0000000000113987

AUTHOR

Roberto Pallini

showing 7 related works from this author

Cilium induction triggers differentiation of glioma stem cells

2020

Glioblastoma multiforme (GBM) possesses glioma stem cells (GSCs) that promote self-renewal, tumor propagation, and relapse. GBM has a poor prognosis, and currently, there are no curative options exist. Understanding the mechanisms of GSCs self-renewal can offer targeted therapeutic interventions. However, insufficient knowledge of the fundamental biology of GSCs is a significant bottleneck hindering these efforts. Here, we show that patient-derived GSCs recruit an elevated level of proteins that ensure the temporal cilium disassembly, leading to suppressed ciliogenesis. Depleting the cilia disassembly complex components at the ciliary base is sufficient to induce ciliogenesis in a subset of…

endocrine system0303 health sciencesPoor prognosisCiliumfungiCilium disassemblyBiologymedicine.diseaseCell biology03 medical and health sciences0302 clinical medicineGentamicin protection assay030220 oncology & carcinogenesisGliomaCiliogenesismedicineStem cellCiliary base030304 developmental biology
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Cilium induction triggers differentiation of glioma stem cells.

2020

Glioblastoma multiforme (GBM) possesses glioma stem cells (GSCs) that promote self-renewal, tumor propagation, and relapse. Understanding the mechanisms of GSCs self-renewal can offer targeted therapeutic interventions. However, insufficient knowledge of GSCs' fundamental biology is a significant bottleneck hindering these efforts. Here, we show that patient-derived GSCs recruit elevated levels of proteins that ensure the temporal cilium disassembly, leading to suppressed ciliogenesis. Depleting the cilia disassembly complex components is sufficient to induce ciliogenesis in a subset of GSCs via relocating platelet-derived growth factor receptor-alpha (PDGFR-α) to a newly induced cilium. Im…

endocrine systemmedicine.medical_treatmentBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesMice0302 clinical medicineGentamicin protection assayGliomaCiliogenesisCell Line TumormedicineAnimalsHumansCell Self Renewal030304 developmental biologyCell Proliferation0303 health sciencesBrain NeoplasmsCiliumGrowth factorfungiBrainCell DifferentiationGliomaCilium disassemblyCell cyclemedicine.diseaseCell biology030220 oncology & carcinogenesisNeoplastic Stem CellsStem cellNeoplasm Recurrence LocalGlioblastomaCell reports
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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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Cancer stem cell analysis and clinical outcome in patients with glioblastoma multiforme

2008

Abstract Purpose: Cancer stem cells (CSC) are thought to represent the population of tumorigenic cells responsible for tumor development. The stem cell antigen CD133 identifies such a tumorigenic population in a subset of glioblastoma patients. We conducted a prospective study to explore the prognostic potential of CSC analysis in glioblastoma patients. Experimental Design: We investigated the relationship between the in vitro growth potential of glioblastoma CSCs and patient death or disease progression in tumors of 44 consecutive glioblastoma patients treated with complete or partial tumorectomy followed by radiotherapy combined with temozolomide treatment. Moreover, we evaluated by immun…

OncologyAdultMaleCancer Researchmedicine.medical_specialtyPathologyAC133 Antigen; Adult; Aged; Antigens CD; Brain Neoplasms; Female; Glioblastoma; Glycoproteins; Humans; Ki-67 Antigen; Male; Middle Aged; Multivariate Analysis; Neoplastic Stem Cells; Peptides; Prospective Studiesmedicine.medical_treatmentPopulationAntigens CDCancer stem cellInternal medicinemedicineHumansAC133 AntigenProspective StudiesAntigensProspective cohort studyeducationAgedGlycoproteinseducation.field_of_studyTemozolomideSettore MED/08 - ANATOMIA PATOLOGICAbusiness.industryBrain NeoplasmsHazard ratioMiddle AgedGliobastoma MultiformeCDRadiation therapyKi-67 AntigenOncologyMultivariate AnalysisNeoplastic Stem CellsImmunohistochemistryFemaleStem cellbusinessGlioblastomaPeptidesmedicine.drug
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A BMP7 Variant Inhibits Tumor Angiogenesis In Vitro and In Vivo through Direct Modulation of Endothelial Cell Biology

2015

Bone morphogenetic proteins (BMPs), members of the TGF-β superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Using an in vitro co-culture endothelial cord formation assay, we investigated the role of a BMP7 variant (BMP7v) in VEGF, bFGF, and tumor-driven angiogenesis. BMP7v treatment led to disruption of neo-endothelial cord formation and regression of existing VEGF and bFGF cords in vitro. Using a series of tumor cell models capable of driving angiogenesis in vitro, BMP7v treatment completely blocked cord formation. Pre-treatment of endothelial cells with BMP7v significantly reduced their cord forming ability, indicating …

Genetics and Molecular Biology (all)MaleVascular Endothelial Growth Factor AFibroblast Growth FactorAngiogenesisBone Morphogenetic Protein 7Nudelcsh:MedicineSmad ProteinsFibroblast growth factorBiochemistryNeovascularizationMiceCell Movementlcsh:ScienceBMP7 Angiogenesis TumorTumorMultidisciplinaryCell DeathNeovascularization PathologicMedicine (all)Cell migrationCell biologyEndothelial stem cellSettore MED/26 - NEUROLOGIAVascular endothelial growth factor ADrug CombinationsAdipose TissueAdipose Tissue; Animals; Bone Morphogenetic Protein 7; Cell Death; Cell Line Tumor; Cell Movement; Cell Proliferation; Collagen; Drug Combinations; Endothelial Cells; Fibroblast Growth Factor 2; Glioblastoma; Human Umbilical Vein Endothelial Cells; Humans; Laminin; Male; Mice Nude; Neoplastic Stem Cells; Neovascularization Pathologic; Neovascularization Physiologic; Proteoglycans; Receptor Fibroblast Growth Factor Type 1; Signal Transduction; Smad Proteins; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Xenograft Model Antitumor Assays; Biochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)Neoplastic Stem CellsFibroblast Growth Factor 2ProteoglycansCollagenmedicine.symptomReceptorType 1Research ArticleSignal TransductionMice NudeNeovascularization PhysiologicBMP7BiologyCell LineSettore MED/04 - PATOLOGIA GENERALECell Line TumormedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansAgricultural and Biological Sciences (all); Biochemistry Genetics and Molecular Biology (all); Medicine (all)Receptor Fibroblast Growth Factor Type 1PhysiologicNeovascularizationCell ProliferationPathologicMatrigelBiochemistry Genetics and Molecular Biology (all)lcsh:REndothelial CellsKinase insert domain receptorVascular Endothelial Growth Factor Receptor-2Xenograft Model Antitumor AssaysAgricultural and Biological Sciences (all)lcsh:QAngiogenesisLamininGlioblastomaPLoS ONE
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Abstract B5: A BMP7 variant inhibits angiogenesis in vitro and in vivo in part by downregulating VEGFR2 and FGFR1 expression in endothelial cells.

2013

Abstract Glioblastoma multiforme (GBM), the most aggressive glioma, requires active angiogenesis for growth and survival. Bone morphogenetic proteins (BMPs), members of the TGF-β superfamily, have numerous biological activities including control of growth, differentiation, and vascular development. Previously, we demonstrated the use of a BMP7 variant (BMP7v) to differentiate glioblastoma stem-like cells (GSLCs) and significantly reduce their tumorigenic potential (Tate and Pallini et al. 2012). Using an in vitro co-culture endothelial cord formation assay, a surrogate of angiogenesis, and its cognate in vivo model, we investigated the role of BMP7v in VEGF, basic FGF (bFGF), tumor-driven a…

Cancer ResearchMatrigelbiologyAngiogenesisSMADFibroblast growth factorReceptor tyrosine kinaseEndothelial stem cellOncologyIn vivoMothers against decapentaplegic homolog 4Immunologybiology.proteinCancer researchMolecular Cancer Therapeutics
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Tumour vascularization via endothelial differentiation of glioblastoma stem-like cells

2010

Glioblastoma is a highly angiogenetic malignancy, the neoformed vessels of which are thought to arise by sprouting of pre-existing brain capillaries. The recent demonstration that a population of glioblastoma stem-like cells (GSCs) maintains glioblastomas indicates that the progeny of these cells may not be confined to the neural lineage. Normal neural stem cells are able to differentiate into functional endothelial cells. The connection between neural stem cells and the endothelial compartment seems to be critical in glioblastoma, where cancer stem cells closely interact with the vascular niche and promote angiogenesis through the release of vascular endothelial growth factor(VEGF) and str…

EndotheliumAngiogenesisTransplantation HeterologousSettore MED/27 - NEUROCHIRURGIAMice TransgenicMice SCIDBiologyModels BiologicalMiceVasculogenesisNeural Stem CellsMice Inbred NODCell Line TumormedicineAnimalsHumansCell LineageVasculogenic mimicryglioblastoma tumor vascularizationIn Situ Hybridization FluorescenceChromosome AberrationsMultidisciplinaryNeovascularization PathologicEndothelial CellsCell DifferentiationVascular endothelial growth factor BEndothelial stem cellVascular endothelial growth factor Amedicine.anatomical_structureVascular endothelial growth factor CTumor Markers BiologicalImmunologyCancer researchEndothelium VascularGlioblastomaNeoplasm TransplantationNature
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