Search results for "Neoplasms"

showing 10 items of 7988 documents

Differential binding cell-SELEX method to identify cell-specific aptamers using high-throughput sequencing

2018

AbstractAptamers have in recent years emerged as a viable alternative to antibodies. High-throughput sequencing (HTS) has revolutionized aptamer research by increasing the number of reads from a few (using Sanger sequencing) to millions (using an HTS approach). Despite the availability and advantages of HTS compared to Sanger sequencing, there are only 50 aptamer HTS sequencing samples available on public databases. HTS data in aptamer research are primarily used to compare sequence enrichment between subsequent selection cycles. This approach does not take full advantage of HTS because the enrichment of sequences during selection can be due to inefficient negative selection when using live…

0301 basic medicineComputer scienceAptamerlcsh:MedicineGenomicsComputational biologyCell selexLigandsArticleDNA sequencingCell Line03 medical and health sciencessymbols.namesakeNegative selectionDrug Delivery Systems0302 clinical medicineCell Line TumorHumansGenomic librarylcsh:ScienceCarcinoma Renal CellSelection (genetic algorithm)Gene LibrarySanger sequencingMultidisciplinaryMolecular medicinelcsh:RSELEX Aptamer TechniqueHigh-throughput screeningComputational BiologyHigh-Throughput Nucleotide SequencingNucleotide MetabolismGenomicsAptamers NucleotideFlow CytometryMolecular medicineKidney Neoplasms030104 developmental biologyDrug DesignDrug deliverysymbolsNucleic Acid Conformationlcsh:QFunctional genomics030217 neurology & neurosurgerySystematic evolution of ligands by exponential enrichment
researchProduct

The good and bad of targeting cancer-associated extracellular matrix

2017

The maintenance of tissue homeostasis requires extracellular matrix (ECM) remodeling. Immune cells actively participate in regenerating damaged tissues contributing to ECM deposition and shaping. Dysregulated ECM deposition characterizes fibrotic diseases and cancer stromatogenesis, where a chronic inflammatory state sustains the ECM increase. In cancer, the ECM fosters several steps of tumor progression, providing pro-survival and proliferative signals, promoting tumor cell dissemination via collagen fibers or acting as a barrier to impede drug diffusion. Interfering with processes leading to chronic ECM deposition, as occurring in cancer, might allow the simultaneous targeting of both pri…

0301 basic medicineContext (language use)BiologyExtracellular matrix03 medical and health sciencesImmune systemNeoplasmsDrug DiscoverymedicineTumor MicroenvironmentAnimalsHumansPharmacology; Drug Discovery3003 Pharmaceutical ScienceMyeloid CellsReceptorTissue homeostasisPharmacologyTumor microenvironmentDrug Discovery3003 Pharmaceutical ScienceCancermedicine.diseaseCell biologyExtracellular Matrix030104 developmental biologyTumor progressionImmunology
researchProduct

Prevention from radiation damage by natural products

2018

Abstract Background Radiotherapy is a mainstay of cancer treatment since decades. Ionizing radiation (IR) is used for destruction of cancer cells and shrinkage of tumors. However, the increase of radioresistance in cancer cells and radiation toxicity to normal tissues are severe concerns. The exposure to radiation generates intracellular reactive oxygen species (ROS), which leads to DNA damage by lipid peroxidation, removal of thiol groups from cellular and membrane proteins, strand breaks and base alterations. Hypothesis Plants have to deal with radiation-induced damage (UV-light of sun, other natural radiation sources). Therefore, it is worth speculating that radioprotective mechanisms ha…

0301 basic medicineCurcuminAntioxidantDNA damagemedicine.medical_treatmentPhytochemicalsPharmaceutical ScienceSilibininRadiation-Protective AgentsAscorbic AcidBiologyPharmacologyAntioxidantsLipid peroxidation03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNeoplasmsRadioresistanceStilbenesDrug DiscoverymedicineHumansRadiation InjuriesFlavonoidsPharmacologyRadiotherapyRadiochemistryPolyphenolsPlantsAscorbic acid030104 developmental biologyComplementary and alternative medicinechemistryResveratrol030220 oncology & carcinogenesisCancer cellCurcuminMolecular MedicineLipid PeroxidationReactive Oxygen SpeciesDNA DamagePhytomedicine
researchProduct

NF-κB Is a Potential Molecular Drug Target in Triple-Negative Breast Cancers.

2017

Breast cancer continues to cause significant burden in global health morbidity and mortality. Triple-negative breast cancers (TNBCs) are highly aggressive with poor prognosis and are characterized by lack of expression of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor (Her-2). TNBCs are often resistant to cytotoxic chemotherapy and pose major difficulty in achieving personalized medicine due to their molecular heterogeneity. There is increasing evidence that the aberrant activation of nuclear factor (NF)-κB signaling is a frequent characteristic of TNBCs. We evaluated the effects of different potential NF-κB inhibitors, such as bisindolylmaleimide I (BI…

0301 basic medicineCurcuminEstrogen receptorTriple Negative Breast NeoplasmsPharmacologydiagnostics drug targets NF-kB signaling personalized medicine triple-negative breast cancerBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBreast cancerCell Line TumorMG132Progesterone receptorGeneticsmedicineGene silencingHumansPrecision MedicineMolecular BiologyTriple-negative breast cancerbusiness.industryCyclohexanonesNF-kappa BCancermedicine.disease030104 developmental biologychemistry030220 oncology & carcinogenesisBenzamidesProteasome inhibitorCancer researchMolecular MedicineFemalebusinessBiotechnologymedicine.drugSignal TransductionOmics : a journal of integrative biology
researchProduct

Transcutaneous immunization with CD40 ligation boosts cytotoxic T lymphocyte mediated antitumor immunity independent of CD4 helper cells in mice.

2018

Transcutaneous immunization (TCI) is a novel vaccination strategy that utilizes skin-associated lymphatic tissue to induce immune responses. Employing T-cell epitopes and the TLR7 agonist imiquimod onto intact skin mounts strong primary, but limited memory CTL responses. To overcome this limitation, we developed a novel imiquimod-containing vaccination platform (IMI-Sol) rendering superior primary CD8+ and CD4+ T-cell responses. However, it has been unclear whether IMI-Sol per se is restricted in terms of memory formation and tumor protection. In our present work, we demonstrate that the combined administration of IMI-Sol and CD40 ligation unleashes fullblown specific T-cell responses in th…

0301 basic medicineCytotoxicity ImmunologicGraft RejectionSkin NeoplasmsOvalbuminmedicine.medical_treatmentT cellImmunologyCD40 Ligand610 MedizinMelanoma ExperimentalPriming (immunology)Gene ExpressionAdministration Cutaneous03 medical and health sciencesMice0302 clinical medicineImmune system610 Medical sciencesmedicineImmunology and AllergyCytotoxic T cellAnimalsSkinCD40ImiquimodMembrane GlycoproteinsbiologyT-Lymphocytes Helper-InducerAllograftsMice Inbred C57BLCTL*030104 developmental biologymedicine.anatomical_structureToll-Like Receptor 7biology.proteinCancer researchImmunizationImmunotherapyAdjuvantImmunologic MemoryCD8030215 immunologyCD27 LigandT-Lymphocytes CytotoxicEuropean journal of immunologyReferences
researchProduct

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
researchProduct

The MRN complex is transcriptionally regulated by MYCN during neural cell proliferation to control replication stress

2015

The MRE11/RAD50/NBS1 (MRN) complex is a major sensor of DNA double strand breaks, whose role in controlling faithful DNA replication and preventing replication stress is also emerging. Inactivation of the MRN complex invariably leads to developmental and/or degenerative neuronal defects, the pathogenesis of which still remains poorly understood. In particular, NBS1 gene mutations are associated with microcephaly and strongly impaired cerebellar development, both in humans and in the mouse model. These phenotypes strikingly overlap those induced by inactivation of MYCN, an essential promoter of the expansion of neuronal stem and progenitor cells, suggesting that MYCN and the MRN complex migh…

0301 basic medicineDNA ReplicationTranscription GeneticDNA damageDNA repairDNA-Binding ProteinCell Cycle ProteinsBiology03 medical and health sciencesMRE11 Homologue ProteinCell Cycle ProteinStrand-Break Repair; N-Myc; Dna-Replication; Human Neuroblastoma; Feingold-Syndrome; C-Myc; Mre11-Rad50-Nbs1 Complex; Targeted Disruption; Genomic Instability; Embryonic LethalityHumansProgenitor cellMolecular BiologyneoplasmsCells CulturedNuclear ProteinCell ProliferationGeneticsNeuronsOncogene ProteinsOriginal PaperMRE11 Homologue ProteinN-Myc Proto-Oncogene ProteinCell growthDNA Repair EnzymeDNA replicationOncogene ProteinNuclear ProteinsCell BiologyNeuronCell biologyAcid Anhydride HydrolasesDNA-Binding Proteins030104 developmental biologyDNA Repair EnzymesMRN complexGene Expression RegulationRad50HumanCell Death and Differentiation
researchProduct

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
researchProduct

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
researchProduct

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
researchProduct