Appeal No. 2004-1346 Page 20
Application No. 08/971,338
that GDF-[]1 is required for the proper development and positioning of organs
during embryogenesis … it has now been confirmed that aberrant expression of
GDF-1 has significant and substantial effects on embryonic development.” In
support of this assertion appellant attempts to draw a nexus between the results
in Rankin, and appellant’s specification (page 2, lines 25-29), wherein appellant
discloses, GDF-1 “like other members of this [TGF-β] superfamily, are [sic] likely
[to] play an important role in mediating developmental decisions related to cell
differentiation.”
We disagree with appellant’s assertions. As the examiner points out
(Answer, page 21), “[a]ppellant is relying upon the filing date of the ultimate
parent application, 07/538,372, filed 6/15/90. The Rankin et al. (March 2000)
[reference] was published well [(10 years)] after the effective filing date of the
instant invention and the abstract itself admits that the function of GDF-1 was not
known when discovered by [the] inventor Lee. [6]” According to Rankin (Abstract),
“[o]ur findings suggest that Gdf1 acts early in the pathway of gene activation that
leads to the establishment of left-right asymmetry.” Appellant admits (Brief, page
11), “the appellant has not asserted that the specification teaches that GDF-1
regulates left-right patterning or axis formation in mice.” Rather it is appellant’s
position that Rankin merely provides proof that appellant’s prediction that GDF-1
plays a role in embryonic development is correct. Id. Specifically, appellant
asserts (id.), “the specification discloses at the paragraph bridging pages 12-13
6 Specifically, the Rankin abstract (published a decade after the effective filing date of the instant
application) expressly states, endnotes omitted, emphasis added, GDF-1 “is a TGF-β family
member of unknown function that was originally isolated from an early mouse embryo cDNA
library….”
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