0000000000341816

AUTHOR

Cesare Peschle

showing 9 related works from this author

Identification and expansion of human colon-cancer-initiating cells

2007

Colon carcinoma is the second most common cause of death from cancer. The isolation and characterization of tumorigenic colon cancer cells may help to devise novel diagnostic and therapeutic procedures. Although there is increasing evidence that a rare population of undifferentiated cells is responsible for tumour formation and maintenance, this has not been explored for colorectal cancer. Here, we show that tumorigenic cells in colon cancer are included in the high-density CD133+ population, which accounts for about 2.5% of the tumour cells. Subcutaneous injection of colon cancer CD133+ cells readily reproduced the original tumour in immunodeficient mice, whereas CD133- cells did not form …

AC133 Antigen; Animals; Antigens CD; Cell Differentiation; Cell Line Tumor; Cell Proliferation; Colonic Neoplasms; Glycoproteins; Humans; Mice; Mice SCID; Neoplasm Transplantation; Neoplastic Stem Cells; Peptides; Phenotype; Transplantation Heterologous; MultidisciplinaryColorectal cancerCellular differentiationPopulationTransplantation HeterologousTumor initiationMice SCIDBiologyColon carcinomasmedicine.disease_causeSCIDCell LineMiceSide populationCancer stem cellAntigens CDSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicineAnimalsHumansAC133 AntigenAntigenseducationCell ProliferationGlycoproteinseducation.field_of_studyTransplantationHeterologousTumorMultidisciplinaryCancerCell Differentiationmedicine.diseaseCDPhenotypeImmunologyColonic NeoplasmsCancer researchNeoplastic Stem CellsCarcinogenesisPeptidesNeoplasm Transplantation
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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CD95 DISC formation and internalizzation occur in lipid rafts of typeI and typeII cells

2004

We investigated the membrane localization of CD95 in type I and type II cells, which differ in their ability to recruit and activate caspase-8. We found that CD95 was preferentially located in lipid rafts of type I cells, while it was present both in raft and non-raft plasma membrane sub-domains of type II cells. After stimulation, CD95 located in phospholipid-rich plasma membrane was recruited to lipid rafts in both types of cells. Similarly, CD95 cross-linking resulted in caspase-independent translocation of FADD/MORT1 and caspase-8 to the lipid rafts, which was prevented by a death domain-defective receptor. CD95 internalization was then rapid in type I and delayed in type II cells and s…

CD95Caspase-8Lipid rafts
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Apoptotic role of Fas/Fas ligand system in the regulation of erythropoiesis

1999

Abstract The possible involvement of Fas and Fas ligand (FasL) in the regulation of erythropoiesis was evaluated. Immunohistochemistry of normal bone marrow specimens revealed that several immature erythroblasts undergo apoptosis in vivo. Analysis of bone marrow erythroblasts and purified progenitors undergoing unilineage erythroid differentiation showed that Fas is rapidly upregulated in early erythroblasts and expressed at high levels through terminal maturation. However, Fas crosslinking was effective only in less mature erythroblasts, particularly at basophilic level, where it induced apoptosis antagonized by high levels of erythropoietin (Epo). In contrast, FasL was selectively induced…

medicine.medical_specialtyPopulationImmunologyBiologyBiochemistryFas ligandReticulocyteSettore MED/04 - PATOLOGIA GENERALEInternal medicinehemic and lymphatic diseasesmedicineCytotoxic T celleducationeducation.field_of_studyhemic and immune systemsCell BiologyHematologyCell biologyHaematopoiesismedicine.anatomical_structureEndocrinologyErythropoietinApoptosisErythropoiesismedicine.drugcirculatory and respiratory physiology
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IL-4 protects tumor cells from anti-CD95 and chemotherapeutic agents via up-regulation of antiapoptotic proteins

2004

Abstract We recently proposed that Th1 and Th2 cytokines exert opposite effects on the pathogenesis and clinical outcome of organ-specific autoimmunity by altering the expression of genes involved in target cell survival. Because a Th2 response against tumors is associated with poor prognosis, we investigated the ability of IL-4 to protect tumor cells from death receptor- and chemotherapy-induced apoptosis. We found that IL-4 treatment significantly reduced CD95 (Fas/APO-1)- and chemotherapeutic drug-induced apoptosis in prostate, breast, and bladder tumor cell lines. Analysis of antiapoptotic protein expression revealed that IL-4 stimulation resulted in up-regulation of cellular (c) FLIP/F…

MaleINFILTRATING LYMPHOCYTESCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsCARCINOMA-CELLSBiologySIGNALING PATHWAYSDownregulation and upregulationCell Line TumorImmunology and AllergyHumansfas ReceptorNON-HODGKINS-LYMPHOMACANCER PATIENTSReceptorBCL-2 PROTEINInterleukin 4EtoposideIL-4 apoptosis cancer stem cellsSettore MED/04 - Patologia GeneraleCHRONIC LYMPHOCYTIC-LEUKEMIAIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalProstatic NeoplasmsFas receptorRecombinant ProteinsCell biologyUp-RegulationProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureFlipCancer researchT-CELLSCamptothecinFemaleInterleukin-4FLICE-INHIBITORY PROTEINSignal transductionCarrier ProteinsRENAL-CELL
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Heart infarct in NOD-SCID mice: therapeutic vasculogenesis by transplantation of human CD34+ cells and low dose CD34+KDR+ cells

2004

Hematopoietic (Hem) and endothelial (End) lineages derive from a common progenitor cell, the hemangioblast: specifically, the human cord blood (CB) CD34+KDR+ cell fraction comprises primitive Hem and End cells, as well as hemangioblasts. In humans, the potential therapeutic role of Hem and End progenitors in ischemic heart disease is subject to intense investigation. Particularly, the contribution of these cells to angiogenesis and cardiomyogenesis in myocardial ischemia is not well established. In our studies, we induced myocardial infarct (MI) in the immunocompromised NOD-SCID mouse model, and monitored the effects of myocardial transplantation of human CB CD34+ cells on cardiac function.…

Vascular Endothelial Growth Factor AneoangiogenesisTime FactorsAngiogenesisCell TransplantationHeart VentriclesCD34Myocardial InfarctionAntigens CD34ApoptosisMice SCIDBiologySCIDPeripheral blood mononuclear cellBiochemistryCulture Media Serum-FreeSerum-FreeCell FusionMiceVasculogenesisMice Inbred NODparasitic diseasesGeneticsAnimalsHumansVentricular Functionendothelial precursorsCell LineageProgenitor cellAntigensMolecular Biologyneoangiogenesis endothelial precursors hematopoietic stem cellsHemodynamicsFetal BloodVascular Endothelial Growth Factor Receptor-2Coculture Techniqueshematopoietic stem cellsCulture MediaTransplantationAutocrine CommunicationCord bloodImmunologycardiovascular systemCancer researchHemangioblastInbred NODCD34neoangiogenesis; endothelial precursors; hematopoietic stem cells; Animals; Antigens CD34; Apoptosis; Autocrine Communication; Cell Fusion; Cell Lineage; Coculture Techniques; Culture Media Serum-Free; Fetal Blood; Heart Ventricles; Hemodynamics; Humans; Mice; Mice Inbred NOD; Mice SCID; Myocardial Infarction; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Ventricular Function; Cell Transplantation; Biotechnology; Biochemistry; Molecular Biology; GeneticsBiotechnology
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CD95 death-inducing signaling complex formation and internalization occur in lipid rafts of type I and type II cells

2004

We investigated the membrane localization of CD95 in type I and type II cells, which differ in their ability to recruit and activate caspase-8. We found that CD95 was preferentially located in lipid rafts of type I cells, while it was present both in raft and non-raft plasma membrane sub-domains of type II cells. After stimulation, CD95 located in phospholipid-rich plasma membrane was recruited to lipid rafts in both types of cells. Similarly, CD95 cross-linking resulted in caspase-independent translocation of FADD/MORT1 and caspase-8 to the lipid rafts, which was prevented by a death domain-defective receptor. CD95 internalization was then rapid in type I and delayed in type II cells and s…

Death Domain Receptor Signaling Adaptor ProteinsEndosomeT-Lymphocytesmedia_common.quotation_subjectImmunologyApoptosisReceptors Tumor Necrosis FactorCell LineMembrane MicrodomainsSettore MED/04 - PATOLOGIA GENERALECell Line TumorReceptorsHumansImmunology and Allergyfas ReceptorFADDInternalizationLipid raftLipid raftsDeath domainmedia_commonTumorbiologyVesicleFas receptorEndocytosisCell biologyProtein TransportCholesterolCD95 death-inducing signaling complexCaspasesCD95biology.proteinlipids (amino acids peptides and proteins)biological phenomena cell phenomena and immunityCaspase-8Tumor Necrosis FactorCaspase-8; CD95; Lipid rafts; Apoptosis; Caspases; Cell Line Tumor; Cholesterol; Death Domain Receptor Signaling Adaptor Proteins; Humans; Membrane Microdomains; Protein Binding; Protein Transport; Receptors Tumor Necrosis Factor; T-Lymphocytes; fas Receptor; Endocytosis; Signal Transduction; Immunology and Allergy; ImmunologyProtein BindingSignal TransductionEuropean Journal of Immunology
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Transplantation of low dose CD34+KDR+ cells promotes vascular and muscular regeneration in ischemic limbs.

2004

Hematopoietic progenitor cell transplantation can contribute to revascularization of ischemic tissues. Yet, the optimal cell population to be transplanted has yet to be determined. We have compared the therapeutic potential of two subsets of human cord blood CD34+ progenitors, either expressing the VEGF-A receptor 2 (KDR) or not. In serum-free starvation culture, CD34+KDR+ cells reportedly showed greater resistance to apoptosis and ability to release VEGF-A, as compared with CD34+KDR- cells. When injected into the hind muscles in immunodeficient SCIDbg mice subjected to unilateral ischemia, a low number (10(3)) of CD34+KDR+ cells improved limb salvage and hemodynamic recovery better than a …

Pathologymedicine.medical_specialtyAngiogenesismedicine.medical_treatmentPopulationMuscle Fibers SkeletalIschemiaNeovascularization PhysiologicAntigens CD34ApoptosisRevascularizationBiochemistryMiceIschemiaGeneticsmedicineAnimalsHumansRegenerationeducationMuscle SkeletalMolecular Biologyeducation.field_of_studybusiness.industryRegeneration (biology)Stem CellsHemodynamicsKinase insert domain receptorExtremitiesmedicine.diseaseFetal BloodFibrosisVascular Endothelial Growth Factor Receptor-2TransplantationImmunologyStem cellbusinessBiotechnologyStem Cell TransplantationFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Human Fetal Aorta Contains Vascular Progenitor Cells Capable of Inducing Vasculogenesis, Angiogenesis, and Myogenesis in Vitro and in a Murine Model …

2007

Vasculogenesis, the formation of blood vessels in embryonic or fetal tissue mediated by immature vascular cells (ie, angioblasts), is poorly understood. We report the identification of a population of vascular progenitor cells (hVPCs) in the human fetal aorta composed of undifferentiated mesenchymal cells that coexpress endothelial and myogenic markers. Under culture conditions that promoted cell differentiation, hVPCs gave rise to a mixed population of mature endothelial and mural cells when progenitor cells were stimulated with vascular endothelial growth factor-A or platelet-derived growth factor-betabeta. hVPCs grew as nonadherent cells and, when embedded in a three-dimensional collagen…

Vascular Endothelial Growth Factor AAngiogenesisBecaplerminNeovascularization PhysiologicAntigens CD34BiologyMuscle DevelopmentMural cellPathology and Forensic MedicineAngiopoietin-2MiceFetusVasculogenesisAntigens CDIschemiaAnimalsHumansCell LineageAC133 AntigenProgenitor cellAortaCells CulturedGlycoproteinsPlatelet-Derived Growth FactorStem CellsProto-Oncogene Proteins c-sisVascular Endothelial Growth Factor Receptor-2Cell biologyEndothelial stem cellVascular endothelial growth factor BVascular endothelial growth factor AVascular endothelial growth factor CImmunologyBlood VesselsPeptidesBiomarkersRegular ArticlesThe American Journal of Pathology
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