Search results for "leukemia cells"

showing 8 items of 8 documents

ROLE OF EXOSOMES RELEASED BY CHRONIC MYLEOGENOUS LEUKEMIA CELLS IN THE MODULATION OF TUMOR MICROENVIROMENT

2010

Exosomeschronic myelogenous leukemia cells
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Antiproliferative Properties of a Few Auranofin-Related Gold(I) and Silver(I) Complexes in Leukemia Cells and their Interferences with the Ubiquitin …

2020

A group of triethylphosphine gold(I) and silver(I) complexes, structurally related to auranofin, were prepared and investigated as potential anticancer drug candidates. The antiproliferative properties of these metal compounds were assessed against two leukemia cell lines, i.e., CCRF-CEM and its multidrug-resistant counterpart, CEM/ADR5000. Interestingly, potent cytotoxic effects were disclosed for both series of compounds against leukemia cells, with IC50 values generally falling in the low-micromolar range, the gold derivatives being on the whole more effective than the silver analogues. Some initial structure-function relationships were drawn. Subsequently, the ability of the study compo…

ProteasesProteasome Endopeptidase ComplexAuranofinSilverleukemia cellsPharmaceutical Sciencemetal complexesantiproliferative propertiesArticleAnalytical ChemistryMetallcsh:QD241-44103 medical and health sciencesInhibitory Concentration 500302 clinical medicineGold Compoundslcsh:Organic chemistryCell Line TumorDrug DiscoverymedicineCytotoxic T cellHumansPhysical and Theoretical Chemistry030304 developmental biologyCell Proliferationproteasome inhibition0303 health sciencesLeukemiaChemistryUbiquitinOrganic Chemistryauranofinmedicine.diseaseauranofin metal complexes proteasome inhibition leukemia cells antiproliferative propertiesDrug Resistance MultipleLeukemiaProteasomeBiochemistryChemistry (miscellaneous)Drug Resistance Neoplasm030220 oncology & carcinogenesisvisual_artvisual_art.visual_art_mediumauranofin;metal complexes; proteasome inhibition; leukemia cells; antiproliferative propertiesMolecular MedicineGoldSelectivitymedicine.drugMolecules
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Carboxyamidotriazole inhibits cell growth of imatinib-resistant chronic myeloid leukaemia cells including T315I Bcr-Abl mutant by a redox-mediated me…

2010

Mutation of the Bcr–Abl oncoprotein is one of most frequent mechanisms by which chronic myelogenous leukemia (CML) cells become resistant to imatinib. Here, we show that treat- ment of cell lines harbouring wild type or mutant BCR–ABL with carboxyamidotriazole (CAI), a calcium influx and signal transduction inhibitor, inhibits cell growth, the expres- sion of Bcr–Abl and its downstream signalling, and induces apoptosis. Moreover, we show that CAI acts by increasing intracellular ROS. Clinically significant, CAI has also inhibitory effects on T315I Bcr–Abl mutant, a mutation that causes CML cells to become insensitive to imatinib and second generation abl kinase inhibitors.

Cancer Researchbcr-abl Carboxyamidotriazole chronic myeloid leukemia cells imatinibBlotting WesternFusion Proteins bcr-ablAntineoplastic AgentsApoptosisSignal transduction inhibitorBiologyPiperazineschemistry.chemical_compoundMicehemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsCell ProliferationSettore MED/04 - Patologia GeneraleABLCarboxyamidotriazoleCell growthWild typeImatinibTriazolesmedicine.diseaseImatinib mesylatePyrimidinesOncologychemistryDrug Resistance NeoplasmBenzamidesMutationCancer researchImatinib MesylateReactive Oxygen SpeciesOxidation-ReductionChronic myelogenous leukemiamedicine.drug
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Prodrug based on halloysite delivery systems to improve the antitumor ability of methotrexate in leukemia cell lines

2021

The prodrug approach, as well as the development of specific systems able to deliver a chemotherapeutic agent in the target site, decreasing the side effects often associated with its administration, are still a challenging. In this context, both methotrexate drug molecules (MTX) and biotin ligand moieties, whose receptors are overexpressed on the surface of several cancer cells, were loaded on halloysite nanotubes (HNTs) to develop nanomaterial based on multifunctional and "smart" delivery systems. To highlight the crucial role played by biotin, carrier systems based on HNTs and MTX were also synthetized. In detail, several approaches were envisaged: i) a supramolecular interaction between…

LeukemiaNanotubesHalloysite nanotubesBiotinAntineoplastic AgentsSurfaces and InterfacesGeneral MedicineSettore CHIM/06 - Chimica OrganicaCell LineDrug delivery systemsColloid and Surface ChemistryMethotrexateSpectroscopy Fourier Transform InfraredSettore BIO/14 - FarmacologiaClayHumansProdrugsPhysical and Theoretical ChemistryLeukemia cellsProdrugBiotechnologySettore CHIM/02 - Chimica Fisica
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V gamma 9V delta 2 T lymphocytes efficiently recognize and kill zoledronate-sensitized, imatinib-sensitive, and imatinib-resistant chronic myelogenou…

2010

Abstract Imatinib mesylate (imatinib), a competitive inhibitor of the BCR-ABL tyrosine kinase, is highly effective against chronic myelogenous leukemia (CML) cells. However, because 20–30% of patients affected by CML display either primary or secondary resistance to imatinib, intentional activation of Vγ9Vδ2 T cells by phosphoantigens or by agents that cause their accumulation within cells, such as zoledronate, may represent a promising strategy for the design of a novel and highly innovative immunotherapy capable to overcome imatinib resistance. In this study, we show that Vγ9Vδ2 T lymphocytes recognize, trogocytose, and efficiently kill imatinib-sensitive and -resistant CML cell lines pre…

gamma delta T cells Imatinib Leukemia cellsAdultmedicine.medical_treatmentImmunologyMice SCIDLymphocyte ActivationZoledronic AcidPiperazinesMicehemic and lymphatic diseasesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineImmunology and AllergyAnimalsHumansneoplasmsCells CulturedDiphosphonatesbusiness.industryImidazolesImatinibReceptors Antigen T-Cell gamma-deltaImmunotherapymedicine.diseaseIn vitroCoculture TechniquesDrug Resistance MultipleLeukemiaImatinib mesylatePyrimidinesCell cultureDrug Resistance NeoplasmImmunologyBenzamidesCancer researchImatinib MesylatebusinessK562 CellsTyrosine kinasemedicine.drugChronic myelogenous leukemiaT-Lymphocytes CytotoxicJournal of immunology (Baltimore, Md. : 1950)
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Exosomal shuttling of miR-126 in endothelial cells modulates adhesive and migratory abilities of chronic myelogenous leukemia cells.

2014

BACKGROUND: Recent findings indicate that exosomes released from cancer cells contain microRNAs (miRNAs) that may be delivered to cells of tumor microenvironment. RESULTS: To elucidate whether miRNAs secreted from chronic myelogenous leukemia cells (CML) are shuttled into endothelial cells thus affecting their phenotype, we first analysed miRNAs content in LAMA84 exosomes. Among the 124 miRNAs identified in LAMA84 exosomes, we focused our attention on miR-126 which was found to be over-overexpressed in exosomes compared with producing parental cells. Transfection of LAMA84 with Cy3-labelled miR-126 and co-culture of leukemia cells with endothelial cells (EC) confirmed that miR-126 is shuttl…

Cancer ResearchEndothelial cellsChronic Myelogenous Leukemia CellsVascular Cell Adhesion Molecule-1Exosomes; Chronic Myelogenous Leukemia; microRNA;BiologyExosomesCell MovementSettore BIO/13 - Biologia ApplicataCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineHumansChronic Myelogenous LeukemiamiRNATumor microenvironmentExosomes; Endothelial cells; Chronic Myelogenous Leukemia Cells; miRNAmicroRNAResearchTransfectionmedicine.diseaseChemokine CXCL12MicrovesiclesExosomeMicroRNAsLeukemiamedicine.anatomical_structureOncologyCell cultureCancer cellCancer researchMolecular MedicineBone marrowChronic myelogenous leukemia
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Role of exosomes released by chronic myelogenous leukemia cells in angiogenesis

2012

The present study is designed to assess if exosomes released from Chronic Myelogenous Leukemia (CML) cells may modulate angiogenesis. We have isolated and characterized the exosomes generated from LAMA84 CML cells and demonstrated that addition of exosomes to human vascular endothelial cells (HUVEC) induces an increase of both ICAM-1 and VCAM-1 cell adhesion molecules and interleukin-8 expression. The stimulation of cell-cell adhesion molecules was paralleled by a dose-dependent increase of adhesion of CML cells to a HUVEC monolayer. We further showed that the treatment with exosomes from CML cells caused an increase in endothelial cell motility accompanied by a loss of VE-cadherin and β-ca…

Cancer ResearchAngiogenesisVascular Cell Adhesion Molecule-1BiologyExosomesArticleExosomes Chronic Myelogenous Leukemia Cells Endothelial cells Tumor MicroenvironmentMiceAntigens CDCell Movementhemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineCell AdhesionHuman Umbilical Vein Endothelial CellsTumor MicroenvironmentAnimalsHumansCell adhesionbeta CateninMatrigelTumor microenvironmentNeovascularization PathologicCell adhesion moleculeInterleukin-8medicine.diseaseCadherinsIntercellular Adhesion Molecule-1MicrovesiclesCell biologyEndothelial stem cellDrug CombinationsOncologyGene Expression RegulationCancer researchProteoglycansCollagenLamininChronic myelogenous leukemia
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EXOSOMES RELEASED BY K562 CHRONIC MYELOID LEUKEMIA CELLS PROMOTE ENDOTHELIAL CELL TUBULAR DIFFERENTIATION THROUGH UPTAKE AND CELL-TO-CELL TRANSFER

2011

Settore BIO/13 - Biologia ApplicataK562MYELOID LEUKEMIA CELLS
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