Appeal No. 2003-1170 Page 2
Application No. 08/817,192
Galton et al. (Galton), “Polymorphisms of the Lipoprotein Lipase Gene and Premature
Atherosclerosis,” Journal of Internal Medicine, Vol. 236, Suppl. 736, pp. 63-68 (1994)
Orkin et al. (Orkin), Report and Recommendations of the Panel to Assess the NIH
Investment in Research on Gene Therapy, issued by the U.S. National Institutes of
Health on December 7, 1995
Verma et al. (Verma), “Gene Therapy-Promises, Problems and Prospects,” Nature, Vol.
389, pp. 239-242 (Sept. 1997)
Claims 50 through 57 stand rejected under 35 U.S.C. § 112, first paragraph
(enablement). We reverse.
Background
The present invention involves the human lipoprotein lipase gene. As explained
by appellants:
It has now been found that a single point mutation in the human
lipoprotein lipase gene which results in an A - G nucleotide change at
codon 291 (nucleotide 1127) of the lipoprotein lipase gene, and a
substitution of serine for the normal asparagine in the lipoprotein lipase
gene product is seen with increased frequency in patients with coronary
artery disease, and is associated with an increased susceptibility to
coronary artery disease, including in particular premature atherosclerosis.
This is expressed as a diminished catalytic activity of lipoprotein lipase,
lower HDL-cholesterol levels and higher triglyceride levels.
Specification, page 2, lines 16-22.
The claimed invention under review in this appeal involves a method of gene
therapy in which a defined replacement lipoprotein lipase gene is expressed in an
individual in which the lipoprotein lipase enzyme has a serine residue present at amino
acid 291 to produce a more fully functional lipoprotein lipase enzyme.
Discussion
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