Appeal 2007-1149
Application 10/066,273
that Appellants have demonstrated that PRO444 is involved in cancer or
pathogenic angiogenesis, and therefore that inhibition of PRO444 would be
effective in these conditions.
However, Appellants have provided an assay indicating that PRO444
“act[s] to induce the expression of c-fos in pericyte cells” (Specification
142). The Specification states that polypeptides having this activity “would
be expected to be useful for the treatment of conditions where induced
angiogenesis would be beneficial including, for example, wound healing”
(id.).
The references cited by the Examiner support Appellants’ position
that inducers of c-fos expression in pericytes stimulate angiogenesis. In
particular, Sakurai indicates that its findings “support the view that . . .
induction of c-fos mRNA is an important step in the induction of VEGF
expression in retinal pericytes,” VEGF being “a key growth factor for retinal
neovascularization” (Sakurai 2779-2780). In addition, we do not agree with
the Examiner that Sakurai demonstrates that “not all the factors that activate
c-fos . . . induce VEGF” (Answer 12). As noted by the Examiner, Sakurai
states that several prostaglandins induced c-fos mRNA (Sakurai 2777) and
that one of them, PGD2, was shown to induce VEGF mRNA (id. at 2779).
However, we agree with Appellants that Sakurai does not state that the other
prostaglandins do not induce VEGF mRNA (Br. 15-16). Instead, there is no
indication in Sakurai that the effect of these other prostaglandins on inducing
VEGF mRNA was tested.
In addition, Otani indicates that Angiotensin II (AII) “induces VEGF
in retinal microcapillary pericytes” and “is reported to stimulate the
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