Appeal No. 1999-0339
Application 07/903,588
progression. Thus, while it may be true that some other gene, genes or gene fragments
may be present on the 4.0 and 7.5 kb TaqI fragments we don’t know what those other
genes are. What we do know from Bièche’s studies, however, is that the met proto-
oncogene is present, and that breast cancer prognosis is decreased when one copy of
the met proto-oncogene is lost. Thus, we conclude that the teachings of the Bièche
would have suggested to those of ordinary skill in the art that the met proto-oncogene is
involved in breast cancer.
As to the appellants’ argument that Bièche did not suggest that one could predict
cancer progression measuring the abundance of the met gene per se (Brief, p. 7), we
direct attention to our discussion above wherein we point out that Bièche makes several
references to the loss of heterozygosity as being a reflection of the loss of the met
proto-oncogene. The loss of heterozygosity; i.e., the loss of one of two copies of the
gene, manifestly reflects a decrease in the abundance of the met proto-oncogene in the
breast tumor tissue.
The appellants argue that Bièche limited their study to DNA samples from
patients having a heterzygous (LS) genotype for the TaqI restriction fragment length
polymorphism (RFLP) on chromosome 7q31 and that identification of the specific gene
involved in the genetic loss would be essential for the examination of patients having a
homozygous (LL or SS) genotype. Brief, pp. 7-8. We find this argument unpersuasive.
As pointed out by the examiner, claim 1 is not limited to patients having a homozygous
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