Ex Parte Qu et al

Board of Patent Appeals and Interferences

Nov 12, 2008

10714508 (B.P.A.I. Nov. 12, 2008)

UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE BOARD OF PATENT APPEALS
AND INTERFERENCES
__________

Ex parte KEVIN Z. QU and ANTHONY SFERRUZZA
__________

Appeal 2008-3490
Application 10/714,508
Technology Center 1600
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Decided: November 12, 2008
__________

Before ERIC GRIMES, RICHARD M. LEBOVITZ, and MELANIE L.
McCOLLUM, Administrative Patent Judges.

McCOLLUM, Administrative Patent Judge.

DECISION ON APPEAL
This is an appeal under 35 U.S.C. § 134 involving claims to a
genotype determination method. The Examiner has rejected the claims as
obvious. We have jurisdiction under 35 U.S.C. § 6(b). We reverse.
STATEMENT OF THE CASE
The angiotensin converting enzyme (ACE) “gene is present in the
population as different allelic variants. A variant of particular interest
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clinically is the presence or absence of a 287 base pair (‘bp’) non-coding
fragment within Intron 16.” (Spec. ¶ 0005.) “When this 287 bp sequence is
present in an ACE gene, the genotype is designated ‘I’ for ‘insertion’;
conversely, when this 287 bp sequence is absent in an ACE gene, the
genotype is designated ‘D’ for ‘deletion’” (id.). “Because the genome
contains two copies of each gene, referred to as ‘alleles,’ possible ACE
genotypes with regard to this variant are D/D, I/D, and I/I” (id.).
Claims 2 and 40-72 are pending and on appeal. We will focus on
claim 2, which reads as follows:
2. A method of determining an angiotensin converting enzyme (ACE)
genotype in a sample, comprising:
amplifying DNA in a single amplification reaction from the sample
with a first pair of flanking primers that hybridize to nucleic acid sequences
flanking an ACE gene sequence, and a third primer that specifically binds to
said ACE gene sequence and together with one of the flanking primers
forms a second pair of primers; and
detecting a homozygous ACE genotype by the production of one or
two amplification products and a heterozygous ACE genotype by the
production of three amplification products.
Claims 2, 40-48, 50, and 67-70 stand rejected under 35 U.S.C.
§ 103(a) as obvious over Lindpaintner1 in view of Lin2 (Ans. 3).
Claims 2, 40-48, 50, and 67-70 stand rejected under 35 U.S.C.
§ 103(a) as obvious over Teranishi3 in view of Lin (id. at 7).

1 Klaus Lindpaintner et al., A Prospective Evaluation of an Angiotensin-
Converting-Enzyme Gene Polymorphism and the Risk of Ischemic Heart
Disease, 332 THE NEW ENGLAND JOURNAL OF MEDICINE 706-711 (1995).
2 Mei-Hui Lin et al., Real-time PCR for rapid genotyping of angiotensin-
converting enzyme insertion/deletion polymorphism, 34 CLINICAL
BIOCHEMISTRY 661-666 (2001).
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Claims 49 and 54-59 stand rejected under 35 U.S.C. § 103(a) as
obvious over Lindpaintner in view of Lin, Soubrier,4 and Buck5 (id. at 11).
Claims 62-65 stand rejected under 35 U.S.C. § 103(a) as obvious over
Lindpaintner in view of Lin and van Bockxmeer6 (id. at 15).
Claim 66 stands rejected under 35 U.S.C. § 103(a) as obvious over
Lindpaintner in view of Lin, van Bockxmeer, Soubrier, and Buck (id. at 18).
Claims 2, 40-48, 50, and 67-70 stand rejected under 35 U.S.C.
§ 103(a) as obvious over Lin in view of Hiratsuka7 (id. at 21).
Claims 49 and 51-61 stand rejected under 35 U.S.C. § 103(a) as
obvious over Lin in view of Hiratsuka, Soubrier, and Buck (id. at 25).
Claims 62-65 stand rejected under 35 U.S.C. § 103(a) as obvious over
Lin in view of Hiratsuka and van Bockxmeer (id. at 33).
Claim 66 stands rejected under 35 U.S.C. § 103(a) as obvious over
Lin in view of Hiratsuka, van Bockxmeer, Soubrier, and Buck (id. at 36).
3 Megumi Teranishi et al., Insertion/deletion angiotensin converting enzyme
gene polymorphism affects the microvascular structure of the kidney in
patients with nondiabetic renal disease, 17 JOURNAL OF HYPERTENSION 351-
356 (1999).
4 US 5,736,323, Apr. 7, 1998.
5 G.A. Buck et al., Design Strategies and Performance of Custom DNA
Sequencing Primers, 27 BIOTECHNIQUES 528-536 (1999).
6 Frank M. van Bockxmeer et al., Angiotensin-Converting Enzyme and
Apolipoprotein E Genotypes and Restenosis After Coronary Angioplasty, 92
CIRCULATION 2066-71 (1995).
7 Masahiro Hiratsuka et al., Detection of Angiotensin-Converting Enzyme
Insertion/Deletion Polymorphisms Using Real-Time Polymerase Chain
Reaction and Melting Curve Analysis with SYBR Green I on a GeneAmp
5700, 289 ANALYTICAL BIOCHEMISTRY 300-303 (2001).
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Claims 71 and 72 stand rejected under 35 U.S.C. § 103(a) as obvious
over Lin in view of Hiratsuka (id. at 39).
LINDPAINTNER OR TERANISHI WITH LIN
The Examiner rejects claims 2, 40-48, 50, and 67-70 under 35 U.S.C.
§ 103(a) as obvious in view of Lindpaintner and Lin and as obvious in view
of Teranishi and Lin. The Examiner also rejects claims 49, 54-59, and 62-66
under 35 U.S.C. § 103(a) as obvious in view of Lindpaintner and Lin and
further in view of one or more of Soubrier, Buck, and van Bockxmeer.
The Examiner relies on both Lindpaintner and Teranishi for teaching:
a method of determining an angiotensin converting enzyme
genotype in a sample comprising: a) amplifying DNA from the
sample with a i) first pair of flanking primers that hybridize to
nucleic acid sequences flanking an ACE gene sequence, and
ii) a third primer that specifically binds to said ACE gene
sequence and together with one of the flanking primers forms a
second pair of primers . . . ; and b) detecting a[n] . . . ACE
genotype by the production of . . . amplification products.
(Id. at 4 and 7-8.) The Examiner finds that neither Lindpaintner nor
Teranishi “teach that the amplification reaction is carried out with three
separate primers in a single amplification reaction” (id. at 6 and 10).
The Examiner relies on Lin for teaching “amplification using three
primers simultaneously in a single amplification reaction” (id.). In
particular, the Examiner finds that “Lin teaches a method of determining an
angiotensin converting enzyme (ACE) genotype in a sample comprising:
amplifying DNA in a single amplification reaction from a sample” (id.).
The Examiner concludes that it would have been prima facie obvious
“to have incorporated the genotyping analysis of the ACE genotype, with
three primers included in a PCR reaction simultaneously taught by Lin into
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the method of ACE genotyping with Lindpaint[n]er [or Teranishi]” (id.). In
particular, the Examiner finds:
Considering the potential for high throughput analysis using the
real-time and multiplexed method taught by Lin and the
significant time saving provided by multiplexing the
amplification using the three primers simultaneously, it would
have been obvious to extend the method of Lindpaint[n]er or
Lin to achieve two I amplicons and a single D amplicon in a
single amplification reaction.
(Id. at 44-45.) In addition, the Examiner finds:
When Teranishi is combined with the three primer, single
amplification method taught by Lin, a method that comprises
two insertion specific amplicons together with a deletion
specific amplicon is achieved. The result of this combination of
references yields genotype analysis comprising two amplicons
in I allele homozygotes, a single amplicon in D allele
homozygotes and three amplicons in I/D heterozygotes.
(Id. at 47.)
Appellants contend that none of Lindpaintner, Teranishi, and Lin
teaches a method that produces two amplicons from the I-allele in a single
PCR reaction (App. Br. 14 and 24). Appellants also contend that there
would have been no motivation to combine Lin’s real-time PCR method
with the two-step methods of Lindpaintner and Teranishi (id. at 15 and 24).
Issue
The issue is whether the Examiner has set forth a prima facie case that
it would have been obvious to both amplify DNA in a single amplification
reaction using three primers and detect a homozygous genotype by the
production of one or two amplification products and a heterozygous
genotype by the production of three amplification products.
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Findings of Fact
1. Lindpaintner discloses that the angiotensin converting enzyme
(ACE) gene “contains a polymorphism based on the presence (insertion [I])
or absence (deletion [D]) within an intron of a 287-base-pair (bp) nonsense
DNA domain, resulting in three genotypes (DD and II homozygotes, and DI
heterozygotes)” (Lindpaintner 706).
2. Lindpaintner discloses determining ACE genotypes by
identifying the D and I alleles based on PCR amplification “of the respective
fragments from intron 16 of the ACE gene and size fractionation and
visualization by electrophoresis” (id. at 707).
3. Specifically, Lindpaintner discloses using a “primer pair to
amplify the D and I alleles, resulting in 319-bp and 597-bp amplicons,
respectively. . . . The amplification products of the D and I alleles were
identified by 300-nm ultraviolet transillumination as distinct bands.” (Id.)
4. In addition, Lindpaintner discloses:
Because the D allele in heterozygous samples is preferentially
amplified, each sample found to have the DD genotype was
subjected to a second, independent PCR amplification with a
primer pair that recognizes an insertion-specific sequence. . . .
The reaction yields a 335-bp amplicon only in the presence of
an I allele, and no product in samples homozygous for DD. . . .
This procedure correctly identified the 4 to 5 percent of samples
with the DI genotype that are misclassified as DD with the
insertion-spanning primers.
(Id. at 707-708.)
5. Teranishi also discloses determining the I/D, II, and DD
genotypes of the ACE gene by PCR (Teranishi 352).
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6. Teranishi discloses a first PCR reaction using sense and
antisense primers, resulting in “a 190 bp fragment in the absence of the
insertion and a 490 bp fragment in the presence of the insertion” (id.)
7. Teranishi also discloses a second PCR reaction in which “the
sense primer was replaced by an insertion-specific primer. . . . A 408 bp
PCR product indicates the presence of at least one I allele.” (Id.)
8. Lin discloses genotyping the “ACE[ ]gene I/D allele by real-
time PCR and melting curve analysis” (Lin 662 (emphasis omitted)).
9. To conduct PCR, Lin discloses adding ACE1, ACE2, and
ACE3 primers to the reaction mixture (id.).
10. Lin’s ACE1 and ACE3 primers flank an intron 16 sequence of
the ACE gene. Lin’s ACE2 primer binds to this ACE intron 16 sequence.
(Id. at 663: Fig. 1.)
11. Using these primers, Lin discloses the amplification of a 65 bp
PCR product for the I allele and an 84 bp PCR product for the D allele (id. at
664).
12. Specifically, Lin discloses that “the II alleles produced a
distinct melting peak at 73.9°C, while the DD alleles individual generated a
melting peak at 76.2°C” (id. at 663).
13. With regard to an individual having an I/D allele, Lin discloses
forming “two melting peaks at 73.9°C and 76.2°C corresponding to the I and
D allele” (id. at 662).
14. Based on the size of the I/D insertion (287 bp), Lin’s 65 bp
PCR product for the I allele must be the product of the ACE2 and ACE3
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primers, not of the ACE1 and ACE3 primers (id. at 663: Fig. 1; see also
Ans. 24 and Reply Br. 9).
15. Lin compares its real-time technique to conventional PCR with
“primers situated outside the insertion/deletion area in intron 16 of the ACE
gene, [which results in] a PCR product of 490 base pairs (bp) and 190 bp
represent[ing] the insertion and deletion allele, respectively” (id. at 662).
16. In the context of this conventional PCR, Lin states:
With the smaller size of PCR product, the D allele may be
preferentially amplified in the heterozygote individuals giving
rise to mistyping of ID individuals in approximately 5% of
cases. . . . To avoid this mistyping, each sample found to have
the DD genotype was subjected to a second independent PCR
amplification with a set of primers that recognize an insertion-
specific sequence.
(Id.)
17. Lin discloses that, “[w]ith the real-time PCR method, [they]
were able to rapidly and accurately complete the genotyping of the 40
specimens in one round of real-time PCR,” including the I/D specimens that
had been mistyped as DD by the first amplification step of conventional
PCR (id. at 663).
18. Lin states that the mistyping “problem arose due to the different
size of I and D allele PCR products” (id. at 664).
19. However, Lin states that, with their real-time PCR, “the PCR
product is relatively small (65 bp for I allele and 84 bp for D allele) and the
preferential amplification of either I or D allele is negligible. This potential
problem was further overcome by optimization of the primers
concentration.” (Id.)
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Analysis
A claim “composed of several elements is not proved obvious merely
by demonstrating that each of its elements was, independently, known in the
prior art.” KSR Int’l v. Teleflex Inc., 127 S. Ct. 1727, 1741 (2007). The
relevant question is “whether there was an apparent reason to combine the
known elements in the fashion claimed by the patent at issue.” Id.
As admitted by the Examiner (Ans. 6 and 10), neither Lindpaintner
nor Teranishi discloses amplifying DNA in a single amplification reaction
with a first pair of flanking primers that hybridize to nucleic acid sequences
flanking a gene sequence and a third primer that specifically binds to the
gene sequence, as recited in claims 2 and 67. Instead, Lindpaintner and
Teranishi each discloses a two step amplification, where the first step uses
flanking primers to form a D amplicon and a longer I amplicon and the
second step uses an internal primer together with another primer to form a
shorter I amplicon (Findings of Fact (FF) 2-7). If these two steps were
combined in a single amplification reaction under conditions in which all
three of these products (and no other products) are formed, the amplification
would result in a single amplicon for homozygous DD individuals, two
different amplicons for homozygous II individuals, and three amplicons for
heterozygous I/D individuals. However, we agree with Appellants that the
Examiner has not set forth a prima facie case that it would have been
obvious to modify Lindpaintner or Teranishi to combine their two
amplification steps into a single amplification reaction under conditions in
which all three of these products are formed.
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In particular, neither Lindpaintner nor Teranishi teach or suggest
combining these two amplification steps into one reaction. Instead, both
references disclose that the steps are conducted as separate amplification
reactions (FF 4 and 7). In addition, Lindpaintner discloses that the second
amplification reaction serves to correctly identify samples with a DI
genotype that, due to preferential amplification, are misclassified as DD by
the first amplification step (FF 4). The Examiner has not provided an
adequate explanation as to whether this purpose can be achieved by
combining the amplification steps in a single reaction under conditions in
which the heterozygous genotype forms three amplification products.
Lin discloses accurately genotyping specimens in one round of real-
time PCR (FF 17). However, Lin discloses detecting one amplification
product for each of the II and DD alleles (i.e., the homozygous ACE
genotypes) and two amplification products for the I/D allele (i.e., the
heterozygous ACE genotype) (FF 11-13). Lin does not disclose the
production of three amplicons. As a result, the Examiner has not shown
that, if Lindpaintner or Teranishi is modified to include a single
amplification reaction using three primers as described in Lin, it would have
been obvious to detect a homozygous genotype by the production of one or
two amplification products and a heterozygous genotype by the production
of three amplification products, as recited in claims 2 and 67. For at least
these reasons, we reverse the rejections of claims 2 and 67 and of claims 40-
48, 50, and 68-70, which depend from either claim 2 or claim 67, under 35
U.S.C. § 103(a) as obvious in view of Lindpaintner and Lin and as obvious
in view of Teranishi and Lin.
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Claim 62 is directed to a method for identifying a patient with a
heightened risk of suffering from a disease. The method includes
determining the ACE genotype in a sample by the steps recited in claim 2.
We have already concluded that the Examiner has not set forth a prima facie
case that claim 2 would have been obvious in view of Lindpaintner and Lin.
The Examiner relies on van Bockxmeer for additional limitations recited in
claim 62, and has not pointed to any disclosure in this reference that would
make up for the deficiencies discussed above (Ans. 15-17). Thus, we
conclude that the Examiner has not set forth a prima facie case that claim 62
and claims 63-65, which depend from claim 62, would have been obvious in
view of Lindpaintner, Lin, and van Bockxmeer. We therefore reverse the
obviousness rejection of these claims in view of these references.
Claims 49 and 54-59 depend from claim 2 and claim 66 depends from
claim 63. We have already concluded that the Examiner has not set forth a
prima facie case that claims 2 and 63 would have been obvious over
Lindpaintner, Lin, and van Bockxmeer. The Examiner relies on Soubrier
and Buck for limitations recited in dependent claims, and has not pointed to
any disclosure in these references that would make up for the deficiencies
discussed above (Ans. 11-15 and 18-20). Thus, we conclude that the
Examiner has not set forth a prima facie case that claims 49, 54-59, and 66
would have been obvious over Lindpaintner and Lin in view of the
additional references applied therewith. We therefore reverse the
obviousness rejection of these claims in view of these references.
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LIN AND HIRATSUKA
The Examiner rejects claims 2, 40-48, 50, and 67-72 under 35 U.S.C.
§ 103(a) as obvious over Lin in view of Hiratsuka. The Examiner also
rejects claims 49 and 51-66 under 35 U.S.C. § 103(a) as obvious over Lin in
view of Hiratsuka and further in view of one or more of Soubrier, Buck, and
van Bockxmeer.
The Examiner relies on Lin for teaching “amplification using three
primers simultaneously in a single amplification reaction for the
determination of angiotensin converting enzyme genotype” (Ans. 21).
Specifically, the Examiner finds:
Lin teaches a method of determining an angiotensin converting
enzyme genotype in a sample comprising: a) amplifying DNA
from the sample with a i) first pair of flanking primers that
hybridize to nucleic acid sequences flanking an ACE gene
sequence, and ii) a third primer that specifically binds to said
ACE gene sequence and together with one of the flanking
primers forms a second pair of primers . . . ; and b) detecting a
homozygous ACE genotype by the production of one or two
amplification products.
(Id.) The Examiner also finds:
The multiplexed real-time PCR amplification technique taught
by Lin genotypes the samples using three primers, however
only detects two of the three potential amplification products -
the deletion allele, a product of the amplification using ACE1
and ACE3 when the insertion is not present, resulting in an
amplicon of 84 base pairs in length and the insertion allele, a
product of the ACE2 (insertion specific) primer and ACE3,
resulting in an amplicon of 65 base pairs in length.
(Id. at 24.)
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The Examiner relies on Hiratsuka for teaching “a similar method of
genotype analysis and [for] teach[ing] very similar flanking primers which
amplify the same general region of the ACE gene sequence” (id.). The
Examiner finds:
Unlike Lin, Hiratsuka detects two amplicons, both products of
the ‘ACE1’ and ‘ACE3’ primers - an insertion allele, where the
full length product of the flanking primers produces an
amplicon of 373 base pairs in length when the insertion is
present, and a deletion allele, where the product of the flanking
primer produces an amplicon of 85 base pairs in length when
the insertion is not present.
(Id.) The Examiner finds that “combining these amplicons with the
amplicons provided by Lin would produce three amplification products in
the heterozygote - 2 products for the I allele and 1 for the D allele” (id. at
23).
The Examiner concludes:
It would have been prima facie obvious . . . to have extended
the genotyping analysis of the ACE genotype, with three
primers included in a PCR reaction simultaneously taught by
Lin to incorporate the third amplicon comprising the product of
the ACE1 and ACE3 primers in the presence of the 287 bp Alu
insertion, resulting in an amplicon of 373 basepairs as taught by
Hiratsuka.
(Id. at 23-24.) In particular, the Examiner states that it would have been
prima facie obvious “that the placement of the primers taught by Lin, using
the conditions and primer concentrations taught by Hiratsuka would produce
a set of amplicons wherein the presence of three amplicons is indicative of a
heterozygous genotype with a reasonable expectation for success” (id. at
25).
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Appellants contend that the “question here is not whether a third
amplicon could have been produced by Lin from the ACE1-ACE3 primer
pair (clearly it is possible), but rather, whether one would have been
motivated to produce such an amplicon and whether it would be useful in
Lin’s method” and that “the answer to both questions is no” (Reply Br. 11).
In particular, Appellants contend that “there is no motivation to produce a
second amplicon from the I-allele because it may confound identification of
the characteristic I- and D-allele amplicons already produced, but would not
provide any additional information” (id.).
Issue
The issue is whether the Examiner has set forth a prima facie case that
it would have been obvious to modify Lin to detect a heterozygous genotype
by the production of three amplification products.
Findings of Fact
20. Hiratsuka discloses “the analysis of ACE insertion/deletion
polymorphisms” by performing PCR using a forward and reverse primer and
melting curve analysis (Hiratsuka 301).
21. Hiratsuka discloses that the resulting “373-bp fragment
corresponded to the I allele, whereas the 85-bp fragment corresponded to the
D allele” (id.).
Analysis
As noted above, a claim “composed of several elements is not proved
obvious merely by demonstrating that each of its elements was,
independently, known in the prior art.” KSR Int’l v. Teleflex Inc., 127 S. Ct.
1727, 1741 (2007). The relevant question is “whether there was an apparent
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reason to combine the known elements in the fashion claimed by the patent
at issue.” Id.
Lin discloses genotyping the “ACE[ ]gene I/D allele by real-time PCR
and melting curve analysis” (FF 8). To conduct PCR, Lin discloses adding
ACE1, ACE2, and ACE3 primers to the reaction mixture (FF 9). Lin’s
ACE1 and ACE3 primers flank an intron 16 sequence of the ACE gene and
its ACE2 primer binds to this ACE intron 16 sequence (FF 10). Using these
primers, Lin discloses detecting one amplification product for each of the II
and DD alleles (i.e., the homozygous ACE genotypes) and two amplification
products for the I/D allele (i.e., the heterozygous ACE genotype) (FF 11-13).
Lin does not disclose amplifying the I allele with flanking primers ACE1
and ACE3 (FF 14).
Hiratsuka discloses amplifying the I allele with flanking primers
(FF 20-21). However, the Examiner has not provided a sufficient reason for
one of ordinary skill in the art to vary the primer concentrations and/or other
conditions in Lin in order to amplify the I allele with flanking primers ACE1
and ACE3. In particular, Lin specifically discloses optimizing the primer
concentrations to overcome preferential amplification between the two PCR
products formed in its reaction (FF 19). The Examiner has not explained
why one of ordinary skill in the art would have instead used “the conditions
and primer concentrations taught by Hiratsuka” (Ans. 25). For at least these
reasons, we reverse the rejection of claims 2 and 67 and of claims 40-48, 50,
and 68-72, which depend from either claim 2 or claim 67, under 35 U.S.C.
§ 103(a) as obvious over Lin in view of Hiratsuka.
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As discussed above, the method of claim 62 includes determining the
ACE genotype in a sample by the steps recited in claim 2. We have already
concluded that the Examiner has not set forth a prima facie case that claim 2
would have been obvious over Lin in view of Hiratsuka. The Examiner
relies on van Bockxmeer for additional limitations recited in claim 62, and
has not pointed to any disclosure in this reference that would make up for
the deficiencies discussed above (Ans. 33-36). Thus, we conclude that the
Examiner has not set forth a prima facie case that claim 62 and claims 63-65,
which depend from claim 62, would have been obvious over Lin in view of
Hiratsuka and van Bockxmeer. We therefore reverse the obviousness
rejection of these claims in view of these references.
Claims 49 and 51-61 depend from claim 2 and claim 66 depends from
claim 63. We have already concluded that the Examiner has not set forth a
prima facie case that claims 2 and 63 would have been obvious over Lin,
Hiratsuka, and van Bockxmeer. The Examiner relies on Soubrier and Buck
for limitations recited in dependent claims, and has not pointed to any
disclosure in these references that would make up for the deficiencies
discussed above (Ans. 25-32 and 36-39). Thus, we conclude that the
Examiner has not set forth a prima facie case that claims 49, 51-61, and 66
would have been obvious over Lin and Hiratsuka in view of the additional
references applied therewith. We therefore reverse the obviousness rejection
of these claims in view of these references.
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CONCLUSION
The Examiner has not shown that the claims would have been obvious
to a person of ordinary skill in the art based on the applied references. We
therefore reverse the rejections of claims 2 and 40-72.
REVERSED
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