Search results for "Cancer"

showing 10 items of 11546 documents

STAT1 Isoforms Differentially Regulate NK Cell Maturation and Anti-tumor Activity

2020

Natural killer (NK) cells are important components of the innate immune defense against infections and cancers. Signal transducer and activator of transcription 1 (STAT1) is a transcription factor that is essential for NK cell maturation and NK cell-dependent tumor surveillance. Two alternatively spliced isoforms of STAT1 exist: a full-length STAT1α and a C-terminally truncated STAT1β isoform. Aberrant splicing is frequently observed in cancer cells and several anti-cancer drugs interfere with the cellular splicing machinery. To investigate whether NK cell-mediated tumor surveillance is affected by a switch in STAT1 splicing, we made use of knock-in mice expressing either only the STAT1α (S…

0301 basic medicineCytotoxicity ImmunologicLymphomaNK cellsCell MaturationMice0302 clinical medicineInterferonImmunology and AllergyProtein IsoformsSTAT1Immunologic SurveillanceOriginal ResearchBone Marrow TransplantationReceptors InterferonInterleukin-15Mice KnockoutLymphopoiesisinterferonInterferon-Stimulated Gene Factor 3Cell biologySpecific Pathogen-Free OrganismsKiller Cells NaturalSTAT1 Transcription FactorOrgan SpecificityMHC class ISignal transductionsignal transductionmedicine.druglcsh:Immunologic diseases. AllergyLymphoid TissueImmunologyBiologyLymphocyte Depletion03 medical and health sciencesInterleukin-15 Receptor alpha SubunitCell Line TumormedicineAnimalsTranscription factorInnate immune systemisoformsMice Inbred C57BL030104 developmental biologyCancer cellSTAT proteinbiology.proteinlcsh:RC581-607IL-15RαSpleen030215 immunologyFrontiers in Immunology
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Tumor- and cytokine-primed human natural killer cells exhibit distinct phenotypic and transcriptional signatures.

2019

An emerging cellular immunotherapy for cancer is based on the cytolytic activity of natural killer (NK) cells against a wide range of tumors. Although in vitro activation, or "priming," of NK cells by exposure to pro-inflammatory cytokines, such as interleukin (IL)-2, has been extensively studied, the biological consequences of NK cell activation in response to target cell interactions have not been thoroughly characterized. We investigated the consequences of co-incubation with K562, CTV-1, Daudi RPMI-8226, and MCF-7 tumor cell lines on the phenotype, cytokine expression profile, and transcriptome of human NK cells. We observe the downregulation of several activation receptors including CD…

0301 basic medicineCytotoxicity ImmunologicPhysiologymedicine.medical_treatmentCytotoxicityGene ExpressionNK cellsLymphocyte ActivationToxicologyPathology and Laboratory MedicineMolecular biology assays and analysis techniquesChemokine receptor0302 clinical medicineNeoplasmsImmune PhysiologyCellular typesGene Regulatory NetworksIL-2 receptorReceptorInnate Immune SystemMultidisciplinaryNucleic acid analysisQImmune cellsRRNA analysisKiller Cells NaturalCytokinePhenotype030220 oncology & carcinogenesisMCF-7 CellsMedicineCytokinesWhite blood cellsTumor necrosis factor alphaImmunotherapyInflammation MediatorsResearch ArticleCell signalingCell biologyBlood cellsScienceImmunologyCD16BiologyResearch and Analysis Methods03 medical and health sciencesExtraction techniquesCell Line TumormedicineGeneticsHumansMolecular Biology TechniquesMolecular BiologySecretionMedicine and health sciencesBiology and life sciencesMolecular DevelopmentNKG2DRNA extraction030104 developmental biologyAnimal cellsImmune SystemCancer researchK562 CellsTranscriptomePhysiological ProcessesDevelopmental BiologyCloningPloS one
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Class I histone deacetylases regulate p53/NF-κB crosstalk in cancer cells

2016

The transcription factors NF-κB and p53 as well as their crosstalk determine the fate of tumor cells upon therapeutic interventions. Replicative stress and cytokines promote signaling cascades that lead to the co-regulation of p53 and NF-κB. Consequently, nuclear p53/NF-κB signaling complexes activate NF-κB-dependent survival genes. The 18 histone deacetylases (HDACs) are epigenetic modulators that fall into four classes (I-IV). Inhibitors of histone deacetylases (HDACi) become increasingly appreciated as anti-cancer agents. Based on their effects on p53 and NF-κB, we addressed whether clinically relevant HDACi affect the NF-κB/p53 crosstalk. The chemotherapeutics hydroxyurea, etoposide, an…

0301 basic medicineDNA damageApoptosisModels BiologicalHistone Deacetylases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorNeoplasmsHumansHydroxyureaEpigeneticsTranscription factorCellular SenescenceEtoposidebiologyNF-kappa BNF-κBCell Cycle CheckpointsDNA NeoplasmCell BiologyHDAC6Gene Expression Regulation NeoplasticHistone Deacetylase InhibitorsCrosstalk (biology)030104 developmental biologyHistonechemistry030220 oncology & carcinogenesisMutationCancer cellbiology.proteinCancer researchTumor Suppressor Protein p53VidarabineDNA DamageSignal TransductionCellular Signalling
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In Vitro Study of the Cytotoxic, Cytostatic, and Antigenotoxic Profile of Hemidesmus indicus (L.) R.Br. (Apocynaceae) Crude Drug Extract on T Lymphob…

2018

In traditional Indian medicine, the crude drug Hemidesmus indicus root—commonly known as Indian sarsaparilla—is used alone or in poly-herbal preparations for the treatment of a wide range of diseases. The present study focuses on the cancer chemopreventive and therapeutic potential of H. indicus extracts on an acute lymphoblastic leukemia cell line (CCRF-CEM). With this aim in mind, we subjected H. indicus roots to two subsequent extractions (hydro-alcoholic extraction and soxhlet extraction). As DNA damage is an important prerequisite for the induction of mutations/cancer by genotoxic carcinogens, cancer chemoprevention may be achieved by preventing genotoxicity. Through an integrated …

0301 basic medicineDNA damageCell SurvivalHealth Toxicology and MutagenesisPhytochemicalsHemidesmus indicus; cancer cells; apoptosis; cell cycle; genotoxicity; antigenotoxicityantigenotoxicitylcsh:MedicineCancer cellCrude drugPharmacologymedicine.disease_causeToxicologyProtective AgentsPlant RootsArticleNOHemidesmus indicus03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansCarcinogenHemidesmus indicusHemidesmusbiologyChemistryPlant Extractslcsh:RgenotoxicityapoptosisApoptosiHemidesmus indicuCell cyclePrecursor Cell Lymphoblastic Leukemia-Lymphomabiology.organism_classificationAntineoplastic Agents Phytogenic030104 developmental biologyApoptosis030220 oncology & carcinogenesisCancer cellcancer cellscell cycleGenotoxicity<i>Hemidesmus indicus</i>; cancer cells; apoptosis; cell cycle; genotoxicity; antigenotoxicityDNA DamageToxins
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Modification of DNA structure by reactive nitrogen species as a result of 2-methoxyestradiol–induced neuronal nitric oxide synthase uncoupling in met…

2020

Abstract 2-methoxyestradiol (2-ME) is a physiological anticancer compound, metabolite of 17β-estradiol. Previously, our group evidenced that from mechanistic point of view one of anticancer mechanisms of action of 2-ME is specific induction and nuclear hijacking of neuronal nitric oxide synthase (nNOS), resulting in local generation of nitro-oxidative stress and finally, cancer cell death. The current study aims to establish the substantial mechanism of generation of reactive nitrogen species by 2-ME. We further achieved to identify the specific reactive nitrogen species involved in DNA-damaging mechanism of 2-ME. The study was performed using metastatic osteosarcoma 143B cells. We detected…

0301 basic medicineDNA damageClinical BiochemistryBone NeoplasmsNitric Oxide Synthase Type INitric OxideBiochemistryNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePeroxynitrous AcidHumansMTT assayViability assaylcsh:QH301-705.5Reactive nitrogen speciesSettore CHIM/02 - Chimica FisicaOsteosarcomalcsh:R5-920Settore BIO/16 - Anatomia UmanaOrganic ChemistryDNAReactive Nitrogen Species2-MethoxyestradiolPeroxynitrous acid030104 developmental biologychemistrylcsh:Biology (General)Settore CHIM/03 - Chimica Generale E InorganicaCancer cellBiophysicslcsh:Medicine (General)030217 neurology & neurosurgeryPeroxynitrite2 methoxyestradiol nitric oxide chemotherapyResearch PaperRedox Biology
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Inherent and toxicant-provoked reduction in DNA repair capacity: A key mechanism for personalized risk assessment, cancer prevention and intervention…

2018

Abstract Genomic investigations reveal novel evidence which indicates that genetic predisposition and inherent drug response are key factors for development of cancer and for poor response to therapy. However, mechanisms for these outcomes and interactions with environmental factors have not been well-characterized. Therefore, cancer risk, prevention, intervention and prognosis determinations have still mainly been based on population, rather than on individualized, evaluations. The objective of this review was to demonstrate that a key mechanism which contributes to the determination is inherent and/or toxicant-provoked reduction in DNA repair capacity. In addition, functional and quantita…

0301 basic medicineDNA repairCarcinogenesisPopulationDNA repairBioinformaticsRisk AssessmentHazardous Substances03 medical and health sciencesCarcinogenesis DNA methylation DNA repair microRNA Personalized medicine Precision medicine Public Health Environmental and Occupational Health0302 clinical medicineNeoplasmsMedicineAnimalsHumansEpigeneticsLymphocyteseducationeducation.field_of_studyCancer preventionDNA methylationmicroRNAbusiness.industryMechanism (biology)Precision medicineEnvironmental and Occupational HealthPublic Health Environmental and Occupational HealthComputational BiologyPrecision medicinePersonalized medicine030104 developmental biology030220 oncology & carcinogenesisDNA methylationBiological AssayPersonalized medicinePublic HealthbusinessDNA Damage
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Fruit and vegetable consumption and health outcomes: an umbrella review of observational studies

2019

The aim of this study was to provide a comprehensive evaluation of current evidence on fruit and vegetable consumption and health outcomes. A systematic search for quantitative syntheses was performed. Several criteria, including study design, dose-response relationship, heterogeneity and agreement of results over time, and identification of potential confounding factors, were used to assess the level of evidence. The strongest (probable) evidence was found for cardiovascular disease protection; possible evidence for decreased risk of colon cancer, depression and pancreatic diseases was found for fruit intake; and colon and rectal cancer, hip fracture, stroke, depression and pancreatic dise…

0301 basic medicineDatabases FactualColorectal cancerHealth BehaviorDiseasemeta-analysiCOLORECTAL-CANCER0302 clinical medicineRisk FactorsVegetablesMedicinevegetableSettore MED/49 - Scienze Tecniche Dietetiche ApplicateDepression (differential diagnoses)Randomized Controlled Trials as TopicMOLECULAR-MECHANISMSDepressionCOLON-CANCERConfoundingcohort study; evidence; Fruit; meta-analysis; umbrella review; vegetable; Food Sciencecohort study; evidence; Fruit; meta-analysis; umbrella review; vegetable; Cardiovascular Diseases; Colonic Neoplasms; Databases Factual; Depression; Diet Healthy; Health Behavior; Humans; Observational Studies as Topic; Pancreatic Diseases; Randomized Controlled Trials as Topic; Risk Factors; Fruit; VegetablesObservational Studies as TopicCardiovascular DiseasesMeta-analysisColonic NeoplasmsDiet HealthyCohort studyCANCER-RISKBLADDER-CANCER030209 endocrinology & metabolismDIETARY POLYPHENOLSDatabases03 medical and health sciencesLUNG-CANCEREnvironmental healthcohort studyHumansCORONARY-HEART-DISEASEFactualHealthy030109 nutrition & dieteticsumbrella reviewbusiness.industryevidencePancreatic DiseasesEvidence-based medicinemedicine.diseaseDietmeta-analysisFruitObservational studyDOSE-RESPONSE METAANALYSISbusinessGASTRIC-CANCERFood Science
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NOTCH signalling in ovarian cancer angiogenesis

2020

The Notch signalling pathway is involved in the new vessel formation process by regulating tip and stalk cells, which are key cells in the sprout formation. This process is essential in both normal ovary and cancer angiogenesis and is regulated by Notch-VEGF crosstalk. Furthermore, Notch has been linked in ovary with stem cell maintenance and epithelial mesenchymal transition processes. Dysregulation of the Notch pathway is frequent in ovarian cancer (OC) and it has been associated with impaired survival and advanced stages or lymph node involvement. Notch also plays a role in chemoresistance to platinum. In this context, this pathway has emerged as an attractive target for precision medici…

0301 basic medicineDemcizumabAngiogenesisNotch signaling pathway610 Medicine & healthContext (language use)General MedicineBiologymedicine.disease10174 Clinic for Gynecology03 medical and health sciencesReview Article on Ovarian Cancer: State of the Art and Perspectives of Clinical Research030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesismedicineCancer researchEpithelial–mesenchymal transitionStem cellOvarian cancerGamma secretaseAnnals of Translational Medicine
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Contribution of allelic imbalance to colorectal cancer

2018

Point mutations in cancer have been extensively studied but chromosomal gains and losses have been more challenging to interpret due to their unspecific nature. Here we examine high-resolution allelic imbalance (AI) landscape in 1699 colorectal cancers, 256 of which have been whole-genome sequenced (WGSed). The imbalances pinpoint 38 genes as plausible AI targets based on previous knowledge. Unbiased CRISPR-Cas9 knockout and activation screens identified in total 79 genes within AI peaks regulating cell growth. Genetic and functional data implicate loss of TP53 as a sufficient driver of AI. The WGS highlights an influence of copy number aberrations on the rate of detected somatic point muta…

0301 basic medicineDenmarkLoss of HeterozygosityGeneral Physics and AstronomyAllelic ImbalanceLoss of heterozygosityGenotypeddc:576.5RNA Small Interferinglcsh:ScienceRNA Small Interfering/geneticsGeneticsMultidisciplinaryQGenomicsPhenotype3. Good healthGENOMEPhenotypesyöpägeenitAllelic ImbalanceTumor Suppressor Protein p53/geneticsColorectal NeoplasmsChromosomes Human Pair 8GENESDNA Copy Number VariationsGenotypeScienceTranscription Factors/geneticsGenomicscolorectal cancerBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins p21(ras)Proto-Oncogene Proteins p21(ras)/genetics03 medical and health sciencesmedicineHumansPoint MutationGenetic Predisposition to DiseaseGenepaksusuolisyöpäChromosome AberrationsWhole Genome SequencingHUMAN-COLONGene Expression ProfilingPoint mutationCancerGeneral Chemistrymedicine.diseaseColorectal Neoplasms/geneticsENHANCERS030104 developmental biologyCELLSlcsh:Q3111 BiomedicineTumor Suppressor Protein p53CRISPR-Cas SystemsmutaatiotTranscription FactorsMicrosatellite Repeats
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Circadian rhythms in the pathogenesis of gastrointestinal diseases

2018

The etiology of digestive pathologies such as irritable bowel syndrome (IBS), inflammatory bowel diseases (IBD) and cancer is not yet fully understood. In recent years, several studies have evidenced circadian variations in mechanisms involved in digestive health. In situations of disturbed circadian rhythms (chronodisruption) where the central clock and the peripheral clocks receive incoherent signals, the synchronicity is lost producing implications for health. This lack of coordination could alter the tissue function and cause long term damage to the organs. Life habits such as sleep, physical exercise, social interaction, and feeding times are determinants for stability and integrity of…

0301 basic medicineDigestive cancersGastrointestinal DiseasesPhysical exerciseBioinformaticsInflammatory bowel diseaseInflammatory bowel diseasePathogenesis03 medical and health sciencesCircadian ClocksmedicineHumansCircadian rhythmsCircadian rhythmHealthy LifestyleDigestive cancerIrritable bowel syndromebusiness.industryGastroenterologyLong term damageGeneral Medicinemedicine.diseaseCircadian RhythmGastrointestinal TractIrritable bowel syndrome030104 developmental biologyEditorialEtiologybusinessWorld Journal of Gastroenterology
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