Search results for "Cance"

showing 10 items of 12092 documents

DNA methylation of shelf, shore and open sea CpG positions distinguish high microsatellite instability from low or stable microsatellite status colon…

2019

Aim: To investigate the genome-wide methylation of genetically characterized colorectal cancer stem cell (CR-CSC) lines. Materials & methods: Eight CR-CSC lines were isolated from primary colorectal cancer (CRC) tissues, cultured and characterized for aneuploidy, mutational status of CRC-related genes and microsatellite instability (MSI). Genome-wide DNA methylation was assessed by MethylationEPIC microarray. Results: We describe a distinctive methylation pattern that is maintained following in vivo passages in immune-compromised mice. We identified an epigenetic CR-CSC signature associated with MSI. We noticed that the preponderance of the differentially methylated positions do not re…

0301 basic medicineCancer ResearchMicroarrayColorectal cancercolon cancer stem cellsSocio-culturaleBiologyEpigenesis Genetic03 medical and health sciencesMice0302 clinical medicineGeneticsmedicineAnimalsHumansEpigeneticsneoplasmsMSIMSSMicrosatellite instabilityMethylationcolon cancer stem cells DNA methylation MSI MSSDNA Methylationmedicine.diseasedigestive system diseases030104 developmental biologyCpG siteDrug Resistance Neoplasm030220 oncology & carcinogenesisDNA methylationColonic NeoplasmsCancer researchNeoplastic Stem CellsMicrosatelliteHeterograftsCpG IslandsMicrosatellite Instabilitycolon cancer stem cellEpigenomics
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Myeloid Cell-Derived Reactive Oxygen Species Induce Epithelial Mutagenesis

2017

Increased oxidative stress has been suggested to initiate and promote tumorigenesis by inducing DNA damage and to suppress tumor development by triggering apoptosis and senescence. The contribution of individual cell types in the tumor microenvironment to these contrasting effects remains poorly understood. We provide evidence that during intestinal tumorigenesis, myeloid cell-derived H2O2 triggers genome-wide DNA mutations in intestinal epithelial cells to stimulate invasive growth. Moreover, increased reactive oxygen species (ROS) production in myeloid cells initiates tumor growth in various organs also in the absence of a carcinogen challenge in a paracrine manner. Our data identify an i…

0301 basic medicineCancer ResearchMyeloidDNA damageApoptosismedicine.disease_causeMice03 medical and health sciencesParacrine signallingmedicineAnimalsMyeloid Cellschemistry.chemical_classificationReactive oxygen speciesTumor microenvironmentChemistryEpithelial CellsHydrogen PeroxideCell BiologyMice Mutant StrainsCell biologyOxidative Stress030104 developmental biologymedicine.anatomical_structureOncologyMutagenesisMutationTumor necrosis factor alphaReactive Oxygen SpeciesCarcinogenesisOxidative stressDNA DamageSignal TransductionCancer Cell
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Bacitracin and Rutin Regulate Tissue Factor Production in Inflammatory Monocytes and Acute Myeloid Leukemia Blasts

2021

Simple Summary Aberrant tissue factor (TF) expression by transformed myeloblasts and inflammatory monocytes contributes to coagulation activation in acute myeloid leukemia (AML). TF procoagulant activity (PCA) is regulated by protein disulfide isomerase (PDI), an oxidoreductase with chaperone activity, but its specific role in AML-associated TF biology is unclear. Here, we provide novel mechanistic insights into this interrelation. We show that bacitracin and rutin, two pan-inhibitors of the PDI family, prevent lipopolysaccharide (LPS)-induced monocyte TF production under inflammatory conditions and constitutive TF expression by THP1 cells and AML blasts, thus exerting promising anticoagula…

0301 basic medicineCancer ResearchMyeloidDaunorubicinacute myeloid leukemia030204 cardiovascular system & hematologyPeripheral blood mononuclear cellArticleFlow cytometry03 medical and health sciencesTissue factor0302 clinical medicineDownregulation and upregulationhemic and lymphatic diseasesmedicinecoagulationProtein disulfide-isomeraseRC254-282medicine.diagnostic_testChemistryrutinNeoplasms. Tumors. Oncology. Including cancer and carcinogensMyeloid leukemiatissue factorprotein disulfide isomeraseMolecular biology030104 developmental biologymedicine.anatomical_structureOncologyinflammationtissue factor; protein disulfide isomerase; acute myeloid leukemia; coagulation; inflammation; rutin; monocytesmonocytesmedicine.drugCancers
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Imiquimod inhibits growth and induces differentiation of myeloid leukemia cell lines

2018

Background: The antitumoral effects of different Toll-like receptor (TLRs) agonists is mediated by activating immune responses to suppress tumors growth, although TLR ligands may also have a direct effect on tumoral cells. Given that TLR signaling induces hematopoietic cell differentiations this may serve as a novel differentiation therapeutic approach for AML. Methods: We investigated the effects of agonists for the ten human TLRs on the proliferation, apoptosis, cell cycle and differentiation of ten different types of myeloid leukemia cell lines (HL-60, U-937, KG-1, KG-1a, K-562, Kasumi-1, EOL-1, NB4, MOLM-13 and HEL). Proliferation was measured using the CellTiter 96 (R) Aqueous One Solu…

0301 basic medicineCancer ResearchMyeloidImiquimodlcsh:RC254-282Flow cytometry03 medical and health sciences0302 clinical medicineToll-like receptorGeneticsmedicineCytotoxic T cellMyeloid leukemia cell lineslcsh:QH573-671Toll-like receptorImiquimodmedicine.diagnostic_testChemistryCell growthlcsh:CytologyMyeloid leukemiaCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisCancer researchPrimary Researchmedicine.drugCancer Cell International
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Transcriptional Profiles and Stromal Changes Reveal Bone Marrow Adaptation to Early Breast Cancer in Association with Deregulated Circulating microRN…

2020

Abstract The presence of a growing tumor establishes a chronic state of inflammation that acts locally and systemically. Bone marrow responds to stress signals by expanding myeloid cells endowed with immunosuppressive functions, further fostering tumor growth and dissemination. How early in transformation the cross-talk with the bone marrow begins and becomes detectable in blood is unknown. Here, gene expression profiling of the bone marrow along disease progression in a spontaneous model of mammary carcinogenesis demonstrates that transcriptional modifications in the hematopoietic compartment occurred as early as preinvasive disease stages. The transcriptional profile showed downregulation…

0301 basic medicineCancer ResearchMyeloidStromal cellInflammationApoptosisBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaCXCR403 medical and health sciencesMice0302 clinical medicineBone MarrowmedicineBiomarkers TumorTumor Cells CulturedAnimalsHumansCirculating MicroRNACell ProliferationMice Inbred BALB CInnate immune systemGene Expression ProfilingAcquired immune systemAdaptation PhysiologicalXenograft Model Antitumor AssaysGene Expression Regulation NeoplasticHaematopoiesis030104 developmental biologymedicine.anatomical_structureOncologyTrascriptional profiles early brest cancer microRNAs030220 oncology & carcinogenesisCancer researchFemaleBone marrowmedicine.symptomStromal CellsTranscriptomeCancer research
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Nicotinamide Phosphoribosyltransferase Acts as a Metabolic Gate for Mobilization of Myeloid-Derived Suppressor Cells

2019

Abstract Cancer induces alteration of hematopoiesis to fuel disease progression. We report that in tumor-bearing mice the macrophage colony-stimulating factor elevates the myeloid cell levels of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway, which acts as negative regulator of the CXCR4 retention axis of hematopoietic cells in the bone marrow. NAMPT inhibits CXCR4 through a NAD/Sirtuin 1–mediated inactivation of HIF1α-driven CXCR4 gene transcription, leading to mobilization of immature myeloid-derived suppressor cells (MDSC) and enhancing their production of suppressive nitric oxide. Pharmacologic inhibition or myeloid-specific ablation …

0301 basic medicineCancer ResearchMyeloidmedicine.medical_treatmentNudeNicotinamide phosphoribosyltransferaseApoptosisColorectal NeoplasmInbred C57BLMicechemistry.chemical_compound0302 clinical medicineTumor Cells CulturedHematopoiesiNicotinamide PhosphoribosyltransferaseInbred BALB CMice Inbred BALB CCulturedbiologySarcomaTumor CellsHaematopoiesismedicine.anatomical_structureOncology030220 oncology & carcinogenesisSirtuinFemaleSarcoma ExperimentalColorectal NeoplasmsAnimals; Apoptosis; Cell Proliferation; Colorectal Neoplasms; Female; Hematopoiesis; Humans; Mammary Neoplasms Experimental; Mice; Mice Inbred BALB C; Mice Inbred C57BL; Mice Nude; Myeloid-Derived Suppressor Cells; NAD; Nicotinamide Phosphoribosyltransferase; Sarcoma Experimental; Signal Transduction; Tumor Cells Cultured; Xenograft Model Antitumor AssaysHumanSignal TransductionMice NudeExperimental03 medical and health sciencesmedicineMyeloid-Derived Suppressor CellAnimalsHumansCell ProliferationAnimalMyeloid-Derived Suppressor CellsMammary NeoplasmsApoptosiMammary Neoplasms ExperimentalImmunotherapyNADXenograft Model Antitumor AssaysHematopoiesisMice Inbred C57BL030104 developmental biologychemistrybiology.proteinCancer researchMyeloid-derived Suppressor CellNAD+ kinaseBone marrowCancer Research
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From ancient herb to modern drug: Artemisia annua and artemisinin for cancer therapy.

2017

Artemisia annua L. is used throughout Asia and Africa as tea and press juice to treat malaria and related symptomes (fever, chills). Its active ingredient, artemisinin (ARS), has been developed as antimalarial drug and is used worldwide. Interestingly, the bioactivity is not restricted to malaria treatment. We and others found that ARS-type drugs also reveal anticancer in vitro and in vivo. In this review, we give a systematic overview of the literature published over the past two decades until the end of 2016. Like other natural products, ARS acts in a multi-specific manner against tumors. The cellular response of ARS and its derivatives (dihydroartemisinin, artesunate, artemether, arteeth…

0301 basic medicineCancer ResearchNecroptosismedicine.medical_treatmentArtemisia annuaDihydroartemisininPharmacologyArtemisia annua03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNeoplasmsmedicineHumansArtemetherArtemisininPI3K/AKT/mTOR pathwaybiologybiology.organism_classificationArtemisininsNeoplasm ProteinsGene Expression Regulation NeoplasticDrug repositioningOxidative Stress030104 developmental biologychemistryArtesunate030220 oncology & carcinogenesismedicine.drugSeminars in cancer biology
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Parthenolide and DMAPT exert cytotoxic effects on breast cancer stem-like cells by inducing oxidative stress, mitochondrial dysfunction and necrosis

2016

Triple-negative breast cancers (TNBCs) are aggressive forms of breast carcinoma associated with a high rate of recidivism. In this paper, we report the production of mammospheres from three lines of TNBC cells and demonstrate that both parthenolide (PN) and its soluble analog dimethylaminoparthenolide (DMAPT) suppressed this production and induced cytotoxic effects in breast cancer stem-like cells, derived from dissociation of mammospheres. In particular, the drugs exerted a remarkable inhibitory effect on viability of stem-like cells. Such an effect was suppressed by N-acetylcysteine, suggesting a role of reactive oxygen species (ROS) generation in the cytotoxic effect. Instead z-VAD, a ge…

0301 basic medicineCancer ResearchNecrosismedicine.disease_causeCancer -- Treatmentchemistry.chemical_compoundOnium CompoundsMedicineCytotoxic T cellBreast -- CancerMembrane Potential Mitochondrialchemistry.chemical_classificationSuperoxideMitochondrial DNAMitochondriaNeoplastic Stem CellsFemaleOriginal Articlemedicine.symptomOligopeptidesSesquiterpenesCell SurvivalNF-E2-Related Factor 2ImmunologyBreast NeoplasmsReal-Time Polymerase Chain Reaction03 medical and health sciencesCellular and Molecular NeuroscienceDownregulation and upregulationCell Line TumorHumansParthenolideparthenolide cancer stem cell triple-negative breast cancer reactive oxygen species nuclear factor erythroid 2-related factor 2Fluorescent DyesReactive oxygen speciesbusiness.industryAcetophenonesNADPH OxidasesCell BiologyCell nuclei -- AbnormalitiesOxidative Stress030104 developmental biologychemistryApocyninImmunologyCancer researchReactive Oxygen SpeciesbusinessOxidative stressTranscription FactorsCell Death & Disease
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Isolation, culture and analysis of adult subependymal neural stem cells

2016

Individual cells dissected from the subependymal neurogenic niche of the adult mouse brain proliferate in medium containing basic fibroblast growth factor (bFGF) and/or epidermal growth factor (EGF) as mitogens, to produce multipotent clonal aggregates called neurospheres. These cultures constitute a powerful tool for the study of neural stem cells (NSCs) provided that they allow the analysis of their features and potential capacity in a controlled environment that can be modulated and monitored more accurately than in vivo. Clonogenic and population analyses under mitogen addition or withdrawal allow the quantification of the self-renewing and multilineage potency of these cells and the id…

0301 basic medicineCancer ResearchNeurogenesisCellular differentiationBasic fibroblast growth factorPopulationCell Culture TechniquesBiologyMice03 medical and health scienceschemistry.chemical_compoundNeural Stem CellsEpendymaNeurosphereSubependymal zoneAnimalsHumanseducationMolecular BiologyNeuronseducation.field_of_studyNeurogenesisCell DifferentiationCell BiologyNeural stem cellCell biologyAdult Stem Cells030104 developmental biologychemistryImmunologyDevelopmental BiologyAdult stem cellDifferentiation
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Effects of the MDM-2 inhibitor Nutlin-3a on PDAC cells containing and lacking WT-TP53 on sensitivity to chemotherapy, signal transduction inhibitors …

2019

Abstract Mutations at the TP53 gene are readily detected (approximately 50–75%) in pancreatic ductal adenocarcinoma (PDAC) patients. TP53 was previously thought to be a difficult target as it is often mutated, deleted or inactivated on both chromosomes in certain cancers. In the following study, the effects of restoration of wild-type (WT) TP53 activity on the sensitivities of MIA-PaCa-2 pancreatic cancer cells to the MDM2 inhibitor nutlin-3a in combination with chemotherapy, targeted therapy, as well as, nutraceuticals were examined. Upon introduction of the WT-TP53 gene into MIA-PaCa-2 cells, which contain a TP53 gain of function (GOF) mutation, the sensitivity to the MDM2 inhibitor incre…

0301 basic medicineCancer ResearchNutlin-3aSettore MED/09 - Medicina Internaendocrine system diseasesmedicine.medical_treatmentmedicine.disease_causePiperazinesTargeted therapy0302 clinical medicineTP53MutationbiologyChemistryImidazolesProto-Oncogene Proteins c-mdm2OxaliplatinTargeted TherapeuticsDrug sensitivity; Nutlin-3a; Nutraceuticals; Targeted therapeutics; TP53030220 oncology & carcinogenesisMolecular MedicineMdm2NutraceuticalNutraceuticalsSignal transductionCarcinoma Pancreatic DuctalSignal Transductionmedicine.drugDrug sensitivityAntineoplastic AgentsIrinotecan03 medical and health sciencesCell Line TumorPancreatic cancerGeneticsmedicineHumansMolecular BiologyneoplasmsChemotherapymedicine.diseasedigestive system diseasesOxaliplatinPancreatic Neoplasms030104 developmental biologyCell cultureDietary Supplementsbiology.proteinCancer researchTERAPÊUTICA MÉDICATumor Suppressor Protein p53
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