Search results for "breast neoplasms"

showing 10 items of 804 documents

Effects of zoledronic acid on proteinase plasma levels in patients with bone metastases.

2006

Background: The effects of the bisphosphonate derivative zoledronic acid (ZA) on the > circulating levels of matrix metalloproteinase-2 (MMP-2), matrix metallo-proteinases-9 > (MMP-9), cathepsin B (Cath B) and urokinase-type plasminogen activator (uPA) in > patients with bone metastasis (BMTS) and the possible correlation with the symptomatic > response induced by this drug in these patients were evaluated. Patients and Methods: > Proteinase levels were determined by enzyme-linked immunosorbent assay (ELISA) in the > plasma of 30 patients with painful bone metastases from breast or prostate cancer > undergoing multiple treatment with ZA (4 mg i.v., every 4 weeks). Healthy subjects > (HS) of…

Aged 80 and overMaleBone Density Conservation AgentsDiphosphonatesZoledronic > acidImidazolesProstatic NeoplasmsBone NeoplasmsBreast NeoplasmsMiddle AgedProteinaseZoledronic AcidCathepsin BMatrix > metalloproteinase-9Matrix Metalloproteinase 9Matrix metalloproteinase-2Bone metastasiBisphosphonates; Bone metastasis; Cathepsin B; Matrix metalloproteinase-2; Matrix > metalloproteinase-9; Proteinases; Urokinase-type plasminogen activator; Zoledronic > acidHumansMatrix Metalloproteinase 2BisphosphonateFemaleUrokinase-type plasminogen activatorAged
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Cellular stress induces cap-independent alpha-enolase/MBP-1 translation.

2015

AbstractMyc promoter-binding protein-1 (MBP-1) is a shorter protein variant of the glycolytic enzyme alpha-enolase. Although several lines of evidence indicate that MBP-1 acts as a tumor suppressor, the cellular mechanisms and signaling pathways underlying MBP-1 expression still remain largely elusive. To dissect these pathways, we used the SkBr3 breast cancer cell line and non-tumorigenic HEK293T cells ectopically overexpressing alpha-enolase/MBP-1. Here, we demonstrate that induced cell stresses promote MBP-1 expression through the AKT/PERK/eIF2α signaling axis. Our results contribute to shedding light on the molecular mechanisms underlying MBP-1 expression in non-tumorigenic and cancer c…

Alpha-enolaseCellEukaryotic Initiation Factor-2Alternative translationBiochemistryeIF-2 KinaseBreast cancerHEK293 CellStructural BiologyProtein IsoformsbiologyMedicine (all)Translation (biology)Recombinant ProteinEndoplasmic Reticulum StressRecombinant ProteinsNeoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation Neoplasticmedicine.anatomical_structureFemaleSignal transductionMyc promoter-binding protein-1Breast NeoplasmHumanSignal TransductionCell SurvivalDNA-Binding ProteinRecombinant Fusion ProteinsBiophysicsBreast NeoplasmsNeoplasm ProteinGeneticCell Line TumorEndoplasmic reticulum streGeneticsmedicineBiomarkers TumorHumansGene SilencingMolecular BiologyProtein kinase BTumor Suppressor ProteinTumor Suppressor ProteinsHEK 293 cellsProtein IsoformCell BiologySettore BIO/18 - GeneticaHEK293 CellsBiophysicGene Expression RegulationPhosphopyruvate HydrataseCancer cellbiology.proteinUnfolded protein responseCancer researchProto-Oncogene Proteins c-aktRecombinant Fusion ProteinFEBS letters
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Receptor Activator of NF-kB (RANK) Expression in Primary Tumors Associates with Bone Metastasis Occurrence in Breast Cancer Patients

2011

Background\ud Receptor activator of NFkB (RANK), its ligand (RANKL) and the decoy receptor of RANKL (osteoprotegerin, OPG) play a pivotal role in bone remodeling by regulating osteoclasts formation and activity. RANKL stimulates migration of RANK-expressing tumor cells in vitro, conversely inhibited by OPG.\ud \ud Materials and Methods\ud We examined mRNA expression levels of RANKL/RANK/OPG in a publicly available microarray dataset of 295 primary breast cancer patients. We next analyzed RANK expression by immunohistochemistry in an independent series of 93 primary breast cancer specimens and investigated a possible association with clinicopathological parameters, bone recurrence and surviv…

Anatomy and PhysiologyMicroarraysSettore MED/06 - Oncologia MedicaCancer TreatmentLigandsMetastasisBone remodelingMetastasisBasic Cancer ResearchBreast TumorsBone and Soft Tissue SarcomasNeoplasm MetastasisMusculoskeletal SystemOligonucleotide Array Sequence AnalysisMultidisciplinaryPredictive markerReceptor Activator of Nuclear Factor-kappa BQRBone metastasisMiddle AgedImmunohistochemistryGene Expression Regulation NeoplasticOncologyRANKLMedicineFemaleResearch Articlemusculoskeletal diseasesmedicine.medical_specialtyHistologyScienceBone NeoplasmsBreast NeoplasmsBiologyBreast cancerAntibody TherapySDG 3 - Good Health and Well-beingOsteoprotegerinInternal medicinemedicineHumansRNA MessengerBoneBiologyAgedBreast cancer bone metastasis RANK-RANKLRANK LigandOsteoprotegerinComputational BiologyCancers and NeoplasmsRANK Ligandmedicine.diseaseEndocrinologyCancer researchbiology.protein
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Angiogenic activity of breast cancer patients' monocytes reverted by combined use of systems modeling and experimental approaches.

2015

Angiogenesis plays a key role in tumor growth and cancer progression. TIE-2-expressing monocytes (TEM) have been reported to critically account for tumor vascularization and growth in mouse tumor experimental models, but the molecular basis of their pro-angiogenic activity are largely unknown. Moreover, differences in the pro-angiogenic activity between blood circulating and tumor infiltrated TEM in human patients has not been established to date, hindering the identification of specific targets for therapeutic intervention. In this work, we investigated these differences and the phenotypic reversal of breast tumor pro-angiogenic TEM to a weak pro-angiogenic phenotype by combining Boolean m…

AngiogenesisQH301-705.5In silicoBreast NeoplasmsMice TransgenicKaplan-Meier EstimateBiologyModels BiologicalMonocytesCell Line03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicineBreast cancerGeneticsmedicineAnimalsHumansBiology (General)Molecular BiologyEcology Evolution Behavior and Systematics030304 developmental biology0303 health sciencesTumor microenvironmentEcologyNeovascularization PathologicComputational BiologyNeoplasms ExperimentalTumor-DerivedMiddle Agedmedicine.diseasePhenotype3. Good healthGene expression profilingPhenotypeComputational Theory and Mathematics030220 oncology & carcinogenesisModeling and SimulationImmunologyCancer researchCytokinesFemaleSignal transductionResearch ArticleSignal TransductionPLoS Computational Biology
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Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1.

2015

How dying tumor cells get noticed Besides killing tumor cells directly, some chemotherapies, such as anthracyclines, also activate the immune system to kill tumors. Vacchelli et al. discovered that in mice, anthracycline-induced antitumor immunity requires immune cells to express the protein formyl peptide receptor 1 (FPR1). Dendritic cells (DCs) near tumors expressed especially high amounts of FPR1. DCs normally capture fragments of dying tumor cells and use them to activate nearby T cells to kill tumors, but DCs lacking FPR1 failed to do this effectively. Individuals with breast or colon cancer expressing a variant of FPR1 and treated with anthracyclines showed poor metastasis-free and ov…

AnthracyclineColorectal cancermedicine.medical_treatmentT-LymphocytesBreast Neoplasmsmicrofluidic chipchemotherapyPolymorphism Single NucleotideFormyl peptide receptor 1immune responseMiceImmune systemImmunityCell Line TumorNeoplasmsmedicineLeukocytesAnimalsHumansAnthracyclinesAllelesAnnexin A1ChemotherapyMultidisciplinarybusiness.industryDendritic Cellsmedicine.diseaseReceptors Formyl PeptideImmunity InnateChemotherapy AdjuvantCancer cellImmunologyCancer researchFemalebusinessColorectal NeoplasmsAdjuvantFPR1 microfluidicScience (New York, N.Y.)
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Anti-cancer activity of di- and tri-organotin(IV) compounds with D-(+)-Galacturonic acid on human tumor cells

2018

Abstract We have compared the anti-proliferative activity in vitro, of R2SnGala (1-3) [R = Me, n-Bu, Ph] and novel R3SnGala (4, 5) [R = Me, n-Bu] with D-(+)-Galacturonic acid [HGala; Galaq-, q = (2) and (1) for R2SnGala and R3SnGala, respectively] compounds, towards human tumor cell lines of intestinal carcinoma (HCT-116) and breast adenocarcinoma (MCF-7). The new synthesized 4 and 5 compounds were characterized, in solution, by 1H, 13C and 119Sn NMR, that showed that HGala acts as monoanionic moiety and evidenced the dynamic behavior of the compounds, due to inter-conversions involving the anomeric carbon atom of the ligand. Cell viability, apoptosis induction and cell cycle distribution w…

Anti cancerCarbohydrateCell SurvivalHCT-116Antineoplastic AgentsApoptosisBreast NeoplasmsOrganotin(IV)Adenocarcinoma010402 general chemistry01 natural sciencesBiochemistryFlow cytometryInorganic ChemistryOrganotin(IV); D-(+)-Galacturonic acid; NMR; Anti cancer; HCT-116; MCF-7Intestinal NeoplasmsmedicineOrganotin CompoundsCytotoxic T cellHumansViability assayCytotoxicityD-(+)-Galacturonic acidmedicine.diagnostic_testAnti-proliferative010405 organic chemistryCell growthChemistryHexuronic AcidsMCF-7 .Cell cycleHCT116 CellsMolecular biologyNMR0104 chemical sciencesCell cultureApoptosisSettore CHIM/03 - Chimica Generale E InorganicaMCF-7 CellsMCF-7Caco-2 Cells
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Chemotherapy and immunomodulation: from immunogenic chemotherapies to novel therapeutic strategies.

2013

Anticancer immunityCancer ResearchOrganoplatinum Compoundsmedicine.medical_treatmentBreast NeoplasmsT-Lymphocytes RegulatoryImmunomodulationChemoimmunotherapyNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansAnthracyclinesCyclophosphamideChemotherapyCell Deathbusiness.industryImmunosuppressionInflammasomeGeneral MedicineOxaliplatinOncologyImmunologyMyeloid-derived Suppressor CellFemaleFluorouracilbusinessImmunosuppressive Agentsmedicine.drugFuture oncology (London, England)
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Folate-targeted supramolecular vesicular aggregates as a new frontier for effective anticancer treatment in in vivo model.

2012

Abstract Supramolecular vesicular aggregates (SVAs), made up by self-assembling liposomes and polyasparthydrazide co-polymers conjugated to folic acid molecules were extensively investigated in this manuscript as potential active targeting formulation for anticancer drug delivery. Folate-targeted systems (FT-SVAs) were used to treat breast cancer and to further proof the potential in vivo administration of these systems for the therapeutic treatment for several aggressive solid tumors. The physicochemical and technological parameters of FT-SVAs are suitable for their potential in vivo administration. The chemotherapeutic activity of GEM-loaded FT-SVAs was increased during in vivo experiment…

Antimetabolites AntineoplasticStereochemistryPharmaceutical ScienceBreast NeoplasmsMice SCIDDeoxycytidinechemistry.chemical_compoundMiceBreast cancerDrug Delivery SystemsFolic AcidPharmacokineticsIn vivoMice Inbred NODPEG ratiomedicineAnimalsHumansLiposomeDrug CarriersGeneral Medicinemedicine.diseaseXenograft Model Antitumor AssaysGemcitabineGemcitabinePLGANylonsHydrazineschemistryDrug deliveryLiposomesCancer researchMCF-7 CellsFemaleFolate supramolecular vescicular aggregates anticancer treatmentBiotechnologymedicine.drugEuropean journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V
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Recent advances in computational design of potent aromatase inhibitors: open-eye on endocrine-resistant breast cancers.

2019

Introduction: The vast majority of breast cancers (BC) are estrogen receptor positive (ER+). The most effective treatments to fight this BC type rely on estrogen deprivation therapy, by inhibiting the aromatase enzyme, which performs estrogen biosynthesis, or on blocking the estrogens signaling path via modulating/degrading the estrogen's specific nuclear receptor (estrogen receptor-?, ER?). While being effective at early disease stage, patients treated with aromatase inhibitors (AIs) may acquire resistance and often relapse after prolonged therapies. Areas covered: In this compendium, after an overview of the historical development of the AIs currently in clinical use, and of the computati…

Antineoplastic Agents Hormonalmedicine.drug_classCYP450sEstrogen receptorallostery; aromatase inhibitors; Breast cancer; CYP450s; ligand-based and structure-based drug design; molecular dynamics; virtual screeningBreast NeoplasmsMolecular Dynamics SimulationBioinformatics03 medical and health sciencesBreast cancer0302 clinical medicineBreast cancerDrug DiscoverymedicineEndocrine systemHumansAromataseSurvival rate030304 developmental biologyCause of deathNeoplasm Staging0303 health sciencesallosterybiologybusiness.industryAromatase Inhibitorsvirtual screeningmedicine.diseaseligand-based and structure-based drug designmolecular dynamicsSurvival RateNuclear receptorEstrogenDrug Resistance Neoplasm030220 oncology & carcinogenesisDrug Designbiology.proteinFemalebusinessExpert opinion on drug discovery
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Artesunate Activates Mitochondrial Apoptosis in Breast Cancer Cells via Iron-catalyzed Lysosomal Reactive Oxygen Species Production

2011

The antimalarial agent artesunate (ART) activates programmed cell death (PCD) in cancer cells in a manner dependent on the presence of iron and the generation of reactive oxygen species. In malaria parasites, ART cytotoxicity originates from interactions with heme-derived iron within the food vacuole. The analogous digestive compartment of mammalian cells, the lysosome, similarly contains high levels of redox-active iron and in response to specific stimuli can initiate mitochondrial apoptosis. We thus investigated the role of lysosomes in ART-induced PCD and determined that in MCF-7 breast cancer cells ART activates lysosome-dependent mitochondrial outer membrane permeabilization. ART impac…

AutophagosomeProgrammed cell deathEndosomeIronArtesunateApoptosisBreast NeoplasmsMitochondrionBiologyBiochemistryPermeabilityAntimalarialsCell Line TumorLysosomemedicineHumansEnzyme InhibitorsMolecular BiologyAutophagyChloroquineCell BiologyArtemisininsMitochondriaCell biologymedicine.anatomical_structureApoptosisMitochondrial MembranesCancer cellFemaleMacrolidesLysosomesReactive Oxygen SpeciesJournal of Biological Chemistry
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