Ex Parte Hogan - Page 13


              Appeal No. 2006-1517                                                                  Page 13                 
              Application No. 09/976,423                                                                                    

                     Thus, Rosen teaches that a polymorphism in the TNF-α gene is informative in                            
              predicting which livers are more likely to be reinfected in HCV-infected patients, but that                   
              polymorphisms in the TNF-β gene are not.  In view of Rosen’s teaching that TNF-β-                             
              specific primers are useless for predicting likelihood of HCV reinfection, we conclude                        
              that the examiner has not adequately explained why Rosen would have led a person                              
              skilled in the art to package primers specific for both TNF-α and TNF-β into a kit.                           
                     Like Rosen, Tarkowski teaches PCR primers for amplifying parts of the TNF-α                            
              and TNF-β genes.  See pages 2078-2079.  Tarkowski analyzed the association                                    
              between aspects of Alzheimer’s disease (AD) and polymorphisms in the TNF-α and                                
              TNF-β genes, but concluded that “the levels of these cytokines did not differ significantly                   
              in patients displaying different alleles of the TNF gene.”  Abstract.  See also page 2080,                    
              right-hand column, second full paragraph:                                                                     
                     [T]he frequencies of TNFα1 versus TNFα2 alleles did not differ between                                 
                     patients with AD and control subjects, suggesting a lack of association                                
                     between TNF polymorphism and the susceptibility for AD.  The intrathecal                               
                     TNFα levels or the degree of cognitive deficit did not differ significantly                            
                     between the groups of AD patients with different TNFα or TNFβ gene                                     
                     polymorphism, suggesting a lack of association between TNF                                             
                     polymorphism and the clinical severity of AD.                                                          
              (Emphases added.)                                                                                             
                     Thus, Tarkowski teaches that the TNF-α and TNF-β polymorphisms that were                               
              examined were not associated with either the susceptibility to or the clinical severity of                    
              Alzheimer’s disease in potential patients.  In view of this teaching, we conclude that the                    
              examiner has not adequately explained why Tarkowski would have led a skilled worker                           
              to package the TNF-α- and TNF-β-specific primers disclosed by Tarkowski into a kit.                           







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