Appeal No. 1999-1330
Application No. 08/527,373
(Brief, paragraph bridging pages 6-7). However, as pointed out by the examiner, this
article was published two years prior to the publication date of Wills (Answer, page 16).
Further to the extent that Jung would have suggested that there was no relationship
between the amount of wild-type p53 present in a tumor cell and the cell's susceptibility
to treatment with either chemotherapy or radiation, both later published articles of Wills
and Nabeya reasonably establish the significance of the presence in a tumor cell of
wild-type p53 and the susceptibility of that cell to damage due to chemotherapeutic
agents and radiation therapy which is not rebutted by subsequent evidence. Further,
we read Jung somewhat differently from appellants. We note, for example, the
statement (page 6393, column 1, first full paragraph):
Recently, Kastan et al. (20) have reported that p53 may play
a role in cellular response to gamma-radiation damage.
Cells that either lack p53 gene expression or overexpress a
mutant p53 do not exhibit a G1 arrest, but G2 arrest is
unaffected. This suggests that wild-type p53 may be
involved in DNA synthesis inhibition following radiation
damage of DNA and provide a cell cycle "check point" (21).
The fidelity of DNA repair during cell cycle arrest may play a
role in the capacity of cells to tolerate radiation injury and
therefore have an impact on radiation sensitivity. In this
study, we investigated alterations of the p53 gene and
correlated these to the response of cells to ionizing radiation
by analyzing the p53 gene in six human SCC cell lines
characterized as RS or RR.
The conclusion reached by Jung and quoted by appellants (Brief, page 7) that
"Jung indicates clearly that there is no correlation between mutations in the p53 gene
and radiation sensitivity or radiation resistance," does not appear to have resulted from
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