Appeal 2007-1149
Application 10/066,273
expression of c-fos and c-jun and their respective proteins, c-Fos and c-Jun,
which constitute the heterodimer complex called AP-1” (Otani 1196-1197).
Otani states that the data “suggest a predominant role of AP-1 . . . in AII
induction of VEGF” in bovine retinal microcapillary pericytes (id. at 1977).
Thus, both Sakurai and Otani appear to support Appellants’ position that
inducers of c-fos expression in pericytes stimulate angiogenesis. (Br. 14-
18.)
Therefore, we agree that those skilled in the art would reasonably
accept the Specification’s assertion that PRO444 is a stimulator of
angiogenesis. The Examiner has provided no basis for doubting that
stimulating angiogenesis is useful in, for example, wound healing, and
therefore is a specific and substantial utility.
The Examiner cites Orlandini as disclosing that VEGF expression in
fibroblasts is unaffected by c-fos. We disagree. Granted, Orlandini states
that, “in vitro, the VEGF mRNA level is not affected by c-fos” (Orlandini
11680). However, Orlandini recognizes that this is in contrast with
observations that VEGF mRNA “is elevated in papillomas originating from
c-fos wild-type cells with respect to papillomas originating from c-fos-
deficient cells” (id.). Orlandini concludes that “[i]t is likely that other events
must happen before VEGF is induced during tumor progression since this
effect can only be observed in vivo” (id.). Thus, we agree with Appellants
(Br. 20-21) that Orlandini does not disclose that expression of c-fos in
fibroblasts is unaffected by c-fos, merely that it is unaffected in vitro.
The Examiner cites Diaz-Flores and Ozerdem as evidence that “the
involvement of pericytes in angiogenesis is controversial and not fully
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