Appeal No. 2006-1565 Page 5
Application No. 09/757,610
directed to treating restenosis (claim 13), or treating bacterial or fungal infections (claim
9), by inhibiting GS-FDH.
With respect to the remaining claims, some of which are limited to killing cancer
cells or reducing their rate of proliferation by inhibiting GS-FDH, the examiner cites
Dermer1 as evidence that “‘petri dish cancer is really a poor representation of
malignancy, with characteristics profoundly different from the human disease’” (Answer,
page 4, and Dermer, column 1). The examiner’s implication, of course, is that the in vitro
examples in the specification would not be predictive of in vivo results in a cancer
patient. Nevertheless, we agree with appellants that “Dermer is not specific enough to
the facts of the instant case” (Reply Brief, page 4) to cast doubt on any assertions in the
specification as to the scope of enablement.
According to the specification, GS-FDH is a highly conserved enzyme that
protects many types of cells (bacterial, fungal, plant, mammalian) from nitrosative stress
(Specification, pages 4 and 33). The examples in the specification appear to
demonstrate that inhibition or reduction of GS-FDH activity in cells of various types (not
just malignant cells) makes the cells more susceptible to the lethal or detrimental effects
of nitrosative stress. See e.g., the in vitro examples on pages 33-36 of the specification.
The examiner has not begun to explain the relevance of Dermer’s general comments
regarding “long-term cell cultures [that] began their careers as stand-ins for real cancer
based only investigator faith” (id.) to any of the examples in the specification.
1 G.B. Dermer, “Another Anniversary for the War on Cancer,” Bio/Technology, Vol. 12, p. 320 (March 12,
1994).
Page: Previous 1 2 3 4 5 6 7 Next
Last modified: November 3, 2007