Appeal No. 2006-0275 Page 9
Application No. 09/964,667
characteristic of Alzheimer’s disease, and also exhibit increased levels of cell
death through apoptosis (id., page 46). The specification does not indicate
whether AD7c-NTP is over-expressed in neuroectodermal tumor cells, malignant
astrocytoma cells, and glioblastoma cells (all malignant cells of neural origin), or
whether the level of expression is comparable to that of normal neurons.
In our view, it is reasonable for the examiner to question whether “any
particular cancer disease [ ] has as its causation, an overexpression of AD7c-
NTP” (Answer, page 7). Moreover, we note that the specification teaches that
that inhibition of AD7c-NTP expression should result in “the reduction of
frequency of . . . nerve cell death” (Specification, page 6). That is, inhibition of
AD7c-NTP expression should result in a reduction in the frequency of apoptosis,
generally considered a desirable process in destroying tumor cells. Thus, in our
view, it is reasonable for the examiner to question appellants’ “conclu[sion] that
interfering with AD7c-NTP expression through the use of antisense
oligonucleotides and ribozymes would effectively treat neuroectodermal tumors,
malignant astrocytomas and glioblastomas” (Reply Brief, page 4).
We find that the examiner has set forth a reasonable basis for his
conclusion that the scope of protection provided by the claims is not adequately
enabled by the description of the invention provided in the specification, which
appellants have not rebutted by evidence or argument. Accordingly, the rejection
of the claims under 35 U.S.C. § 112, first paragraph, for lack of enablement is
affirmed.
Page: Previous 1 2 3 4 5 6 7 8 9 10 11 Next
Last modified: November 3, 2007