Appeal No. 2003-2091 Page 3
Application No. 09/266,465
Claims 9-13 stand rejected under 35 U.S.C. § 112, second paragraph, as
indefinite.
We affirm the indefiniteness rejection but reverse all of the rejections over the
prior art.
Background
“Adenoviral vectors have become one of the leading vectors for gene transfer,
especially in gene therapy contexts.” Specification, page 1. “Several studies have
demonstrated the ability of adenovirus-mediated wild-type p53 [tumor suppressor]
replacement gene therapy to induce . . . apoptosis in malignant cells carrying p53 gene
mutations.” Id.
“Apoptosis, or programmed cell death, is an essential occurring process for
normal embryonic development . . . and suppressing carcinogenesis.” Id., page 2.
“[L]ittle is known of the mechanisms by which wild-type p53 induces apoptosis. It
appears that p53 induces apoptosis, at least in part, by up-regulating proapoptotic
members of the Bcl-2 family of proteins.” Id., page 1.
“Bcl-2 acts to suppress cell death triggered by a variety of stimuli. . . . [T]here is
a family of Bcl-2 cell death regulatory proteins which share in common structural and
sequence homologies. These different family members have been shown to either
possess similar functions to Bcl-2 or counteract Bcl-2 function and promote cell death.”
Id., page 2. “One such family member having Bcl-2 counteracting function is Bax.” Id.
Other proapoptotic members of the Bcl-2 family include Bak, Bad, Bid, Bik, and Harikiri.
Specification, pages 21-22.
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