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 .
DETAILED ACTION
The amendment filed on 07/21/2025 has been entered.
Applicant’s election without traverse of Group I, claims 12-15, 18, 19, 24-27, 31, 36-38, 43, 45, 47, 52, 74, 75, 92, 120, and 121, in the reply filed on 03/25/2025 is acknowledged.
Applicant is reminded that upon the cancelation of claims to a non-elected invention, the inventorship must be corrected in compliance with 37 CFR 1.48(a) if one or more of the currently named inventors is no longer an inventor of at least one claim remaining in the application. A request to correct inventorship under 37 CFR 1.48(a) must be accompanied by an application data sheet in accordance with 37 CFR 1.76 that identifies each inventor by his or her legal name and by the processing fee required under 37 CFR 1.17(i).
Claims 1-11, 16-17, 20-23, 28-30, 32-35, 39-42, 44, 46, 48-51, 53-91, 74-75 93-119, and 122-171 are canceled in the claim set filed on 07/21/2025.
Claims 43 and 45, remain withdrawn without traverse as being drawn to nonelected inventions.
Claims 12-15, 18-19, 24-27, 31, 36-38, 47, 52, 92, 120, and 121 are currently under examination.
Response to the Arguments
Claims 12-13, 25, 92, 120, and 121 were amended by applicant in the claim set filed on 07/21/2025 and no new matter was added.
Claim amendments filed on 07/21/2025 overcome all of the previous claim objections.
Applicant’s arguments regarding previous rejection(s) of claim(s) 12-15, 18-19, 24-27, 31, 36-38, 47, 52, 92, 120, and 121 under 35 U.S.C. 102 or 103 have been fully considered and are persuasive. Applicant’s argument on Pg. 8-11, states that “Applicant notes that claims 12, 13, 120, and 121 have been amended to incorporate an element from previous claims 74 and 75, neither of which was included in the instant rejection. The remaining claims depend directly or indirectly from claim 12. For at least these reasons, Applicant respectfully submits that the amended claims are novel over Ladanyi and thus respectfully requests that the Examiner withdraw the rejection.” The 35 U.S.C. 102 and 103 rejections documented in the previously mailed non-final have been withdrawn in light of applicants claim amendments and arguments on Pg. 8-11. However, upon further consideration and search, new grounds of rejection are made as documented below in the 35 U.S.C. 103 rejection in this office action on Pg. 4-19.
The rejections documented below in this Final Office Action are necessitated by claim amendments filed on 07/21/2025.
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.
Claims 12-15,18-19, 24-27, 37, 47, 52, 92 and 120-121 are rejected under 35 U.S.C. 103 as being obvious over Ladanyi et al. (“Ladanyi”, U.S. Patent No. 5,670,317, Sep. 23, 1997) in view of Artomov et al. (“Artomov” U.S. Patent App. Pub. No. US 2019/0030147 A1, Jan. 31, 2019).
Ladanyi discloses a method comprising an isolated nucleic acid molecule encoding a chimeric EWS-WT1 protein. This invention also provides an isolated protein which is a chimeric EWS-WT1 protein. This invention further provides method of diagnosing a desmoplastic small round cell tumor in a subject which comprises detecting in a sample from the subject a nucleic acid molecule encoding a chimeric EWS-WT1 protein positive detection indicating the presence of desmoplastic small round cell tumor. This invention also provides a method of inhibiting the growth of a neoplastic cell, wherein the cell is characterized by the presence of a chimeric EWS-WT1 protein which comprises contacting an antibody which specifically recognizes the chimeric EWS-WT1 fusion protein under suitable conditions so that an antibody-antigen complex is formed, thereby inhibiting the growth of the neoplastic cell (Abstract).
Regarding claims 12, Ladanyi teaches a method of diagnosing a desmoplastic small round cell tumor in a subject which comprises detecting in a sample from the subject a nucleic acid molecule encoding a chimeric EWS-WT1 protein (e.g., Pg. 15 col. 2 ln 52-55). Ladanyi teaches a method of inhibiting the growth of a neoplastic cell wherein the cell is characterized by the presence of a chimeric EWS-WT1 protein which comprises contacting an antibody conjugated to a therapeutic agent, wherein the antibody recognizes the chimeric EWS-WT1 protein under suitable conditions so that an antibody-antigen complex is formed, thereby inhibiting the growth of the neoplastic cell. (e.g., Pg. 17 col. 8 ln 25-32; Pg. 15 col. 2 ln 57-61). Thus, Ladanyi teaches a method of treating or delaying progression of cancer, comprising:(a) detecting an Ewing sarcoma breakpoint region I- Wilms tumor protein (EWSR1-WT1) fusion gene encoding a neoantigen in a sample from an individual; and (b) administering to the individual an effective amount of a treatment.
Ladanyi does not explicitly teach a method comprising (b) administering to the individual an effective amount of checkpoint inhibitor.
Artomov discloses methods that relate to constructing therapeutic fusion-specific vaccine libraries, selecting a therapeutic fusion-specific vaccine for a cancer patient, and/or constructing a de nova therapeutic fusion-specific vaccine for patients having a gene fusion that is absent from a fusion specific vaccine library (Abstract).
Regarding claim 12, Artomov teaches a method comprising “treatment for a patient with cancer”. (e.g., Pg. 16., para. 87). Artomov teaches a method comprising “suitable therapies… include but are not limited to immunotherapies, for example checkpoint blockade therapies, for example, but not limited to, anti-PD1 (e.g., nivolumab (Opdivo®), pembrolizumab (Keytruda®), pidilizumab etc.), anti-CTLA4 (e.g., ipilimumab (Yervoy®), tremelimumab), or other checkpoint inhibitors such as BMS-936559, MPDL3280A, MEDI4736, MSB0010718C, IMP321, MGA271” (Para. 91). Thus, Ladanyi and Artomov teach a method comprising (b) administering to the individual an effective amount of checkpoint inhibitor.
Therefore, it would have been obvious to someone of ordinary skill in the art before the effective filing date of the claimed invention to have modified the method of treating and/or delaying progression of a cancer comprising EWSR1-WT1 as taught by Ladanyi to incorporate the method of treatment with checkpoint inhibitor(s) as taught by Artomov and provide an effective checkpoint inhibitor treatment for cancer comprising the gene fusion. Doing so would improve the effective treatment regime outcome against cancer evasion.
The teachings of Ladanyi and Artomov are documented above in the rejection of claim 12 under 35 U.S.C. 103. Claims 14-15,18-19, 24-27, 37, 47, 52 and 92 depend on claim 12. Claims 13 and 120-121 are independent claims.
Regarding claim 13, Ladanyi teaches a method of diagnosing a desmoplastic small round cell tumor in a subject which comprises detecting in a sample from the subject a nucleic acid molecule encoding a chimeric EWS-WT1 protein (e.g., Pg. 15 col. 2 ln 52-55). Ladanyi teaches a method of inhibiting the growth of a neoplastic cell wherein the cell is characterized by the presence of a chimeric EWS-WT1 protein which comprises contacting an antibody conjugated to a therapeutic agent, wherein the antibody recognizes the chimeric EWS-WT1 protein under suitable conditions so that an antibody-antigen complex is formed, thereby inhibiting the growth of the neoplastic cell. (e.g., Pg. 17 col. 8 ln 25-32; Pg. 15 col. 2 ln 57-61). Thus, Ladanyi and Artomov teach a method of treating or delaying progression of cancer, comprising:(a) acquiring knowledge of an Ewing sarcoma breakpoint region 1 - Wilms tumor protein (EWSRI-WT1) fusion gene encoding a neoantigen in a sample from an individual; and (b) responsive to said knowledge, administering to the individual an effective amount of a treatment comprising a checkpoint inhibitor.
Regarding claim 14, Ladanyi teaches a method wherein diagnosing a desmoplastic small round cell tumor in a subject which comprises detecting in a sample from the subject a nucleic acid molecule encoding a chimeric EWS-WT1 protein (e.g., Pg. 14, col. 2, ln 52-55). Ladanyi teaches a method wherein tumor and normal tissue samples were collected (e.g., Pg. 20, col. 13, ln 55). Thus, Ladanyi and Artomov teach a method comprising, prior to detecting the presence of an EWSRI-WTI1 fusion gene encoding a neoantigen in the sample, obtaining the sample from the individual.
Regarding claim 15, Ladanyi teaches a method wherein tumor and normal tissue samples were collected (e.g., Pg. 20, col. 13, ln 55). Thus, Ladanyi and Artomov teach a method wherein the sample is: (a) a blood, bone marrow, tumor, or tissue sample; (b) from amniotic fluid, blood, plasma, serum, semen, lymphatic fluid, cerebral spinal fluid, ocular fluid, urine, saliva, stool, mucus, sweat, blood, skin, hair, hair follicles, saliva, oral mucous, vaginal mucus, sweat, tears, epithelial tissues, urine, semen, seminal fluid, seminal plasma, prostatic fluid, Cowper's fluid, excreta, biopsy, ascites, cerebrospinal fluid, or lymph; or (c) a biopsy or formalin-fixed paraffin-embedded (FFPE) sample.
Regarding claim 18, Ladanyi teaches a method wherein DNA isolated from frozen tumor (e.g., Pg. 19, col. 12, ln 9-10). Thus, Ladanyi and Artomov teach a method wherein the presence of an EWSR1-WT1 fusion gene is detected in DNA or RNA from the sample.
Regarding claim 19, Ladanyi teaches a method wherein Direct sequencing of purified recombinant plasmid DNA was carried out by PCR (e.g., Pg. 20, col. 13, ln 12-13). Direct sequencing is interpreted as Sanger sequencing. Thus, Ladanyi and Artomov teach a method wherein the presence of an EWSR1-WT1 fusion gene is detected: (a) in cell-free DNA (cfDNA), (b) in DNA by next-generation sequencing (NGS), polymerase chain reaction (PCR), Sanger sequencing, or fluorescence in situ hybridization (FISH); or (c) in RNA by RNA-sequencing (RNA-seq), polymerase chain reaction (PCR), Sanger sequencing, or fluorescence in situ hybridization (FISH).
Regarding claim 24, Artomov teaches a method comprising identifying long peptides at fusion breakpoints and predicting peptide binding affinity to MHC class I proteins (e.g., Pg. 13, para. 46; Figure 1). Thus, Ladanyi and Artomov teach a method wherein the neoantigen binds, or is predicted to bind, a major histocompatibility complex (MHC) class I molecule of the individual.
Regarding claim 25, Artomov teaches a method comprising determining peptide binding affinity to MHC proteins using biochemical techniques in vitro (e.g., Pg. 13, para. 46). Artomov teaches a method wherein peptides with predicted IC50 <500 nM are considered to bind to HLA proteins. In some embodiments, peptides with predicted IC50<50 nM are considered as strong binders to HLA proteins (e.g., Pg. 26, para. 201). Both KD and IC50 are interpreted to describe binding affinity. Thus, Ladanyi and Artomov teach a method wherein the neoantigen binds, or is predicted to bind, an MHC class I molecule of the individual with a dissociation constant (KD) of 50 nM or less.
Regarding claim 26, Artomov teaches method wherein information relating to one or more HLA alleles of the cancer patient are obtained by analysis (e.g., Pg. 10, para. 10). Artomov teaches method comprising determining a binding affinity of peptide-HLA class I major genes comprising HLA-A, HLA-B, and/or HLA-C. (e.g., Pg. 22, para. 48). Thus, Ladanyi and Artomov teach a method comprising: genotyping one or more human leukocyte antigen (HLA)-A, HLA-B, and HLA-C alleles from the sample from the individual.
Regarding claim 27, Artomov teaches a method wherein a patient is selected for vaccination with a therapeutic fusion-specific vaccine from the fusion-specific vaccine library if the patient has one or more HLA proteins that can effectively bind and present to the immune system one or more fusion-derived neoantigens that are present in the library. (e.g., Pg.15 para. 68). Thus, Ladanyi and Artomov teach a method wherein:(a) the cancer does not comprise a loss-of-heterozygosity at an HLA-A, HLA-B, or HLA- C allele that encodes an MHC class I molecule to which the neoantigen binds, or is predicted to bind; or(b) the cancer comprises a loss-of-heterozygosity at one or more, but not all, of HLA-A, HLA-B, or HLA-C allele(s) that encode an MHC class I molecule to which the neoantigen binds, or is predicted to bind; or(c) the cancer does not comprise a loss-of-function mutation in a CIITA or B2M gene.
Regarding claim 37, Ladanyi teaches a method wherein EWS and the WT1 genes in DSRCT were initially examined in five DSRCT tissue samples. Ladanyi teaches the results confirmed the presence of a consistent fusion of the EWS and WT1 genes in DSRCT (e.g., Pg. 14, col. 2, ln 18-21). Thus, Ladanyi and Artomov teach a method wherein the cancer is a desmoplastic small round cell tumor (DSRCT).
Regarding claim 47, Ref teaches a method wherein EWS and WT1 specific probes and comparison of restriction map data indicated a fusion of the two genes with expected breakpoints within the intron between exons 7 and 8 of EWS and the intron between exons 7 and 8 of WT1 (FIG. 5B) (e.g., Pg. 22, col. 17, ln 29-33; Figure 5 B). Thus, Ladanyi and Artomov teach a method wherein EWSR1-WT1 fusion gene:(a) comprises a coding sequence of EWSR1 at the 5' end and a coding sequence of WT1 at the 3' end or (c) is formed via breakpoints in intron 7 of EWSR1 and intron 7 of WT1.
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Regarding claim 52, Ladanyi teaches a method comprising a 100% query match to the 9 aa of SEQ ID No. 1 (instant case) to SEQ ID No. 19 of U.S. Patent 5670317 (e.g., Sequence search result 1, see image below). Thus, Ladanyi and Artomov teach a method wherein: (a) the
neoantigen comprises at least 5 contiguous amino acids from the sequence SSYGQQSEK (SEQ ID NO:1).
Regarding claim 92, Artomov teaches a method wherein treatment comprises treating a patient with a fusion-derived peptide or vaccine composition in combination with one or more additional therapies. Artomov teaches a method wherein vaccination of a patient is combined with one or more targeted therapies, chemotherapies, radiation, immunotherapy, or with hematopoietic stem cell transplantation. Artomov teaches a method wherein suitable therapies that can be combined with vaccination include but are not limited to immunotherapies, for example checkpoint blockade therapies (e.g., Pg. 16. para. 91). Thus, Ladanyi and Artomov teach a method further comprising administering an additional anti-cancer therapy to the individual.
Regarding claims 120, Ladanyi teaches a method of diagnosing a desmoplastic small round cell tumor in a subject which comprises detecting in a sample from the subject a nucleic acid molecule encoding a chimeric EWS-WT1 protein (e.g., Pg. 15 col. 2 ln 52-55). Ladanyi teaches a method of inhibiting the growth of a neoplastic cell wherein the cell is characterized by the presence of a chimeric EWS-WT1 protein which comprises contacting an antibody conjugated to a therapeutic agent, wherein the antibody recognizes the chimeric EWS-WT1 protein under suitable conditions so that an antibody-antigen complex is formed, thereby inhibiting the growth of the neoplastic cell. (e.g., Pg. 17 col. 8 ln 25-32; Pg. 15 col. 2 ln 57-61). Thus, Ladanyi and Artomov teach a method of treating or delaying progression of cancer, comprising:(a) detecting a Ewing sarcoma breakpoint region 1 (EWSR1) fusion gene encoding a neoantigen in a sample from an individual; and (b) administering to the individual an effective amount of a treatment comprising a cancer checkpoint inhibitor.
Regarding claim 121, Ladanyi teaches a method of diagnosing a desmoplastic small round cell tumor in a subject which comprises detecting in a sample from the subject a nucleic acid molecule encoding a chimeric EWS-WT1 protein (e.g., Pg. 15 col. 2 ln 52-55). Ladanyi teaches a method of inhibiting the growth of a neoplastic cell wherein the cell is characterized by the presence of a chimeric EWS-WT1 protein which comprises contacting an antibody conjugated to a therapeutic agent, wherein the antibody recognizes the chimeric EWS-WT1 protein under suitable conditions so that an antibody-antigen complex is formed, thereby inhibiting the growth of the neoplastic cell. (e.g., Pg. 17 col. 8 ln 25-32; Pg. 15 col. 2 ln 57-61). Thus, Ladanyi and Artomov teach a method of treating or delaying progression of cancer, comprising:(a) acquiring knowledge of a Ewing sarcoma breakpoint region 1 (EWSR1) fusion gene encoding a neoantigen in a sample from an individual; and (b) responsive to said knowledge, administering to the individual an effective amount of a treatment comprising a cancer checkpoint inhibitor.
Response to Arguments
Applicant' s arguments filed on 07/21/2025 (Pg. 9-10) with respect to claims 12-15,18-19, 24-27, 37, 47, 52, 92 and 120-121 have been considered but do not apply to the new grounds of rejections. To clarify some instances argued in the response filed 07/21/20205 that remain relevant to the new grounds of 103 rejection documented in this Final Office Action, examiner’s responses to each relevant argument made by Applicant are provided below:
Applicants’ argument: “To the extent that the rejection would apply to amended claims 12, 13, 120, and 121, Applicant respectfully submits that the amended claims are not obvious over Ladanyi in view of Artomov because, based on the combination of references, one of ordinary skill in the art would not be motivated to treat a cancer having an EWSRJ-WTJ fusion gene encoding a neoantigen with an effective amount of a checkpoint inhibitor.” (Pg. 9)
Examiner’s Response: Applicant’s arguments with respect to claim amendments to claims 12-12 and 120-121 have been considered but do not apply to the new ground of rejection. Note, “comprising” is interpreted as an open-ended transitional term that does not exclude additional, unrecited elements or method steps. See MPEP 2111.03. Thus, the mere presence of the checkpoint inhibitor administration whether in combination or alone is sufficiently obvious enough for a skilled artisan to treat a subject with cancer.
Claims 31, 36 and 38 are rejected under 35 U.S.C. 103 as being unpatentable over Ladanyi et al. (“Ladanyi”, U.S. Patent No. 5,670,317, Sep. 23, 1997) in view of Artomov et al. (“Artomov” U.S. Patent App. Pub. No. US 2019/0030147 A1, Jan. 31, 2019), as applied to claim 12-15,18-19, 24-27, 37, 47, 52, 92 and 120-121, and further in view of Cote et al. (“Cote”, (2018). Next‐generation sequencing for patients with sarcoma: A single center experience. The oncologist, 23(2), 234-242.).
The teachings of Ladanyi and Artomov are documented above in the rejection of claims 12-15,18-19, 24-27, 37, 47, 52, 92 and 120-121 under 35 U.S.C. 103. Claims 31, 36 and 38 depend on claim 12. Claim 38 depends on claim clam 37, which depends on claim 12.
Ladanyi and Artomov do not explicitly teach a method further comprising “determining a tumor mutational burden (TMB) from the sample from the individual” and/or “determining microsatellite instability (MSI) from the sample from the individual”.
Cote discloses a method comprising targeted NGS for patients with sarcoma. Mutations were readily detected and 75 (representing 40% of patients) were testable for therapeutic effect using existing drugs within the confines of a clinical trial. These data indicate that targeted NGS is a useful tool in potentially routing patients to mutation specific clinical trials (Abstract- Conclusion).
Regarding claim 31, Cote teaches a method wherein tumor mutational burden (TMB) was calculated (e.g., Pg. 235, Tumor Mutational Burden and Microsatellite Status, para. 1). Thus, Ladanyi, Artomov and Cote teach a method comprising determining a tumor mutational burden (TMB) from the sample from the individual.
Regarding claim 36, Cote teaches a method wherein tumors were classified as microsatellite unstable high (MSI-H) or microsatellite stable (MSS) (e.g., Pg. 236, Tumor Mutational Burden and Microsatellite Status, para. 1). Thus, Ladanyi, Artomov and Cote teach a method comprising determining microsatellite instability (MSI) from the sample from the individual.
Regarding claim 38, Cote teaches a method wherein microsatellite instability data were available on 50 of the patient samples. Microsatellite instability was stable for all tested samples. Stable is interpreted as not instable, therefore DSRCT was not characterized by MSI. (e.g., Pg. 241, para. 2). Thus, Ladanyi, Artomov and Cote teach a method wherein the cancer is a DSRCT, and wherein the DSRCT is characterized by a low TMB and/or is not characterized by microsatellite instability (MSI).
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the claimed invention modify the method of treating and/or delaying progression of a cancer comprising EWSR1-WT1 as taught by Ladanyi and Artomov to incorporate the method comprising TMB and MSI determination as taught by Cote to have yielded the predictable result of adding to the parameters used to assess an effective and targeted therapeutic for the cancer. Doing so would allow for the predictable outcome of determining the specificity of a therapeutic for a particular cancer patient.
Response to Arguments
Applicant' s arguments filed on 07/21/2025 (Pg.10) with respect to claims 31, 36 and 38 have been considered but do not apply to the new grounds of rejections. To clarify some instances argued in the response filed 07/21/20205 that remain relevant to the new grounds of 103 rejection documented in this Final Office Action, examiner’s responses to each relevant argument made by Applicant are provided below:
“The Examiner has not identified any disclosure in Cote related to administration of a checkpoint inhibitor. Cote discloses that the checkpoint inhibitor pembrolizumab "was recently approved by the FDA for tumors that are MSI-H" (Cote at page 241, right column, 2nd full paragraph). However, Cote states that all of the patients it analyzed had tumors that were MSI stable (MSS), not MSI-H. See Cote at Abstract and page 241, right column, 2nd full paragraph. Based on these teachings, one of skill in the art would not be motivated to treat a cancer with an EWSRJ-WTJ fusion gene encoding a neoantigen using a checkpoint inhibitor as recited in the amended claims.
Examiner’s Response: Applicant’s arguments with respect to claim(s) 31, 36 and 38 have been considered but do not apply to the new grounds of rejection. In response to applicant's arguments against the references individually, one cannot show nonobviousness by attacking references individually where the rejections are based on combinations of references. See In re Keller, 642 F.2d 413, 208 USPQ 871 (CCPA 1981); In re Merck & Co., 800 F.2d 1091, 231 USPQ 375 (Fed. Cir. 1986).
Conclusion of Response to Arguments
In view of the amendments, new grounds of rejections and above responses to arguments, no claims are in condition for allowance.
Conclusion
Applicant's amendment necessitated the new ground(s) of rejection presented in this Office action. Accordingly, THIS ACTION IS MADE FINAL. See MPEP § 706.07(a). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KENDRA R VANN-OJUEKAIYE whose telephone number is (571)270-7529. The examiner can normally be reached M-F 9:00 AM- 5:00 PM.
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Winston Shen can be reached at (571)272-3157. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/KENDRA R VANN-OJUEKAIYE/Examiner, Art Unit 1682 /WU CHENG W SHEN/Supervisory Patent Examiner, Art Unit 1682
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