Search results for "Chronic myeloid leukemia"

showing 10 items of 25 documents

Interleukin 3- receptor targeted exosomes inhibit in vitro and in vivo chronic myelogenous Leukemia cell growth

2017

Despite Imatinib (IM), a selective inhibitor of Bcr-Abl, having led to improved prognosis in Chronic Myeloid Leukemia (CML) patients, acquired resistance and long-term adverse effects is still being encountered. There is, therefore, urgent need to develop alternative strategies to overcome drug resistance. According to the molecules expressed on their surface, exosomes can target specific cells. Exosomes can also be loaded with a variety of molecules, thereby acting as a vehicle for the delivery of therapeutic agents. In this study, we engineered HEK293T cells to express the exosomal protein Lamp2b, fused to a fragment of Interleukin 3 (IL3). The IL3 receptor (IL3-R) is overexpressed in CML…

0301 basic medicineMedicine (miscellaneous)PharmacologyEngineered exosomeExosomesInterleukin 3Antineoplastic AgentMiceHEK293 Cellhemic and lymphatic diseasesDrug CarrierPharmacology Toxicology and Pharmaceutics (miscellaneous)Drug CarriersChronic myeloid leukemiaMyeloid leukemiaChronic myeloid leukemia; Drug delivery; Drug resistance; Engineered exosomes; Interleukin 3; Animals; Antineoplastic Agents; Cell Line Tumor; Cell Proliferation; Disease Models Animal; Drug Carriers; Exosomes; HEK293 Cells; Heterografts; Humans; Imatinib Mesylate; Leukemia Myelogenous Chronic BCR-ABL Positive; Mice; Receptors Interleukin-3; Treatment Outcome3. Good healthTreatment OutcomeImatinib MesylateHeterograftsHeterograftResearch Papermedicine.drugHumanEngineered exosomesAntineoplastic Agents03 medical and health sciencesIn vivoCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineAnimalsHumansneoplasmsInterleukin 3.Interleukin 3Cell Proliferationbusiness.industryAnimalImatinibmedicine.diseaseMicrovesiclesReceptors Interleukin-3ExosomeDisease Models AnimalHEK293 Cells030104 developmental biologyImatinib mesylateDrug resistanceCancer cellDrug deliverybusinessChronic myelogenous leukemia
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BCR-ABL1 Doubling-Times and Halving-Times May Predict CML Response to Tyrosine Kinase Inhibitors

2019

In Chronic Myeloid Leukemia (CML), successful treatment requires accurate molecular monitoring to evaluate disease response and provide timely interventions for patients failing to achieve the desired outcomes. We wanted to determine whether measuring BCR-ABL1 mRNA doubling-times (DTs) could distinguish inconsequential rises in the oncogene’s expression from resistance to tyrosine kinase inhibitors (TKIs). Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment. Patients were subdivided in two groups: those with a confirmed rise in BCR-ABL1 transcripts without MR3.0 loss and those failing IM. We found …

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtyDisease ResponseChronic Myeloid LeukemiaBCR-ABL1/ABL1IShalving-timelcsh:RC254-28203 medical and health sciences0302 clinical medicineInternal medicinehemic and lymphatic diseasesBCR-ABL1/ABL1; IS; Chronic Myeloid Leukemia; Doubling-time; Halving-time; Tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineDoubling timeOriginal ResearchBCR-ABL1/ABL1Oncogenebusiness.industryMyeloid leukemialcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensDiscontinuationdoubling-time030104 developmental biologyImatinib mesylateOncology030220 oncology & carcinogenesisCohortISBCR-ABL1/ABL1 ISbusinessTyrosine kinaseFrontiers in Oncology
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Management of Ponatinib in Patients with Chronic Myeloid Leukemia with Cardiovascular Risk Factors

2019

Cardiovascular (CV) adverse events are considered common complications of ponatinib treatment. Recently, it has been demonstrated that ponatinib dose reductions in definite settings can obtain optimal responses and lower ponatinib-related CV events. In this study, we describe the management of 5 patients with chronic myeloid leukemia treated with ponatinib, from second to fourth line of tyrosine kinase inhibitor therapy, carrying high pre-ponatinib CV risk, who obtained optimal molecular response and developed no CV adverse event during follow-up. Among these 5 patients, 2 had diagnosis of ischemic heart disease and underwent percutaneous angioplasty, 2 had type 2 diabetes and arterial hype…

0301 basic medicinemedicine.medical_specialtymedicine.drug_class030106 microbiologyCardiovascular risk factorsType 2 diabetesDiseaseTyrosine-kinase inhibitorSettore MED/15 - Malattie Del Sangue03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineDrug DiscoverymedicinePharmacology (medical)In patientAdverse effectPharmacologybusiness.industryPonatinibChronic myeloid leukemiaMyeloid leukemiaGeneral Medicinemedicine.diseaseCardiovascular riskInfectious DiseasesOncologychemistry030220 oncology & carcinogenesisPonatinibbusiness
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Late onset of unilateral optic disk edema secondary to treatment with imatinib mesylate

2017

Key Clinical Message Prompt ophthalmology evaluation and immediate imatinib suspension should be suggested at any time of tyrosine kinase inhibitor therapy in patients with visual deficit, as it may be a clinical manifestation of optic disk edema, and suspension may help in prompt recovery.

Adverse event0301 basic medicinegenetic structuresmedicine.drug_classOptic Disk EdemaLate onsetCase ReportClinical manifestationCase ReportsTyrosine-kinase inhibitor03 medical and health sciences0302 clinical medicinechronic myeloid leukemiatyrosine kinase inhibitorsmedicineIn patientAdverse effectbusiness.industryoptic disk edemaImatinibGeneral Medicineeye diseases030104 developmental biologyImatinib mesylateimatiniboptic nerve edemaAnesthesiaAdverse events030221 ophthalmology & optometrybusinessmedicine.drugClinical Case Reports
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BCL2 gene polymorphisms and splicing variants in chronic myeloid leukemia.

2015

Recent data suggest that constitutional genetic variation in the antiapoptotic BCL2 gene could be associated with the susceptibility to develop chronic myeloid leukemia (CML) and the clinical outcome in several hematological malignancies. The present study examines whether BCL2 single nucleotide polymorphisms (SNPs) predispose to CML or may potentially influence the disease characteristics at diagnosis. Notably, no association was observed between the four candidate BCL2 SNPs and the risk of developing CML. Instead, the 4777C>A (rs2279115) and the 5735A>G (rs1801018) SNPs were significantly associated with the disease risk profile as determined by the Sokal score. We found that such polymor…

Cancer ResearchBCL2business.industryAlternative splicingChronic myeloid leukemiaClinical courseMyeloid leukemiaSingle-nucleotide polymorphismHematologyBioinformaticsSplicingBCL2 Chronic myeloid leukemia Polymorphisms Splicing SusceptibilityOncologyimmune system diseasesSusceptibilityhemic and lymphatic diseasesGenetic variationRNA splicingMedicinebiological phenomena cell phenomena and immunitySokal ScorebusinessPolymorphismsGeneneoplasms
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The new iodoacetamidobenzofuran derivative TR120 decreases STAT5 expression and induces antitumor effects in imatinib-sensitive and imatinib-resistan…

2013

The identification of novel compounds modulating the expression/activity of molecular targets downstream to BCR-ABL could be a new approach in the treatment of chronic myeloid leukemias (CMLs) resistant to imatinib or other BCR-ABL-targeted molecules. Recently, we synthesized a new class of substituted 2-(3,4,5-trimethoxybenzoyl)-2-N,N-dimethylamino-benzo[b]furans, and among these 3-iodoacetylamino-6-methoxybenzofuran-2-yl(3,5-trimethoxyphenyl)methanone (TR120) showed marked cytotoxic activity in BCR-ABL-expressing cells. Interestingly, TR120 was more potent than imatinib in cell growth inhibition and apoptosis induction in both BCR-ABL-expressing K562 and KCL22 cells. Moreover, it showed a…

Cancer ResearchFusion Proteins bcr-ablApoptosisPiperazinesSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundhemic and lymphatic diseasesSTAT5 Transcription FactorCytotoxic T cellPharmacology (medical)Cyclin D1STAT5biologyDrug SynergismCell cycleNeoplasm ProteinsGene Expression Regulation NeoplasticLeukemiaOncologyProto-Oncogene Proteins c-bcl-2BenzamidesImatinib MesylateGrowth inhibitionmedicine.drugbcl-X ProteinDown-RegulationAntineoplastic AgentsBone Marrow CellsResting Phase Cell CycleColony-Forming Units AssayBenzophenonesNecrosisCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansneoplasmsBenzofuransPharmacologyG1 PhaseImatinibBCR-ABL chronic myeloid leukemia imatinib resistance STAT5 tyrosine kinase inhibitorsmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGenes bcl-1Genes bcl-2PyrimidineschemistryApoptosisDrug Resistance NeoplasmSettore BIO/14 - FarmacologiaCancer researchbiology.proteinK562 CellsK562 cells
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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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Biochemical and chemical characterization of Cynara cardunculus L. extract and its potential use as co-adjuvant therapy of chronic myeloid leukemia

2017

Abstract Ethnopharmacological relevance Ancient mediterranean diet was characterized by consuming the spontaneous forms of Cynara cardunculus L. (CCL), commonly called artichoke. Cultivated and/or spontaneous forms of CC studies have demonstrated that methanol extract of CCL flower and/or cynaropicrin showed remarkable anti-proliferative activity in vitro models of leukocyte cancer cell. Aim of the study Chronic myeloid leukemia (CML) is associated with a reciprocal translocation of the long arms of chromosomes 9 and 22 generating the BCR/ABL fusion gene, translated in the p210 BCR/ABL oncoprotein kinase. This chimeric protein is the target of a kinase inhibitor, imatinib, but the developme…

Cynara cardunculus L.Sesquiterpene0301 basic medicineSettore MED/06 - Oncologia MedicaFusion Proteins bcr-ablPharmacologyAntineoplastic AgentLactoneschemistry.chemical_compound0302 clinical medicinehemic and lymphatic diseasesDrug DiscoveryK562 cellABLChemistryChronic myeloid leukemiabreakpoint cluster regionMyeloid leukemiaLactoneCynaropicrinImatinib resistantChemotherapy Adjuvant030220 oncology & carcinogenesisImatinib MesylateChronic myeloid leukemia; Cynara cardunculus L.; Imatinib resistant; K562 cells; P210BCR/ABLoncoprotein; Antineoplastic Agents; Antineoplastic Agents Phytogenic; Cell Survival; Chemotherapy Adjuvant; Cynara; Drug Resistance Neoplasm; Fusion Proteins bcr-abl; Humans; Imatinib Mesylate; K562 Cells; Lactones; Leukemia Myelogenous Chronic BCR-ABL Positive; Plant Extracts; Sesquiterpenes; Pharmacology; Drug Discovery3003 Pharmaceutical ScienceSesquiterpenesHumanmedicine.drugCell SurvivalAntineoplastic AgentsCynaraPlant Extract03 medical and health sciencesLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansViability assayneoplasmsPharmacologyPlant ExtractsCell growthDrug Discovery3003 Pharmaceutical ScienceImatinibAntineoplastic Agents PhytogenicP210BCR/ABLoncoprotein030104 developmental biologyDrug Resistance NeoplasmCancer researchK562 CellsK562 cellsJournal of Ethnopharmacology
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Intracellular retention of ABL kinase inhibitors determines commitment to apoptosis in CML cells

2012

PLoS one 7(7), e40853 (2012). doi:10.1371/journal.pone.0040853

Drugs and DevicesDrug Research and DevelopmentTime Factorsmedicine.drug_classChronic Myeloid LeukemiaIntracellular Spacelcsh:MedicineApoptosisPharmacologyPiperazinesTyrosine-kinase inhibitorHematologic Cancers and Related DisordersCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesLeukemiasmedicineHumansAnnexin A5Proto-Oncogene Proteins c-abllcsh:ScienceProtein Kinase InhibitorsMyeloproliferative DisordersMultidisciplinaryABLDose-Response Relationship DrugCaspase 3Chemistrylcsh:RBiological activityImatinibHematologyrespiratory tract diseasesDasatinibKineticsPyrimidinesImatinib mesylatePharmacodynamicsBenzamidesImatinib MesylateMedicineATP-Binding Cassette Transporterslcsh:QDrug Screening Assays AntitumorSignal transductionIntracellularResearch ArticleSignal Transductionmedicine.drug
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Exosomes released by k562 chronic myeloid leukemia cells promote endothelial cell tubular differentiation through uptake and cell-to-cell transfer

2012

Exosomes, microvesicles of endocytic origin released by normal and tumor cells, play an important role in cell-to-cell ommunication. Angiogenesis has been shown to regulate progression of chronic myeloid leukemia (CML). The mechanism through which this happens has not been elucidated. We isolated and characterized exosomes from K562 CML cells and evaluated their effects on human umbilical endothelial cells (HUVECs). Fluorescent-labeled exosomes were nternalized by HUVECs during tubular differentiation on Matrigel. Exosome localization was perinuclear early in differentiation, moving peripherally in cells undergoing elongation and connection. Exosomes move within and between nanotubular stru…

Exosomes Nanotubes Chronic myeloid leukemia Endothelial cells Tyrosine kinase inhibitors
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