Search results for " Humans"

showing 10 items of 2466 documents

CD90+ liver cancer cells modulate endothelial cell phenotype through the release of exosomes containing H19 lncRNA

2015

Background CD90+ liver cancer cells have been described as cancer stem-cell-like (CSC), displaying aggressive and metastatic phenotype. Using two different in vitro models, already described as CD90+ liver cancer stem cells, our aim was to study their interaction with endothelial cells mediated by the release of exosomes. Methods Exosomes were isolated and characterized from both liver CD90+ cells and hepatoma cell lines. Endothelial cells were treated with exosomes, as well as transfected with a plasmid containing the full length sequence of the long non-coding RNA (lncRNA) H19. Molecular and functional analyses were done to characterize the endothelial phenotype after treatments. Results …

Cancer ResearchAngiogenesisAngiogenesis; CD90+ liver cancer cells; Exosomes; Long-non-coding RNA H19; Antigens Thy-1; Cell Adhesion; Cell Line Tumor; Endothelial Cells; Exosomes; Human Umbilical Vein Endothelial Cells; Humans; Liver Neoplasms; RNA Long Noncoding; Phenotype; Molecular Medicine; Oncology; Cancer ResearchBiologyCD90+ liver cancer cellsExosomesCell LineSettore BIO/13 - Biologia ApplicataCancer stem cellCell Line TumormedicineCell AdhesionHuman Umbilical Vein Endothelial CellsHumansCD90AntigensThy-1TumorExosomes Long-non-coding RNA H19 CD90+ liver cancer cells AngiogenesisResearchLiver NeoplasmsCancerEndothelial Cellsmedicine.diseaseMicrovesiclesCell biologyEndothelial stem cellPhenotypeOncologyembryonic structuresThy-1 AntigensRNAMolecular MedicineRNA Long NoncodingLong NoncodingAngiogenesisStem cellLiver cancerLong-non-coding RNA H19Molecular Cancer
researchProduct

Genetic evolution of T-cell resistance in the course of melanoma progression

2014

Abstract Purpose: CD8+ T lymphocytes can kill autologous melanoma cells, but their activity is impaired when poorly immunogenic tumor phenotypes evolve in the course of disease progression. Here, we analyzed three consecutive melanoma lesions obtained within one year of developing stage IV disease for their recognition by autologous T cells. Experimental Design: One skin (Ma-Mel-48a) and two lymph node (Ma-Mel-48b, Ma-Mel-48c) metastases were analyzed for T-cell infiltration. Melanoma cell lines established from the respective lesions were characterized, determining the T-cell–stimulatory capacity, expression of surface molecules involved in T-cell activation, and specific genetic alteratio…

Cancer ResearchB7 Antigensmedicine.medical_treatmentMedizinGene ExpressionT-Lymphocyte Subsetshemic and lymphatic diseasesCluster AnalysisLymphocytesNeoplasm MetastasisLymph nodeMelanomaTumorImmunogenicityMelanomaSingle Nucleotidemedicine.anatomical_structurePhenotypeButorphanolOncologyDisease ProgressionCytokinesEvolutionT cellHuman leukocyte antigenBiologyPolymorphism Single NucleotideArticleCell LineEvolution MolecularLymphocytes Tumor-InfiltratingCell Line TumormedicineHumansGenetic Predisposition to DiseaseTumor-InfiltratingAllelePolymorphismneoplasmsAllelesNeoplasm StagingHistocompatibility Antigens Class IMolecularImmunotherapymedicine.diseaseAlleles; B7 Antigens; Butorphanol; Cell Line Tumor; Cluster Analysis; Cytokines; Disease Progression; Gene Expression; Genetic Predisposition to Disease; Histocompatibility Antigens Class I; Humans; Lymphocytes Tumor-Infiltrating; Melanoma; Mutation; Neoplasm Metastasis; Neoplasm Staging; Phenotype; Polymorphism Single Nucleotide; T-Lymphocyte Subsets; beta 2-Microglobulin; Evolution Molecular; Oncology; Cancer ResearchImmunologyMutationbeta 2-MicroglobulinCD8
researchProduct

Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment: the challenge ahead

2015

Goodson, William H. et al.

Cancer ResearchCarcinogenesis[SDV]Life Sciences [q-bio]METHOXYCHLOR-INDUCED ALTERATIONSReviewPharmacologyMESH: Carcinogens EnvironmentalCarcinogenic synergiesChemical mixturesNeoplasmsMESH: AnimalsMESH: NeoplasmsCarcinogenesiRisk assessmentCancerACTIVATED PROTEIN-KINASESMedicine (all)Low dose1. No povertyCumulative effectsBREAST-CANCER CELLSGeneral MedicineEnvironmental exposureMESH: CarcinogenesisBIO/10 - BIOCHIMICAEPITHELIAL-MESENCHYMAL TRANSITION3. Good health[SDV] Life Sciences [q-bio]Environmental CarcinogenesisESTROGEN-RECEPTOR-ALPHARisk assessmentHumanMESH: Environmental ExposureENDOCRINE-DISRUPTING CHEMICALSTARGETING TISSUE FACTOR[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPrototypical chemical disruptorsExposure[SDV.CAN] Life Sciences [q-bio]/CancerEnvironmental healthmedicine[SDV.EE.SANT] Life Sciences [q-bio]/Ecology environment/HealthCarcinogenEnvironmental carcinogenesis[SDV.EE.SANT]Life Sciences [q-bio]/Ecology environment/HealthMESH: HumansAnimalPOLYBROMINATED DIPHENYL ETHERSCancerEnvironmental Exposuremedicine.diseaseMESH: Hazardous SubstancesCarcinogens EnvironmentalMIGRATION INHIBITORY FACTORVASCULAR ENDOTHELIAL-CELLSHazardous SubstanceNeoplasmCarcinogenesis
researchProduct

CD38/CD31, the CCL3 and CCL4 chemokines, and CD49d/vascular cell adhesion molecule-1 are interchained by sequential events sustaining chronic lymphoc…

2009

AbstractCD38 and CD49d are associated negative prognosticators in chronic lymphocytic leukemia (CLL). Despite evidence that both molecules are involved in interactions occurring between CLL and normal cells in the context of CLL-involved tissues, a functional link is still missing. Using gene expression profiles comparing CD38+CD49d+ versus CD38−CD49d− CLL cells, we showed overexpression of the CCL3 and CCL4 chemokines in cells from the former group. These chemokines were also up-regulated by CD38 signals in CLL; moreover, CCL3 was expressed by CLL cells from bone marrow biopsies (BMB) of CD38+CD49d+ but not CD38−CD49d− cases. High levels of CCR1 and, to a lesser extent, CCR5, the receptors…

Cancer ResearchChemokineChronic lymphocytic leukemiaIntegrin alpha4ApoptosisCD38immune system diseaseshemic and lymphatic diseasesReceptorsChronicMacrophages; Apoptosis; Membrane Glycoproteins; Humans; Integrin alpha4; Antigens CD38; Vascular Cell Adhesion Molecule-1; Endothelial Cells; Receptors Chemokine; Antigens CD31; Cell Survival; Bone Marrow Cells; Leukemia Lymphocytic Chronic B-Cell; Antigens CD; Up-Regulation; Chemokine CCL4; Chemokine CCL3; Cell LineChemokine CCL4Chemokine CCL3Membrane GlycoproteinsLeukemiaCell adhesion moleculehemic and immune systemsLymphocyticCDUp-RegulationPlatelet Endothelial Cell Adhesion Molecule-1Leukemiamedicine.anatomical_structureOncologyChemokineReceptors ChemokineTumor necrosis factor alphaStromal cellCell SurvivalVascular Cell Adhesion Molecule-1Bone Marrow CellsBiologyCell LineAntigens CDmedicineHumansAntigensMonocyteMacrophagesB-CellEndothelial Cellsmedicine.diseaseADP-ribosyl Cyclase 1Leukemia Lymphocytic Chronic B-CellCLL integrins chemokines CD49d CD38 prognosis.Cancer researchbiology.proteinCD31Settore MED/15 - Malattie del SangueCD38
researchProduct

Effects of resveratrol analogs on cell cycle progression, cell cycle associated proteins and 5fluoro-uracil sensitivity in human derived colon cancer…

2009

International audience; Epidemiological studies suggested that trans-resveratrol, a wine grape component, could prevent malignant tumor development. This compound also demonstrated cytostatic and cytotoxic effects on tumor cells in vitro. To obtain trans-resveratrol derivatives with a better cellular uptake and enhanced antiproliferative effects, we synthesized a triacetate derivative as well as an oligomer, epsilon-viniferin and its acetylated form, epsilon-viniferin penta-acetate. We also obtained vineatrol, a wine grape shoot extract that associates several polyphenols that may act synergistically, including trans-resveratrol and epsilon-viniferin. We show here that resveratrol triacetat…

Cancer ResearchCyclin AFluorescent Antibody TechniqueCell Cycle ProteinsMESH: Cell CycleMESH: Flow CytometryMESH : Blotting WesternResveratrolmedicine.disease_causeWine grapeMESH: Drug SynergismImmunoenzyme Techniqueschemistry.chemical_compoundMESH: PhenolsMESH : Cell Cycle ProteinsMESH : Tumor Cells CulturedMESH: StilbenesStilbenesTumor Cells CulturedMESH : Cell ProliferationMESH: Fluorescent Antibody TechniqueMESH: Antimetabolites AntineoplasticbiologyKinaseMESH : Antimetabolites AntineoplasticCell Cyclefood and beveragesDrug SynergismCell cycleFlow CytometryMESH : Colonic NeoplasmsOncologyBiochemistryColonic NeoplasmsMESH : FluorouracilFluorouracilMESH : PhenolsAntimetabolites AntineoplasticMESH : Drug SynergismMESH : Flow CytometryBlotting WesternMESH : ImmunoprecipitationMESH : StilbenesMESH: Cell Cycle ProteinsPhenolsMESH : Immunoenzyme TechniquesMESH: Cell ProliferationMESH : Cell Cycle[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologymedicineHumansImmunoprecipitationMESH: Blotting Western[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Tumor Cells CulturedKinase activityMESH: Immunoenzyme Techniques[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyBenzofuransCell ProliferationMESH: Colonic NeoplasmsMESH: HumansMESH : BenzofuransMESH: ImmunoprecipitationMESH : HumansMESH: BenzofuransMESH : Fluorescent Antibody TechniquechemistryResveratrolCell culturebiology.proteinCarcinogenesisMESH: Fluorouracil
researchProduct

Cancer stem cell definitions and terminology:the devil is in the details

2012

The cancer stem cell (CSC) concept has important therapeutic implications, but its investigation has been hampered both by a lack of consistency in the terms used for these cells and by how they are defined. Evidence of their heterogeneous origins, frequencies and their genomic, as well as their phenotypic and functional, properties has added to the confusion and has fuelled new ideas and controversies. Participants in The Year 2011 Working Conference on CSCs met to review these issues and to propose a conceptual and practical framework for CSC terminology. More precise reporting of the parameters that are used to identify CSCs and to attribute responses to them is also recommended as key t…

Cancer ResearchGeneral MathematicsACUTE MYELOID-LEUKEMIAPERIPHERAL-BLOODBiologyAnimals; Cell Differentiation; Cell Transformation Neoplastic; Clonal Evolution; Humans; Neoplastic Stem Cells; Terminology as Topic; Oncology; Cancer ResearchBioinformaticsCell TransformationSomatic evolution in cancerTumor Initiating CellsTerminologyClonal EvolutionIN-VITRO PROPAGATIONPHENOTYPIC HETEROGENEITYREPOPULATING CELLSConsistency (negotiation)Cancer stem cellCancer stem cells (CSC)Settore MED/04 - PATOLOGIA GENERALETerminology as TopicmedicineAnimalsHumansIn patientACUTE LYMPHOBLASTIC-LEUKEMIAGENE-EXPRESSIONConfusionSettore MED/04 - Patologia GeneraleMELANOMA-CELLSCognitive scienceNeoplasticAnimalApplied MathematicsSTEM/PROGENITOR CELLSCell DifferentiationTUMOR-INITIATING CELLSPeripheral bloodCell Transformation Neoplasticcancer stem cells differentiation tumor definitionsOncologyNeoplastic Stem CellsNeoplastic Stem Cellmedicine.symptomHuman
researchProduct

Novel insulin receptor substrate 1 and 2 variants in breast and colorectal cancer

2013

The insulin/insulin-like growth factor pathway is involved in breast and colorectal cancer (CRC) development. In the present study, we analyzed the coding region and short intron-exon borders of the insulin receptor substrate 1 and 2 (IRS‑1 and IRS‑2) genes in 12 cell lines derived from breast cancer (BC), 14 cell lines derived from CRC and 33 primary CRCs. The nucleotide variants identified in BC were 3 in IRS‑1, 1 of which (p.Arg267Cys) was novel and with a pathogenic potential as predicted by in silico analysis and 6 in IRS‑2. Twenty‑one variants in IRS‑1 and 18 in IRS‑2 were identified in the CRC samples. These included 11 novel IRS‑1 variants detected exclusively in CRCs, which include…

Cancer ResearchInsulin Receptor Substrate ProteinsSettore MED/06 - Oncologia MedicaIn silicoMutation MissenseBreast NeoplasmsColorectal NeoplasmBiologymedicine.disease_causeFrameshift mutationBreast cancerBreast cancerMCF-7 CellCell Line TumormedicineHumansMissense mutationFrameshift MutationInsulin Receptor Substrate ProteinSequence DeletionGeneticsMutationCaco-2 CellPolymorphism GeneticCancerGenetic VariationInsulin receptor substrate 1ArticlesGeneral MedicineInsulin receptor substrate 2HCT116 Cellsmedicine.diseaseColorectal cancerIRS1Mutagenesis InsertionalCell Transformation NeoplasticHT29 CellOncologyHCT116 CellBreast cancer; Colorectal cancer; Insulin receptor substrate 1; Insulin receptor substrate 2; Breast Neoplasms; Caco-2 Cells; Cell Line Tumor; Cell Transformation Neoplastic; Colorectal Neoplasms; Female; Frameshift Mutation; Genetic Variation; HCT116 Cells; HT29 Cells; Humans; Insulin Receptor Substrate Proteins; MCF-7 Cells; Mutagenesis Insertional; Mutation Missense; Polymorphism Genetic; Sequence Deletion; Signal Transduction; Cancer Research; OncologyInsulin Receptor Substrate ProteinsMCF-7 CellsFemaleCaco-2 CellsColorectal NeoplasmsHT29 CellsBreast NeoplasmHumanSignal Transduction
researchProduct

Patterns of Carbon-Bound Exogenous Compounds in Patients with Lung Cancer and Association with Disease Pathophysiology.

2021

Abstract Asymptomatic anthracosis is the accumulation of black carbon particles in adult human lungs. It is a common occurrence, but the pathophysiologic significance of anthracosis is debatable. Using in situ high mass resolution matrix-assisted laser desorption/ionization (MALDI) fourier-transform ion cyclotron resonance (FT-ICR) mass spectrometry imaging analysis, we discovered noxious carbon-bound exogenous compounds, such as polycyclic aromatic hydrocarbons (PAH), tobacco-specific nitrosamines, or aromatic amines, in a series of 330 patients with lung cancer in highly variable and unique patterns. The characteristic nature of carbon-bound exogenous compounds had a strong association wi…

Cancer ResearchLung NeoplasmsNitrosaminesDNA damageCarcinogenesismedicine.disease_causeMass SpectrometryTobacco UseMetabolomeTumor MicroenvironmentMedicineHumansCarcinogenesis; Carcinoma Squamous Cell/chemically induced; Carcinoma Squamous Cell/metabolism; Carcinoma Squamous Cell/pathology; Humans; Idiopathic Pulmonary Fibrosis/chemically induced; Idiopathic Pulmonary Fibrosis/metabolism; Idiopathic Pulmonary Fibrosis/pathology; Lung Neoplasms/chemically induced; Lung Neoplasms/metabolism; Lung Neoplasms/pathology; Mass Spectrometry; Metabolome; Nitrosamines/adverse effects; Polycyclic Aromatic Hydrocarbons/adverse effects; Retrospective Studies; Tobacco Use; Tumor MicroenvironmentPolycyclic Aromatic HydrocarbonsLung cancer610 Medicine & healthRetrospective StudiesAnthracosisLungbusiness.industrymedicine.diseasePathophysiologyIdiopathic Pulmonary Fibrosismedicine.anatomical_structureOncologyTumor progressionCancer researchCarcinoma Squamous CellMetabolome570 Life sciences; biologybusinessCarcinogenesis
researchProduct

In vivo targeting of human neutralizing antibodies against CD55 and CD59 to lymphoma cells increases the antitumor activity of rituximab.

2007

AbstractAn in vivo model of human CD20+ B-lymphoma was established in severe combined immunodeficiency mice to test the ability of human neutralizing miniantibodies to CD55 and CD59 (MB55 and MB59) to enhance the therapeutic effect of rituximab. The miniantibodies contained single-chain fragment variables and the hinge-CH2-CH3 domains of human IgG1. LCL2 cells were selected for the in vivo study among six B-lymphoma cell lines for their high susceptibility to rituximab-dependent complement-mediated killing enhanced by MB55 and MB59. The cells injected i.p. primarily colonized the liver and spleen, leading to the death of the animals within 30 to 40 days. Thirty percent of mice receiving bio…

Cancer ResearchLymphoma B-Cellmedicine.drug_classmedicine.medical_treatmentAntineoplastic AgentsCD59 AntigensAntigens CD59Mice SCIDPharmacologyMonoclonal antibodyAntigens CD55Antineoplastic AgentAntibodies Monoclonal Murine-DerivedMicerituximabIn vivomedicineAnimalsHumansantibodies against CD55 and CD59CD20Severe combined immunodeficiencyMice Inbred BALB CbiologyCD55 AntigensAnimalAntibody-Dependent Cell CytotoxicityAntibodies MonoclonalImmunotherapyrituximab; antibodies against CD55 and CD59medicine.diseaseDisease Models AnimalOncologyAnimals; Antibodies Monoclonal; Antibodies Monoclonal Murine-Derived; Antibody-Dependent Cell Cytotoxicity; Antigens CD55; Antigens CD59; Antineoplastic Agents; Disease Models Animal; Female; Humans; Lymphoma B-Cell; Mice; Mice Inbred BALB C; Mice SCID; Rituximab; Cancer Research; OncologyMonoclonalImmunologybiology.proteinRituximabFemaleAntibodymedicine.drugHuman
researchProduct

SOCS2 controls proliferation and stemness of hematopoietic cells under stress conditions and its deregulation marks unfavorable acute leukemias

2015

Abstract Hematopoietic stem cells (HSC) promptly adapt hematopoiesis to stress conditions, such as infection and cancer, replenishing bone marrow–derived circulating populations, while preserving the stem cell reservoir. SOCS2, a feedback inhibitor of JAK–STAT pathways, is expressed in most primitive HSC and is upregulated in response to STAT5-inducing cytokines. We demonstrate that Socs2 deficiency unleashes HSC proliferation in vitro, sustaining STAT5 phosphorylation in response to IL3, thrombopoietin, and GM-CSF. In vivo, SOCS2 deficiency leads to unrestricted myelopoietic response to 5-fluorouracil (5-FU) and, in turn, induces exhaustion of long-term HSC function along serial bone marro…

Cancer ResearchMyeloidSuppressor of Cytokine Signaling ProteinsMice TransgenicNeoplasm ProteinMiceBone MarrowSuppressor of Cytokine Signaling ProteinmedicineAnimalsHumansMEF2 Transcription FactorThrombopoietinSTAT5Cell ProliferationRegulation of gene expressionABLLeukemiabiologyMEF2 Transcription FactorsAnimalMedicine (all)Animals; Bone Marrow; Cell Differentiation; Cell Proliferation; Fluorouracil; Gene Expression Regulation Neoplastic; Hematopoietic Stem Cells; Humans; Leukemia; MEF2 Transcription Factors; Mice; Mice Transgenic; Neoplasm Proteins; Neoplastic Stem Cells; Suppressor of Cytokine Signaling Proteins; Cancer Research; Oncology; Medicine (all)breakpoint cluster regionCell DifferentiationHematopoietic Stem CellHematopoietic Stem CellsNeoplasm ProteinsGene Expression Regulation NeoplasticHaematopoiesismedicine.anatomical_structureOncologyImmunologybiology.proteinCancer researchNeoplastic Stem CellsFluorouracilNeoplastic Stem CellStem cellHuman
researchProduct