Appeal No. 2002-1631 Page 2
Application No. 08/213,433
based on a non-enabling disclosure.
We reverse the rejection.
BACKGROUND
“Chemical carcinogenesis is a multistep process that includes initiation,
promotion and progression . . . with the rate-limiting steps in multistage carcinogenesis
occurring during the promotion and progression phases. Numerous studies have
shown that tumor promotion is a long term process that is partially reversible and that
requires chronic exposure to tumor promoter.” Specification, page 1. “[S]everal genes
that may be involved in tumor promotion or progression have been shown to respond to
AP-1,” a heterodimeric transcriptional activator formed from the phosphoprotein
products of two proto-oncogenes: c-jun and c-fos. Id., pages 1 and 2.
“Recent studies of the c-jun proto-oncogene have revealed that the regions
critical for transcriptional activation include the dimerization domain, the DNA-binding
domain, and an area within the amino terminal half of the c-jun protein that functions as
a transcriptional activation domain.” It has been demonstrated that “regions of c-jun
required for transcriptional activation are the same as those required for c-jun/ras-
induced transformation . . . suggesting that c-jun might transform cells by altering gene
expression through dysregulated DNA transcription;” it has also been demonstrated that
“a dominant negative c-jun mutant which specifically blocked AP-1 activity also blocked
H-ras plus c-jun induced cellular co-transformation.” Specification, page 3.
“[T]he present invention relates to methods of . . . treating carcinogenesis in
mammals via the use of dominant negative deletion mutants of c-jun as therapeutic
agents.” Specification, page 8. As explained by the examiner, “[t]he invention lies in
the realm of gene therapy;” thus, “to be effective, sufficient nucleic acid [ ] encoding a c-
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