DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Claims 7, 10-11, and 14 are pending and under examination. Claims 7 and 14 are amended. Claims 1-6, 8-9, 12-13, and 15 are canceled.
Continued Examination Under 37 CFR 1.114
A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on 3/10/26 has been entered.
Priority
The instant application 17/907,791 filed on 8/29/22 is a 371 US national phase of PCT/KR2021/002276 filed on 2/24/21, and claims foreign priority to KR10-2020-0024778 filed on 2/28/20 and KR10-2021-0015216 filed on 2/3/21. The priority date is determined to be 2/24/21 in the absence of a copy certified translation of KR10-2020-0024778 and/or KR10-2021-0015216.
Receipt is acknowledged of KR10-2020-0024778 and KR10-2021-0015216 certified copies of papers required by 37 CFR 1.55. Priority Documents were electronically retrieved by USPTO from participating IP office on 8/29/22.
Should applicant desire to obtain the benefit of foreign priority under 35 U.S.C. 119(a)-(d) prior to declaration of an interference, a certified English translation of the foreign application must be submitted in reply to this action. 37 CFR 41.154(b) and 41.202(e).
Failure to provide a certified translation may result in no benefit being accorded for the non-English application.
Response to Arguments
Applicant’s arguments, see pages 5-11, filed 1/4/26, with respect to the rejections of claims 7, 10-11, and 14 under 35 USC 103 have been fully considered and are found persuasive. Therefore, the rejections documented in the Non-Final mailed 12/12/25 have been withdrawn. However, upon further consideration, new grounds of rejections necessitated by claim amendments are made in this Final Office Action.
Claim Rejections - 35 USC § 112 – Written Description
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 10-11 and 14 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
This 112(a) rejection is necessitated by claim amendments filed 1/4/26.
Claims 10-11 and 14 recite administration of “an anticancer agent”, with claims 11 and 14 reciting specific anticancer agents selected from doxorubicin, paclitaxel, vincristine, daunorubicin, vinblastine, actinomycin-D, docetaxel, etoposide, teniposide, bisantrene, imatinib, cisplatin, and 5-fluorouracil.
Per MPEP 2163.05(II):
The introduction of claim changes which involve narrowing the claims by introducing elements or limitations which are not supported by the as-filed disclosure is a violation of the written description requirement of 35 U.S.C. 112(a) or pre-AIA 35 U.S.C. 112, first paragraph. See, e.g., Fujikawa v. Wattanasin, 93 F.3d 1559, 1571, 39 USPQ2d 1895, 1905 (Fed. Cir. 1996) (a "laundry list" disclosure of every possible moiety for every possible position does not constitute a written description of every species in a genus because it would not "reasonably lead" those skilled in the art to any particular species); and Regents of the Univ. of Minnesota v. Gilead Scis., Inc., 61 F.4th 1350, 1356-58, 2023 USQ2d 269 (Fed. Cir. 2023). (emphasis added)
It is noted that the specification only provides written description of administration of siTINAGL1, however, does not reasonably convey possession of the claimed pharmaceutical composition further comprising an anticancer agent. The Specification provides for a laundry list of a large genus of potential anticancer agents (page 8, lines 4-6) without describing their use in the claimed pharmaceutical composition, lacking representative examples, protocols, dosages, or other description showing the inventors had possession of the full claimed subject matter at the time of filing.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claim 7 is rejected under 35 U.S.C. 103 as being unpatentable over Sun et al. (2019; NPL citation 3 in IDS filed on 8/29/22; “TINAGL1 promotes hepatocellular carcinogenesis through the activation of TGF-β signaling-medicated VEGF expression”; Cancer Management and Research 2019:11 767–775; https://doi.org/10.2147/CMAR.S190390) in view of Ge et al. and associated Dataset D6 excerpt (2018; NPL citations W and X on page 1 of PTO-892 filed 7/14/25; “A proteomic landscape of diffuse-type gastric cancer”; Nat Commun 9, 1012 (2018). https://doi.org/10.1038/s41467-018-03121-2), and Madar et al. (2013; NPL citation U on page 1 of PTO-892 filed 7/14/25; "'Cancer associated fibroblasts' - more than meets the eye"; Trends in Molecular Medicine, Volume 19, Issue 8; Pages 447-453; https://doi.org/10.1016/j.molmed.2013.05.004).
This 103 rejection is necessitated by claim amendments filed 1/4/26.
(i) Sun et al. teaches that “TINAGL1 promotes hepatocellular carcinogenesis through the activation of TGF-β signaling-medicated VEGF expression” (Title).
Relevant to claim 7, Sun et al. Abstract teaches "TINAGL1 knockdown suppressed HCC cell growth, proliferation, and migration and induced apoptosis in HCC cells, whereas TINAGL1 overexpression had opposite effects. In addition, inhibition of TINAGL1 retarded xenograft tumor growth in a nude mouse model."
This teaching reads on claim 7 A method of treating… comprising administering a pharmaceutical composition comprising an effective amount of a TINAGL1 inhibitor as an active ingredient to a subject in need of treating.
Further relevant to claim 7, Sun et al. Figure 4E Western blot and associated caption teach si-TINAGL1 knockdown expression.
This teaching reads on claim 7 wherein the TINAGL1 inhibitor is siRNA that specifically bind to TINAGL1 protein or a gene encoding the protein, and wherein the TINAGL1 inhibitor inhibits secretion and expression of TINAGL1 protein or a gene encoding the protein.
(ii) Sun et al. is silent to specifics regarding diffuse type gastric cancer. However, these limitations were known in the prior art and taught by Ge et al.
Relevant to claim 7, Ge et al. Abstract teaches that “Here we present a dataset from 84 DGC [diffuse-type gastric cancer] patients, composed of a proteome of 11,340 gene products and mutation information of 274 cancer driver genes covering paired tumor and nearby tissue…"
Further relevant to claim 7, Ge et al. teaches "Cancer driver pathways, including transforming growth factor (TGF), WNT, NOTCH and interferon (IFN), were up-regulated in DGC with prominent increase in proteins at ligand and receptor levels (Fig. 2e), suggesting the dysregulation of these important cancer driver pathways from the most up-stream in DGC" (page 4, column 1, paragraph 1).
Further relevant to claim 7, Ge et al. Supplementary Data 2, Dataset D6 page 5 teaches that TINAGL1 is one of 2,538 gene products that show Tumor to Nearby tissue protein expression ratio of >3 or <1/3 in at least 8 patients.
Sun et al. teaches that TINAGL1 upregulation is associated with prognostic prediction in hepatocellular carcinogenesis and impacts the TGF-β/Smad3/VEGF metastasis pathway. Although the instant invention is directed towards diffuse type gastric cancer, Ge et al. teaches that the TGF pathways “were up-regulated in DGC” and that TINAGL1 protein expression is detectably different between paired tumor and nearby tissues. Therefore, the skilled artisan would find it obvious to use TINAGL1 as a target for treatment of diffuse type gastric cancer because Sun et al. teaches that TINAGL1 is upregulated in highly metastatic tumors and promotes metastasis via the TGF pathways, and Ge et al. teaches that diffuse type gastric cancer is characterized by upregulation of TGF pathways with detectably distinct paired tumor-nearby tissue TINAGL1 expression.
Thus, these combined teachings read on claim 7 with regards to TINAGL1 association with diffuse type gastric cancer.
(iii) Sun et al. in view of Ge et al. is silent to specifics regarding cancer-associated fibroblasts (CAF). However, these limitations were known in the prior art and taught by Madar et al.
Relevant to claim 7, Madar et al. Abstract teaches that "Cancer associated fibroblasts (CAFs) are a subpopulation of cells that reside within the tumor microenvironment and promotes the transformation process by encouraging tumor growth, angiogenesis, inflammation, and metastasis. CAF-specific proteins serve as both prognostic markers and targets for anticancer drugs."
(iv) Although Sun et al. and Ge et al. do not explicitly teach cancer-associated fibroblasts, this limitation would have been prima facie obvious to the skilled artisan. It is noted that Sun et al., Ge et al., and Madar et al. are all analogous disclosures to the instant cancer field.
The skilled artisan would have been motivated to combine the analogous art. Sun et al. Abstract teaches that “Tubulointerstitial nephritis antigen-like 1 (TINAGL1) is an extracellular matrix protein that plays an important role in cell adhesion and therefore modulates cell proliferation, migration, and differentiation. In addition, it is frequently upregulated in highly metastatic tumors.” As Madar et al. teaches that cancer associated fibroblasts are associated with key factors within cancer pathogenesis (such as metastasis), and Sun et al. teaches that TINAGL1 upregulation is associated with highly metastatic tumors, the skilled artisan would be motivated to assess the Madar et al. cancer associated fibroblasts within the methodologies rendered obvious by Sun et al. in view of Ge et al. The skilled artisan would be motivated to mitigate the encouragement of “tumor growth, angiogenesis, inflammation, and metastasis”.
The skilled artisan would have a reasonable expectation of success based on the disclosures of Sun et al. in view of Ge et al. and Madar et al., as discussed in the preceding paragraphs.
Claims 10-11 and 14 are rejected under 35 U.S.C. 103 as being unpatentable over Sun et al. (2019; NPL citation 3 in IDS filed on 8/29/22; “TINAGL1 promotes hepatocellular carcinogenesis through the activation of TGF-β signaling-medicated VEGF expression”; Cancer Management and Research 2019:11 767–775; https://doi.org/10.2147/CMAR.S190390) in view of Ge et al. and associated Dataset D6 excerpt (2018; NPL citations W and X on page 1 of PTO-892 filed 7/14/25; “A proteomic landscape of diffuse-type gastric cancer”; Nat Commun 9, 1012 (2018). https://doi.org/10.1038/s41467-018-03121-2), and Madar et al. (2013; NPL citation U on page 1 of PTO-892 filed 7/14/25; "'Cancer associated fibroblasts' - more than meets the eye"; Trends in Molecular Medicine, Volume 19, Issue 8; Pages 447-453; https://doi.org/10.1016/j.molmed.2013.05.004), as applied to claim 7 above, and further in view of Babu et al. (2017; "Combinatorial therapeutic approaches with RNAi and anticancer drugs using nanodrug delivery systems". Drug Dev Ind Pharm. 2017 Sep;43(9):1391-1401. doi: 10.1080/03639045.2017.1313861).
The teachings of Sun et al. in view of Ge et al. and Madar et al. are applied to instantly rejected claims 10-11 and 14 as they were previously applied to claim 7 as rendering obvious a method of treating diffuse type gastric cancer.
Sun et al. in view of Ge et al. and Madar et al. is silent to specifics regarding anticancer agents (claims 10-11 and 14). However, these limitations were known in the prior art and taught by Babu et al.
Relevant to claims 10 and 14, Babu et al. Abstract teaches “Combining siRNA and other therapeutic agents can overcome the multidrug resistance (MDR) phenomenon by simultaneously silencing genes and enhancing chemotherapeutic activity. Moreover, the therapeutic efficiency of anticancer drugs can be significantly improved by additive or synergistic effects induced by siRNA and combined therapies.”
This teaching reads on claim 10 wherein the pharmaceutical composition further comprises an anticancer agent; and claim 14 wherein the pharmaceutical composition further comprises an anticancer agent.
Relevant to claims 11 and 14, Babu et al. teaches co-administrations of siRNA and doxorubicin (page 1393, column 2, paragraph 2); paclitaxel (page 1395); docetaxel (page 1393, column 1, paragraph 3); and cisplatin (page 1395, column 1, paragraph 5).
These teachings read on claim 11 wherein the anticancer agent is selected from the group consisting of doxorubicin, paclitaxel… docetaxel… cisplatin; and claim 14 wherein the anticancer agent is selected from the group consisting of doxorubicin, paclitaxel… docetaxel.
Although Sun et al., Ge et al., and Madar et al. do not explicitly teach anticancer agents, this limitation would have been prima facie obvious to the skilled artisan. It is noted that Sun et al., Ge et al., Madar et al., and Babu et al. are all analogous disclosures to the instant cancer field.
The skilled artisan would have been motivated to combine the analogous art. Babu et al. Abstract teaches “Combining siRNA and other therapeutic agents can overcome the multidrug resistance (MDR) phenomenon by simultaneously silencing genes and enhancing chemotherapeutic activity. Moreover, the therapeutic efficiency of anticancer drugs can be significantly improved by additive or synergistic effects induced by siRNA and combined therapies.” Thus, the skilled artisan would be motivated to include the Babu et al. anticancer combination therapy within the methodologies rendered obvious by modified-Sun et al. in order to overcome multidrug resistance and improve therapeutic efficacy.
The skilled artisan would have a reasonable expectation of success based on the disclosures of Sun et al. in view of Ge et al., and Madar et al., and further in view of Babu et al., as discussed in the preceding paragraphs.
Conclusion
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/SARAH JANE KENNEDY/Examiner, Art Unit 1682
/WU CHENG W SHEN/Supervisory Patent Examiner, Art Unit 1682
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