Search results for "Camptothecin"

showing 10 items of 93 documents

Utilizing inherent fluorescence of therapeutics to analyze real-time uptake and multi-parametric effector kinetics.

2011

Abstract The precise detection of pharmaceutical drug uptake and knowledge of a drug’s efficacy at the single-cell level is crucial for understanding a compound’s performance. Many pharmaceutical drugs, like the model substances Doxorubicin, Mitoxantrone or Irinotecan, have a distinctive natural fluorescence that can be readily exploited for research purposes. Utilizing this respective natural fluorescence, we propose a method analyzing simultaneously in real-time the efficiency, effects and the associated kinetics of compound-uptake and efflux in mammalian cells by flow cytometry. We show that real-time flow cytometric quantification of compound-uptake is reliably measured and that analyzi…

DrugPharmaceutical drugCell Survivalmedia_common.quotation_subjectmedicine.medical_treatmentKineticsAntineoplastic AgentsComputational biologyBiologyPharmacologyIrinotecanGeneral Biochemistry Genetics and Molecular BiologyFluorescenceFlow cytometryCell Line TumormedicineHumansMolecular Biologymedia_commonmedicine.diagnostic_testEffectorBiological TransportFlow CytometryFluoresceinsFluorescenceDrug Resistance MultipleMultiple drug resistanceKineticsDoxorubicinDrug Resistance NeoplasmCamptothecinEffluxMitoxantroneSingle-Cell AnalysisReactive Oxygen SpeciesMethods (San Diego, Calif.)
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Selected Secondary Plant Metabolites for Cancer Therapy

2015

Secondary plant metabolites reveal numerous biological activities making them attractive as resource for drug development of human diseases. As the majority of cancer drugs clinically established during the past half century is derived from nature, cancer researchers worldwide try to identify novel natural products as lead compounds for cancer therapy. Natural products are considered as promising cancer therapeutics, either as single agents or in combination protocols, to enhance the antitumor activity of additional therapeutic modalities. Most natural compounds exert pleotrophic effects and modulate various signal transduction pathways. A better understanding of the complex mechanisms of a…

Drugmedia_common.quotation_subjectPhytochemicalsApoptosisDrug developmentResveratrolBiologyPharmacologychemistry.chemical_compoundBetulinic acidmedicineddc:610media_commonlcsh:R5-920Epidermal growth factor receptorCancerBioactivity-guided fractionationmedicine.diseaseSmall moleculeTargeted tumor therapyComplementary and alternative medicinechemistryDrug developmentDrug resistanceCancer celllcsh:Medicine (General)Camptothecinmedicine.drugWorld Journal of Traditional Chinese Medicine
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The CD95/CD95 ligand system is not the major effector in anticancer drug-mediated apoptosis.

1998

Many anticancer drugs are able to induce apoptosis in tumor cells but the mechanisms underlying this phenomenon are poorly understood. Some authors reported that the p53 tumor suppressor gene may be responsible for drug-induced apoptosis; however, chemotherapy-induced apoptosis can also be observed in p53 negative cells. Recently, doxorubicin (DXR) was reported to induce CD95L expression to mediate apoptosis through the CD95/CD95L system. Thus, an impairment of such a system may be involved in drug resistance. We evaluated the in vitro antitumor activity of several cytotoxic drugs on two human p53-negative T-cell lymphoma cell lines, the HUT78-B1 CD95L-resistant cell line and the HUT78 pare…

Fas Ligand ProteinCaspase 3Antineoplastic AgentsApoptosismedicineTumor Cells CulturedCytotoxic T cellHumansfas ReceptorCytotoxicityMolecular BiologyEtoposideEtoposideMembrane GlycoproteinsChemistryCaspase 3Cell BiologyFas receptorCaspase InhibitorsProto-Oncogene Proteins c-bcl-2Cell cultureApoptosisDoxorubicinCaspasesCancer researchTumor Suppressor Protein p53Camptothecinmedicine.drugCell death and differentiation
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Enzyme-responsive silica mesoporous supports capped with azopyridinium salts for controlled delivery applications

2012

11 páginas, 7 figuras, 3 tablas y 2 esquemas

INGENIERIA DE LA CONSTRUCCIONCell SurvivalPyridinesmedia_common.quotation_subjectenzymesNanoparticleNanotechnologyPyridinium Compoundsmesoporous materialsCatalysisgated materialsHeLachemistry.chemical_compoundQUIMICA ORGANICAQUIMICA ANALITICAmedicineRhodamine BHumansGated materialsInternalizationAzopyridinium derivativemedia_commonbiologyChemistryRhodaminesOrganic ChemistryQUIMICA INORGANICAGeneral Chemistrybiology.organism_classificationSilicon DioxideCombinatorial chemistryMesoporous materialsEnzymesazopyridinium derivativeDrug deliveryDrug deliveryMCF-7 CellsNanoparticlesnanoparticlesMesoporous materialOxidoreductasesAzo CompoundsPorosityCamptothecinIntracellularmedicine.drugHeLa Cells
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Amidase-responsive controlled release of antitumoral drug into intracellular media using gluconamide-capped mesoporous silica nanoparticles

2012

MCM-41 silica nanoparticles were used as inorganic scaffolding to prepare a nanoscopic-capped hybrid material S1, which was able to release an entrapped cargo in the presence of certain enzymes, whereas in the absence of enzymes, a zero release system was obtained. S1 was prepared by loading nanoparticles with Safranine O dye and was then capped with a gluconamide derivative. In the absence of enzymes, the release of the dye from the aqueous suspensions of S1 was inhibited as a result of the steric hindrance imposed by the bulky gluconamide derivative, the polymerized gluconamide layer and the formation of a dense hydrogen-bonded network around the pore outlets. Upon the addition of amidase…

INGENIERIA DE LA CONSTRUCCIONMaterials scienceCell SurvivalNanoparticleAntineoplastic AgentsElectron Microscopy Service of the UPVGluconatesAmidaseAmidohydrolasesHydrolysisQUIMICA ORGANICAEnzymatic hydrolysisPeptide bondOrganic chemistryHumansGeneral Materials ScienceDrug effectsMicroscopy ConfocalQUIMICA INORGANICAHydrogen BondingMesoporous silicaSilicon DioxideControlled releaseCombinatorial chemistryMCF-7 CellsNanoparticlesCamptothecinHybrid materialLysosomesPorosityHeLa Cells
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[Apoptosis of human leukemic cells induced by topoisomerase I and II inhibitors].

1996

International audience; Comparison between five human leukemic lines (BV173, HL60, U937, K562, KCL22) suggest that the main determinant of their sensitivity to topoisomerase I (camptothecin) and II (VP-16) inhibitors is their ability to regulate cell cycle progression in response to specific DNA damage, then to die through apoptosis: the more the cells inhibit cell cycle progression, the less sensitive they are. The final pathway of apoptosis induction involves a cytoplasmic signal, active at neutral pH, needing magnesium, sensitive to various protease inhibitors and activated directly by staurosporine. Modulators of intracellular signaling (calcium chelators, calmodulin inhibitors, PKC mod…

Leukemia[SDV]Life Sciences [q-bio]Cell CycleApoptosisCell DifferentiationDNA Neoplasm[SDV.BC]Life Sciences [q-bio]/Cellular BiologyStaurosporine[SDV] Life Sciences [q-bio]AlkaloidsDNA Topoisomerases Type IIDNA Topoisomerases Type ITumor Cells CulturedHumansTopoisomerase II InhibitorsCamptothecinTopoisomerase I Inhibitors[SDV.BC] Life Sciences [q-bio]/Cellular BiologyProtein Kinase CEtoposideSignal Transduction
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TNF-alpha gene promoter polymorphisms and risk of venous thromboembolism in gastrointestinal cancer patients undergoing chemotherapy

2013

Abstract Background TNF-α has been proposed as a predictive factor for venous thromboembolism (VTE). Genetic polymorphisms could regulate TNF-α production. However, the relationship between TNFA gene variants and VTE is not clarified. This study aims to investigate the predictive role of five different TNFA gene promoter SNPs, or their haplotype combination(s), for a first VTE episode in gastrointestinal cancer out-patients treated with chemotherapy. Patients and methods Serum TNF-α levels and TNFA -863C/A, -857C/T, -376G/A, -308G/A and -238G/A gene promoter polymorphisms were retrospectively evaluated in 314 subjects, including 157 controls and 157 Caucasian patients with histologically di…

MaleAntimetabolitesSettore MED/06 - Oncologia Medicamedicine.medical_treatmentchemotherapyGastroenterologysingle nucleotide polymorphismschemotherapy; gastrointestinal cancer; single nucleotide polymorphisms; tumour necrosis factor-α; venous thromboembolismsingle nucleotide polymorphismPhytogenic80 and overtumour necrosis factor-αPromoter Regions GeneticGastrointestinal NeoplasmsAged 80 and overHazard ratioSingle NucleotideHematologyMiddle AgedAntineoplasticChemotherapy regimenOncologyFemaleFluorouracilmedicine.drugAdultRiskAntimetabolites Antineoplasticmedicine.medical_specialtygastrointestinal cancervenous thromboembolismAntineoplastic AgentsSingle-nucleotide polymorphismIrinotecanPolymorphism Single NucleotidePromoter RegionsGeneticInternal medicinemedicineHumansGenetic Predisposition to DiseaseGastrointestinal cancercardiovascular diseasesPolymorphismRetrospective StudiesAgedChemotherapyTumor Necrosis Factor-alphabusiness.industryHaplotypeOdds ratiomedicine.diseaseAntineoplastic Agents PhytogenicIrinotecanHaplotypesCase-Control StudiesImmunologyCamptothecinHuman medicinePolymorphism Single Nucleotide; Antimetabolites Antineoplastic; single nucleotide polymorphisms; Humans; Retrospective Studies; Aged; Promoter Regions Genetic; Haplotypes; Aged 80 and over; Adult; gastrointestinal cancer; Genetic Predisposition to Disease; Male; tumour necrosis factor-α; Tumor Necrosis Factor-alpha; Venous Thromboembolism; Camptothecin; chemotherapy; Risk; Fluorouracil; Case-Control Studies; Gastrointestinal Neoplasms; Middle Aged; venous thromboembolism; Antineoplastic Agents Phytogenic; Femalebusiness
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Phase I study of FOLFIRI plus pimasertib as second-line treatment for KRAS-mutated metastatic colorectal cancer

2015

BACKGROUND: The mitogen-activated protein kinase (MAPK) pathway has been implicated in the molecular pathogenesis of human cancers, including metastatic colorectal cancer (mCRC). This provides a rationale for the development of MAPK-targeted agents such as pimasertib. METHODS: Patients with KRAS mutant mCRC were treated in the second-line setting with FOLFIRI (5-fluorouracil/folinic acid/irinotecan) plus pimasertib. The primary objective of the safety run-in phase was to determine the maximum-tolerated dose (MTD) and the recommended phase II dose of pimasertib combined with FOLFIRI. RESULTS: Sixteen patients were enrolled in the trial. Ten and six patients were treated daily with 45 and 60 …

MaleCancer ResearchColorectal cancermedicine.medical_treatmentLeucovorinColorectal NeoplasmPharmacologymedicine.disease_causepimasertibcombination therapyAntineoplastic Combined Chemotherapy ProtocolsNeoplasm Metastasiscombination therapy second-line treatmentAged 80 and overProto-Oncogene ProteinCetuximabKRAS-mutated metastatic colorectal cancerMedicine (all)MEK inhibitorMiddle AgedNeoplasm MetastasiTreatment OutcomeOncologyFluorouracilFOLFIRISecond-line treatmentFemaleFluorouracilKRASColorectal NeoplasmsPimasertibHumanmedicine.drugNiacinamideProto-Oncogene Proteins p21(ras)FOLFIRIProto-Oncogene ProteinsmedicineHumansCombination therapyneoplasmsAgedChemotherapyMEK inhibitorAntineoplastic Combined Chemotherapy Protocolbusiness.industryKRAS -mutated metastatic colorectal cancerGenes raras Proteinmedicine.diseasedigestive system diseasesGenes rassecond-line treatmentMutationras ProteinsClinical StudyCancer researchCamptothecinHuman medicinebusinessCamptothecinThe British journal of cancer
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Immune-modulating effects of the newest cetuximab-based chemoimmunotherapy regimen in advanced colorectal cancer patients.

2012

Cetuximab is a human-murine chimeric monoclonal antibody to the epidermal growth factor receptor, active for advanced colorectal cancer treatment in combination with chemotherapy. Cetuximab mainly acts by inhibiting epidermal growth factor receptor-mediated pathways in cancer cells; however, in the human host, its IgG1 backbone may offer additional antitumor activity that includes FcγRs-mediated antibody-dependent cell cytotoxicity, phagocytosis, cross priming, and tumor-specific T-cell-mediated immune response. These mechanisms are still under active investigation. At this purpose, we have performed an immunologic investigation in advanced colon cancer patients enrolled in an ongoing phase…

MaleCancer Researchmedicine.medical_treatmentCetuximabPharmacologyDeoxycytidineAldesleukinT-Lymphocyte SubsetsImmunology and AllergyCytotoxic T cellEpidermal growth factor receptorChemoimmunotherapybiologyCetuximabAntibodies MonoclonalMiddle AgedRecombinant ProteinsAdvanced Colorectal CancerErbB ReceptorsKiller Cells NaturalFemaleFluorouracilImmunotherapyAntibodyColorectal NeoplasmsImmune-modulating Effectmedicine.drugImmunologyAntineoplastic AgentsAntibodies Monoclonal HumanizedIrinotecanDrug Administration ScheduleImmunomodulationImmune systemCell Line TumormedicineHumansPharmacologyEpidermal growth factor receptorPolychemotherapybusiness.industryImmunotherapyDendritic CellsColorectal cancerGemcitabineCase-Control StudiesCancer cellbiology.proteinInterleukin-2CamptothecinbusinessJournal of immunotherapy (Hagerstown, Md. : 1997)
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IL-4 protects tumor cells from anti-CD95 and chemotherapeutic agents via up-regulation of antiapoptotic proteins

2004

Abstract We recently proposed that Th1 and Th2 cytokines exert opposite effects on the pathogenesis and clinical outcome of organ-specific autoimmunity by altering the expression of genes involved in target cell survival. Because a Th2 response against tumors is associated with poor prognosis, we investigated the ability of IL-4 to protect tumor cells from death receptor- and chemotherapy-induced apoptosis. We found that IL-4 treatment significantly reduced CD95 (Fas/APO-1)- and chemotherapeutic drug-induced apoptosis in prostate, breast, and bladder tumor cell lines. Analysis of antiapoptotic protein expression revealed that IL-4 stimulation resulted in up-regulation of cellular (c) FLIP/F…

MaleINFILTRATING LYMPHOCYTESCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsCARCINOMA-CELLSBiologySIGNALING PATHWAYSDownregulation and upregulationCell Line TumorImmunology and AllergyHumansfas ReceptorNON-HODGKINS-LYMPHOMACANCER PATIENTSReceptorBCL-2 PROTEINInterleukin 4EtoposideIL-4 apoptosis cancer stem cellsSettore MED/04 - Patologia GeneraleCHRONIC LYMPHOCYTIC-LEUKEMIAIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalProstatic NeoplasmsFas receptorRecombinant ProteinsCell biologyUp-RegulationProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureFlipCancer researchT-CELLSCamptothecinFemaleInterleukin-4FLICE-INHIBITORY PROTEINSignal transductionCarrier ProteinsRENAL-CELL
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