Search results for "Tumor Physiology"

showing 6 items of 6 documents

Carboxyamidotriazole-Orotate Inhibits the Growth of Imatinib-Resistant Chronic Myeloid Leukaemia Cells and Modulates Exosomes-Stimulated Angiogenesis

2012

The Bcr/Abl kinase has been targeted for the treatment of chronic myelogenous leukaemia (CML) by imatinib mesylate. While imatinib has been extremely effective for chronic phase CML, blast crisis CML are often resistant. New therapeutic options are therefore needed for this fatal disease. Although more common in solid tumors, increased microvessel density was also reported in chronic myelogenous leukaemia and was associated with a significant increase of angiogenic factors, suggesting that vascularity in hematologic malignancies is a controlled process and may play a role in the leukaemogenic process thus representing an alternative therapeutic target. Carboxyamidotriazole-orotate (CTO) is …

MaleResearch ValidityPhysiologyAngiogenesisTumor PhysiologyFusion Proteins bcr-ablCancer Treatmentlcsh:MedicinePharmacologyExosomesCardiovascular PhysiologyBiochemistryPiperazinesHematologic Cancers and Related DisordersMicechemistry.chemical_compoundCell Movementhemic and lymphatic diseasesMolecular Cell BiologyBasic Cancer ResearchMedicine and Health SciencesPhosphorylationPost-Translational ModificationExtracellular Signal-Regulated MAP Kinaseslcsh:ScienceChronic Myelogenous LeukemiaMultidisciplinaryABLNeovascularization PathologicGene Expression Regulation LeukemicChemistryHematologyResearch AssessmentOncologyBenzamidesImatinib MesylateMedicineOncology AgentsAntiangiogenesis Therapymedicine.drugResearch ArticleChronic Myeloid LeukemiaAntineoplastic AgentsResearch and Analysis MethodsCell GrowthCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveLeukemiasCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansRNA MessengerPhosphotyrosineBiologyCell ProliferationOrotic AcidTumor microenvironmentCarboxyamidotriazoleInterleukin-8lcsh:RBiology and Life SciencesProteinsCancers and NeoplasmsImatinibTriazolesmedicine.diseaseXenograft Model Antitumor AssaysRetractionExosomePyrimidinesImatinib mesylateDrug Resistance NeoplasmCarboxyamidotriazole Orotatelcsh:QAngiogenesisCell Adhesion MoleculesProto-Oncogene Proteins c-aktDevelopmental BiologyChronic myelogenous leukemiaPLoS ONE
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Glucocorticoid receptor knockdown decreases the antioxidant protection of B16 melanoma cells: an endocrine system-related mechanism that compromises …

2014

We previously reported an interorgan system in which stress-related hormones (corticosterone and noradrenaline), interleukin-6, and glutathione (GSH) coordinately regulate metastatic growth of highly aggressive B16-F10 melanoma cells. Corticosterone, at levels measured in tumor-bearing mice, also induces apoptotic cell death in metastatic cells with low GSH content. In the present study we explored the potential role of glucocorticoids in the regulation of metastatic cell death/survival during the early stages of organ invasion. Glucocorticoid receptor (GCR) knockdown decreased the expression and activity of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting step in GSH synthesis, in …

MaleTumor PhysiologyGlutathione reductaseCancer TreatmentMelanoma ExperimentalGene Expressionlcsh:MedicineBiochemistryAntioxidantsMetastasisAnalytical Chemistrychemistry.chemical_compoundOxidative DamageMiceGlucocorticoid receptorSpectrum Analysis TechniquesCell SignalingNeoplasmsMolecular Cell BiologyBasic Cancer ResearchMedicine and Health SciencesNeoplasm Metastasislcsh:Sciencechemistry.chemical_classificationMultidisciplinaryCell DeathGlutathione peroxidaseEndocrine TherapyFlow CytometryGlutathioneChemistrymedicine.anatomical_structureOncologyResearch DesignSpectrophotometryPhysical SciencesCytophotometryGlucocorticoidmedicine.drugResearch ArticleSignal Transductionmedicine.medical_specialtyEndotheliumClinical Research DesignCell SurvivalGlutamate-Cysteine LigaseDown-RegulationEndocrine SystemBiologyResearch and Analysis MethodsCell LineReceptors GlucocorticoidInternal medicineCell Line TumormedicineGeneticsAnimalsHumansAnimal Models of DiseaseOncogenic Signalinglcsh:RBiology and Life SciencesEndothelial CellsGlutathioneCell BiologyMice Inbred C57BLEndocrinologyHEK293 CellschemistryCell cultureCancer cellAnimal Studieslcsh:QEndothelium VascularCytometryPLoS ONE
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Factors Determining Sensitivity and Resistance of Tumor Cells to Arsenic Trioxide

2012

Previously, arsenic trioxide showed impressive regression rates of acute promyelocytic leukemia. Here, we investigated molecular determinants of sensitivity and resistance of cell lines of different tumor types towards arsenic trioxide. Arsenic trioxide was the most cytotoxic compound among 8 arsenicals investigated in the NCI cell line panel. We correlated transcriptome-wide microarray-based mRNA expression to the IC(50) values for arsenic trioxide by bioinformatic approaches (COMPARE and hierarchical cluster analyses, Ingenuity signaling pathway analysis). Among the identified pathways were signaling routes for p53, integrin-linked kinase, and actin cytoskeleton. Genes from these pathways…

MicroarraysTumor PhysiologyCancer Treatmentlcsh:MedicineToxicologyArsenicalschemistry.chemical_compoundArsenic TrioxideBasic Cancer ResearchRNA NeoplasmArsenic trioxidelcsh:ScienceOligonucleotide Array Sequence AnalysisMultidisciplinaryintegumentary systemCytotoxinsOxidesTransfectionNeoplasm ProteinsGene Expression Regulation NeoplasticActin CytoskeletonOncologyMedicineThioredoxinSignal TransductionResearch Articleinorganic chemicalsAcute promyelocytic leukemiaToxic Agentschemistry.chemical_elementAntineoplastic AgentsBiologyComplementary and Alternative MedicineCell Line TumormedicineHumansRNA MessengerBiologyArseniclcsh:RComputational BiologyCancers and Neoplasmsmedicine.diseaseActin cytoskeletonMolecular biologychemistryDrug Resistance NeoplasmApoptosisCell culturelcsh:QPLoS ONE
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Ultrasound-Guided Intramural Inoculation of Orthotopic Bladder Cancer Xenografts: A Novel High-Precision Approach

2013

Orthotopic bladder cancer xenografts are essential for testing novel therapies and molecular manipulations of cell lines in vivo. Current xenografts rely on tumor cell inoculation by intravesical instillation or direct injection into the bladder wall. Instillation is limited by the lack of cell lines that are tumorigenic when delivered in this manner. The invasive model inflicts morbidity on the mice by the need for laparotomy and mobilization of the bladder. Furthermore this procedure is complex and time-consuming. Three bladder cancer cell lines (UM-UC1, UM-UC3, UM-UC13) were inoculated into 50 athymic nude mice by percutaneous injection under ultrasound guidance. PBS was first injected b…

PathologyMouseTumor PhysiologyCancer Treatmentlcsh:MedicineMiceBasic Cancer ResearchMedicineUltrasonicslcsh:ScienceBladder Cancer and Urothelial Neoplasias of the Urinary TractMultidisciplinaryUltrasoundAnimal ModelsBladder CancerOncolytic VirusesOncologySurgery Computer-AssistedMedicineOncology AgentsFemaleImmunotherapyResearch Articlemedicine.drugmedicine.medical_specialtyClinical Research DesignUrologyTransplantation HeterologousModel OrganismsIn vivoCell Line TumorAnimalsHumansBioluminescence imagingddc:610Animal Models of DiseaseBiologyCell ProliferationCisplatinBladder cancerbusiness.industrylcsh:RCancers and NeoplasmsChemotherapy and Drug Treatmentmedicine.diseaseGemcitabineOncolytic virusTransplantationGenitourinary Tract TumorsUrinary Bladder NeoplasmsFeasibility Studieslcsh:QbusinessPLoS ONE
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MMP-10/stromelysin-2 promotes invasion of head and neck cancer.

2011

BackgroundPeriostin, IFN-induced transmembrane protein 1 (IFITM1) and Wingless-type MMTV integration site family, member 5B (Wnt-5b) were previously identified as the invasion promoted genes of head and neck squamous cell carcinoma (HNSCC) by comparing the gene expression profiles between parent and a highly invasive clone. We have previously reported that Periostin and IFITM1 promoted the invasion of HNSCC cells. Here we demonstrated that Wnt-5b overexpression promoted the invasion of HNSCC cells. Moreover, stromelysin-2 (matrix metalloproteinase-10; MMP-10) was identified as a common up-regulated gene among Periostin, IFITM1 and Wnt-5b overexpressing HNSCC cells by using microarray data s…

Tumor PhysiologyClone (cell biology)p38 Mitogen-Activated Protein KinasesMetastasisMetastasisMolecular Cell BiologyBasic Cancer ResearchNeoplasm MetastasisRegulation of gene expressionGene knockdownMultidisciplinaryHead and Neck cancerQRTransfectionHead and Neck TumorsExtracellular MatrixUp-RegulationGene Expression Regulation NeoplasticOncologyHead and Neck NeoplasmsGene Knockdown TechniquesCarcinoma Squamous CellMedicineResearch ArticleScience490Oral MedicineBiologyPeriostinHead and Neck Squamous Cell CarcinomaMatrix Metalloproteinase 10stomatognathic systemSettore MED/28 - Malattie OdontostomatologicheCell Line TumormedicineCancer Detection and Diagnosisotorhinolaryngologic diseasesHumansNeoplasm Invasiveness490BiologyExtracellular Matrix AdhesionsProtein Kinase InhibitorsneoplasmsMicroarray analysis techniquesCancers and Neoplasmsmedicine.diseaseMolecular biologyHead and neck squamous-cell carcinomaAntigens DifferentiationWnt Proteinsstomatognathic diseasesCancer researchCell Adhesion MoleculesPLoS ONE
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Acidic Environment Leads to ROS-Induced MAPK Signaling in Cancer Cells

2011

Tumor micromilieu often shows pronounced acidosis forcing cells to adapt their phenotype towards enhanced tumorigenesis induced by altered cellular signalling and transcriptional regulation. In the presents study mechanisms and potential consequences of the crosstalk between extra- and intracellular pH (pH(e), pH(i)) and mitogen-activated-protein-kinases (ERK1/2, p38) was analyzed. Data were obtained mainly in AT1 R-3327 prostate carcinoma cells, but the principle importance was confirmed in 5 other cell types. Extracellular acidosis leads to a rapid and sustained decrease of pH(i) in parallel to p38 phosphorylation in all cell types and to ERK1/2 phosphorylation in 3 of 6 cell types. Furth…

Tumor PhysiologyIntracellular Spacelcsh:MedicineSignal transductionERK signaling cascadeMolecular cell biologyNeoplasmsBasic Cancer ResearchTumor MicroenvironmentSignaling in Cellular ProcessesPhosphorylationCyclic AMP Response Element-Binding ProteinCreb Signalinglcsh:ScienceCellular Stress ResponsesMultidisciplinaryKinaseMechanisms of Signal TransductionSignaling cascadesHydrogen-Ion ConcentrationProtein-Tyrosine KinasesCell biologyOncologyMedicinePhosphorylationMitogen-Activated Protein KinasesSodium-Potassium-Exchanging ATPaseIntracellularResearch ArticleCell SurvivalMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesIntracellular pHBiologyCREBModels BiologicalCell GrowthDogsCell Line TumorAnimalsHumansProtein Kinase InhibitorsBiologyPI3K/AKT/mTOR pathwaylcsh:RRatsEnzyme ActivationCancer cellbiology.proteinlcsh:QExtracellular SpaceReactive Oxygen SpeciesAcidsPLoS ONE
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