Ex Parte Gutin et al

Patent Trial and Appeal Board

May 12, 2017

13310916 (P.T.A.B. May. 12, 2017)

United States Patent and Trademark Office
UNITED STATES DEPARTMENT OF COMMERCE
United States Patent and Trademark Office
Address: COMMISSIONER FOR PATENTS
P.O.Box 1450
Alexandria, Virginia 22313-1450
www.uspto.gov
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
3314-01-1U 1392
EXAMINER
HARWARD, SOREN T
ART UNIT PAPER NUMBER
1631
MAIL DATE DELIVERY MODE
13/310,916 12/05/2011 Alexander Gutin
05/12/201726698 7590
MYRIAD GENETICS INC.
INTELLECTUAL PROPERTY DEPARTMENT
320 WAKARA WAY
SALT LAKE CITY, UT 84108
05/12/2017 PAPER
Please find below and/or attached an Office communication concerning this application or proceeding.
The time period for reply, if any, is set in the attached communication.
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte ALEXANDER GUTIN, JERRY LANCHBURY,
SUSANNE WAGNER, and VICTOR ABKEVICH
Appeal 2017-0005751
Application 13/310,916
Technology Center 1600
Before RICHARD M. LEBOVITZ, JEFFREY N. FREDMAN, and
RICHARD J. SMITH, Administrative Patent Judges.
LEBOVITZ, Administrative Patent Judge.
DECISION ON APPEAL
This appeal involves claims directed to a method of screening for
cancer comprising analyzing a sample for gene mutations. The Examiner
rejected the claims under 35 U.S.C. §§ 101 and 103. We have jurisdiction
under 35 U.S.C. § 6(b). The rejections are affirmed.
as the real-1 The Appeal Brief (“Appeal Br.”) 3 lists Myriad Genetics, Inc.,
party-in-interest.
Appeal 2017-000575
Application 13/310,916
STATEMENT OF THE CASE
Appellants appeal from the Examiner’s final rejection (“Final Act.”)
of claims 7, 9, 10, 16, 18, 20 and 26—31. The claims stand rejected as
follows:
1. Claims 7, 18 and 20 under pre-AIA 35 U.S.C. § 103(a) as obvious
in view of Gocke, et al. (US 2009/0298085 Al, publ. Dec. 3, 2009;
“Gocke”); Ogechi N. lkediobi et al. {Mutation analysis of 24 known cancer
genes in the NCI-60 cell line set, Molecular Cancer Therapeutics,
5(11):2606—12, ©2006 American Association for Cancer Research;
“lkediobi”); Hillan (WO 2007/001868 Al, publ. Jan. 4, 2007; “Hillan”); and
Daniele Soria et al. (A Comparison of Three Different Methods for
Classification of Breast Cancer Data, 2008 Seventh International
Conference on Machine Learning and Applications, 619—24; © IEEE,
“Soria”) as “evidenced” by Duda et al. (Pattern Classification, Second
Edition, pp. 29-31, 615, © 2001 John Wiley & Sons, Inc; “Duda”).
2. Claims 9, 10, and 16 under pre-AIA 35 U.S.C. § 103(a) as obvious
in view of Gocke, lkediobi, Hillan, Soria (“as evidenced by Duda”), and
Pressman (US 2005/0282201 Al, publ. Dec. 22, 2005).
3. Claims 26, 30 and 31 under pre-AIA 35 U.S.C. § 103(a) as obvious
in view of Gocke, lkediobi, Hillan, and Soria.
4. Claims 27—29 under pre-AIA 35 U.S.C. § 103(a) as obvious in
view of Gocke, lkediobi, Hillan, Soria, and Pressman.
5. Claims 7, 9, 10, 16, 18, 20 and 26—31 are rejected under 35
U.S.C. 1101 because the claimed inventions are directed to non-statutory
subject matter.
2
Appeal 2017-000575
Application 13/310,916
There are only two independent claims involved in the appeal, claims
7 and 26. All the rejections are based on the same set of four publications
(Gocke, lkediobi, Hillan, Soria), with the same rationale for each, except
rejections 2 and 4 cite Pressman to reach limitations in dependent claims.
The dependent claims, however, were not argued separately nor did
Appellants address the rejections separately. Consequently, we have
considered all four obviousness rejections together.
Claim 7 and 26 involve similar steps. Claim 7 recites a specific
formula to calculate cancer type; claim 26 does not recite the formula.
Claim 7 is representative and is reproduced below:
7. A method of screening patients for cancer comprising:
(1) analyzing in a sample from a bodily fluid a panel of
genes comprising the APC, EGFR, KRAS, PTEN, and TP53 genes
and at least one gene chosen from the group consisting of the
AIM/1, CDKN2A, FBN2, FBXW7, FU13479, IDH1, PIK3CA,
PIK3R1, RBI, SMAD4, TGFBR2, and TNN genes; wherein
(a) the APC gene is analyzed by sequencing all
coding exons of the APC gene;
(b) the PTEN gene is analyzed by sequencing all
coding exons of the PTEN gene;
(c) the EGFR gene is analyzed by genotyping said
sample for a mutation resulting in the L858R amino acid variant;
(d) the KRAS gene is analyzed by genotyping said
sample for a mutation resulting in either the G12C/S/R or the
G12D/V/A amino acid variant; and
(e) the TP53 gene is analyzed by sequencing all
coding exons of the TP53 gene;
(2) (a) diagnosing the presence of cancer or a high
likelihood of cancer in a patient in whose sample a mutation was
detected in step (1) in at least one of said APC, EGFR, KRAS,
PTEN, or TP53 genes; or
3
Appeal 2017-000575
Application 13/310,916
(2) (b) diagnosing the absence of cancer or a low likelihood
of cancer in a patient in whose sample no mutation was detected
in step (1) in any of said A PC, EGFR, KRAS, PTEN, and TP53
genes; and
(3) calculating a first likelihood said patient diagnosed
with cancer in step (2)(a) has cancer ci using the formula: wherein
the product is taken over all of the genes in said panel mutated in
the sample (7=7, 2, ..., n), the sum is taken over all cancer types t,
M(g/ ci) is the frequency of somatic mutations in each gene g of
said panel of genes in cancer type Ci, and Po(ci) is the a priori
probability of cancer ci given that the patient has a cancer; and;
(4) calculating a second likelihood said patient
diagnosed with cancer in step (2)(a) has cancer c2 using the
formula: wherein the product is taken over all of the genes in said
panel mutated in the sample (7=7, 2, ..., n), the sum is taken over
all cancer types t, M(g/ c2) is the frequency of somatic mutations
in each gene g of said panel of genes in cancer type c2, and Po(c2)
is the a priori probability of cancer C2 given that the patient has a
cancer; and
(5) diagnosing said patient with cancer ci if said first
likelihood calculated in step (3) is greater than said second
likelihood calculated in step (4).
OBVIOUSNESS REJECTIONS
Claim 7 is directed to a method of screening patients for cancer. The
method has five steps. In the first step (1), a sample from a body fluid is
analyzed for the presence of six genes: (a) APC, (b) PTEN, (c) EGFR; (d)
KRAS; (e) TP53; and (f)2 “at least one gene chosen from the group
consisting of’ a list of 12 genes. The EGFR and KRAS genes are analyzed
for the presence of specific amino acid mutations. In step (2), the presence
2 The first five genes in the claim are designated in the claim as (a) to (e).
The sixth gene is not designated with a letter; for reference, “(f)” has been
added to the sixth gene.
4
Appeal 2017-000575
Application 13/310,916
or absence of cancer is determined by the detection of a gene mutation in
one of the six recited genes. The likelihood of the patient having a cancer
type Ci or C2 is further determined using a specific equation recited in the
claim (steps (3)-(4)).
The Examiner found that Gocke describes isolating tumor-derived
nucleic acids from a blood sample, and identifying mutated alleles in the
sample, meeting the first step of claim 7 of “analyzing in a sample from a
bodily fluid a panel of genes.” Final Act. 5. The Examiner also found that
Gocke’s method is a “method of screening patients for cancer” as recited in
the preamble of claim 7 because Gocke teaches that presence mutations in
the blood sample can be used to detect cancerous cells anywhere in the body
and screen for individuals at risk for cancer and premalignant conditions. Id.
The Examiner found the Gocke teaches screening for (a) APC, (d)
KRAS, (e) KRAS, and (f) PI6 (also known as the CDKN2A gene), the latter
which is one member of the list of 12 genes. Id.
The Examiner found that Gocke does not describe screening for
oncogenic mutations in (b) PTEN and (c) EGFR as in step (1) of the claim.
The Examiner also found that Gocke does not describe determining the
likelihood of a cancer type ci or C2 as recited in steps (3) to (5) of claim 7.
Id.
To meet mutational screening step (1), the Examiner cited fkediobi
which discloses a list of 24 cancer genes (Table 2) that includes all of the
claimed genes: (a) APC, (b) PTEN, (c) EGFR; (d) KRAS; (e) TP53; and (f)
P16 (also known as the CDKN2A gene). Id. The Examiner stated that the
specifically claimed EGFR and KRAS amino acid mutations are not taught
5
Appeal 2017-000575
Application 13/310,916
by either Gocke or Ikediobi, but found that Hillan teaches screening for
these oncogenic mutations. Id.
The Examiner found that the equation recited in steps (3) and (4) for
calculating the likelihood of a cancer type using the frequency of mutation in
the six genes is Bayes classifier and further found that Soria describes the
recited classifier to classify cancers based on biomarker data. Id. at 6.
Based on these findings, the Examiner made well-reasoned, fact-based
statements explaining the reason to have modified Gocke’s method to have
arrived at the claimed invention. The Examiner concluded that one of
ordinary skill in the art would have had reason “to modify the method of
Gocke to also detect oncogenic mutations in EGFR, KRAS and PTEN genes,
as taught by Ikediobi and Hillan, because Ikediobi and Hillan teach that
mutations in these genes are characteristic of various types of cancers.” Id.
at 7. The Examiner further found that the skilled worker would have had
reason to apply Soria’s teaching to Gocke to determine the likelihood of a
specific cancer type as in steps (3)—(5) of claim 7 “because Soria teaches that
the naive Bayes classifier is a simple yet effective method of classifying
cancers based on a biomarker profile.” Furthermore, the Examiner stated
there was a reasonable expectation of success that Soria’s classifier would
predict the likelihood of a cancer type because “Ikediobi teaches that
mutation profiles differ among cancer types such that they can be used to
classify cancer types” and Soria teaches that the Bayes classifier “is
amenable to classifying discrete data (such as mutation profiles).” Id. at 8.
6
Appeal 2017-000575
Application 13/310,916
DISCUSSION
Appellants contend that the Examiner erred in not considering the
claim as whole. Appeal Br. 14. Appellants argue that “[njothing cited in the
record suggests the specific panel of genes and mutations recited in the
claims has any special significance or utility in screening for cancer.” Id. at
6. (Emphasis added).
This argument does not persuade us that the Examiner erred in
rejecting the claims as obvious.
As established by the Examiner, Gocke describes a method that
involves “analyzing” genes “in a sample from a bodily fluid” to screen
patients for cancer as required by claim 7. For example, Gocke teaches “the
detection, identification, or monitoring of the existence, progression or
clinical status of benign, premalignant, or malignant neoplasms in humans or
other animals that contain a mutation that is associated with the neoplasm,
through detection of the mutated nucleic acid of the neoplasm in plasma or
serum fractions.” Gocke 13. Gocke teaches that the detected mutations
comprise genes associated with neoplasms and oncogenes. Id. Tflf 3, 24.
While Gocke gives examples of several different oncogenes to test for the
presence of in blood plasma or serum 18, 24, 41, 67, 68), the disclosure
is broader and there is no indication that Gocke is limited to these examples.
To the contrary, Gocke discloses a “useful application of this invention is to
identify mutant oncogenes or tumor-associated DNA,” indicating that Gocke
is not limited to the small subset of oncogenes disclosed in it. Id. 136.
Ikediobi identified “24 known cancer genes” whose presence were
determined in a cell lines used to test for anticancer drugs. Ikediobi 2606,
2609 (Table 2). These 24 genes include all six genes recited in claim 7.
7
Appeal 2017-000575
Application 13/310,916
Appellants state that it “is very clear that none of these references [Gocke,
Ikediobi, and Hillan] individually teaches the panel recited in the claims.”
Reply Br. 9. However, Table 2 of Ikediobi shows APC, CDKN2A, EGFR,
KRAS, PTEN, and TP53 as recited in claim 7. Appellants have no basis for
denying that Ikediobi tests for all six genes recited in claim 7.
While Ikediobi’s panel contains more than the six genes recited in
claim 7, as discussed by the Examiner, the claim is open-ended and does not
exclude the presence of additional genes in the gene panel. Specifically, the
claim recites “a panel of genes comprising” the six specific genes; the term
“comprising” is open-ended3 and permits the inclusion of additional genes.
In addition, for the sixth gene designated (f) herein, the claim recites “at
least one gene chosen from the group,” indicating that more than one gene in
the group may be included in the panel. Accordingly, Appellants’ argument
about a “specific” and “minimal” panel of genes (Appeal Br. 14) is
inconsistent with the plain language of the claim which permits the presence
of other genes in the gene panel. For this reason, the panel of 24 genes
described by Ikediobi which includes the six recited genes reads directly on
the claim, and the only issue is whether such panel would have been obvious
to use in Gocke’s method. As discussed above, the Examiner provided a
fact-based explanation as to why it would have been obvious to use
Ikediobi’s genes in Gocke’s method. Final Act. 7; Ans. 9. Since Gocke
does not limit its method to the specific genes disclosed in it, and
3 In re Baxter, 656 F.2d 679, 686—87 (CCPA 1981)(“As long as one of the
monomers in the reaction is [claimed] propylene, any other monomer may
be present, because the term ‘comprises’ permits the inclusion of other steps,
elements, or materials.”); see also MPEP § 2111.03 (Ninth Edition).
8
Appeal 2017-000575
Application 13/310,916
specifically teaches analyzing for the presence of oncogenes, there is
adequate reason to have used the 24 oncogenes described in Ikediobi in
Gocke’s method. See also Ans. 7—8 explaining why it would have been
obvious to test for EGFR in Gocke’s method.
Appellants contend that the recited “specific minimal combination of
genes” enabled the detection of “unexpectedly high proportion of cancers
(nearly 95%) and to specify which cancer for which a particular patient has
screened positive.” Appeal Br. 14. However, Appellants did not direct our
attention in the Appeal Brief to the evidence of unexpected results.
An applicant cannot prove unexpected results with attorney
argument and bare statements without objective evidentiary
support. See In re Lindner, 59 C.C.P.A. 920, 457 F.2d 506, 508
(CCPA 1972); In re Geisler, 116 F.3d 1465 (Fed. Cir. 1997)
(“attorney argument [is] not the kind of factual evidence that is
required to rebut a prima facie case of obviousness”); In re Soni,
54 F.3d 746, 750 (Fed. Cir. 1995) (“It is well settled that
unexpected results must be established by factual evidence. Mere
argument or conclusory statements ... [do] not suffice.”) (quoting
In re De Blauwe, 736 F.2d 699, 705 (Fed. Cir. 1984)).
CFMT, Inc. v. Yieldup Intern. Corp., 349 F.3d 1333, 1342 (Fed. Cir. 2003).
Appellants contend that Ikediobi “teaches away from the specific
combination of genes recited in the claims” because oncogenic mutations in
EGFR were not found. Appeal Br. 15.
Appellants’ argument is not supported factually. The following
disclosure from Ikediobi demonstrates the error in Applicant’s argument.
Specifically, Ikediobi expressly disclosed that mutations in EGFR are
associated with cancer:
Response to two other kinase inhibitors, gefitinib and erlotinib,
has been linked to activating mutations in the epidermal growth
9
Appeal 2017-000575
Application 13/310,916
factor receptor (EGFR) gene in patients with lung
adenocarcinoma (17).
Ikediobi. at 2607. Even absent this teaching, Hillan was cited by the
Examiner for teaching EGFR oncogenic mutations. Hillan 3. Thus,
oncogenic mutations in EGFR were known at the time of the invention.
Moreover, neither reference criticizes, discredits or otherwise discourages
the use of oncogenic EGFR mutations in Gocke’s method. See In re Fulton,
391 F.3d 1195, 1201 (Fed. Cir. 2004).
Ikediobi simply did not observe any of the known oncogenic
mutations in the cell lines they tested. However, Ikediobi observed EGFR
variants that merited further study. Ikediobi teaches:
An additional 19 tentative oncogenic variants were identified,
including missense variants in the receptor tyrosine kinase genes
EGFR, ERBB2, and FLT3.
Id. at 2609.
The receptor tyrosine kinases are perhaps the most
successfully exploited set of molecular targets in cancer to date.
Several family members (EGFR, ERBB2, FLT3, KIT, MET, and
PDGFRA) were included in the set of 24 genes assessed. No
mutations identical to those most frequently reported (17) were
seen. However, several interesting variants were identified. In
EGFR, two amino acid substitutions, p.P753S in the SK-MEL-
28 melanoma and p.T75 II in the RPMI-8226 myeloma line, were
identified within the region of the kinase domain frequently
affected by in-frame deletions. Both residues are subject to
missense substitution as part of more complex deletion/
substitution mutations in lung adenocarcinoma. 14 Further
investigation of those lines for sensitivity to EGFR inhibitors and
the potential role of EGFR mutations in a subset of melanoma
and myeloma are warranted.
Id. at 2611.
10
Appeal 2017-000575
Application 13/310,916
Accordingly, EGFR would not have been omitted from the panel of
24 oncogenes disclosed by Ikediobi.
Appellants also contend that Ikediobi “does not teach or suggest
screening for the specific recited oncogenic mutations in EGFR to detect
occult cancer.” Appeal Br. 15—16. However, as discussed above, Ikediobi
expressly teaches that EGFR cancer mutations were known, and Ikediobi
screened tumor cell lines for mutations in the EGFR gene. Hillan, as found
by the Examiner, teaches known mutations in EGFR associated with cancer,
including the recited mutations. Appellants did not identify an error in the
Examiner’s reliance on Hillan. Consequently, there was adequate reason,
based on Ikediobi’s teaching to test for EGFR mutations, to search for the
specific EGFR mutations identified in Hillan.
For the foregoing reasons, the obviousness rejections 1—4 of claims 7
and 26 are affirmed.
Appellants did not provide separate arguments for the dependent
claims in the Appeal Brief. In the Reply Brief, Appellants state that the
dependent claims do not “rise or fall with the independents,” but provide no
argument why they do not. Reply Br. 10. “A statement which merely points
out what a claim recites will not be considered an argument for separate
patentability of the claim.” 37 C.F.R. 41.37(1 )(iv). Consequently, claims 9,
10, 16, 18, 20, and 27-—31 fall with claims 7 and 26.
SECTION 101 PATENT INELIGIBILITY REJECTION
The Examiner rejected the claims under 35U.S.C. § 101 as directed to
non-statutory subject matter. Final Act. 2. Specifically, the Examiner found
that the claims “do not amount to significantly more than the abstract idea of
11
Appeal 2017-000575
Application 13/310,916
an algorithm that calculates the likelihood that a patient has cancer,” and that
the additional steps in the claim involving the analysis of genes in a sample
were conventional at the time of the invention. Id. at 3. The Examiner also
found that the claims “do not recite something significantly different than
the natural correlation between genetic mutations and the particular type of
cancer (or absence thereof).” Id. The Examiner stated that the claims are
“directed to steps of observing this natural principle through well-
understood, routine and conventional means (i.e. genotyping a panel of
genes for a patient).” Id. The Examiner also stated “no elements of the
claim actually apply this observation in a practical manner; they simply
calculate the likelihood of the particular type of cancer given the observation
. . . Hence, the claims lack any element that would render them significantly
more than a natural correlation.” Id. at 3^4.
Discussion
To determine whether a claim is eligible for patent under 35 U.S.C.
§ 101, a two-step analysis is necessary. As set forth in Alice Corp. Pty. Ltd.
v. CLSBankInt 7, 134 S. Ct. 2347, 2355 (2014):
First, we determine whether the claims at issue are directed to
one of those patent-ineligible concepts [e.g., a law of nature,
natural phenomenon, or abstract idea]. If so, we then ask, what
else is there in the claims before us? . . . We have described step
two of this analysis as a search for an inventive concept—i.e., an
element or combination of elements that is sufficient to ensure
that the patent in practice amounts to significantly more than a
patent upon the ineligible concept itself.
Id. (alterations, citations, and quotation marks omitted).
Mayo
12
Appeal 2017-000575
Application 13/310,916
Appellants contend that the claims are eligible for a patent under
Mayo Collaborative Services v. Prometheus Laboratories, Inc., 132 S. Ct.
1289, 1297 (2012). We thus begin our discussion with Mayo.
In Mayo, the claim comprised steps of administering a drug to a
subject and determining the levels of the metabolite of drug in the subject.
The metabolite levels were used in a “wherein” clause to determine a need to
increase or decrease the amount of drug subsequently administered to the
subject. Mayo, 132 S.Ct. at 1295. The Supreme Court held that the
wherein clauses “simply tell a doctor about the relevant natural laws, at most
adding a suggestion that he should take those laws into account when
treating his patient.” Id. at 1297. Further, the Court wrote:
Prometheus’ patents set forth laws of nature — namely,
relationships between concentrations of certain metabolites in
the blood and the likelihood that a dosage of a thiopurine drug
will prove ineffective or cause harm. Claim 1, for example,
states that if the levels of 6—TG in the blood (of a patient who has
taken a dose of a thiopurine drug) exceed about 400 pmol per
8x108 red blood cells, then the administered dose is likely to
produce toxic side effects. While it takes a human action (the
administration of a thiopurine drug) to trigger a manifestation of
this relation in a particular person, the relation itself exists in
principle apart from any human action. The relation is a
consequence of the ways in which thiopurine compounds are
metabolized by the body—entirely natural processes. And so a
patent that simply describes that relation sets forth a natural law.
Id. at 1296-97.
In this case, the claims are similar to those in Mayo because they
involve a “relation itself [which] exists in principle apart from any human
action” (id.), namely the relationship between the naturally-occurring gene
mutations detected in step (1) and the correlation of these gene mutations
13
Appeal 2017-000575
Application 13/310,916
with the presence or likelihood of cancer in the subsequent steps of the
claims.
Appellants attempt to distinguish Mayo, stating that the claims in
Mayo “were directed to the law of nature itself because the entire process
recited in the claims was routine in the art and the only ‘new’ element was
‘wherein’ clauses that were literally a statement of the law of nature.”
Appeal Br. 12. However, Appellants ignore that the first step of the analysis
under Alice and Mayo is to determine whether the claims are directed to an
abstract idea or natural phenomenon, and then to consider whether the claim
as a whole make it patentable. Thus, while the conventionality of a step is
pertinent to the analysis, it must first be decided if the claim falls within a
judicial exception to patent eligibility. In this case, we have found that the
claim falls within the judicial exception.
Appellants also contend that the claims are directed to a “concrete”
laboratory process involving the physical analysis of multiple genes. Appeal
Br. 11; Reply Br. 6. Apparently, Appellants mean to distinguish the claims
from being a purely abstract idea. However, Mayo was also directed to
concrete process of administering a drug and the determining the
metabolites levels of the drug in the subject, but such “concreteness” did not
deter the Court from deciding that claim was directed to a natural law
because the recited steps simply represented mining information about the
natural relationship between drug and metabolite levels. In this case, we
find the same problem: the manipulative, physical steps of the claim are
performed to extract information about a natural relationship between cancer
and gene mutations.
14
Appeal 2017-000575
Application 13/310,916
Diehr
Appellants contend that the claims are eligible for a patent for the
same reason as in Diamond v. Diehr, 101 S.Ct. 1048 (1981) (“Diehr”).
Appeal Br. 7.
In Diehr, the claims were directed to a method of operating a rubber­
molding press of precision molded compounds. Application of Diehr, 602
F.2d 982, 983—984 (CCPA 1979) (“Application of Diehr”; lower court
decision; Diehr did not reproduce the claims, but Application of Diehr did.)
The temperature in the mold during the rubber-molding process was
constantly determined and provided to a digital computer. Application of
Diehr, id. The computer calculated the Arrhenius equation for the reaction
time during the cure using the temperature and used the equation to
determine when to open the press. Application of Diehr, id.
Although the claim recited a mathematical algorithm, namely the
Arrhenius equation, the Court held that the claim was eligible for a patent.
[W]hen a claim containing a mathematical formula implements
or applies that formula in a structure or process which, when
considered as a whole, is performing a function which the patent
laws were designed to protect (e. g., transforming or reducing an
article to a different state or thing), then the claim satisfies the
requirements of § 101
Diehr, 101 S.Ct. at 1059-60.
In this case, as found by the Examiner, the presence of mutations are
used to determine the presence of cancer, and further used to determine the
cancer type (ci or C2) (in claim 7, a specific equation is used; claim 26 does
not require a specific equation). However, the determination steps are
mental steps, i.e., a decision based on the mutations detected in the sample
of the subject, and do not involve a change to an article or other concrete
15
Appeal 2017-000575
Application 13/310,916
object as it did in Diehr, or to how the process of analyzing for the presence
of the genes is carried out in step (1) of claims 1 and 26. The Court
emphasized that the process in Diehr was to make rubber, and the
mathematical formula was simply used to determine when to open the mold
so over curing did not occur. Id. at 1057. Thus, while Appellants assert that
the claim is like the claim in Diehr and not Mayothey have not have
factually distinguished Mayo, except to say the claimed method improves a
laboratory diagnostic process. Appeal Br. 11. However, an improvement in
a diagnostic process, it insufficient basis alone to impart eligibility for the
reasons set forth in Mayo. Indeed, in Mayo, the improvement guided how
subsequent drug administration steps were subsequently carried out, but,
here, neither claim 7 not claim 26 use the diagnostic process to modify the
“concrete” steps of the gene analysis step.
Appellants’ further reliance on dependent claims which recite
“recommending, prescribing, ordering, or performing a diagnostic test for
the presence of cancer cj to confirm the presence of cancer cj in said patient”
as additional evidence of patent eligibility is unpersuasive because such
steps do not influence how the gene analysis and detecting is carried out, but
rather represent simply another diagnostic step to discern a natural
relationship between the cancer and a diagnostic test.
Appellants also state the claims are like Diehr because the algorithm
is not at the point of novelty. Reply Br. 7. However, even if this is true, this
does not change the fact that the rejected claims in this appeal are directed to
a correlation between mutated genes and cancer presence and cancer type,
which fundamentally reflects a natural process of the genes involved in
cancer.
16
Appeal 2017-000575
Application 13/310,916
The second step of the patent eligibility analysis requires a
determination of whether the claims do significantly more than simply
describe the abstract idea or natural law. Mayo Collaborative Services v.
Prometheus Laboratories, Inc., 132 S.Ct. 1289, 1297 (2012). In Mayo, the
administering and determining steps were found by the Court to be “well-
understood, routine, conventional activity previously engaged in by
scientists who work in the field.” Mayo, 132 S.Ct. at 1298. Citing earlier
cases decided by the Court, the Court held that “Purely ‘conventional or
obvious’ ‘[pre]-solution activity’ is normally not sufficient to transform an
unpatentable law of nature into a patent-eligible application of such a law.”
Id. at 1298. The Court wrote:
The upshot is that the three steps simply tell doctors to gather
data from which they may draw an inference in light of the
correlations. To put the matter more succinctly, the claims
inform a relevant audience about certain laws of nature; any
additional steps consist of well-understood, routine,
conventional activity already engaged in by the scientific
community; and those steps, when viewed as a whole, add
nothing significant beyond the sum of their parts taken
separately. For these reasons we believe that the steps are not
sufficient to transform unpatentable natural correlations into
patentable applications of those regularities.
Id.
In this case, step (1) of claims 7 and 26 comprise the routine and
conventional activity of analyzing a sample for presence of a mutation in six
specifically recited gene. As discussed above, Gocke discloses analyzing
samples for the presence of oncogenic mutations in plasma or serum (Gocke
13), providing adequate evidence to establish to establish the
conventionality of the step. The data collected about the detection of
mutations is utilized in step (2) to diagnose a cancer or the likelihood of a
17
Appeal 2017-000575
Application 13/310,916
cancer. Claim 7 recites specific equations to accomplish the diagnosis. The
“diagnosing” step is also accomplished Gocke. The use of biological
markers to classify cancer was also well-known as shown by Soria.
Appellants emphasize that the claims are not just analyzing any gene,
but recites a specific panel and specific mutations within the panel. Appeal.
Br. 9-10. Appellants did not articulate the significance of this argument,
but it appears to be part of their contention that the Examiner did not
consider the claim as a whole {id. at 7), and the whole involves a panel of
genes and specific gene mutations. However, as discussed above, a panel of
genes that includes all the claimed genes is described by Ikediobi and the
claims utilize the gene panel in the manner described by Gocke. It is true
that neither publications identifies the specific EGR and KRAS mutations
recited in the claim, but these were known to be oncogenic mutations and
Gocke expressly teaches screening for oncogenic mutations.
Appellants also contend the claims do not raise preemption concerns.
Reply Br. 9.
As discussed in Ariosa Diagnostics, Inc. v. Sequenom, Inc., 788 F.3d
1371, 1379 (Fed. Cir. 2015), “While preemption may signal patent
ineligible subject matter, the absence of complete preemption does not
demonstrate patent eligibility.” Moreover, Ariosa held: “Where a patent’s
claims are deemed only to disclose patent ineligible subject matter under the
Mayo framework, as they are in this case, preemption concerns are fully
addressed and made moot.” Id. Consequently, since the subject matter is
ineligible for a patent under the Alice/Mayo, we need not address the
preemption concern.
For the foregoing reasons, we affirm the rejection under 35 U.S.C. §
18
Appeal 2017-000575
Application 13/310,916
101 because the claims are ineligible for patent as being directed to a natural
phenomenon, a judicially-recognized exception to the statute.
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)(l)(iv).
AFFIRMED
19