Appeal No. 1999-1732
Application No. 08/308,879
tumors in vivo. Phares found that PGF caused regression of most of the mammary tumors
induced by DMBA or NMU, and that endogenous growth hormone serum levels were also
reduced. The Answer also relied on Phares for teaching that growth hormone has been
implicated as a growth stimulant for rat mammary tumors and for human breast cancer
cells, which may be due to its regulatory influence prolactin receptors. The reference also
states that NMU-induced mammary tumors are regressed by the inhibition of growth
hormone release from the hypothesis with somatostatin, leading to the conclusion that
growth hormone plays an active role in mammary tumor formation. The Answer
acknowledges that the reference does not teach the use of a growth hormone receptor
antagonist to regress mammary tumor cell growth, but asserts that a “routineer would
reasonably expect that the removal of [growth hormone] influence at the [prolactin] and
estrogen receptors located on mammary tumor cells will cause tumor regression because
decreased serum levels of [growth hormone] and, then, reduced activity at the receptors,
has been shown to regress mammary tumors.” Answer, pages 4-5.
The Answer characterizes Chen as teaching a bovine growth hormone antagonist,
wherein three substitutions have been made. Watahiki is then relied upon for teaching the
identity of growth hormones across several species, and that if the mutations had been
made to human growth hormone, one of the substitutions would have been G120R.
The rejection concludes that it would have been obvious to the ordinary artisan to
substitute the PGF as used by Phares to reduce growth hormone levels with the growth
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