Appeal No. 2002-1299 Page 3
Application No. 08/962,740
transgenic mice. See Durbin, bridging paragraph, pages 443-444. The
examiner explains (Answer, page 3), Stat1
is a gene product which interacts with interferon to change the viral
tropism of the cell containing the Stat1, i.e. places the cells in an
antiviral state. Therefore, a cell or cell line which does not produce
the Stat1 product, i.e. a null allele, would be more susceptible to
viral infection and replication thus being a good vehicle for viral
production.
According to the examiner (Answer, bridging paragraph, pages 3-4), while
“Durbin speaks to the development and utility of cell lines with such an allele …
[the reference] does not teach developing a cell line from the mice.”
To make up for the deficiency in Durbin, the examiner relies on Leder,
Jallat and Todaro. According to the examiner (Answer, page 4), Leder, Jallat
and Todaro teach the production of cell lines from transgenic mice.
Claim 1:
In response to the rejection of record, appellants argue (Brief, page 4):
Durbin does not disclose or suggest making an immortalized Stat1
deficient cell line. … Durbin never discloses or suggests any
reason to prepare an immortalized Stat1-deficient cell line. Thus,
Durbin clearly does not suggest an immortalized Stat1-deficient cell
line or the utility of such immortalized cell line as hosts for
producing viral stocks, for producing recombinant viral vectors, or
for detecting viruses and the like.
In addition, appellants argue (id.), “Leder, Jallat and Todaro, do not remedy the
deficiencies of Durbin as none of these references relate to Stat1-deficient
transgenic animals or cell lines.” According to appellants (Brief, page 5), “[t]he
question here is not whether the cell line of the Stat1-deficient mouse disclosed
in Durbin could be immortalized, but whether one would have been motivated to
perform such immortalization of Durbin’s Stat1-deficient cell line based on Jallat,
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