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    Histone deacetylase as a therapeutic target.
        
        Trends Endocrinol. Metab. 12, 294-300 (2001)
    
    
    
	    The maintenance of health depends on the coordinated and tightly regulated expression of genetic information. Certain forms of leukemia have become paradigms for the pathogenic role of aberrant repression of differentiation genes. In these acute leukemias, fusion proteins generated by chromosomal translocations no longer function as transcriptional activators, but instead repress target genes by recruiting histone deacetylases (HDACs). The potential benefit of HDAC inhibition has been established by the use of enzyme inhibitors in vitro and in a single reported case of experimental therapy. Because recently identified HDAC inhibitors appear to overcome many drawbacks of early inhibitory compounds in clinical use, the stage is set to test the therapeutic value of HDAC inhibition in leukemias and in other diseases, including solid tumors and aberrant hormonal signaling. This review summarizes the range of diseases expected to respond to HDAC inhibition.
	
	
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        Publication type
        Article: Journal article
    
 
    
        Document type
        Scientific Article
    
 
     
    
     
     
    
    
        Language
        english
    
 
    
        Publication Year
        2001
    
 
     
    
        HGF-reported in Year
        0
    
 
    
    
        ISSN (print) / ISBN
        1043-2760
    
 
    
        e-ISSN
        1879-3061
    
 
    
     
     
	     
	 
	 
     
	
    
        Quellenangaben
        
	    Volume: 12,  
	    Issue: 7,  
	    Pages: 294-300 
	    
	    
	
    
 
    
         
        
            Publisher
            Elsevier
        
 
         
	
         
         
         
         
         
	
         
         
         
    
         
         
         
         
         
         
         
    
        Reviewing status
        Peer reviewed
    
 
     
     
     
     
     
     	
    
        PubMed ID
        11504668
    
    
        Erfassungsdatum
        2001-12-31