Appeal No. 2006-0298 Page 5
Application No. 10/021,955
In rejecting the claims, however, the examiner appears to have examined
the full scope of the claims, and has not limited the analysis to the claims as they
read on the elected group of SEQ ID NO. 76, nor as they read on the elected
species 247∆C. For example, as to the nature of the invention, the examiner
states that the claims are drawn “to a method of detecting the presence or
absence of any mutation in a periaxin polynucleotide and its association with any
myelinopathy.” Examiner’s Answer, page 4. The examiner states further that
“the specification has not established that a statistically significant association
exists between all of the specific mutations disclosed in the specification, and any
myelinopathy, or any specific myelinopathy, or that a predictable correlation can
be made as to an association between any mutation in the periaxin gene and any
myelinopathy or any specific myelinopathy.” Id. at 5.
In addition, the rejection only briefly touches on the elected subject matter
and the elected species, that is, the claims as they read on SEQ ID NO. 76 and
247∆C, respectively. Thus, the examiner states in the Examiner’s Answer that:
- The specification asserts that based on the common known methods in
the art, mutations in other periaxin polynucleotide sequences (for
example SEQ ID No. 76) could be detected. The specification
discloses mutations in SEQ ID No. 1 and extrapolates the use of
similar techniques to detect mutations in other periaxin polynucleotides
(for example SEQ ID NO. 76). (Pages 4-5)
- It is clear from the teachings in Table-2, that the mere presence of an
alteration in periaxin such as substitution or deletion is not indicative of
myelinopathy. Further, with regard to the 2145T->A and 274 ∆C
mutation in claim 36, and the R196X, C715X, or R82FSX96, the
specification has provided no data as to whether these mutations are
even associated with myelinopathy. (Page 10).
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