Interference 104,066
We recognize that Lee’s position is premised on its contention that Vogelstein’s
claimed invention is generic with respect to that of Lee. Throughout its brief, Lee
characterizes Vogelstein’s claims as being directed to a generic method of supplying
wild-type p53 gene function to a cell which has lost said gene function by virtue of a
mutation in a p53 gene. LB, pp. 4-19. According to Lee, its claims are directed to a
method of treating mammalian cancer cells in vivo; whereas, Vogelstein’s claims are
said to be directed to a method of supplying p53 gene function to any tumor cell,
benign9 or malignant, for diagnostic, prophylactic or therapeutic purposes. Thus, Lee
anticipate or render obvious each of Lee’s claims designated as corresponding to the
count. Thus, whether Lee’s invention was unobviousness (and novel) at the time the
Lee application was filed, is immaterial to the issue presented by the belated motion.
9 We point out that Lee’s arguments in its brief for final hearing that the tumor
cells recited in Vogelstein’s claims refer to both benign (non-cancerous) and malignant
(cancerous) tumors (e.g., LB, para. bridging pp. 15-16), were not raised in Lee’s belated
motion 1. Accordingly, since these arguments could have been raised in the original
motion, but were not, they have not been considered by the merits panel. 37 C.F.R. §
1.655(b). Moreover, assuming, arguendo, that these arguments were properly raised in
the belated motion, we would find them unpersuasive for several reasons.
First, Lee has not presented any evidence that (i) those of ordinary skill in the art
would have understood the tumor cells recited in Vogelstein’s claims 11-23 to refer to
benign tumors; or (ii) benign tumors lack p53 gene function. Thus, we find that Lee
relies only on attorney argument to support its contentions. To that end, we point out
that arguments of counsel are accorded little, or no, evidentiary weight. Meitzner v.
Mindick, 549 F.2d 775, 782, 193 USPQ 17, 22 (CCPA 1977), cert. denied, 434 U.S.
854, 195 USPQ 465 (1977).
Second, Lee’s arguments are inconsistent with the evidence of record. We
direct attention to Lee’s exhibits LX 2002, 2003, 2006, 2010, 2013 and 2016 which
disclose the role of the p53 gene as a tumor suppressor gene and that mutations in
said gene result in the development of a malignant phenotype. See, LX2006 which lists
numerous common cancers in the U.S. which lack p53 gene function and, especially,
Table II which highlights the advances in p53 gene research over a sixteen (16) year
period. Consistent with the teachings of Lee’s exhibits we note that the VACO 235
adenoma cell line disclosed in Vogelstein’s specification which is said to be “a benign
8
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