyOxidative phosphorylationlcsh:BiochemistryNitrosative stre03 medical and health sciencesHumansHemoglobinReactive oxygen speciesKetocholesterolNADPH Oxidases030104 developmental biologychemistrybiology.proteinTriolPhosphatidylinositol 3-KinaseNitric Oxide SynthaseEryptosiProto-Oncogene Proteins c-aktCholestanolsCellular Physiology and Biochemistry
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Protective and regenerative effects of a novel medical device against esophageal mucosal damage using in vitro and ex vivo models.

2020

Gastroesophageal reflux disease (GERD) is a common digestive disorder that causes esophagitis and injuries to the esophageal mucosa. GERD symptoms are recurrent during pregnancy and their treatment is focused on lifestyle changes and nonprescription medicines. The aim of this study was to characterize the mechanism of action of a new patented medical device, an oral formulation containing hyaluronic acid, rice extract, and amino acids dispersed in a bioadhesive polymer matrix, by assessing its protective effects in in vitro and ex vivo models of esophageal mucosa damage. Acidic bile salts and pepsin cocktail (BSC) added to CP-A and COLO-680 N esophagus cells were used as an in vitro GERD mo…

0301 basic medicineEsophageal MucosaHyaluronic acidRM1-950PharmacologyPermeability03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePepsinCell Line TumorDigestive disorderHyaluronic acidMedicineHumansRegenerationEsophagusAmino AcidsHyaluronic AcidEvans BlueMedical devicePharmacologybiologybusiness.industryBioadhesive polymer; Gastroesophageal reflux disease (GERD); Hyaluronic acid; Medical device; Rice extractPlant ExtractsRice extractAdhesivenessOryzaGeneral MedicineBioadhesive polymermedicine.diseaseGastroesophageal reflux disease (GERD)digestive system diseases030104 developmental biologymedicine.anatomical_structurechemistryEquipment and Supplies030220 oncology & carcinogenesisbiology.proteinGERDGastroesophageal RefluxTherapeutics. PharmacologybusinessWound healingEx vivoBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
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Stopping injection attacks with code and structured data

2018

Injection attacks top the lists of the most harmful software vulnerabilities. Injection vulnerabilities are both commonplace and easy to exploit, which makes development of injection protection schemes important. In this article, we show how injection attacks can be practically eliminated through the use of structured data paired with cryptographic verification codes upon transmission. peerReviewed

0301 basic medicineExploitComputer scienceCross-site scriptingCryptographyComputer securitycomputer.software_genreSQL injection03 medical and health sciences0302 clinical medicineSoftwareSQL injectionCode (cryptography)Cryptographic hash functionProof-carrying codeproof-carrying codetietoturvaSQLbusiness.industryXSS030104 developmental biologyinjection030220 oncology & carcinogenesiscryptographic hashbusinesscomputer
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Integrative analysis of structural variations using short-reads and linked-reads yields highly specific and sensitive predictions.

2020

Genetic diseases are driven by aberrations of the human genome. Identification of such aberrations including structural variations (SVs) is key to our understanding. Conventional short-reads whole genome sequencing (cWGS) can identify SVs to base-pair resolution, but utilizes only short-range information and suffers from high false discovery rate (FDR). Linked-reads sequencing (10XWGS) utilizes long-range information by linkage of short-reads originating from the same large DNA molecule. This can mitigate alignment-based artefacts especially in repetitive regions and should enable better prediction of SVs. However, an unbiased evaluation of this technology is not available. In this study, w…

0301 basic medicineFalse discovery rateComputer scienceArtificial Gene Amplification and ExtensionPolymerase Chain ReactionDatabase and Informatics MethodsSequencing techniques0302 clinical medicineBreast TumorsBasic Cancer ResearchMedicine and Health SciencesDNA sequencingBiology (General)EcologyHigh-Throughput Nucleotide SequencingGenomicsDNA Neoplasm3. Good healthIdentification (information)OncologyComputational Theory and MathematicsModeling and SimulationMCF-7 CellsFemaleSequence AnalysisResearch ArticleBioinformaticsQH301-705.5Breast NeoplasmsGenomicsComputational biologyResearch and Analysis MethodsHuman Genomics03 medical and health sciencesCellular and Molecular NeuroscienceCancer GenomicsGenomic MedicineBreast CancerGeneticsDNA Barcoding TaxonomicHumansMolecular Biology TechniquesMolecular BiologyEcology Evolution Behavior and SystematicsWhole genome sequencingLinkage (software)Whole Genome SequencingGenome HumanDideoxy DNA sequencingGenetic Diseases InbornCancers and NeoplasmsBiology and Life SciencesComputational BiologyStatistical modelSequence Analysis DNARepetitive RegionsLogistic Models030104 developmental biologyGenomic Structural VariationHuman genomeSequence Alignment030217 neurology & neurosurgeryPLoS Computational Biology
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ADAM10 in Alzheimer's disease: Pharmacological modulation by natural compounds and its role as a peripheral marker.

2019

Abstract Alzheimer’s disease (AD) represents a global burden in the economics of healthcare systems. Amyloid-β (Aβ) peptides are formed by amyloid-β precursor protein (AβPP) cleavage, which can be processed by two pathways. The cleavage by the α-secretase A Disintegrin And Metalloprotease 10 (ADAM10) releases the soluble portion (sAβPPα) and prevents senile plaques. This pathway remains largely unknown and ignored, mainly regarding pharmacological approaches that may act via different signaling cascades and thus stimulate non-amyloidogenic cleavage through ADAM10. This review emphasizes the effects of natural compounds on ADAM10 modulation, which eventuates in a neuroprotective mechanism. M…

0301 basic medicineFarmacologiaADAM10DiseaseRM1-950Natural compoundsCleavage (embryo)NeuroprotectionCatechin03 medical and health sciencesADAM10 ProteinAmyloid beta-Protein Precursor0302 clinical medicineAlzheimer DiseaseDisintegrinHumansSenile plaquesPharmacological modulationPharmacologyMetalloproteinaseAmyloid beta-PeptidesbiologyChemistryPlant ExtractsADAM10ProteinsGinkgo bilobaMembrane ProteinsGeneral Medicineα-SecretaseAlzheimer's disease030104 developmental biologyMalaltia d'AlzheimerNeuroprotective Agents030220 oncology & carcinogenesisPharmaceuticalbiology.proteinTherapeutics. PharmacologyAmyloid Precursor Protein SecretasesNeuroscienceAlzheimer’s diseaseProteïnesBiomarkersBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
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FGFR a promising druggable target in cancer: Molecular biology and new drugs.

2017

Abstract: Introduction: The Fibroblast Growth Factor Receptor (FGFR) family consists of Tyrosine Kinase Receptors (TKR) involved in several biological functions. Recently, alterations of FGFR have been reported to be important for progression and development of several cancers. In this setting, different studies are trying to evaluate the efficacy of different therapies targeting FGFR. Areas Covered: This review summarizes the current status of treatments targeting FGFR, focusing on the trials that are evaluating the FGFR profile as inclusion criteria: Multi-Target, Pan-FGFR Inhibitors and anti-FGF (Fibroblast Growth Factor)/FGFR Monoclonal Antibodies. Expert opinion: Most of the TKR share …

0301 basic medicineFibroblast Growth FactorDruggabilityFibroblast growth factorTyrosine-kinase inhibitorReceptor tyrosine kinase0302 clinical medicineNeoplasmsFGFR inhibitorsFGFMolecular Targeted TherapyCancerCancer; FGF; FGFR; FGFR inhibitors; Drug Resistance Neoplasm; Fibroblast Growth Factors; Gene Fusion; Humans; Molecular Targeted Therapy; Mutation; Neoplasms; Protein Kinase Inhibitors; Receptors Fibroblast Growth Factor; Signal Transduction; Hematology; Oncology; Geriatrics and GerontologybiologyFGFRHematologyFGFR inhibitorOncologyFibroblast growth factor receptor030220 oncology & carcinogenesisembryonic structuresSignal transductionbiological phenomena cell phenomena and immunityGene FusionHumanSignal Transductionmusculoskeletal diseasesanimal structuresmedicine.drug_classProtein Kinase Inhibitor03 medical and health sciencesmedicineHumansProtein Kinase InhibitorsCancer; FGF; FGFR; FGFR inhibitorsbusiness.industryCancermedicine.diseaseMolecular biologyReceptors Fibroblast Growth FactorFibroblast Growth Factors030104 developmental biologyDrug Resistance NeoplasmCancer cellMutationbiology.proteinNeoplasmHuman medicineGeriatrics and GerontologybusinessCritical reviews in oncology/hematology
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Numerical Treatment of the Filament-Based Lamellipodium Model (FBLM)

2017

We describe in this work the numerical treatment of the Filament-Based Lamellipodium Model (FBLM). This model is a two-phase two-dimensional continuum model, describing the dynamics of two interacting families of locally parallel F-actin filaments. It includes, among others, the bending stiffness of the filaments, adhesion to the substrate, and the cross-links connecting the two families. The numerical method proposed is a Finite Element Method (FEM) developed specifically for the needs of this problem. It is comprised of composite Lagrange–Hermite two-dimensional elements defined over a two-dimensional space. We present some elements of the FEM and emphasize in the numerical treatment of t…

0301 basic medicineFinite element spaceNumerical analysisPiecewise constant approximationMechanicsFinite element methodQuantitative Biology::Cell BehaviorQuantitative Biology::Subcellular ProcessesPiecewise linear functionProtein filament03 medical and health sciences030104 developmental biology0302 clinical medicineClassical mechanics030220 oncology & carcinogenesisBending stiffnessLamellipodiumMathematics
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