Appeal No. 1996-3330 Application 07/861,458 several C.elegans genes, including deg-1, mec-4, mec-6, which are involved in neuronal degeneration . . . Chalfie et al. suggest in said Abstract and on page 415, second-to-last paragraph, that study of such genes would be desirable because of a possible correlation with several human diseases. However, in our opinion, Chalfie stops short of suggesting that the corresponding gene might be found in or should be isolated from the human genome. At page 410, column 1, first full paragraph, Chalfie states that "[i]nsights into how genetic lesions can lead to neuronal degeneration could be obtained by studying animal models with similar defects." Thus, we read Chalfie as suggesting the use of C. elegans as a model for studying disease conditions in humans which might share a genetic cause. We find no suggestion in Chalfie that one should try to isolate or identify homologues, in humans, of those genes identified in C. elegans. Goddard is relied upon, by the examiner, as teaching that C. elegans has DNA sequences related to a human gene and the use of nucleic acid probes based on a first organism to obtain and sequence hybridization signals from a second organism. (Answer, page 5). The examiner, also, notes that Goddard teaches the desirability of studying an organism of intermediate complexity between the other two organism. (Answer, page 6). However, as pointed out by appellants, both Chalfie and Goddard are "silent as to the subject matter of this invention, namely, how to clone an unknown gene in a higher organism which is homologous to an identified gene in a lower organism." (Brief, page 7Page: Previous 1 2 3 4 5 6 7 8 9 10 11 NextLast modified: November 3, 2007