Search results for "cancer cell"

showing 10 items of 756 documents

Role of S128R polymorphism of E-selectin in colon metastasis formation.

2007

The extravasation of cancer cells is a key step of the metastatic cascade. Polymorphisms in genes encoding adhesion molecules can facilitate metastasis by increasing the strength of interaction between tumor and endothelial cells as well as impacting other properties of cancer cells. We investigated the Ser128Arg (a561c at the nucleotide level) polymorphism in the E-selectin gene in patients with metastatic colon cancer and its functional significance. Genotyping for a561c polymorphism was performed on 172 cancer patients and on an age-matched control population. The colon cancer group was divided into groups with (M+) and without observable metastasis (M−). For in vitro functional assays, …

MaleCancer ResearchColorectal cancerBiologyArginineTransfectionMetastasise-SELECTIN; COLON CANCER METASTASISSettore BIO/13 - Biologia ApplicataCell MovementE-selectinmedicineCell AdhesionSerineTumor Cells CulturedHumansNeoplasm MetastasisPolymorphism GeneticCell adhesion moleculeCancerTransfectionMiddle Agedmedicine.diseaseExtravasationColon Carcinoma E-Selectin Metastasis PolymorphismPhenotypeOncologyImmunologyCancer cellColonic NeoplasmsCancer researchbiology.proteinFemaleE-SelectinSignal TransductionInternational journal of cancer
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l-glutamine: a major substrate for tumor cells in vivo?

1987

From 65 human breast cancer xenografts investigated, a net glutamine uptake was found in 13 tumors (mean +/- SE: 15.7 +/- 4.5 nmol/g per min) whereas a net release (22.5 +/- 3.3 nmol/g per min) was observed in 40 tumors. In 12 tumors neither a significant net uptake nor a net release was obvious. There is experimental evidence that glutamine is taken up by cancer cells only at arterial concentrations greater than 0.5 mM. Another parameter determining glutamine utilization by tumor cells may be the tissue oxygenation. In hypoxic or anoxic tumor areas, glutamine oxidation is unlikely since oxygen is required for the reoxidation of coenzymes which are reduced in the course of this metabolic pa…

MaleCancer Researchmedicine.medical_specialtyGlutamineTransplantation HeterologousOxygenechemistry.chemical_elementBreast NeoplasmsBiologyModels BiologicalOxygenOxygen ConsumptionCarcinosarcomaIn vivoInternal medicinemedicineAnimalsHumanscomputer.programming_languageGlutaminolysisRats Inbred StrainsGeneral MedicineHydrogen-Ion ConcentrationTumor OxygenationRatsGlutamineTransplantationEndocrinologyOncologychemistryCancer cellFemaleEnergy MetabolismcomputerMathematicsNeoplasm TransplantationJournal of Cancer Research and Clinical Oncology
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Effects of phenylbutyrate on proliferation and apoptosis in human prostate cancer cells in vitro and in vivo.

1999

Phenylbutyrate (PB) is a potent differentiating agent and currently under investigation for the treatment of prostate cancer (CaP) and other malignancies. We have studied the impact of PB in vitro and in vivo on differentiation, proliferation and apoptosis in the LNCaP and LuCaP 23.1 prostate cancer xenograft models. In vitro we found that i) PB increased PSA secretion/cell, ii) inhibited cell proliferation in a time- and dose-dependent manner resulting in a cell cycle arrest in G1-phase and iii) induced apoptosis at concentrations of 2.5 mM after 3 days of treatment. In PB treated animals tumor growth stabilized or regressed. Combination of castration and PB treatment had a synergistic ant…

MaleCancer Researchmedicine.medical_specialtyProgrammed cell deathTransplantation HeterologousMice NudeAntineoplastic AgentsApoptosisBiologyPhenylbutyrateMiceProstate cancerIn vivoInternal medicineLNCaPTumor Cells CulturedmedicineAnimalsHumansMice Inbred BALB CCell growthCell CycleProstatic NeoplasmsCancerCell Differentiationmedicine.diseasePhenylbutyratesDisease Models AnimalEndocrinologyOncologyCancer cellAndrogensCancer researchCell DivisionNeoplasm TransplantationInternational Journal of Oncology
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Immune-modulating effects of the newest cetuximab-based chemoimmunotherapy regimen in advanced colorectal cancer patients.

2012

Cetuximab is a human-murine chimeric monoclonal antibody to the epidermal growth factor receptor, active for advanced colorectal cancer treatment in combination with chemotherapy. Cetuximab mainly acts by inhibiting epidermal growth factor receptor-mediated pathways in cancer cells; however, in the human host, its IgG1 backbone may offer additional antitumor activity that includes FcγRs-mediated antibody-dependent cell cytotoxicity, phagocytosis, cross priming, and tumor-specific T-cell-mediated immune response. These mechanisms are still under active investigation. At this purpose, we have performed an immunologic investigation in advanced colon cancer patients enrolled in an ongoing phase…

MaleCancer Researchmedicine.medical_treatmentCetuximabPharmacologyDeoxycytidineAldesleukinT-Lymphocyte SubsetsImmunology and AllergyCytotoxic T cellEpidermal growth factor receptorChemoimmunotherapybiologyCetuximabAntibodies MonoclonalMiddle AgedRecombinant ProteinsAdvanced Colorectal CancerErbB ReceptorsKiller Cells NaturalFemaleFluorouracilImmunotherapyAntibodyColorectal NeoplasmsImmune-modulating Effectmedicine.drugImmunologyAntineoplastic AgentsAntibodies Monoclonal HumanizedIrinotecanDrug Administration ScheduleImmunomodulationImmune systemCell Line TumormedicineHumansPharmacologyEpidermal growth factor receptorPolychemotherapybusiness.industryImmunotherapyDendritic CellsColorectal cancerGemcitabineCase-Control StudiesCancer cellbiology.proteinInterleukin-2CamptothecinbusinessJournal of immunotherapy (Hagerstown, Md. : 1997)
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Adipose stem cell niche reprograms the colorectal cancer stem cell metastatic machinery.

2021

Obesity is a strong risk factor for cancer progression, posing obesity-related cancer as one of the leading causes of death. Nevertheless, the molecular mechanisms that endow cancer cells with metastatic properties in patients affected by obesity remain unexplored. Here, we show that IL-6 and HGF, secreted by tumor neighboring visceral adipose stromal cells (V-ASCs), expand the metastatic colorectal (CR) cancer cell compartment (CD44v6 + ), which in turn secretes neurotrophins such as NGF and NT-3, and recruits adipose stem cells within tumor mass. Visceral adipose-derived factors promote vasculogenesis and the onset of metastatic dissemination by activation of STAT3, which inhibits miR-200…

MaleCancer microenvironmentobesityStromal cellColorectal cancerScienceSettore MED/50 - Scienze Tecniche Mediche ApplicateGeneral Physics and AstronomyAdipose tissueMice SCIDSCIDmetastasis.General Biochemistry Genetics and Molecular BiologyArticleMiceVasculogenesisSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansNeoplasm MetastasisStem Cell NicheZinc Finger E-box Binding Homeobox 2Tumor microenvironmentMultidisciplinarybusiness.industryHepatocyte Growth FactorInterleukin-6Stem CellsQadipose stromal cellCancerCD44v6General Chemistrymedicine.diseaseCellular ReprogrammingColorectal cancerMicroRNAsAdipose TissueCancer cellColonic NeoplasmsCancer researchNeoplastic Stem Cellsconsensus molecular subtypeStem cellSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratoriobusinessNature communications
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Curcumin inhibits in vitro and in vivo chronic myelogenous leukemia cells growth : a possible role for exosomal disposal of miR-21

2015

// Simona Taverna 1 , Marco Giallombardo 1 , Marzia Pucci 1 , Anna Flugy 1 , Mauro Manno 2 , Samuele Raccosta 2 , Christian Rolfo 3 , Giacomo De Leo 1 , Riccardo Alessandro 1, 4 1 Dipartimento di Biopatologia e Metodologie Biomediche, Sezione di Biologia e Genetica, Universita di Palermo, Italy 2 Istituto di Biofisica, CNR, Palermo, Italy 3 Phase I - Early Clinical Trials Unit Oncology Department and Center of Oncological Research (CORE), University Hospital Antwerp & Antwerp University, Belgium 4 Istituto di Biomedicina e Immunologia Molecolare (IBIM), Consiglio Nazionale delle Ricerche, Palermo, Italy Correspondence to: Riccardo Alessandro, e-mail: riccardo.alessandro@unipa.it Keywords: e…

MaleCurcuminexosomes microRNAs CML curcumin miR-21exosomesMice SCIDBiologyTransfectionMiceRandom Allocationchemistry.chemical_compoundDownregulation and upregulationLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesmedicineAnimalsHumansCMLBiologyCell ProliferationCell growthTransfectionmedicine.diseaseXenograft Model Antitumor AssaysMolecular biologyMicrovesiclesmicroRNAsOncologychemistryCancer cellCurcuminmiR-21Human medicineK562 CellsResearch PaperChronic myelogenous leukemiaK562 cellsOncotarget
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Molecular Pathways Involved in Prostate Carcinogenesis: Insights from Public Microarray Datasets

2012

PLoS one 7(11), e49831 (2012). doi:10.1371/journal.pone.0049831

MaleEXPRESSIONMicroarrayMicroarraysPopulationlcsh:MedicineBiologyMETABOLISMMalignancyBioinformaticsMetastasisMolecular GeneticsProstate cancerGeneticsCancer GeneticsBiomarkers TumormedicineHumansEpithelial–mesenchymal transitioneducationProstate carcinogenesislcsh:ScienceBiologyCANCER CELLSSIGNATURESOligonucleotide Array Sequence Analysiseducation.field_of_studyMultidisciplinarySystems BiologyProstate CancerCHOLESTEROLlcsh:RComputational BiologyCancers and NeoplasmsProstatic NeoplasmsGenomicsmedicine.diseaseEPITHELIAL-MESENCHYMAL TRANSITIONGene Expression Regulation NeoplasticMODELGenitourinary Tract TumorsCell Transformation NeoplasticOncologyCancer cellBIOLOGICAL PATHWAYSMedicinelcsh:QMetabolic Networks and PathwaysResearch Article
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Heterogeneous activation of MMP-9 due to prostate cancer-bone interaction.

2007

OBJECTIVES To determine whether matrix metalloproteinase (MMP)-9 activation resulting from prostate cancer cell-bone interaction is dependent on the tumor cell type and/or the nature of the bone microenvironment. METHODS In vitro co-cultures of human prostate cancer cells (PC3 and C4-2B) and mouse, human fetal, or human adult tissues were performed. In vivo the tumor cells were intratibially injected in SCID mice or intraosseously inoculated into fetal or adult bone xenografts in SCID mice. MMP-2 and MMP-9 expression and activation were determined by gelatin zymography in conditioned media obtained in vitro and in lysates derived from the in vivo studies at different time points. RESULTS Ac…

MaleFetusPathologymedicine.medical_specialtybusiness.industryUrologyBone metastasisProstatic NeoplasmsMice SCIDMatrix metalloproteinaseBone tissuemedicine.diseaseIn vitroBone and BonesProstate cancerMicemedicine.anatomical_structureMatrix Metalloproteinase 9In vivoCancer cellMedicineAnimalsHumansbusinessCells CulturedUrology
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Regulation of glutathione metabolism in Ehrlich ascites tumour cells.

1992

Glutathione metabolism was studied in cancer cells during the growth of an Ehrlich ascites tumour. GSH, but not GSSG, content decreases when cell proliferation and the rate of protein synthesis in the tumour decrease. This change correlates with a decrease in the rate of GSH synthesis and an increase in glutathione peroxidase and glutathione S-transferase activities. Glutathione efflux from tumour cells seems to co-ordinate with the rate of GSH synthesis. Cysteine, and not methionine, promotes GSH synthesis in tumour cells. However, changes in the rate of GSH synthesis are not due to limitations in the supply of blood cysteine or to changes in the intracellular amino acid pool of the cancer…

MaleGPX1Glutathione reductaseProtein metabolismMice Inbred StrainsBiologyGlucosephosphate DehydrogenaseBiochemistrychemistry.chemical_compoundMiceMethionineReference ValuesAnimalsAmino AcidsCarcinoma Ehrlich TumorMolecular BiologyCells CulturedGlutathione Transferasechemistry.chemical_classificationGlutathione PeroxidaseGlutathione DisulfideGlutathione peroxidaseCell BiologyGlutathioneGlutathioneAcetylcysteineRatsKineticsGlutathione ReductasechemistryBiochemistryLiverCancer cellGlutathione disulfidesense organsCell DivisionCysteineSubcellular FractionsResearch ArticleThe Biochemical journal
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Cancer cells induce immune escape via glycocalyx changes controlled by the telomeric protein TRF2

2019

International audience; Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells with strong immunosuppressive activity that promote tumor growth. In this study, we describe a mechanism by which cancer cells control MDSCs in human cancers by upregulating TRF2, a protein required for telomere stability. Specifically, we showed that the TRF2 upregulation in cancer cells has extratelomeric roles in activating the expression of a network of genes involved in the biosynthesis of heparan sulfate proteoglycan, leading to profound changes in glycocalyx length and stiffness, as revealed by atomic force microscopy. This TRF2-dependent regulation facilitated the recruitment of MDSCs, their …

MaleHSPG;immunosurveillance;MDSC;NK cells;TRF2Mice NudeBiologyGlycocalyxGeneral Biochemistry Genetics and Molecular BiologyMetastasisGlycocalyx03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationNeoplasmsmedicineAnimalsHumansTelomeric Repeat Binding Protein 2STAT3Molecular BiologyCells Cultured030304 developmental biology0303 health sciencesGeneral Immunology and MicrobiologyGeneral NeuroscienceMyeloid-Derived Suppressor CellsArticlesTelomeremedicine.disease3. Good healthImmunosurveillanceGene Expression Regulation NeoplasticMice Inbred C57BLTLR2HEK293 CellsTumor progressionCancer cellCancer researchbiology.proteinNIH 3T3 Cells[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleTumor Escape030217 neurology & neurosurgery
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