Search results for "IMATINIB"

showing 10 items of 108 documents

Galangin increases the cytotoxic activity of imatinib mesylate in imatinib-sensitive and imatinib-resistant Bcr-Abl expressing leukemia cells

2008

Resistance to imatinib mesylate is an emergent problem in the treatment of Bcr-Abl expressing myelogenous leukemias and additional therapeutic strategies are required. We observed that galangin, a non-toxic, naturally occurring flavonoid was effective as anti-proliferative, and apoptotic agent in Bcr-Abl expressing K562 and KCL22 cells and in imatinib mesylate resistant K562-R and KCL22-R cells. Galangin induced an arrest of cells in G0–G1phase of cell cycle and a decrease in pRb, cdk4, cdk1, cycline B levels; moreover, it was able to induce a monocytic differentiation of leukemic Bcr-Abl+ cells. Of note, galangin caused a decrease in Bcl-2 levels and markedly increased the apoptotic activi…

Cancer ResearchSettore MED/17 - Malattie InfettiveSettore MED/06 - Oncologia MedicaApoptosisPharmacologyResting Phase Cell CyclePiperazineschemistry.chemical_compoundCell Line TumorLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansCytotoxic T cellChrysinneoplasmsFlavonoidsLeukemiaG1 PhaseApoptosiCell DifferentiationImatinibmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaGalanginLeukemiaPyrimidinesImatinib mesylateOncologychemistryDrug Resistance NeoplasmImatinibBenzamidesSettore BIO/14 - FarmacologiaImatinib MesylateK562 CellsFisetinBcr-AblK562 cellsmedicine.drugCancer Letters
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Role of adjuvant imatinib dose in radically resected GIST harboring KIT exon 9 mutations

2020

11533 Background: Gastrointestinal stromal tumors (GIST) with a driver mutation in KIT exon 9 (Ex9) represent about 10% of all newly diagnosed cases. In the metastatic setting, Ex9-mutated GIST patients benefit from higher doses of imatinib (800 mg/day vs standard 400 mg/day). The additional therapeutic benefit from a higher dose of imatinib in the adjuvant setting in this molecular subgroup has not been confirmed. Methods: We retrospectively identified 105 patients (pts) with resected Ex9-mutated GIST treated with adjuvant imatinib (800 mg/day or 400 mg/day) in 15 different European centers. Disease-Free Survival (DFS) and Imatinib Failure-Free Survival (IFFS) were calculated and analyzed…

Cancer ResearchStromal cellGiSTbusiness.industrymedicine.medical_treatmentMedizinImatinibNewly diagnosed3. Good health03 medical and health sciencesExon0302 clinical medicineOncology030220 oncology & carcinogenesisMutation (genetic algorithm)medicineCancer research10. No inequalitybusinessAdjuvant030215 immunologymedicine.drug
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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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Efficacy and safety of bosutinib (BOS) for Philadelphia chromosome–positive (Ph+) leukemia in older versus younger patients (pts).

2012

6511 Background: BOS is an oral dual Src/Abl kinase inhibitor with potent activity in Ph+ leukemia. Methods: Efficacy and safety of BOS 500 mg/d was evaluated in older (≥65 y; n = 119) and younger (<65 y; n = 451) pts in 3 cohorts: chronic phase chronic myeloid leukemia (CP CML) after imatinib (IM; CP2L cohort; n = 287); CP CML after IM + dasatinib (DAS) and/or nilotinib (NIL; CP3L cohort; n = 119); and accelerated/blast phase (AP/BP) CML or acute lymphoblastic leukemia after IM ± DAS and/or NIL (ADV cohort; n = 164). Results: Baseline events (≥65 y vs <65 y) included respiratory disorders (35% vs 13%), cardiac disorders (29% vs 9%), and diabetes (4% vs 4%). Median baseline medicatio…

Cancer Researchmedicine.medical_specialtyPediatricsPhiladelphia Chromosome Positivebusiness.industryImatinibmedicine.diseaseGastroenterologyDasatinibLeukemiaOncologyNilotinibhemic and lymphatic diseasesInternal medicineCohortmedicineAdverse effectbusinessBosutinibmedicine.drugJournal of Clinical Oncology
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Hyaluronic acid based nanohydrogels fabricated by microfluidics for the potential targeted release of Imatinib: Characterization and preliminary eval…

2019

Abstract Microfluidics is emerging as an innovative technique for the “on chip” fabrication of nanoparticles for drug delivery applications. Here, by using an amphiphilic derivative of hyaluronic acid as a starting macromolecule, nanohydrogels loaded with Imatinib were produced by the microfluidic procedure in order to develop an innovative therapeutic tool for the treatment of retinal neovascularization. Both cyRGDC functionalized and non-functionalized nanohydrogels were designed and fabricated by using the same technique. The targeting efficiency of the obtained nanosystems was studied in vitro on human retinal pigment epithelial cells (HRPEpiC) and human umbilical vein endothelial cells…

Cell SurvivalDrug CompoundingHyaluronic acidMicrofluidicsMicrofluidicsPharmaceutical ScienceAngiogenesis Inhibitors02 engineering and technologyRetinal Pigment Epithelium030226 pharmacology & pharmacyTHERAPYUmbilical veinANGIOGENESISNeovascularization03 medical and health scienceschemistry.chemical_compoundNanoparticle0302 clinical medicineLab-On-A-Chip DevicesAmphiphileHyaluronic acidmedicineHuman Umbilical Vein Endothelial CellsHumansPEPTIDEDRUG-DELIVERYNeovascularizationDrug CarriersChemistryImatinibHydrogels021001 nanoscience & nanotechnologyRANIBIZUMABVEGFIn vitroChoroidal NeovascularizationNanostructuresINTEGRINSMicrofluidicDrug deliveryImatinibImatinib MesylateFeasibility StudiesNanoparticlesmedicine.symptomTargeted delivery0210 nano-technologyBiomedical engineeringmedicine.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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Drug-related cardiotoxicity for the treatment of haematological malignancies in elderly.

2010

Several publications have focused on the cardiotoxicity of specific classes of haematological therapeutic agents such as antracyclines and cyclofosfamide. Cardiotoxicity of cancer chemotherapeutics is a problem for patients of all ages, but it increases with age. Toxicity can also be developed months after the last chemotherapy dose, and late reactions can be seen years later when they present new-onset cardiomyopathy. No data are available about the cardiotoxicity of non-chemotherapy agents currently used as preferred therapy for haematological malignancy in elderly. In this review we have provided a summary of the cardiovascular toxic effects produced by different drugs and therapeutic ag…

Drugmedicine.medical_specialtyHeart diseaseHeart Diseasesmedicine.medical_treatmentmedia_common.quotation_subjectCardiomyopathyAntineoplastic AgentsPharmacologyCardiotoxinsDrug Delivery SystemsDrug DiscoverymedicineAnimalsHumansIntensive care medicinedrug cardiotoxicity haematological malignanciesmedia_commonAgedPharmacologyCardiotoxicityChemotherapybusiness.industryAge FactorsCancerImatinibmedicine.diseaseHematologic NeoplasmsRituximabbusinessmedicine.drugCurrent pharmaceutical design
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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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Gene Signatures in Gastrointestinal Stromal Tumors

2011

Gastrointestinal stromal tumors (GISTs) constitute a rare heterogeneous group of the most common mesenchymal neoplasm of gastrointestinal tract (GI). GISTs have emerged during the recent years as a distinct sarcoma entity due to advances in the understanding of molecular mechanism of their pathogenesis. They are believed to originate from precursors shared with interstitial cells of Cajal (ICC) – the pacemaker cells of the gut (for which CD117 antigen is the immunohistochemical marker), and they may arise along all GI (most commonly in the stomach or the small bowel) or rarely elsewhere. Their biological behavior is difficult to predict, ranging from clinically benign to malignant. The trea…

Gastrointestinal tractPathologymedicine.medical_specialtyStromal cellGiSTbiologyCD117business.industrymedicine.diseasePrimary tumordigestive system diseasesInterstitial cell of Cajalsymbols.namesakeImatinib mesylatemedicinesymbolsbiology.proteinSarcomabusinessneoplasms
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Predictive Factors of Response to Sunitinib in Imatinib-Resistant Gastrointestinal Stromal Tumors (GISTs): A Multi-Institutional Study

2019

Imatinib 400 mg is the standard of care for medical treatment of advanced GISTs. In the majority of cases, however, GISTs eventually develop resistance to imatinib. The optimal second line treatment has not been established yet and imatinib dose escalation (800 mg) or sunitinib represent two feasible options. The objective of this retrospective, multi-institutional, study is to analyze the validity of several parameters as possible predictive factors of response to sunitinib after imatinib failure. We reviewed 128 metastatic GISTs treated with sunitinib between January 2007 to June 2017. Primary tumour site, metastatic site, c-KIT/PDGFR-α mutational status, PET-FDG status and type…

GiSTSunitinibbusiness.industryImatinibmedicine.diseaseurologic and male genital diseasesImatinib resistantdigestive system diseasesfemale genital diseases and pregnancy complicationsmedicineCancer researchGastrointestinal stromal tumors (GISTs)businessneoplasmsmedicine.drugoncology_oncogenics
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