Search results for "Neoplastic"

showing 10 items of 2901 documents

Crucial Role of Interleukin-4 in the Survival of Colon Cancer Stem Cells

2008

Abstract Colon tumors may be maintained by a rare fraction of cancer stem-like cells (CSC) that express the cell surface marker CD133. Self-renewing CSCs exhibit relatively greater resistance to clinical cytotoxic therapies and recent work suggests that this resistance may be mediated in part by an autocrine response to the immune cytokine interleukin 4 (IL-4). Blocking IL-4 signaling can sensitize CSCs to apoptotic stimuli and increase the in vivo efficacy of cytotoxic therapy. These findings suggest that inhibitors of IL-4 signaling may offer a new therapeutic tool in colon carcinoma. [Cancer Res 2008;68(11):4022–5]

Cancer ResearchCell SurvivalColorectal cancermedicine.medical_treatmentCancerBiologymedicine.diseaseInterleukin-4 colon cancer stem cellsCytokineOncologyCancer stem cellColonic NeoplasmsImmunologyNeoplastic Stem CellsCancer researchmedicineHumansCytotoxic T cellInterleukin-4Stem cellAutocrine signallingInterleukin 4Cancer Research
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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The Impact of Insulin on Low-dose Metronomic Vinorelbine and Mafosfamide in Breast Cancer Cells

2021

Background/aim Breast cancer (BC) may be affected by diabetes and anti-diabetic medication, as well as its therapeutic agents. Low-dose metronomic chemotherapy (LDMC) is an available treatment option in BC. We investigated the impact of insulin on low-dose metronomic vinorelbine and mafosfamide in BC cell lines. Materials and methods Human BC cell lines T-47D, MCF-7, MDA-MB-231, BT-549 and non-tumorigenic breast cell line MCF-10A were exposed to 0.01 μg/ml and 10 μg/ml insulin in combination with low-dose metronomic vinorelbine or mafosfamide. The cell viability was determined after 24-72 hours using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Results Insulin, especi…

Cancer ResearchCell Survivalmedicine.medical_treatmentAntineoplastic AgentsBreast NeoplasmsPharmacologyVinorelbinechemistry.chemical_compoundBreast cancerMafosfamideCell Line TumormedicineHumansInsulinCytotoxic T cellViability assayCyclophosphamidebusiness.industryInsulinVinorelbineGeneral Medicinemedicine.diseaseMetronomic ChemotherapyOncologychemistryAdministration MetronomicFemalebusinessmedicine.drugHormoneAnticancer Research
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Ionizing radiation but not anticancer drugs causes cell cycle arrest and failure to activate the mitochondrial death pathway in MCF-7 breast carcinom…

2001

There is considerable evidence that ionizing radiation (IR) and chemotherapeutic drugs mediate apoptosis through the intrinsic death pathway via the release of mitochondrial cytochrome c and activation of caspases -9 and -3. Here we show that MCF-7 cells that lack caspase-3 undergo a caspase-dependent apoptotic cell death in the absence of DNA fragmentation and alpha-fodrin cleavage following treatment with etoposide or doxorubicin, but not after exposure to IR. Re-expression of caspase-3 restored DNA fragmentation and alpha-fodrin cleavage following drug treatment, but it did not alter the radiation-resistant phenotype of these cells. In contrast to the anticancer drugs, IR failed to induc…

Cancer ResearchCell cycle checkpointAntineoplastic AgentsApoptosisBreast NeoplasmsDNA FragmentationMitochondrionHeLaTransformation GeneticRadiation IonizingGeneticsTumor Cells CulturedHumansMolecular BiologyCaspaseEtoposidebiologyCaspase 3CarcinomaCell CycleMicrofilament ProteinsDNA NeoplasmCell cyclebiology.organism_classificationCaspase 9MitochondriaApoptosisCell cultureDoxorubicinCaspasesImmunologyCancer researchbiology.proteinDNA fragmentationFemaleCarrier ProteinsDNA DamageHeLa CellsOncogene
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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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The human Lgl polarity gene, Hugl-2, induces MET and suppresses Snail tumorigenesis

2012

Lethal giant larvae proteins have key roles in regulating polarity in a variety of cell types and function as tumour suppressors. A transcriptional programme initiated by aberrant Snail expression transforms epithelial cells to potentially aggressive cancer cells. Although progress in defining the molecular determinants of this programme has been made, we have little knowledge as to how the Snail-induced phenotype can be suppressed. In our studies we identified the human lethal giant larvae homologue 2, Hugl-2, (Llgl2/Lgl2) polarity gene as downregulated by Snail. Snail binds E-boxes in the Hugl-2 promoter and represses Hugl-2 expression, whereas removal of the E-boxes releases Hugl-2 from …

Cancer ResearchCell typeMice SCIDSnailmedicine.disease_causeMiceMice Inbred NODbiology.animalChlorocebus aethiopsparasitic diseasesCell polarityGeneticsmedicineAnimalsHumansGenes Tumor SuppressorNeoplasm MetastasisMolecular BiologyTranscription factorCells CulturedRegulation of gene expressionbiologyfungiHEK 293 cellsCell PolarityHep G2 CellsAnatomyProto-Oncogene Proteins c-metXenograft Model Antitumor AssaysPhenotypeUp-RegulationCell biologyGene Expression Regulation NeoplasticCytoskeletal ProteinsCell Transformation NeoplasticHEK293 CellsCOS CellsSnail Family Transcription FactorsCarcinogenesisProtein BindingTranscription FactorsOncogene
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Mitochondrial chaperones in cancer: From molecular biology to clinical diagnostics

2006

Mitochondria are cell organelles involved in processes of cell life and death, and therefore also in tumoral transformation. Indeed, mitochondria dysfunction is a prominent feature of cancer cells. Mitochondrial proteins and DNA have also been previously studied as markers of tumorigenesis. Heat shock proteins (HSPs) are ubiquitous evolutionary conserved proteins. HSPs enhance their expression in stressed cells and they are involved in gene expression regulation, DNA replication, signal transduction, differentiation, apoptosis, cellular senescence or immortalization. This review reflects recent views on the role of some mitochondrial molecular chaperones as prohibitin, mortalin and HSP60/HS…

Cancer ResearchCellBiologyMitochondrionmedicine.disease_causeMitochondrial ProteinsNeoplasmsHeat shock proteinmedicineHumanscancerProhibitinHeat-Shock ProteinsPharmacologyMolecular biologyMitochondriaCell biologyCell Transformation Neoplasticmedicine.anatomical_structureOncologyCancer cellMolecular MedicineHSP60Signal transductionCarcinogenesisMolecular ChaperonesCancer Biology & Therapy
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Osteosarcoma cell-derived exosomes affect tumor microenvironment by specific packaging of microRNAs

2018

Abstract Bone microenvironment provides growth and survival signals essential for osteosarcoma (OS) initiation and progression. OS cells regulate communications inside tumor microenvironment through different ways and, among all, tumor-derived exosomes support cancer progression and metastasis. To define the contribution of OS-derived exosomes inside the microenvironment, we investigated the effects induced in bone remodeling mechanism and tumor angiogenesis. We demonstrated that exosomes promoted osteoclasts differentiation and bone resorption activity. Furthermore, exosomes potentiated tube formation of endothelial cells and increased angiogenic markers expression. We therefore investigat…

Cancer ResearchCellBone NeoplasmsBiologyExosomesmedicine.disease_causeCell MovementSettore BIO/13 - Biologia ApplicataosteosarcomamicroRNABiomarkers TumormedicineHumansexosometumor microenvironmentTelomerase reverse transcriptaseCells CulturedCell ProliferationTube formationTumor microenvironmentNeovascularization PathologicGene Expression ProfilingGeneral Medicinemedicine.diseaseMicrovesiclesGene Expression Regulation NeoplasticMicroRNAsmedicine.anatomical_structureCancer researchmicroRNAs profilingOsteosarcomaEndothelium VascularCarcinogenesis
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Heterogeneous response to differentiation induction with different polar compounds in a clonal rat rhabdomyosarcoma cell line (BA-HAN-1C)

1989

The clonal rat rhabdomyosarcoma cell line BA-HAN-1C was tested for its susceptibility to differentiation induction with different polar compounds. This cell line is composed of proliferating mononuclear tumour cells, some of which spontaneously fuse to form terminally differentiated postmitotic myotube-like giant cells. Exposure of BA-HAN-1C cells to dimethylsulphoxide (DMSO), hexamethylene bisacetamide (HMBA), sodium butyrate (NaBut) and N-monomethylformamide (NMF) resulted in a significant inhibition of proliferation (P less than 0.001) and in a simultaneous increase in differentiation. The response was most pronounced after exposure to NMF as evidenced by a marked increase in the creatin…

Cancer ResearchCellular differentiationAntineoplastic AgentsBiologyPeripheral blood mononuclear cellHexamethylene bisacetamideCell LineCell Fusionchemistry.chemical_compoundAcetamidesRhabdomyosarcomaTumor Cells CulturedAnimalsDimethyl SulfoxideCreatine KinaseCell fusionFormamidesDimethyl sulfoxideCell DifferentiationSodium butyrateMolecular biologyClone CellsRatsButyratesOncologychemistryBiochemistryCell cultureGiant cellButyric AcidResearch ArticleBritish Journal of Cancer
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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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