Xian, Jie
  
(2020)
From clinic to laboratory: Signal transduction analysis and future applications, [Dissertation thesis], Alma Mater Studiorum Università di Bologna. 
 Dottorato di ricerca in 
Scienze biomediche e neuromotorie, 33 Ciclo. DOI 10.48676/unibo/amsdottorato/9535.
  
 
  
  
        
        
        
  
  
  
  
  
  
  
    
  
    
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      Abstract
      Results: Here we reported the first case of EH with multifocal metachronous bone lesions. This case shows the possible existence of multifocal metachronous EH without producing a fatal outcome. FOS gene rearrangement is critical to assistant the diagnosis of EH. On the other hand, we studied inositide signalling in AML, confirming the IC50 of MOLM-13, HL-60, THP-1 and U-937 hematopoietic cell lines when exposed to Azacitidine and Venetoclax. Moreover, Azacitidine and Venetoclax treatment could induce an increase of the Sub-G0/G1 phase, as well as a G0/G1 arrest in MOLM-13 cells and HL-60 cells. At the same time, it seems to prolong the S phase in U-937 cells. Furthermore, the combination therapy was also able to specifically induce myelopoiesis, as MOLM-13 and THP-1 cells showed an increased expression of CD14. Finally, the combined treatment triggers a higher expression of PLC-β1, which activates the signaling pathway to degrade PKCα.
     
    
      Abstract
      Results: Here we reported the first case of EH with multifocal metachronous bone lesions. This case shows the possible existence of multifocal metachronous EH without producing a fatal outcome. FOS gene rearrangement is critical to assistant the diagnosis of EH. On the other hand, we studied inositide signalling in AML, confirming the IC50 of MOLM-13, HL-60, THP-1 and U-937 hematopoietic cell lines when exposed to Azacitidine and Venetoclax. Moreover, Azacitidine and Venetoclax treatment could induce an increase of the Sub-G0/G1 phase, as well as a G0/G1 arrest in MOLM-13 cells and HL-60 cells. At the same time, it seems to prolong the S phase in U-937 cells. Furthermore, the combination therapy was also able to specifically induce myelopoiesis, as MOLM-13 and THP-1 cells showed an increased expression of CD14. Finally, the combined treatment triggers a higher expression of PLC-β1, which activates the signaling pathway to degrade PKCα.
     
  
  
    
    
      Tipologia del documento
      Tesi di dottorato
      
      
      
      
        
      
        
          Autore
          Xian, Jie
          
        
      
        
          Supervisore
          
          
        
      
        
      
        
          Dottorato di ricerca
          
          
        
      
        
      
        
          Ciclo
          33
          
        
      
        
          Coordinatore
          
          
        
      
        
          Settore disciplinare
          
          
        
      
        
          Settore concorsuale
          
          
        
      
        
          Parole chiave
          Epithelioid hemangioma, Acute Myeloid Leukemia, nuclear inositide-dependent pathways, phosphoinositides, cell signalling
          
        
      
        
          URN:NBN
          
          
        
      
        
          DOI
          10.48676/unibo/amsdottorato/9535
          
        
      
        
          Data di discussione
          4 Dicembre 2020
          
        
      
      URI
      
      
     
   
  
    Altri metadati
    
      Tipologia del documento
      Tesi di dottorato
      
      
      
      
        
      
        
          Autore
          Xian, Jie
          
        
      
        
          Supervisore
          
          
        
      
        
      
        
          Dottorato di ricerca
          
          
        
      
        
      
        
          Ciclo
          33
          
        
      
        
          Coordinatore
          
          
        
      
        
          Settore disciplinare
          
          
        
      
        
          Settore concorsuale
          
          
        
      
        
          Parole chiave
          Epithelioid hemangioma, Acute Myeloid Leukemia, nuclear inositide-dependent pathways, phosphoinositides, cell signalling
          
        
      
        
          URN:NBN
          
          
        
      
        
          DOI
          10.48676/unibo/amsdottorato/9535
          
        
      
        
          Data di discussione
          4 Dicembre 2020
          
        
      
      URI
      
      
     
   
  
  
  
  
  
    
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