Appeal No. 1999-0339
Application 07/903,588
deletion of the met proto-oncogene. To that end, we direct attention to (i) “Fig. 1- Loss
of heterozygosity at c-met proto-oncogene,” (ii) Table II “Multivariant Analysis of
Metastasis-Free and Overall Survival in 121 Patients Heterozygous for c-met Proto-
oncogene,” (iii) p. 141, col. 2, last sentence, which in a discussion of Table III states
that the results “indicate[] that the c-met deletion is strongly predictive of metastasis in
patients with grade III tumours,” and (iv) p. 142, col. 1, wherein it states that “Such loss
of heterozygosity on chromosome 7q is consistent with cytogenetic findings in primary
breast tumours, and the frequencies of the c-met deletion may be underestimated
because of cellular heterogeneity of tumour biopsy material.”
Second, it was known in the art, and taught by Bièche, that the met gene located
on chromosome 7q31 is a proto-oncogene. Bièche, p. 140, col. 1, para. 1; Park, the
entire publication. The pmetH probe employed by Bièche was specific for the met
proto-oncogene. Bièche, p. 139, col. 1, para. 1, p. 140, col. 1, para. 2. Thus, it is
reasonable to conclude that the loss of heterozygosity from the region of chromosome
7 which was known to contain the met proto-oncogene would have suggested to those
of ordinary skill in the art that the met proto-oncogene was responsible for the poor
prognosis in the breast cancer patients reported by Bièche.
Third, although it is argued that any one of other genes present on chromosome
7 could be responsible for the initiation of breast malignancies, neither the appellants
nor Dr. Dean state what “other genes” are present that could play a role in tumor
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