Ex Parte Roesch et al

Patent Trial and Appeal Board

Mar 16, 2017

13388583 (P.T.A.B. Mar. 16, 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.
13/388,583 03/05/2012 Alexander O. Roesch WSTR-0047H 1070
26259 7590 03/20/2017
LICATA & TYRRELL P.C.
66 E. MAIN STREET
MARLTON, NJ 08053
EXAMINER
ZARA, JANE J
ART UNIT PAPER NUMBER
1674
NOTIFICATION DATE DELIVERY MODE
03/20/2017 ELECTRONIC
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.
Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the
following e-mail address(es):
PTOactions@licataandtyrrell.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte ALEXANDER O. ROESCH and MEENHARD HERLYN1
Appeal 2016-003769
Application 13/388,583
Technology Center 1600
Before DONALD E. ADAMS, ERIC B. GRIMES, and JOHN E.
SCHNEIDER, Administrative Patent Judges.
GRIMES, Administrative Patent Judge.
DECISION ON APPEAL
This is an appeal under 35U.S.C. § 134 involving claims relating to
cancer treatment, which have been rejected as obvious. We have jurisdiction
under 35 U.S.C. § 6(b). We affirm.
STATEMENT OF THE CASE
The Specification states that “advanced melanomas ... are
notoriously resistant to all available therapies” and that “[ujsing the H3K4
demethylase JARID1B ... as a biomarker, a small subpopulation of slowly-
proliferating melanoma cells has been identified.” (Spec. 114.)
1 Appellants identify the Real Party in Interest as The Wistar Institute.
(Appeal Br. 1.)
Appeal 2016-003769
Application 13/388,583
The Specification states that “[ijsolated JARIDIB-positive melanoma
cells give rise to highly proliferative progeny and show high self-renewal
capacity. . . . [T]he JARID IB-positive subpopulation is essential for
continuous tumor maintenance.” (Id.) “Thus, targeting this subpopulation
of JARID IB-positive cells . . . represents an effective means to exhaust
tumor growth and development.” (Id.)
Claims 73—79 are on appeal. Claims 73 and 74 are illustrative and
read as follows:
Claim 73: A pharmaceutical composition comprising a cancer therapeutic
agent and a JARID IB inhibitor in admixture with a pharmaceutically
acceptable carrier, wherein said composition is formulated for transdermal
or topical administration.
Claim 74: A method for decreasing self-renewal of tumor cells comprising
contacting an esophageal cancer, squamous cell carcinoma, adenocarcinoma,
or melanoma tumor with a JARID IB inhibitor thereby decreasing self-
renewal of the tumor cells.
DISCUSSION
The Examiner has rejected all of the claims on appeal under 35 U.S.C.
§ 103(a) as obvious based on Nakamura2 and Waxman.3 (Ans. 3.) The
Examiner finds that Nakamura teaches treatment of various forms of cancer
using a cancer therapeutic agent and a JARID IB inhibitor, but does not
teach transdermal administration. (Id. at 3 4.) The Examiner finds that
Waxman teaches inhibiting the expression of JARID IB to reduce tumor cell
growth and teaches compositions for topical administration. (Id. at 4.)
2 Nakamura et al., US 2012/0045766 Al, published Feb. 23, 2012.
3 Waxman et al., US 2011/0003753 Al, published Jan. 6, 2011.
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The Examiner concludes that the claimed compositions and methods
would have been obvious
because Nakamura and Waxman teach the role of JARID1B
expression in various forms of cancer, including breast, prostate,
and esophageal cancers, and Waxman teach[es] the routine
experimentation involved in generating pharmaceutical
formulations for administering anticancer agents for treating
various forms of cancer, including transdermal formulations.
(Id.) The Examiner finds that a person of ordinary skill in the art would
have been motivated to combine the references “because JARID1B
overexpression was known in the art to be associated with various forms of
cancer and Waxman teaches combination compositions for cancer therapy.”
(Id.)
We agree with the Examiner that Nakamura and Waxman support a
prima facie case of obviousness. Nakamura discloses that “the expression
level of JARID1B ... is up-regulated compared with normal tissues, in
many types of cancer, including bladder and lung carcinomas.” (Nakamura
137.) Nakamura also discloses that “small interfering RNAs (siRNAs)
targeting JARID1B gene . . . have the ability to inhibit growth of cancerous
cells.” (Id.) “[T]he term ‘siRNA’ refers to a double-stranded RNA
molecule which prevents translation of a target mRNA.” (Id. 1162.)
Nakamura states that “a double-stranded molecule of present
invention may be directly introduced into the cells. . . . Alternatively, ... a
DNA encoding the double-stranded molecule may be introduced into cells as
a vector.” (Id. 1218.) “The present methods can be used to inhibit the
growth or metastasis of cancer expressing JARID1B gene; for example acute
myelogenous leukemia, bladder cancer, breast cancer,” etc. (Id. 1222.)
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Nakamura states that “the double-stranded molecule of the invention
can also be administered to a subject in combination with a pharmaceutical
agent different from the double-stranded molecule,” including chemo­
therapeutic agents. {Id. 1223.) Nakamura discloses that its double-stranded
molecule can be administered by various means, although it does not suggest
topical or transdermal administration. {Id. ]Hf 235—238.)
Waxman discloses “compositions for treating breast cancer . . . [that]
comprise a peptide derived from the mSin3 A interaction domain (SID),
which will be referred to herein as a SID decoy peptide, capable of
interfering with interactions between SID and . . . the transcription repressor
Sin3A.” (Waxman 111.) Waxman states that “[pjolynucleotides can be
administered to cells or subjects and expressed by the cells or subjects,
rather than administering the peptides themselves.” {Id. 147.)
Waxman states that “[pharmaceutical dosage forms containing the
compositions may include at least one isolated peptide of the present
invention, or an isolated polynucleotide encoding the isolated peptide; and a
pharmaceutically acceptable carrier.” {Id. 1 57.) “Oral and transdermal
formulations containing the compositions of the present invention are also
envisioned.” {Id. 1 59.) “Transdermal formulations can be prepared in the
form of a patch, ointment, cream, lotion, solution, tincture, or the like.” {Id.)
Waxman states that its active agents “may be co-administered with one or
more other therapies, such as hormonal therapy, chemotherapy, or radiation
therapy.” {Id. 1 62.)
Waxman also discloses that JARID1B has been found to be
overexpressed in breast cancers, and “in a syngeneic mouse mammary tumor
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model similar to the one used here, stable knockdown of JARID1 []B also
resulted in reduced tumor cell growth.” {Id. 1125.)
We agree with the Examiner that claim 73 would have been obvious
to a person of ordinary skill in the art based on Nakamura and Waxman.
Specifically, Nakamura discloses inhibiting the growth or metastasis of
breast cancer cells by administering a small interfering RNA (siRNA) that
prevents translation of the JARID1B gene, and suggests administering the
siRNA in the form of DNA encoding the siRNA, and in combination with
another cancer therapeutic agent. Waxman teaches administering DNA
encoding a cancer therapeutic agent by transdermal administration, in
combination with a chemotherapeutic agent. Thus, it would have been
obvious to administer DNA encoding Nakamura’s JARIDIB-inhibiting
siRNA, in combination with a chemotherapeutic agent, transdermally.
Appellants argue that Nakamura does not “teach or suggest a
pharmaceutical composition formulated for topical or transdermal
administration as presently claimed” in claim 73 (Appeal Br. 9) and Waxman
“does not teach or suggest a pharmaceutical composition containing a
JARID1B inhibitor” {id. at 10). Appellants argue that “[tjhere is no single
example or suggestion by Waxman et al. of a combination composition
containing a JARID1B inhibitor” and “there is insufficient information and
guidance provided by the combined teachings of the cited references to direct
one of skill in the art to prepare pharmaceutical compositions for transdermal
or topical administration as presently claimed.” {Id. at 11.) Appellants
present the same arguments with respect to claims 75—77. {Id. at 13—16.)
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These arguments are not persuasive. As discussed above, Nakamura
discloses siRNAs that inhibit JARID1B and suggests administering a siRNA
in the form of DNA encoding the siRNA, while Waxman teaches that DNA
encoding a cancer therapeutic agent can be administered transdermally.
Both references teach treating breast cancer. It would have been obvious,
based on the combined teachings of the references, to administer
Nakamura’s siRNA-encoding DNA transdermally. “The test for
obviousness is what the combined teachings of the references would have
suggested to one of ordinary skill in the art.” In re Young, 927 F.2d 588,
591 (Fed. Cir. 1991).
Appellants also argue, with respect to claim 77, that Nakamura does
not “demonstrate inhibition of metastatic progression of any of the cancers
disclosed therein.” (Appeal Br. 15)
Nakamura expressly states, however, that its “methods can be used to
inhibit the growth or metastasis of cancer expressing JARID1B gene; for
example acute myelogenous leukemia, bladder cancer, breast cancer,” etc.
(Nakamura 1222.) “[A] prior art printed publication cited by an examiner is
presumptively enabling barring any showing to the contrary by a patent
applicant.” In re Antor Media Corp., 689 F.3d 1282, 1288 (Fed. Cir. 2012).
Appellants have not shown that Nakamura is not enabling for what it
discloses.
Finally, with respect to claim 77, Appellants cite the Board decision in
Appeal 2011-011328 as holding that treatment of lung and breast cancer
using a histone deacetylase inhibitor cannot be extrapolated to kidney tumor
cells with a reasonable expectation of success. (Appeal Br. 16.) Claim 77,
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however, is not limited to any particular type of cancer and Nakamura
discloses that its method is effective in inhibiting metastasis of a variety of
different cancer types. That disclosure is presumed to be enabled, In re
Antor Media Corp., 689 F.3d at 1288, and Appellants have not shown that it
is not.
With regard to claim 74, Appellants argue that neither Nakamura nor
Waxman “teach or suggest decreasing self-renewal of esophageal cancer,
squamous cell carcinoma, adenocarcinoma, or melanoma tumor cells using a
JARID1B inhibitor.” (Appeal Br. 12.) Appellants also argue that the
references do not suggest “treating” or “inhibiting metastatic progression” of
the same types of cancer, as recited in claims 78 and 79, respectively. (Id. at
17—18.) Also, with respect to claim 74, Appellants argue that, according to
the Specification, “‘self-renewal’ of a JARIDIB-positive cell refers to the
ability of a cell to regenerate to resemble parental tumor heterogeneity as
determined, e.g., by continuous survival of cells in stem cell medium and
cell morphology.”
These arguments are not persuasive. With regard to the types of
cancer recited in claims 74, 78, and 79, Nakamura states that its method “can
be used to inhibit growth or metastasis” of a variety of cancers, “especially
bladder and lung cancer.” (Nakamura 1222.) Nakamura also discloses that
lung tumors arise from, among other things, adenocarcinoma and squamous
cell carcinoma. (Id. at Table 5.) Thus, it would have been obvious to apply
the treatment made obvious by Nakamura and Waxman to patients with lung
cancer, including those lung tumors arising from adenocarcinoma or
squamous cell carcinoma.
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With regard to “self-renewal,” Nakamura discloses that “[t]o
investigate the role of JARID1B in human carcinogenesis, siRNA
oligonucleotide duplexes, to specifically suppress the expression of
JARID1B (siJARIDlB#l . . .)” were tested in three bladder cancer cell lines,
two non-small lung cancer cell lines, and one small lung cancer cell line.
(Nakamura 1 507.) Nakamura reports that “[i]n all cases, the growth of
cancer cells was significantly suppressed after treatment with
siJARIDlB#l.” {Id.)
Appellants’ Specification states that
JARID1B expression can be inhibited using, e.g., antisense,
ribozyme, or RNAi molecules or techniques known in the art. In
particular embodiments, RNA interference or RNAi is
employed. This technique involves introducing into a cell
double-stranded RNA (dsRNA), having a sequence
corresponding to the exonic portion of the target gene. . . .
Typically, siRNAs are about 20 to 23 nucleotides in length.
(Spec. 121.)
As the Specification acknowledges, therefore, the claimed method
encompasses using siRNAs to inhibit expression of JARID1B. Nakamura
discloses using siRNAs to inhibit expression of JARID1B. The method
made obvious by Nakamura and Waxman therefore will have the same
effect as the claimed method, because it treats the same cells with the same
agents. Cf. Bristol-Myers Squibb Co. v. Ben Venue Labs., Inc., 246 F.3d
1368, 1376 (Fed. Cir. 2001) (Preamble language reciting “a method for
treating a cancer patient to effect regression of a taxol-sensitive tumor, said
method being associated with reduced hematologic toxicity” was “only a
statement of purpose and intended result. The expression does not result in a
manipulative difference in the steps of the claim.”). Appellants have not
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shown that the method of claim 74 differs in its manipulative step(s) from
the method made obvious by the prior art.
SUMMARY
We affirm the rejection of claims 73—79 under 35 U.S.C. § 103(a)
based on Nakamura and Waxman.
TIME PERIOD FOR RESPONSE
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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