Ex Parte Ward

Board of Patent Appeals and Interferences

Jul 20, 2012

12120322 (B.P.A.I. Jul. 20, 2012)

UNITED STATES PATENT AND TRADEMARK OFFICE
__________

BEFORE THE BOARD OF PATENT APPEALS
AND INTERFERENCES
__________

Ex parte KENNETH WARD
__________

Appeal 2011-012653
Application 12/120,322
Technology Center 1600
__________

Before DONALD E. ADAMS, FRANCISCO C. PRATS, and
JEFFREY N. FREDMAN, Administrative Patent Judges.

FREDMAN, Administrative Patent Judge.

DECISION ON APPEAL
This appeal under 35 U.S.C. § 134 involves claims to methods of
administering desogestrel to asymptomatic patients at high risk of
developing endometriosis. The methods may include a step of detecting
genetic markers linked to endometriosis in the patient‟s genetic material.
We have jurisdiction under 35 U.S.C. § 6(b). We affirm.
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Statement of the Case
Background
“[T]he present invention relates to specific single nucleotide
polymorphisms (SNPs) in the human genome, their association with
endometriosis and related pathologies, and their use in determining women
at risk for developing endometriosis” (Spec. 1 ¶ 0002).
The Claims
Claims 1-5, 8-14, 17-52, 55-62, and 65-77 are on appeal. Claims 1
and 2 are representative and read as follows:
1. A method of administering a therapeutic, said method
comprising the following steps:
assessing a predisposition for endometriosis in a
subject that does not exhibit an endometriosis symptom, and
administering a therapeutic to said subject.

2. The method of claim 1, wherein said step of assessing
is preceded by the step of detecting in the genetic material of
said subject the presence of at least one genetic marker
correlated with at least one endometriosis related condition.

The Issues
A. The Examiner rejected claims 1-5, 8-14, 17-52, 55-62, 65-70, 73-75,
and 77 under 35 U.S.C. § 103(a) as obvious over De Koning,
1

Treloar,
2
Vigano,
3
and Foster.
4

1
De Koning, WO 00/21511 A2, published Apr. 20, 2000.
2
Treloar et al., Genomewide Linkage Study in 1,176 Affected Sister Pair
Families Identifies a Significant Susceptibility Locus for Endometriosis on
Chromosome 10q26, 77 AM. J. HUM. GENET. 365-376 (2005).
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B. The Examiner rejected claims 71, 72, 75, and 76 under 35 U.S.C.
§ 103(a) as obvious over De Koning, Treloar, Vigano, Foster, and
Affymetrix.
5

A. Obviousness of Claims 1-5, 8-14, 17-52, 55-62, 65-70, 73-75 and 77
The Examiner finds De Koning “teaches a method of treating
endometriosis comprising the administration of a progestogen like
desogestrel” (Ans. 6). The Examiner concedes De Koning does not teach
the use of genetic markers to assess a patient‟s predisposition to
endometriosis (id.).
The Examiner finds Treloar “teaches that endometriosis is [a]
gynecological disease [whose] cause remains uncertain.” (Id.). The
Examiner further finds Treloar teaches endometriosis is a complex genetic
trait (id.). The Examiner notes Treloar discloses “novel positional genetic
variants that influence the risk of developing endometriosis” (id.).
The Examiner finds Vigano teaches “endometriosis is a gynecological
disease with a certain genetic background.” (Id.). The Examiner notes
Treloar discloses a “genetic polymorphism in the ICAM-1 gene domain may
contribute to the susceptibility to endometriosis” (id.). The Examiner further
finds Treloar teaches “[g]enotyping of the patients could be useful to select

3
Vigano et al., Intercellular adhesion molecule-1 (ICAM-1) gene
polymorphisms in endometriosis, 9 MOL. HUM. REPRODUCTION 47-52
(2003).
4
Foster et al., US 2002/0147155 A1, published Oct. 10, 2002.
5
Affymetrix GCS 3000 Instrument System, LABX SCIENTIFIC MARKETPLACE
(June 15, 2006),
http://www.labx.com/v2/adsearch/detail3.cfm?adnumb=291866 [hereinafter
Affymetrix].
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subgroups that could develop a more severe from [sic] of the disease” (id. at
6-7).
The Examiner finds Foster “teaches a method of administering
pharmaceutical compositions to women at high risk of developing
endometriosis” (id. at 7).
Therefore, the Examiner concludes
At the time of invention, it would have been prima facie
obvious for a person of ordinary skill in the art to detect if a
woman, [sic] that does not show any symptoms of
endometriosis, and has genetic markers correlated with increase
[sic] susceptibility to endometriosis as taught by Treolar [sic]
and Vigano, to further assess, based on those genetic markers,
the predisposition for that woman to be susceptible to
endometriosis, as taught by Vigano, and administer a
pharmaceutical composition known to treat or reduce the
conditions associated with endometriosis as taught by Foster,
wherein the drug is desogestrel which according to De Koning
can treat endometriosis, in order to reduce the risk of these
women of developing endometriosis . . . with a reasonable
expectation of success
(Id. at 7-8).
Appellant contends the prior art references cited by the Examiner do
not teach all of the limitations of claims 1, 21, 35, 49, 69, 74 and, thus, do
not teach all of the limitations of their dependent claims (App. Br. 4, 7, 11,
14, 17, 21).
The issue with respect to this rejection is: Does the evidence of record
support the Examiner‟s conclusion that De Koning, Treloar, Vigano, and
Foster render claims 1, 21, 35, 49, 69, and 74 obvious?

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Findings of Fact
1. De Koning teaches the administration of a progestogen, such as
desogestrel, to treat endometriosis (De Koning at 7, lines 3-5, 22-24).
2. Foster teaches “[a] woman at higher than normal risk of
developing endometriosis is a woman at greater risk than the general
population of women of developing endometriosis for the first time” (Foster
4 ¶ 0034) (emphasis added).
3. Foster teaches that even women possessing risk factors
indicating higher than normal risk “will [not] certainly develop the
condition” if it goes untreated (Foster 4 ¶ 0034).
4. Foster teaches risk factors for endometriosis as including “early
menarche (before age 13 years), frequent menstruations (e.g., menstrual
cycles of 27 days or less), unusually long menstrual period (5-7 days or
longer), chronic pelvic pain, especially with stenosis of the external cervical
os, advanced age, Asian race, the presence of Mullerian anomalies (e.g.,
duplicate cervix and vagina), long duration of uninterrupted menstrual
cycles, long duration of intrauterine device (IUD) use, infertility, nulliparity,
only one live birth, or after ten years since the last birth.” (Foster 4 ¶ 0034).
5. Foster teaches “[a] method of preventing endometriosis in a
woman at higher than normal risk of developing endometriosis, comprising:
administering to the woman at higher than normal risk of developing
endometriosis a pharmaceutically acceptable composition . . . to inhibit the
growth or thickening of endometriotic tissue in the woman.” (Foster 9, claim
13).
6. Foster teaches “[f]amilial risk factors can also contribute to a
higher than normal risk of developing endometriosis” (Foster 4 ¶ 0037).
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7. Foster teaches that the “preceding is merely illustrative of
factors that can contribute to a woman being at higher than normal risk of
developing endometriosis, and is not an exhaustive list” (Foster 4 ¶0038).
8. Foster teaches “administering to the woman a pharmaceutically
acceptable composition comprising at least one aryl hydrocarbon receptor
binding ligand, in an amount effective to reduce or prevent the growth or
thickening of endometriotic tissue in the woman” (Foster 3 ¶ 0025).
9. Foster teaches that “preventing endometriosis encompasses
inhibiting or reducing the size of endometriotic tissue present in the woman
and/or preventing the development symptoms of endometriosis, regardless
of whether the size of her endometriotic tissue is actually measured” (Foster
4 ¶ 0032).
10. Treloar teaches the 10q26 chromosomal region exhibits
significant linkage to endometriosis (see Treloar 369-72).
11. Vigano teaches two polymorphisms, R241 and K469, in the
ICAM-1 gene corresponding to an increased risk of endometriosis (Vigano
51).
12. Vigano teaches that “genotyping of the patients could be useful
to select subgroups that could develop a more severe form of the disease”
(Vigano 52).
Principles of Law
To establish a prima facie case of obviousness, the examiner must
find “a reason that would have prompted a person of ordinary skill in the
relevant field to combine the elements in the way the claimed new invention
does.” KSR Intern. Co. v. Teleflex Inc., 550 U.S. 398, 418 (2007).
Emphasizing “an expansive and flexible approach” to the question of
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obviousness, the Supreme Court noted several methods of demonstrating
obviousness, such as identifying a teaching, suggestion, or motivation to
combine the references or through “the mere substitution of one element for
another known in the field” to yield predictable results. Id. at 415-17.
Claim terms are interpreted using the broadest reasonable
interpretation in light of the Specification. See, e.g., In re Hyatt, 211 F.3d
1367, 1372 (Fed. Cir. 2000) (“[D]uring examination proceedings, claims are
given their broadest reasonable interpretation consistent with the
specification.”); see also In re Morris, 127 F.3d 1048, 1054-56 (Fed. Cir.
1997) (“Absent an express definition in their specification, the fact that
appellants can point to definitions or usages that conform to their
interpretation does not make the PTO‟s definition unreasonable when the
PTO can point to other sources that support its definition.”).
Analysis
Claim 1
Foster teaches a “method of preventing endometriosis in a woman at
higher than normal risk of developing endometriosis” wherein a compound
known to treat endometriosis is administered to a woman at high risk (Foster
9, claim 13; FF 2). Foster teaches:
Known risk factors for endometriosis include early menarche
(before age 13 years), frequent menstruations (e.g., menstrual
cycles of 27 days or less), unusually long menstrual period (5-7
days or longer), chronic pelvic pain, especially with stenosis of
the external cervical os, advanced age, Asian race, the presence
of Mullerian anomalies (e.g., duplicate cervix and vagina), long
duration of uninterrupted menstrual cycles, long duration of
intrauterine device (IUD) use, infertility, nulliparity, only one
live birth, or after ten years since the last birth.
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(Foster 4 ¶ 0034; FF 4). Foster teaches that the “preceding is merely
illustrative of factors that can contribute to a woman being at higher than
normal risk of developing endometriosis, and is not an exhaustive list”
(Foster 4 ¶ 0038; FF 7). The Examiner acknowledges that while Foster
teaches an extensive list of risk factors for endometriosis (FF 4), Foster does
not expressly teach the use of genetic risk factors for predisposition to
endometriosis.
Treloar teaches the 10q26 chromosomal region exhibits significant
linkage to endometriosis (see Treloar 369-72; FF 10). Vigano teaches two
polymorphisms, R241 and K469, in the ICAM-1 gene corresponding to an
increased risk of endometriosis (Vigano 51; FF 11). Vigano teaches that
“genotyping of the patients could be useful to select subgroups that could
develop a more severe form of the disease” (Vigano 52; FF 12).
Applying the KSR standard of obviousness to the findings of fact, we
conclude that a person of ordinary skill in the art would have reasonably
have included genetic risk factors in the Foster method of preventing
endometriosis since Vigano teaches “genotyping of the patients could be
useful to select subgroups that could develop a more severe form of the
disease” (Vigano 52; FF 12). The selection of other known risk factors
simply represents the “mere substitution of one element for another known
in the field” to yield a predictable result. KSR, 550 U.S. at 416.
Appellant contends that neither Treloar nor Vigano teach a genetic
basis for determining a woman‟s predisposition to endometriosis (App. Br.
4-5).
We are not persuaded. While this is a limitation of claim 2, not claim
1, Vigano expressly teaches that “genotyping of the patients could be useful
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to select subgroups that could develop a more severe form of the disease”
(Vigano 52; FF 12). The ordinary artisan, at the time of invention, would
reasonably have recognized that the SNP and chromosomal endometriosis
risk markers identified by Treloar and Vigano would have permitted genetic
identification of individuals at greater risk for endometriosis. In
combination with Foster‟s teaching to treat individuals at higher risk (FF 5),
the ordinary artisan would reasonably have performed the genotyping prior
to treatment in order to identify such individuals (FF 5-12).
Appellant contends that “Foster did not teach a method of
administering pharmaceutical compositions to subjects that are
asymptomatic of endometriosis” (App. Br. 6). Appellant proffers the Ward
Declaration
6
which states that “the current state of the art practice in
gynecological medicine is to administer endometriosis therapeutics to only
those patients who exhibit an endometriosis related condition” (App. Br. 7).
Appellant contends that in Foster “the word „prevent‟ cannot be
misconstrued to mean asymptomatic” (App. Br. 7).
We are not persuaded. We have considered the Ward Declaration, but
rather than address the teachings of Foster, the Declaration makes general
statements regarding the state of the art. However, it is Foster upon which
the rejection relies, not the general state of the art, and it is Foster who
teaches to “prevent the growth or thickening of endometriotic tissue in the
woman” (Foster 3 ¶ 0025).
We also find that Appellant‟s interpretation of “prevent” in Foster to
exclude asymptomatic women is objectively unreasonable. As we have just
noted, Foster teaches to “prevent the growth or thickening of endometriotic

6
Ward Declaration, filed Aug. 23, 2010.
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tissue in the woman” (Foster 3 ¶ 0025). Since endometriotic tissue is
normally present in women, preventing the growth or thickening of this
tissue will necessarily include treatment of asymptomatic women. This
understanding is bolstered by Foster‟s list of risk factors, many of which are
entirely asymptomatic. Risk factors such as Mullerian anomalies, advanced
age, being of Asian descent, use of an intrauterine device, uninterrupted
menstrual cycles, only one live birth, and a period of ten years since the last
birth cannot be construed to be symptoms of endometriosis (see Foster 4 ¶
0034; FF 4).
Finally, Appellant‟s reliance on Foster‟s definition of “preventing
endometriosis” in paragraph 32 is misplaced (see, e.g., App. Br. 7). In
paragraph 32, Foster is simply acting as his own lexicographer in expanding
the definition of “preventing” by permitting it alternatively encompass
“inhibiting or reducing the size of endometriotic tissue present in the
woman” or “preventing the development [of] symptoms of endometriosis”
(Foster 4 ¶ 0032; FF 9). The only reasonable interpretation of the second
part of the definition “preventing the development [of] symptoms of
endometriosis” (Foster 4 ¶ 0032; FF 9), is the treatment of asymptomatic
women since otherwise symptoms of endometriosis would develop and
would not have been “prevented” as required by both Foster‟s claims and
Specification.
Claims 21 and 35
While Appellant separately argues claims 21 and 35, the only
difference between these claims and claim 1 is they each recite, respectively,
the administration of an oral contraceptive or an ovulation suppression
substance instead of a therapeutic. The Examiner cites De Koning for the
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use of desogestrel to treat endometriosis (Ans. 6; FF 1). The Examiner noted
desogestrel is both an oral contraceptive and an ovulation suppressant (see
Ans. 8). We conclude that a person of ordinary skill in the art would have
reasonably substituted desogestrel into Foster‟s method of preventing
endometriosis as De Koning teaches desogestrel is an effective treatment for
the disease. Doing so is no more than the “mere substitution of one element
for another known in the field” to yield a predictable result. KSR, 550 U.S.
at 416
Appellant does not contest this assertion. Appellant simply restates the
arguments made with regard to claim 1. Accordingly, for the reasons stated
with regard to claim 1, we are not persuaded by Appellant‟s arguments.
Claim 49
Appellant contends that the combination of De Koning, Treloar,
Vigano, and Foster does not teach the method of claim 49. Claim 49 is
identical to claim 1 with an additional limitation of “detecting in the genetic
material of said subject the presence of at least one genetic marker correlated
with at least one endometriosis related condition” preceding the step of
assessing predisposition (see App. Br. 30-31). Thus, Appellant argues that
the prior art does not teach the detection of a genetic marker correlated to
endometriosis (see App. Br. 14-16).
We are not persuaded. As we discussed above, Treloar teaches the
10q26 chromosomal region exhibits significant linkage to endometriosis (see
Treloar 369-72; FF 10). Treloar discloses, in Table 2, a series of
chromosomal regions and known markers in those regions associating with
endometriosis (see Treloar at 369; FF 6). Treloar specifically stated:
“[a]nalysis of our combined set of families identified significant linkage
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(MLS = 3.16) to a novel susceptibility locus on chromosome 10q26.” (Id. at
372). Vigano teaches two polymorphisms, R241 and K469, in the ICAM-1
gene corresponding to an increased risk of endometriosis (Vigano 51; FF
11). Vigano teaches that “genotyping of the patients could be useful to
select subgroups that could develop a more severe form of the disease”
(Vigano 52; FF 12).
We note the Specification does not provide a definition of the claim
term “marker.” By definition, any disease-associated chromosomal location
is reasonably interpreted as a marker, since neither the claim nor
Specification limit the term “marker” to a SNP. Vigano notes that a marker
“may represent a predisposing factor for endometriosis” (Vigano 51) but
Vigano “cannot rule out that these results may be due to linkage
disequilibrium with other unknown mutations” (Vigano 51). That is, the
mutations may themselves not be the underlying causal mutation, but serve
as markers of a nearby causal mutation. We therefore agree with the
Examiner that as long a location is linked to the presence of a disease, it can
be considered a marker for that disease (see Ans. 16) (stating “[g]enetic
markers [are] indicators of the predisposition to a certain disease or
indicators of how the disease is evolving . . . .”).
Thus, we agree with Examiner that both Treloar and Vigano disclose
genetic markers that correlate with endometriosis.
We also agree with the Examiner that Foster provides sufficient
motivation to utilize genetic markers to assess a patient‟s risk of
endometriosis (see Ans. 7). As noted by the Examiner, Foster teaches
“[f]amilial risk factors can also contribute to a higher than normal risk of
developing endometriosis” (Foster 4 ¶ 0037; FF 6). An ordinary artisan of
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ordinary skill and creativity would reasonably interpret this teaching to
directly suggest the role of genetic influences in a woman‟s predisposition to
endometriosis, such as those identified by Treloar and Vigano (FF 10-12).
Claim 69
Appellant contends that the combination of De Koning, Treloar,
Vigano, and Foster does not teach the method of claim 69 (App. Br. 17-18).
Appellant restates virtually verbatim the arguments proffered with regard to
claim 1 (see id.).
Accordingly, for the reasons stated above with regard to claim 1, we
are not persuaded. We must note claim 69 is broader than claim 1 since it
does not require the administration of a therapeutic; it simply designates one
with an assessed predisposition for endometriosis as a candidate for
treatment (see App. Br. 32). Appellant does not argue whether the cited
prior art discloses “designating said subject as a candidate for administration
of a therapeutic.” Appellant instead argues the administration of a
therapeutic, which is a limitation of claim 1 but not a limitation of claim 69,
and is an argument we have already addressed regarding claim 1 above.
Claim 74
Appellant contends that De Koning, Treloar, Vigano, and Foster do
not teach the method of claim 74 (App. Br. 21-24). Again, Appellant
restates virtually verbatim the argument as to claim 1 (see id.).
Claim 74 is nearly identical to claim 49 as it requires the identification
of a person with a marker correlating to endometriosis (App. Br. 33). The
only difference is it does not require an assessment of predisposition or an
administration of a therapeutic, only the designation of the patient with the
marker as a candidate for endometriosis (id.). Appellant again does not
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argue whether the prior art discloses the designation of a patient as a
candidate; simply arguing the administration of a therapeutic – a limitation
not present in this claim (see App. Br. 24).
We are not persuaded for the reasons given above in response to claim
49.
Conclusion of Law
The evidence of record supports the Examiner‟s conclusion that De
Koning, Treloar, Vigano, and Foster render obvious claims 1, 21, 35, 49, 69,
and 74.
B. Obviousness of Claims 71, 72, 75, and 76 over De Koning, Treloar,
Vigano, Foster, and Affymetrix.
The Examiner finds De Koning, Vigano, Treloar, and Foster “teach all
the limitations of claims 71-72 and 75-76 except for the use on an
Affymetrix GCS 3000 scanner for the detection of genetic markers” (Ans.
12). The Examiner finds the LabX web page “teaches that the Affymetrix
GCS scanner has been used as a gene scanner” (Ans. 12). Therefore, the
Examiner concludes it would have been obvious “to further detect genetic
markers with an apparatus like the Affymetrix GCS 3000” (Ans. 12-13).
The Examiner provides sound fact-based reasoning for combining
Affymetrix with De Koning, Treloar, Vigano, and Foster. We adopt the fact
finding and analysis of the Examiner as our own. Appellant argues the
underlying obviousness rejection over De Koning, Treloar, Vigano, and
Foster, but Appellant does not identify any material defect in the Examiner's
reasoning for combining Affymetrix with De Koning, Treloar, Vigano, and
Foster. Since Appellants only argue the underlying rejection of De Koning,
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Treloar, Vigano, and Foster which we affirmed above, we affirm this
rejection for the reasons stated by the Examiner.
SUMMARY
In summary, we affirm the rejection of claims 1, 21, 35, 49, 69, and 74 under
35 U.S.C. § 103(a) as obvious over De Koning, Treloar, Vigano, and Foster.
Pursuant to 37 C.F.R. § 41.37(c)(1), we also affirm the rejection of claims 2-5, 8-14,
17-20, 22-34, 36-48, 50-52, 55-62, 65-68, 70, 73, 75, and 77 as these claims were
not argued separately.
We also affirm the rejection of claims 71, 72, 75, and 76 under 35
U.S.C. § 103(a) as obvious over De Koning, Treloar, Vigano, Foster, and
Affymetrix.

TIME PERIOD
No time period for taking any subsequent action in connection with this
appeal may be extended under 37 C.F.R. § 1.136(a).

AFFIRMED

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