Search results for "CISPLATIN"

showing 10 items of 267 documents

O6-methylguanine-DNA methyltransferase activity and sensitivity to cyclophosphamide and cisplatin in human lung tumor xenografts

1998

The DNA repair protein O6-methylguanine-DNA methyl-transferase (MGMT) is a main determinant of resistance of cells to the cytostatic effects of O6-alkylguanine-generating alkylating agents. The purpose of our study was to assay MGMT activity in cells of lung cancers and to correlate MGMT levels with chemotherapy response to cyclophosphamide (CTX) and cisplatin (DDP). MGMT levels were determined in 14 human lung tumor xenografts. There was a wide variation of MGMT expression in these tumors, ranging from 10 to 984 fmol/mg protein. There was also a wide range in the sensitivity of the xenografts to CTX and DDP, as measured by specific growth delay. When the MGMT levels of the different xenogr…

Cancer ResearchPathologymedicine.medical_specialtyLung NeoplasmsMethyltransferaseCyclophosphamidemedicine.medical_treatmentTransplantation HeterologousMice NudeAntineoplastic AgentsBiologyMiceO(6)-Methylguanine-DNA Methyltransferasechemistry.chemical_compoundIn vivoCarcinoma Non-Small-Cell LungCarcinomamedicineAnimalsHumansCyclophosphamideneoplasmsCisplatinChemotherapyDose-Response Relationship DrugO-6-methylguanine-DNA methyltransferasemedicine.diseasedigestive system diseasesNitrogen mustardOncologychemistryCancer researchFemaleCisplatinmedicine.drugInternational Journal of Cancer
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Aurora-A Transcriptional Silencing and Vincristine Treatment Show a Synergistic Effect in Human Tumor Cells

2008

Aurora-A is a centrosome-associated serine/threonine kinase that is overexpressed in multiple types of human tumors. Primarily, Aurora-A functions in centrosome maturation and mitotic spindle assembly. Overexpression of Aurora-A induces centrosome amplification and G 2 /M cell cycle progression. Recently, it was observed that overexpression of Aurora-A renders cells resistant to cisplatin (CDDP)-, etoposide-, and paclitaxel-induced apoptosis.Our results indicate that already in initial stages of cancer progression Aurora-A overexpression could have a major role in inducing supernumerary centrosomes and aneuploidy, as shown by immunohistochemistry on tissue sections from various stages of hu…

Cancer ResearchPathologymedicine.medical_specialtyTranscription GeneticApoptosismacromolecular substancesProtein Serine-Threonine KinasesBiologyTransfectionPLK1Aurora KinasesRNA interferenceCell Line TumormedicineHumansGene silencingGene SilencingRNA Small InterferingMitotic catastropheCentrosomeCisplatinCarcinomaCell CycleDrug SynergismAuroraA/stk15centrosome amplificationAneuploidy CINGeneral MedicineCell cycleAneuploidyAntineoplastic Agents PhytogenicGene Expression Regulation NeoplasticSettore BIO/18 - Geneticaenzymes and coenzymes (carbohydrates)OncologyVincristineCentrosomeColonic Neoplasmsembryonic structuresCancer cellCancer researchbiological phenomena cell phenomena and immunityHeLa Cellsmedicine.drugOncology Research Featuring Preclinical and Clinical Cancer Therapeutics
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Downregulation of RhoB GTPase confers resistance to cisplatin in human larygneal carcinoma cells

2009

Acquired resistance to cisplatin represents a major obstacle to an efficient chemotherapy. We found downregulation of RhoB expression in cisplatin-resistant tumor cell lines from different origin. In cisplatin-resistant laryngeal carcinoma subline overexpression of farnesylated or geranylgeranylated RhoB increased cisplatin-induced cell death, while silencing of RhoB expression diminished sensitivity of parental HEp-2 cells via decreased cellular accumulation of cisplatin. However, since RhoB silencing in additional tumor cell lines did not alter their sensitivity to cisplatin, we can assume that RhoB downregulation does not provide general protective role in cell response to cisplatin. Nev…

Cancer ResearchProgrammed cell deathGenetic enhancementRHOBmedicine.medical_treatmentDown-RegulationAntineoplastic AgentsBiologyDownregulation and upregulationCell Line TumormedicineCarcinomaHumansGene silencingrhoB GTP-Binding ProteinLaryngeal NeoplasmsCisplatinChemotherapymedicine.diseaseCell biologyOncologyDrug Resistance NeoplasmCancer researchcisplatin ; drug resistance ; Rho GTPases ; RhoBCisplatinmedicine.drug
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The apoptotic effects of cisplatin and carboplatin in retinoblastoma Y79 cells.

1998

This study demonstrated that cisplatin and carboplatin stimulate apoptosis in human retinoblastoma Y79 cells, cisplatin being the most effective compound. The apoptotic effect appeared after 8 h and then increased in a time-dependent manner. Treatment with cisplatin and carboplatin also provoked an increase in the level of p53 and p21, and a lowering in Bcl-2. The prolonged exposure of Y79 cells to cisplatin induced resistance to cisplatin, carboplatin and etoposide. The basal level of p53 was in resistant cells higher than in untreated cells, while Bcl-2 was not modified. p53 and Bcl-2 levels did not change after treating of resistant cells with cisplatin, carboplatin or etoposide. However…

Cancer ResearchProgrammed cell deathPathologymedicine.medical_specialtyCell Survivalmedicine.medical_treatmentAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundTumor Cells CulturedmedicineHumansEtoposideCisplatinChemotherapyRetinoblastomaDNA NeoplasmCarboplatinProto-Oncogene Proteins c-bcl-2OncologychemistryDrug Resistance NeoplasmApoptosisCell culturecarboplatinCancer researchCisplatinTumor Suppressor Protein p53Camptothecinmedicine.drugInternational Journal of Oncology
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Resistance to diverse apoptotic triggers in multidrug resistant HL60 cells and its possible relationship to the expression of P-glycoprotein, Fas and…

2002

We studied the human HL60 leukemia cell line and its multidrug resistant (MDR) variant HL60R. In contrast to the HL60, HL60R showed an inability to undergo apoptosis from doxorubicin (Dox) or other different stimuli, including cisplatin, Fas ligation and serum withdrawal. HL60R cells lost surface Fas expression, but we found no evidence that Fas/FasL mediates the apoptotic effects of Dox in HL60. P-glycoprotein (P-gp) did not seem to play a major role as a specific inhibitor of apoptosis. In fact, the P-gp inhibitor verapamil reversed only partially the resistance to Dox-induced apoptosis of the MDR cells. In addition, it did not modify the rate of apoptosis induced from the other stimuli i…

Cancer ResearchProgrammed cell deathTime FactorsChromosomal Proteins Non-HistoneSurvivinDown-RegulationAntineoplastic AgentsApoptosisHL-60 CellsNerve Tissue ProteinsBiologyInhibitor of apoptosisFas ligandInhibitor of Apoptosis ProteinsInhibitory Concentration 50SurvivinTumor Cells CulturedHumansATP Binding Cassette Transporter Subfamily B Member 1RNA Messengerfas ReceptorP-glycoproteinInhibitor of apoptosis domainCaspase 3Reverse Transcriptase Polymerase Chain ReactionProteinsFlow CytometryNeuronal Apoptosis-Inhibitory ProteinNeoplasm ProteinsCell biologyProto-Oncogene Proteins c-bcl-2OncologyDoxorubicinDrug Resistance NeoplasmApoptosisCaspasesbiology.proteinInsect ProteinsNAIPCisplatinMicrotubule-Associated ProteinsCancer Letters
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Dendritic cells as mediators of tumor-induced tolerance in metastatic melanoma.

1997

Escape from immune surveillance is critical for tumor progression in metastatic melanoma. We assessed the function of melanoma-derived dendritic cells (DCs) in patients presenting simultaneously with responding (rM) or progressing (pM) melanoma metastases. These rare coincidences allowed us to compare syngeneically the function of tumor DCs. CD83+ DCs were purified freshly from large responding (rDCs) or progressing (pDCs) metastases following chemo-immunotherapy. rDCs were 5 times more potent inducers of allogeneic T-cell proliferation than the pDCs that were used as control. Phenotypic analysis showed a marked depression of CD86 expression on pDCs. Culture supernatants from pM showed prod…

Cancer ResearchT-LymphocytesImmune toleranceImmune systemAntigens CDAntigens NeoplasmAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansAntigen-presenting cellMelanomaCD86Membrane Glycoproteinsbusiness.industryMelanomaInterferon-alphahemic and immune systemsDendritic cellDendritic Cellsmedicine.diseaseInterleukin-10Neoplasm ProteinsTolerance inductionOncologyTumor progressionImmunologyCytokinesInterleukin-2Tumor EscapeB7-2 AntigenCisplatinbusinessCell DivisionInternational journal of cancer
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Curvature increases permeability of the plasma membrane for ions, water and the anti-cancer drugs cisplatin and gemcitabine

2019

ABSTRACTIn this work the permeability of a model asymmetric plasma membrane, for ions, water and the anti-cancer drugs cisplatin and gemcitabine is studied by means of all-atom molecular dynamics simulations. It is shown that permeability of the membranes increases from one to three orders of magnitude upon membrane bending depending on the compound and the sign of curvature. Our results show that the membrane curvature is an important factor which should be considered during evaluation of drug translocation.TOC GRAPHICS

Cell Membrane PermeabilityLipid Bilayerslcsh:MedicineAntineoplastic AgentsMolecular Dynamics SimulationCurvature01 natural sciencesDeoxycytidineArticleSupramolecular assemblyIonMembrane bending03 medical and health sciencesComputational biophysics0103 physical sciencesmedicineAnimalsHumanslcsh:Science030304 developmental biologyCisplatinIons0303 health sciences010304 chemical physicsChemistryCell Membranelcsh:RWaterMembrane structure and assemblyGemcitabineOrders of magnitude (mass)MembraneMembrane curvaturePermeability (electromagnetism)Drug deliveryBiophysicslcsh:QCisplatinmedicine.drugScientific Reports
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Induction of micronucleated and binucleate cells in Chinese hamster ovary (CHO) cells by cis-diamminedichloroplatinum (II): a morphological and morph…

1990

Abstract The mutagenicity and cytotoxicity of cis -diamminedichloroplatinum (II) (cisplatin) at doses of 5, 10 and 20 μg/ml in Chinese hamster ovary (CHO) cells have been examined. A morphological characterization of several cell types induced by cisplatin was carried out. The frequencies of both cells with micronuclei and binucleate cells as a time-dependent parameter have also been studied. Whilst the number of cells with micronuclei was found to decrease with time, the number of binucleate cells increased. The possible kinetic mechanism for the production of binucleate cells and cells with micronuclei is discussed. A morphometric analysis was also performed. The nuclear area in both trea…

Cell NucleusGeneticsCisplatinCis diamminedichloroplatinum iiCell typeMicronucleus TestsDose-Response Relationship DrugChinese hamster ovary cellNuclear areaBiologyToxicologyMolecular biologyCricetinaeMicronucleus testGeneticsmedicineAnimalsCisplatinCytotoxicityInterphaseCell DivisionCells CulturedAfter treatmentmedicine.drugMutation Research/Genetic Toxicology
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Saponins-mediated potentiation of cisplatin accumulation and cytotoxicity in human colon cancer cells.

2002

The triterpene saponins jenisseensosides A, B, C, D were found to increase the accumulation and cytotoxicity of the anticancer agent cisplatin in human colon tumor cells. These compounds are glycosides of quillaic acid whose fucose residue was acylated by a trans- or cis-p methoxycinnamic acid. In contrarst, other saponins derivatives without this acyl moiety were not found to potentiate the accumulation and cytotoxicity of cisplatin. These results suggested the importance of the acyl moiety for activity.

Cell SurvivalSaponinPharmaceutical SciencePlant RootsFucoseAnalytical Chemistrychemistry.chemical_compoundStructure-Activity RelationshipTriterpeneDrug DiscoverymedicineMoietyHumansOleanolic AcidCytotoxicitySilenePlatinumPharmacologychemistry.chemical_classificationCisplatinDose-Response Relationship DrugPlant ExtractsOrganic ChemistryGlycosideBiological activityDrug SynergismSaponinsTriterpenesComplementary and alternative medicinechemistryBiochemistryMolecular Medicinelipids (amino acids peptides and proteins)CisplatinHT29 Cellsmedicine.drugPlanta medica
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Cisplatin sensitivity is related to late DNA damage processing and checkpoint control rather than to the early DNA damage response

2008

The present study aimed at elucidating mechanisms dictating cell death triggered by cisplatin-induced DNA damage. We show that CL-V5B hamster mutant cells, a derivative of V79B, are hypersensitive to cisplatin-induced apoptotic death. CL-V5B cells are characterized by attenuated cisplatin-induced early (2-6 h) stress response, such as phosphorylation of stress-activated protein kinases (SAPK/JNK), ATM and Rad3-related (ATR) protein kinase, histone H2AX and checkpoint kinase-1 (Chk-1). Human FANCC cells also showed a reduced phosphorylation of H2AX and SAPK/JNK at early time point after cisplatin treatment. This was not the case for BRCA2-defective VC-8 hamster cells, indicating that the FA …

Cell cycle checkpointCisplatin-DNA adducts ; DNA repair ; Interstrand cross links ; DNA damage response ; Cell cycle checkpoint ; Cell deathDNA damageDNA repairHealth Toxicology and MutagenesisApoptosisCell LineHistonesDNA AdductsCricetinaeGeneticsmedicineAnimalsHumansCHEK1PhosphorylationMolecular BiologyChromosome AberrationsCisplatinbiologyJNK Mitogen-Activated Protein KinasesDNA replicationG2-M DNA damage checkpointMolecular biologyCell biologyHistonebiology.proteinCisplatinDNA DamageMutagensmedicine.drug
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