Appeal No. 2002-0779 Page 2
Application No. 08/825,746
type p53 protein which is required for non-neoplastic growth of said
cell, whereby wild-type p53 gene function is supplied to the cell.
12. The method of claim 4 wherein said portion corresponds to a region
of the p53 gene in the cell which contains the mutations.
The examiner relies on the following references:
Frömmel et al. (Frömmel), ”An estimate on the effect of point mutation and
natural selection on the rate of amino acid replacement in proteins,” J Mol. Evol.,
Vol. 21, pp. 233-257 (1985)
Bowie et al. (Bowie), ”Deciphering the message in protein sequences: Tolerance
to amino acid substitutions,” Science, Vol. 247, pp. 1306-1310 (1990)
Hollstein et al. (Hollstein), ”p53 Mutations in human cancers,” Science, Vol. 253,
pp. 49-53 (1991)
Ngo et al. (Ngo), ”Computational complexity, protein structure prediction, and the
levinthal paradox,” Birkhäuser Boston, pp. 490-495 (1994)
Hodgson, “Advances in vector systems for gene therapy,” Exp. Opin. Ther.
Patents, Vol. 5, No. 5, pp. 459-468 (1995)
Verma et al. (Verma), ”Gene therapy – promises, problems and prospects,”
Nature, Vol. 389, pp. 239-242 (1997)
Anderson, “Human gene therapy,” Nature, Vol. 392, pp. 25-30 (1998)
Miller et al. (Miller), ”Targeted vectors for gene therapy,” J. FASEB, Vol. 9,
pp.190-199 (1995)
Claims 4 and 12 stand rejected under 35 U.S.C. § 112, first paragraph, as
not enabled by the specification.
We reverse.
Background
The p53 gene encodes a tumor suppressor and the mutation of p53 is
associated with cancer. Specification, page 6 (“[M]utational events associated
with tumorigenesis occur in the p53 gene.”). The specification discloses a
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