Search results for "Neoplastic"

showing 10 items of 2901 documents

Although rare, severe complications following intravesical bacillus Calmette-Guerin treatment should not be overlooked!

2015

An interesting series of 22 patients affected by severe systemic toxicity following bacillus Calmette-Guerin (BCG) intravesical adjuvant therapy for bladder cancer is presented in this issue of Inf...

Microbiology (medical)Malemedicine.medical_specialtyAntineoplastic AgentsGastroenterologySettore MED/24 - UrologiaInternal medicineparasitic diseasesmedicineAdjuvant therapyIntravesical bacillus Calmette-GuerinAnimalsHumansBacillus (shape)Mycobacterium bovisBladder cancerGeneral Immunology and Microbiologybiologybusiness.industryGeneral Medicinebiology.organism_classificationmedicine.diseaseMycobacterium bovisbladder cancer BCG toxicityInfectious DiseasesSystemic toxicityUrinary Bladder NeoplasmsBCG VaccinebusinessBCG vaccineInfectious diseases (London, England)
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Chemoembolization for hepatocellular carcinoma : optimization of the procedure

2011

With 700,000 deaths in 2008, hepatocellular carcinoma is the 3rd most common cause of cancer-related death worldwide. Transarterial chemoembolization is the standard treatment for intermediate-stage hepatocellular carcinoma. This intraarterial treatment is performed by injecting an anticancer drug carried by ethiodized oil or by drug-eluting beads and followed by the occlusion of the artery when ethiodized oil is used. Median survival of patients remains < 2 years, and there is no consensus about the optimal treatment regimen. The aim of our work was to improve the efficacy of transarterial chemoembolization in optimizing the anticancer drug and its carrier.We have demonstrated that idarubi…

Microsphères d’embolisation[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyEthiodized oilLipiodolAgent anticancéreuxHepatocellular carcinoma[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyAntineoplastic agentsChimioembolisationChemoembolizationCarcinome hépatocellulaire
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Pursaethosides A-E, triterpene saponins from Entada pursaetha.

2005

Five new triterpenoid saponins, pursaethosides A-E (1-5), were isolated from the n-BuOH extract of the seed kernels of Entada pursaetha along with the known phaseoloidin. The structures of 1-5 were elucidated mainly by spectroscopic data interpretation and chemical degradation. Pursaethosides C-E (3-5) possess as a common structural feature entagenic acid as aglycon, which is rare among triterpene saponins. Compounds 2-4 and phaesolidin were found to be not cytotoxic when tested against HCT 116 and HT-29 human colon cancer cells.

MimosaSaponinPharmaceutical SciencePharmacognosyEntada pursaethaAnalytical ChemistryTriterpenoidTriterpeneDrug DiscoveryTumor Cells CulturedHumansCameroonNuclear Magnetic Resonance BiomolecularPharmacologychemistry.chemical_classificationPlants MedicinalMolecular StructureOrganic ChemistryGlycosideSaponinsAntineoplastic Agents PhytogenicTerpenoidTriterpenesHuman colon cancerComplementary and alternative medicinechemistryBiochemistryMolecular MedicineDrug Screening Assays AntitumorJournal of natural products
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Deregulated repression of c-Jun provides a potential link to its role in tumorigenesis.

2004

The transcription factor c-Jun cooperates with oncogenic alleles of ras in malignant transformation. Constitutively active Ras causes, via activation of mitogen activated protein kinases, phosphorylation of c-Jun which is essential for subsequent target gene activation and tumorigenesis. Studying the mechanisms controlling c-Jun activity we found that its transcription activation function is actively repressed by a presumably multimeric repressor complex that includes histone deacetylase 3 as a critical subunit. Suppression of c-Jun is relieved by MAP kinase-mediated phosphorylation and/or titration of inhibitor components. The viral tumorigenic counterpart of c-Jun, v-Jun, escapes this inh…

Mitogen-Activated Protein Kinase KinasesTranscriptional ActivationKinaseProtein subunitc-junCell CycleRepressorCell BiologyBiologyHDAC3Histone DeacetylasesMalignant transformationEnzyme ActivationRepressor ProteinsCell Transformation NeoplasticGenes junCancer researchras ProteinsPhosphorylationAnimalsHumansPhosphorylationMolecular BiologyTranscription factorDevelopmental Biology
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Synthesis, cytotoxicity, and inhibitory effects on tubulin polymerization of a new 3-heterocyclo substituted 2-styrylquinazolinones

2004

In order to study the influence of 3-substitution on the cytotoxic activity of 2-styrylquinazolinones, new 6-chloro-2-styryl-3-(heteroaryl)-4(3H)-quinazolinones were synthesized by refluxing equimolar amounts of 6-chloro-2-methyl-3-(heteroaryl)-4(3H)-quinazolinones and benzaldehyde in glacial acetic acid. At 1 microg ml(-1) concentration, almost all 2-styrylquinazolinones showed some cytotoxic activity against the L1210 and K562 leukemia cell lines. However, only 6-chloro-2-styryl-3-(pyrimidin-2yl)-4(3H)-quinazolinone inhibited the growth of these cells by over 50%. This last compound was also the only member of the series that inhibited tubulin polymerization, with an IC(50) value of 5.8 v…

Mitotic indexCell SurvivalPolymersAntineoplastic AgentsSettore BIO/19 - Microbiologia GeneraleMicrotubuleschemistry.chemical_compoundAcetic acidHeterocyclic CompoundsTubulinMicrotubuleDrug DiscoveryTumor Cells CulturedmedicineColchicineAnimalsHumansCytotoxic T cellCytotoxicityPharmacologyMolecular StructureChemistryTubulin ModulatorsOrganic ChemistryBiological activityGeneral MedicineMolecular biologySettore CHIM/08 - Chimica FarmaceuticaTubulin ModulatorsRatsMechanism of actionBiochemistryCell cultureQuinazolinesDrug Screening Assays Antitumormedicine.symptomK562 cells2-Styrylquinazolinones Antimitotic agents Cytotoxic activity MicrotubulesEuropean Journal of Medicinal Chemistry
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Isoindolo[2,1-a]quinoxaline derivatives, novel potent antitumor agents with dual inhibition of tubulin polymerization and topoisomerase I.

2008

Isoindoloquinoxalines 4 and 5 were obtained by refluxing 2-(2'-aminoaryl)-1-cyanoisoindoles 3a- e in acetic or formic acid. All derivatives were screened by the National Cancer Institute (Bethesda, MD) for the in vitro one dose primary anticancer assay against a 3-cell line panel. Compounds 4a- e, screened against a panel of about 60 human tumor cell lines, showed remarkable antineoplastic activity; they had GI 50 values in the low micromolar or submicromolar range and reached, in the case of 4c, nanomolar concentrations on 88% of the 59 tested cell lines. Flow cytometric analysis of cell cycle after treatment with 4c demonstrated an arrest of the cell cycle in G2/M phase. This effect was a…

Mitotic indexMagnetic Resonance SpectroscopySpectrophotometry InfraredPolymersFLUORESCENT-PROBELIGAND-DNA SYSTEMSMitosisCELL-LINESAntineoplastic AgentsACRIDINE-ORANGETopoisomerase-I InhibitorMITOCHONDRIATubulinCell Line TumorQuinoxalinesDrug DiscoveryHumansCytotoxicitybiologyChemistryTopoisomeraseB-DNACell CycleCell cycleAPOPTOSISCDEnzyme ActivationMICROTUBULESBiochemistryMicroscopy FluorescenceCell cultureApoptosisEnzyme inhibitorLINEAR DICHROISM SPECTROSCOPYCaspasesbiology.proteinMolecular MedicineDrug Screening Assays AntitumorTopoisomerase I InhibitorsReactive Oxygen SpeciesJournal of medicinal chemistry
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Steroidal glycosides from Ornithogalum dubium Houtt

2018

The phytochemical study of Ornithogalum dubium Houtt. (Asparagaceae) led to the isolation of five undescribed steroidal glycosides together with two known ones. Their structures were established by using NMR analysis and mass spectrometry as (25R)-3β-hydroxyspirost-5-en-1β-yl O-α-L-arabinopyranosyl-(1 → 2)-α-L-rhamnopyranoside, (25S)-3β-hydroxyspirost-5-en-1β-yl O-β-D-glucopyranosyl-(1 → 6)-β-D-glucopyranoside, (22S)-16β-[(α-L-rhamnopyranosyl)oxy]-22-hydroxycholest-5-en-3β-yl O-β-D-glucopyranosyl-(1 → 4)-β-D-glucopyranoside, (22S,23S)-1β,3β,11α,16β,23-pentahydroxy-5α-cholest-24-en-22β-yl β-D-glucopyranoside, (22S,23S)-3β-[(β-D-glucopyranosyl)oxy]-22,23-dihydroxy-5α-cholest-24-en-16β-yl O-α-…

Models Molecular0106 biological sciencesSteroidal glycosidesStereochemistryAntineoplastic AgentsHL-60 CellsPlant ScienceHorticulture01 natural sciencesBiochemistryAsparagaceaeCarbohydrate ConformationmedicineHumansCytotoxic T cellGlycosidesCytotoxicityMolecular BiologyCisplatinOrnithogalum dubiumbiology010405 organic chemistryChemistryGeneral Medicinebiology.organism_classificationmedicine.disease0104 chemical sciencesLeukemiaPhytochemicalA549 CellsOrnithogalumSteroids010606 plant biology & botanymedicine.drugPhytochemistry
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Modulation of P-glycoprotein activity by novel synthetic curcumin derivatives in sensitive and multidrug-resistant T-cell acute lymphoblastic leukemi…

2016

Abstract Background Multidrug resistance (MDR) and drug transporter P-glycoprotein (P-gp) represent major obstacles in cancer chemotherapy. We investigated 19 synthetic curcumin derivatives in drug-sensitive acute lymphoblastic CCRF–CEM leukemia cells and their multidrug-resistant P-gp-overexpressing subline, CEM/ADR5000. Material and methods Cytotoxicity was tested by resazurin assays. Doxorubicin uptake was assessed by flow cytometry. Binding modes of compounds to P-gp were analyzed by molecular docking. Chemical features responsible for bioactivity were studied by quantitative structure activity relationship (QSAR) analyses. A 7-descriptor QSAR model was correlated with doxorubicin uptak…

Models Molecular0301 basic medicineCurcuminCell SurvivalT cellQuantitative Structure-Activity RelationshipAntineoplastic AgentsPharmacologyPrecursor T-Cell Lymphoblastic Leukemia-LymphomaToxicologyFlow cytometry03 medical and health sciences0302 clinical medicineCell Line TumormedicineHumansDoxorubicinATP Binding Cassette Transporter Subfamily B Member 1CytotoxicityP-glycoproteinPharmacologybiologymedicine.diagnostic_testChemistrymedicine.diseaseDrug Resistance MultipleMultiple drug resistanceLeukemia030104 developmental biologymedicine.anatomical_structureDoxorubicinDrug Resistance NeoplasmCell culture030220 oncology & carcinogenesisbiology.proteinmedicine.drugToxicology and Applied Pharmacology
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Synthesis, Structural Elucidation, and Biological Evaluation of NSC12, an Orally Available Fibroblast Growth Factor (FGF) Ligand Trap for the Treatme…

2016

NSC12 is an orally available pan-FGF trap able to inhibit FGF2/FGFR interaction and endowed with promising antitumor activity. It was identified by virtual screening from a NCI small molecule library, but no data were available about its synthesis, stereochemistry, and physicochemical properties. We report here a synthetic route that allowed us to characterize and unambiguously identify the structure of the active compound by a combination of NMR spectroscopy and in silico conformational analysis. The synthetic protocol allowed us to sustain experiments aimed at assessing its therapeutic potential for the treatment of FGF-dependent lung cancers. A crucial step in the synthesis generated a c…

Models Molecular0301 basic medicineLung NeoplasmssynthesisFGF Lung cancer growth factor chemical characterization synthesisIn silicoAdministration OralAntineoplastic AgentsPharmacologyFibroblast growth factorMiceStructure-Activity Relationship03 medical and health sciences0302 clinical medicineIn vivoDrug DiscoveryTumor Cells CulturedAnimalsHumansFGFStructure–activity relationshipCell ProliferationDose-Response Relationship DrugMolecular Structurechemical characterizationCell growthChemistrygrowth factorLigand (biochemistry)Small moleculeCell biologyFibroblast Growth FactorsCholesterol030104 developmental biologyFibroblast growth factor receptor030220 oncology & carcinogenesisMolecular MedicineDrug Screening Assays AntitumorLung cancerJournal of Medicinal Chemistry
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Targeting Cavity-Creating p53 Cancer Mutations with Small-Molecule Stabilizers: the Y220X Paradigm

2020

We have previously shown that the thermolabile, cavity-creating p53 cancer mutant Y220C can be reactivated by small-molecule stabilizers. In our ongoing efforts to unearth druggable variants of the p53 mutome, we have now analyzed the effects of other cancer-associated mutations at codon 220 on the structure, stability, and dynamics of the p53 DNA-binding domain (DBD). We found that the oncogenic Y220H, Y220N, and Y220S mutations are also highly destabilizing, suggesting that they are largely unfolded under physiological conditions. A high-resolution crystal structure of the Y220S mutant DBD revealed a mutation-induced surface crevice similar to that of Y220C, whereas the corresponding pock…

Models Molecular0301 basic medicineMutantCarbazolesDruggabilityCancer therapyAntineoplastic Agents01 natural sciencesBiochemistryDNA-binding proteinStructure-Activity Relationship03 medical and health sciencesProtein DomainsHumansCancer mutationsThermolabileQD0415Protein Stability010405 organic chemistryChemistryArticlesGeneral MedicineSmall moleculeAffinities0104 chemical sciences030104 developmental biologyGene Expression RegulationMutationBiophysicsMolecular MedicineMutant ProteinsDrug Screening Assays AntitumorTumor Suppressor Protein p53CrystallizationProtein BindingQD0241ACS Chemical Biology
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