Appeal No. 1999-1732
Application No. 08/308,879
hormone, does not contain a sufficient teaching that the claimed result would be obtained.
Thus, the answer fails to set forth a prima facie case that the claims are rendered obvious
by the Kopchick reference.
The treatment of cancers, such as breast cancer, is an unpredictable art. The
somatostatin analogues discussed by Kopchick are hypothesized to inhibit tumor growth
by inhibiting growth hormone secretion. See Kopchick, col. 3, lines 63-65. But that is only
one of a number of hypothesized mechanisms by which somatostatin analogues may
inhibit tumor growth. Even if somatostatin analogues act to inhibit tumor growth by
suppressing serum growth hormone levels, growth hormone antagonists, however, actually
increase the production of endogenous growth hormone in the pituitary, and may lead to
increased serum growth hormone levels. See Cronin Declaration, page 6. Therefore, the
growth hormone antagonists and the somatostatin analogues work by different
mechanisms, and thus the ordinary artisan would not have a reasonable expectation of
success from data produced by somatostatin analogues in inhibiting breast cancer growth
to translate to success with growth hormone antagonists.
The claims were also rejected as obvious over the teachings of the combined
teachings of Phares, Chen and Watahiki.
The Phares reference uses a growth hormone agonist, pleroceroid growth factor
(PGF) to study the effect of endogenous growth hormone levels on the growth of 7, 12,
dimethylbenz(a)anthracene (DMBA)- or N-nitrosomethylurea (NMU)-induced rat mammary
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