Search results for "Multiple"

showing 10 items of 2678 documents

Expression of the IAPs in multidrug resistant tumor cells

2003

We have investigated the expression of the IAPs (inhibitory of apoptosis proteins) in the human HL-60 leukemia and in its multidrug resistant, P-glycoprotein (P-gp) over-expressing variant, HL-60R. HL-60R exhibits resistance to apoptosis induced from P-gp substrate drugs and also from other triggers (cisplatin, TNF-alpha, Fas ligation, TRAIL, IFN-gamma and serum starvation) not related to the multidrug transporter. Except for c-IAP-1 mRNA, HL-60R significantly over-expressed both the mRNAs and the proteins of all the IAPs studied, i.e. c-IAP-1, c-IAP-2, XIAP, NAIP and survivin. Determination of the DNA-binding capacity of NF-kappaB (p50 or p65 subunits) indicated that, while HL-60 cells sho…

Cancer ResearchBlotting WesternCellApoptosisHL-60 CellsBiologyInhibitor of Apoptosis Proteinsmultidrug resistanceSurvivinmedicineHumansRNA MessengerCisplatinOncogeneReverse Transcriptase Polymerase Chain ReactionNF-kappa BProteinsGeneral MedicineIAPCell cycleapoptosiMolecular biologyDrug Resistance MultipleXIAPGene Expression Regulation Neoplasticmedicine.anatomical_structureOncologyDrug Resistance NeoplasmApoptosisCancer researchNAIPmedicine.drugOncology Reports
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Bortezomib: a new pro-apoptotic agent in cancer treatment.

2010

Bortezomib is a proteasome inhibitor. It targets the ubiquitin-proteasome pathway with subsequent inhibition of the degradation of proteins involved in cell cycle regulation and cancer cell survival. The best known molecular mechanism concerns the inhibition of IkappaB breakdown and the related stabilization of NFkappaB, thus preventing its translocation to the nucleus for the activation of downstream pathways. Bortezomib is the only drug in this class which has been approved for clinical use. It has shown an efficient antitumor effect in a phase III clinical trial (APEX) involving relapsed multiple myeloma patients. Response rate, time to progression and overall survival have been improved…

Cancer ResearchCell cycle checkpointSettore MED/06 - Oncologia MedicaAntineoplastic AgentsApoptosisPharmacologyDexamethasoneBortezomibMiceNeoplasmshemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsDrug DiscoverymedicineAnimalsHumansDexamethasoneMultiple myelomaPharmacologyproteasome inhibitionClinical Trials as TopicNeovascularization Pathologicbusiness.industryBortezomibCell CycleNF-kappa Bsolid tumorsmedicine.diseaseBoronic AcidsClinical trialBortezomib; solid tumors; proteasome inhibition.OncologyApoptosisPyrazinesCancer cellProteasome inhibitorCancer researchMultiple MyelomabusinessProteasome InhibitorsBortezomib solid tumors proteasome inhibitionmedicine.drug
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Whole-epigenome analysis in multiple myeloma reveals DNA hypermethylation of B cell-specific enhancers

2015

Abstract Analyzing the DNA methylome of multiple myeloma (MM), a plasma cell neoplasm, by whole-genome bisulfite sequencing and high-density arrays, we observed regional DNA hypermethylation embedded in extensive global hypomethylation. In contrast to the widely reported DNA hypermethylation of promoter-associated CpG islands (CGIs) in cancer, hypermethylated sites in MM as compared to normal plasma cells were located outside CpG islands and were unexpectedly associated with intronic enhancer regions active in normal B cells. Both RNA-seq and in vitro reporter assays indicated that enhancer hypermethylation is globally associated with downregulation of its host genes. ChIP-seq and DNAseI-se…

Cancer ResearchCellular differentiationCèl·lules BADNBisulfite sequencingImmunologyPlasma CellsDown-RegulationBiologyBiochemistryEpigenesis GeneticEpigènesiCell Line TumorGeneticsMielomatosiHumansEpigeneticsEnhancerPromoter Regions GeneticGeneMolecular BiologyGenetics (clinical)EpigenomicsB cellsGenome HumanResearchCell DifferentiationMethylationDNACell BiologyHematologyDNA NeoplasmPlasma cell neoplasmDNA MethylationMolecular biologyMyeloproliferative disordersGene Expression Regulation NeoplasticEnhancer Elements GeneticOncologyCpG siteDNA methylationNeoplastic Stem CellsCpG IslandsMultiple MyelomaEpigenesisTranscription FactorsGenome Research
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Expression of DNA repair proteins hMSH2, hMSH6, hMLH1,O6-methylguanine-DNA methyltransferase and N-methylpurine-DNA glycosylase in melanoma cells wit…

1999

Malignant melanoma is well known for its primary unresponsiveness to chemotherapy. The mechanisms conferring this intrinsic resistance are unclear. In this study, we investigated the role of genes involved in DNA repair in a panel of human melanoma cell variants exhibiting low and high levels of resistance to 4 commonly used drugs in melanoma treatment, i.e., vindesine, etoposide, fotemustine and cisplatin. We show that in melanoma cells exhibiting resistance to cisplatin, etoposide and vindesine, the nuclear content of each of the DNA mismatch repair (MMR) proteins hMLH1, hMSH2 and hMSH6 was reduced by 30–70%. A decreased expression level of up to 80% of mRNAs encoding hMLH1 and hMSH2 was …

Cancer ResearchDNA RepairTranscription GeneticVindesineDNA repairAntineoplastic AgentsBiologyNitrosourea CompoundsDNA GlycosylasesO(6)-Methylguanine-DNA MethyltransferaseOrganophosphorus CompoundsProto-Oncogene ProteinsmedicineHumansRNA MessengerPromoter Regions GeneticMelanomaN-Glycosyl HydrolasesneoplasmsEtoposideAdaptor Proteins Signal TransducingEtoposideCisplatinMelanomaNuclear Proteinsmedicine.diseaseMolecular biologyDrug Resistance Multipledigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinOncologyDNA glycosylaseFotemustineVindesineDNA mismatch repairCisplatinCarrier ProteinsMutL Protein Homolog 1medicine.drugInternational Journal of Cancer
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Type I keratin cDNAs from the rainbow trout: independent radiation of keratins in fish

2002

Five different type I keratins from a teleost fish, the rainbow trout Oncorhynchus mykiss, have been sequenced by cDNA cloning and identified at the protein level by peptide mass mapping using MALDI-MS. This showed that the entire range of type I keratins detected biochemically in this fish has now been sequenced. Three of the keratins are expressed in the epidermis (subtype Ie), whereas the other two occur in simple epithelia and mesenchymal cells (subtype Is). Among the Is keratins is an ortholog of human K18; the second Is polypeptide is clearly distinct from K18. We raised a new monoclonal antibody (F1F2, subclass IgG1) that specifically recognizes trout Is keratins, with negative react…

Cancer ResearchDNA Complementaryanimal structuresType I keratinMolecular Sequence Datamacromolecular substancesBiologyPeptide MappingEvolution MolecularMesodermSpecies SpecificityAntibody SpecificityKeratinAnimalsHumansProtein IsoformsAmino Acid SequenceCloning MolecularMolecular BiologyZebrafishPhylogenyZebrafishMammalschemistry.chemical_classificationGeneticsMultiple sequence alignmentSequence Homology Amino Acidintegumentary systemPhylogenetic treeLampreyAntibodies MonoclonalLampreysEpithelial CellsCell Biologybiology.organism_classificationProtein Structure TertiaryTroutchemistryOrgan SpecificityOncorhynchus mykissSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationSharksKeratinsRainbow troutEpidermisSequence AlignmentDevelopmental BiologyDifferentiation
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From a Better Understanding of the Mechanisms of Action of Histone Deacetylases Inhibitors to the Progress of the Treatment of Malignant Lymphomas an…

2017

Background Notable progress has been made in chemo- and immunotherapy of B-cell lymphomas, but less in the treatment of T-cell lymphomas. Objective Histone deacetylases inhibitors are a potentially useful therapeutic mean, as an epigenetic dysregulation is present in lymphomas, and especially in T-cell types. We aimed to study the progress made in this area. Method A mini-review was achieved using the articles published in PubMed in the last two years and the new patents made in this field. Results Histone deacetylases inhibitors are involved in the derepression of tumor suppressor genes through a histone deacetylase-mediated transcriptional process. Their inhibition is followed by cell cyc…

Cancer ResearchDrug exportmedicine.medical_treatmentCellular differentiationAntineoplastic Agents010402 general chemistryLymphoma T-Cell01 natural sciencesHistone DeacetylasesRomidepsinPatents as TopicDrug DiscoveryPlasma Cell MyelomamedicineAnimalsHumansPharmacology (medical)Epigeneticsbiology010405 organic chemistrybusiness.industryDrug SynergismGeneral MedicineImmunotherapymedicine.diseasePeripheral T-cell lymphoma0104 chemical sciencesHistone Deacetylase InhibitorsHistoneOncologyDrug DesignImmunologyCancer researchbiology.proteinbusinessMultiple Myelomamedicine.drugRecent patents on anti-cancer drug discovery
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Apoptotic effects of thiazolobenzimidazole derivatives on sensitive and multidrug resistant leukaemic cells

2001

We investigated the cytotoxic activity of eight thiazolobenzimidazole derivatives on sensitive HL60 and multidrug-resistant (MDR) (HL60R) leukaemia cell lines. The antitumour effects of these compounds were compared with those of RS-TBZ, a thiazolobenzimidazole derivative, previously described in our reports, that was able to induce apoptosis more markedly in MDR cells than in the parental sensitive cell lines. Only two compounds in this study proved to have interesting effects: (a) the S-enantiomer of TBZ, that was able to induce apoptosis in MDR cells in a slightly more selective manner than TBZ (racemic form); and (b) TBZ-4-OCH3 (TBZ-4-OCH3), that showed cytotoxic and apoptotic effects o…

Cancer ResearchHL60Antineoplastic AgentsHL-60 CellsApoptosisBiologyMultidrug resistanceCaspase 8Anticancer drugschemistry.chemical_compoundAntigenCytotoxic T cellHumansLeukaemiafas ReceptorProgenitor cellLeukemiaCell CycleCaspase InhibitorsDrug Resistance MultipleMultiple drug resistanceThiazolobenzimidazoleThiazolesAnticancer drugs; Apoptosis; Leukaemia; Multidrug resistance; Thiazolobenzimidazole;OncologychemistryCell cultureApoptosisDrug Resistance NeoplasmImmunologyCancer researchBenzimidazoles
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Uncommon Synchronous Association between Ovarian Carcinoma and Gastrointestinal Stromal Tumor: A Case Study and Literature Review

2013

Background The association of gastrointestinal stromal tumors (GIST) and other cancers is well known, but its synchronous occurrence with gynecological malignancies is very uncommon. Usually, the diagnosis is accidentally established. We describe a patient with GIST and concurrent ovarian cancer and discuss the clinical implications of this finding. Case report A 64-year-old woman with a prior diagnosis of ovarian cancer developed a second recurrence after having undergone two operations and adjuvant chemotherapy. While tumor debulking was performed, a small, nonsuspicious lesion was removed from the greater curvature of the stomach. Histology revealed a GIST. Conclusion The association of …

Cancer ResearchPaclitaxelGastrointestinal Stromal TumorsOvariectomyAntigens CD34Carcinoma Ovarian EpithelialCystectomyHysterectomyCarboplatin030218 nuclear medicine & medical imagingNeoplasms Multiple PrimarySalpingectomy03 medical and health sciencesPancreatectomy0302 clinical medicineOvarian cancerSynchronous occurrenceStomach NeoplasmGastrectomyStomach NeoplasmsAntineoplastic Combined Chemotherapy ProtocolsGastrointestinal Stromal TumorBiomarkers TumorHumansNeoplasms Glandular and EpithelialColectomyOvarian NeoplasmsAntineoplastic Combined Chemotherapy ProtocolOvarian NeoplasmGeneral MedicineMiddle AgedImmunohistochemistryProto-Oncogene Proteins c-kitTreatment OutcomeOncologyChemotherapy AdjuvantCA-125 Antigen030220 oncology & carcinogenesisSplenectomyLymph Node ExcisionFemaleHumanTumori Journal
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Altered Expression of c-IAP1, Survivin, and Smac Contributes to Chemotherapy Resistance in Thyroid Cancer Cells

2006

Abstract Resistance to chemotherapy predicts an unfavorable outcome for patients with radioiodine-insensitive thyroid cancer. To investigate the mechanisms underlying this resistance, we evaluated the expression of four different inhibitor of apoptosis proteins, and their antagonist, Smac, in thyroid cancer cells that survived 48 hours of exposure to cisplatin, doxorubicin, or taxol. We found high levels of c-IAP1 after cisplatin treatment and increased expression of survivin following exposure to doxorubicin. Cells that endured treatment with taxol showed reduced expression of Smac and released minimal amounts of this protein from the mitochondria. Down-regulation of c-IAP1 and survivin in…

Cancer ResearchPaclitaxelSurvivinmedicine.medical_treatmentAntineoplastic AgentsX-Linked Inhibitor of Apoptosis ProteinBiologyInhibitor of apoptosisInhibitor of Apoptosis ProteinsMitochondrial ProteinsCell Line TumorSurvivinmedicineHumansGene silencingCytotoxic T cellDoxorubicinThyroid NeoplasmsThyroid cancerCisplatinChemotherapyIntracellular Signaling Peptides and Proteinsmedicine.diseaseDrug Resistance MultipleNeoplasm ProteinsOncologyDoxorubicinDrug Resistance NeoplasmCancer researchCisplatinApoptosis Regulatory ProteinsMicrotubule-Associated Proteinsmedicine.drugCancer Research
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Abstract 5379: Recurrent inactivation of PARD3, a polarity-related gene, in squamous cell carcinomas of the lung.

2013

Abstract In spite of the recent advances in cancer genomics, the genetics underlying the development of lung squamous cell carcinomas (SCC) is still poorly understood. Here, we investigated the contribution of the cell polarity-related gene, PARD3, to lung SCC carcinogenesis. First, we tested for PARD3 alterations in lung cancer cell lines from various histopathological types. The analysis confirmed an intragenic deletion at the H157 cells and unveiled biallelic mutations in another cell line. Both cell lines are SCCs, which circumscribed PARD3 alterations to this lung cancer type. Next, we extended the genetic screening, which included the determination of mutations and of intragenic delet…

Cancer ResearchPathologymedicine.medical_specialtyCell growthCellWild typeCancerBiologymedicine.diseasemedicine.disease_causemedicine.anatomical_structureOncologymedicineCancer researchMultiplex ligation-dependent probe amplificationLung cancerCarcinogenesisGeneCancer Research
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