Appeal No. 1996-2756
Application No. 07/987,235
over other members. In this regard, one may mention by way of example, the ras, ..
[family] of oncogenes. … [T]he ras family, involves the activation of protooncogenes
by a point mutation, which apparently results in the expression of a biologically
abnormal product.
THE REJECTION UNDER 35 U.S.C. § 103:
We begin our review of the rejection of record in light of the disclosure
provided by appellants’ specification. According to the examiner (Answer, page 4)
Weinberg discloses “an antisense oligonucleotide which selectively inhibits the K-
ras oncogene, which encodes a protein of 21,000 molecular weight or p21.” The
examiner notes (id.) that Weinberg discloses that “[t]ransfection of nucleic acid
molecules containing K-ras cDNA in the antisense orientation into SW-2-3 cells …
resulted in the loss of the transformed phenotype normally exhibited by SW-2-3
cells.” The examiner further notes (id.) that Weinberg discloses that “the muscle
actin promoter would be sufficiently active to produce antisense oncogene
transcripts in a quantity sufficient to inhibit the target oncogene.” According to the
examiner (Answer, page 5) Weinberg “does not teaches [sic] the inhibition of
oncogenes by antisense oligonucleotides to introns.”
To make up for the deficiency in Weinberg, the examiner applies (Answer,
page 5) Izant to teach “that antisense RNA to introns, exons and splice junctions
4 Paper No. 27, received July 7, 1995.
4
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