Appeal No. 1999-1732
Application No. 08/308,879
hormone antagonist taught by Chen “because the antagonist would be expected to reduce
[growth hormone] activity or influence at the mammary tumor cell [prolactin] and estrogen
receptors like the reduced serum [growth hormone] levels found after PGF.” Answer, page
5. Because Phares teaches that NMU-induced rat mammary tumors are regressed with
decreased growth hormone influence, the Answer also concludes that there is a
reasonable expectation of success that receptor antagonism would be useful for the
treatment of breast cancer.
Appellants put forth several arguments why the combination of Phares, Chen and
Watahiki do not render the claimed process of inhibiting the growth of breast cancer cells
obvious. In particular, Appellants argue that at most, the combination provides an invitation
to experiment, and thus does not produce a reasonable expectation of success. Again, we
agree, for basically the same reasons discussed above with respect to the rejection over
Kopchick.
As pointed out by Appellants, the PGF used by Phares to treat NMU-induced rat
mammary tumors is a growth hormone agonist. As with the somatostatin analogues,
growth hormone agonists decrease serum growth hormone levels. In contrast, as
explained in the expert declaration, growth hormone antagonists may actually increase
serum growth hormone levels. Moreover, the differences in mechanism between the
growth hormone agonist PGF and growth hormone antagonists are also demonstrated by
the fact that PGF treated animals demonstrate increased growth, whereas growth hormone
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