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 .
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 06/24/2026 has been entered.
Status of the Claims
Claims 1-3, 5-9, 12-14, 25, 28, 42, and 44-49 are pending.
It is noted that while claim 26 is marked as cancelled, the claim limitations have not been deleted. However, because claim 26 depends on claim 15, which itself has been cancelled, claim 26 has been interpreted as cancelled as indicated.
Claim 1, 13, 25, 28, and 42 are newly amended.
Claims 13-14, 25, 28, 42, and 44-49 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 09/11/2025.
Claims 1-3, 5-9 and 12 have been examined on their merits.
Withdrawn Objections & Rejections
The objections and rejections presented herein represent the full set of objections and rejections currently pending in the application. Any objections or rejections not specifically reiterated are hereby withdrawn.
The rejection of claims 1-4, 6-9, and 12 under 35 U.S.C. 103 as being unpatentable over Zhang et al. (US20190106710A1, previously cited) in view of Heikkinen et al. (Human Mutation, 2017, previously cited) and Zhang et al. (Leukemia Research, hereafter “Zhang YC”) as evidenced by Arce et al. (Nature, 2025, previously cited) is withdrawn in order to address the claims as amended.
The rejection of claim 5 under 35 U.S.C. 103 as being unpatentable over Zhang et al. (US20190106710A1, previously cited) in view of Heikkinen et al. (Human Mutation, 2017, previously cited), and Zhang et al. (Leukemia Research, hereafter “Zhang YC”) as evidenced by Arce et al. (Nature, 2025), as applied to claim 1 above, and further in view of Yonekura et al. (BMC Research Notes, 2018, previously cited) is withdrawn in order to address the claims as amended.
Claim Interpretation
In regards to the term “genetic modification”, the specification does not explicitly define this term. While, the term could broadly be defined to refer to any change in the genome of a T cell, including natural mutations, in the art, the term appears to have the specific meaning of using bioengineering techniques in order to introduce changes to a cell’s genome (as in “genetically modified”).
Indeed, as specifically defined by Merriam-Webster (retrieved from internet 09/24/2025, previously cited), the term “genetic modification” means “the modification of an organism's genetic material that involves using applied techniques of genetics and biotechnology to alter or delete a DNA segment or to insert a new DNA segment from a different species in order to express or suppress a targeted trait or traits.”
Furthermore, while the instant specification does not explicitly define “genetic modification”, in regards to the term “modifying’, the specification states, “the phrase ‘modifying’ refers to inducing a structural change in the sequence of the genome at a target genomic region in a T cell” (paragraph [0077]; emphasis added), which implies that modification requires biotechnological manipulation.
Therefore, the term “genetic modification”, has been interpreted as defined by Merriam-Webster, and has been interpreted as requiring a biotechnological step, and is synonymous with “genetically modified”, and has not been interpreted as referring to phenomena such as natural mutations.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claims 1-3, 5-9 and 12 are rejected under 35 U.S.C. 103 as being unpatentable over Zhang et al. (US20190106710A1, previously cited) in view of Krejsgaard et al. (Leukemia, 2008).
In regards to claim 1, Zhang teaches genetically modified cells (claim 12). Zhang teaches that the cells can derived from T-cell lymphoma (paragraph [0048]), and are therefore, T cells.
Zhang teaches that the MED12 (which is a nuclear factor) gene can be specifically targeted for modification (paragraphs [0501, 0509]). Zhang teaches that these cells may be engineered with multiple regulatory elements (claim 1), and therefore, can comprise at least one factor.
A person of ordinary skill in the art would have been motivated to choose MED12 as a target in order to study its effects on T-cell lymphoma. Furthermore, because Zhang explicitly teaches MED12 as a target, it could have been done with predictable results and a reasonable expectation of success.
In regards to the cell type, Zhang is silent as to the specific T cell type.
However, Krejsgaard teaches that Sézary syndrome (SS) is an aggressive variant of cutaneous T cell lymphoma characterized by malignant regulatory T cells (Tregs) (Title, Abstract, p2231). Therefore, a person of ordinary skill in the art would have been motivated to choose Tregs in order to study Treg function in this form of T cell lymphoma. Furthermore, because Zhang teaches that an object the invention is to provide compositions related to generating models to study proliferative disorders and specifically to study T-cell lymphomas (paragraphs [0048-0049]), and because malignant Tregs are known to be involved in T-cell lymphomas, it could have been done with predictable results and a reasonable expectation of success
In regards to claim 2, as above, Zhang teaches that MYB can also be an inhibition target for neoplastic diseases (claim 1; paragraph [0044]; paragraphs [0504, 507]) (of which Sézary syndrome is a known type).
A person of ordinary skill in the art would have been motivated to further target MYB in order to study interactions in the context of this disease state. Furthermore, since Zhang teaches MYB can be a target for inhibition for neoplastic diseases, it could have been done with predictable results and a reasonable expectation of success.
In regards to whether expression of CTLA4 (claim 2) is increased in the T cell relative the expression of CTLA4 in a T cell not comprising the genetic modification or heterologous nucleotide as in claim 2, as above, Applicant should note that this is a natural property of the functioning of the cell.
According to MPEP 2112, “[T]he discovery of a previously unappreciated property of a prior art composition, or of a scientific explanation for the prior art’s functioning, does not render the old composition patentably new to the discoverer.” Atlas Powder Co. v. IRECO Inc., 190 F.3d 1342, 1347, 51 USPQ2d 1943, 1947 (Fed. Cir. 1999). Thus, the claiming of a new use, new function or unknown property which is inherently present in the prior art does not necessarily make the claim patentable. In re Best, 562 F.2d 1252, 1254, 195 USPQ 430, 433 (CCPA 1977). In In re Crish, 393 F.3d 1253, 1258, 73 USPQ2d 1364, 1368 (Fed. Cir. 2004), the court held that the claimed promoter sequence obtained by sequencing a prior art plasmid that was not previously sequenced was anticipated by the prior art plasmid which necessarily possessed the same DNA sequence as the claimed oligonucleotides. The court stated that “just as the discovery of properties of a known material does not make it novel, the identification and characterization of a prior art material also does not make it novel.” Id.
Moreover, there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference. Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003).
In the instant case, the claims suggest that genetic modification of T cell in regards to MED12 and MYB is sufficient to cause subsequent increases in CTLA4 (different genes). Thus, since the T cell as taught above, comprises that genetic modification of T cell in regards to MED12 and MYB it would naturally possess the property of exhibiting increased CTLA4 or IL2RA expression.
Furthermore, as evidenced by Arce et al. (Nature, 2025), perturbance (knockout) of MED12 results in both increases and decreased in CTLA4 and IL2RA over time (Extended Data Fig. 2g; Fig. 2b, p932).
Thus, inhibition of MED12 in T cells itself is sufficient to cause increased expression of CTLA4 in T cells.
In regards to claims 3 and 6-9, Zhang teaches that PTEN can also be an inhibition target for neoplastic diseases (claim 1; paragraph [0044]; paragraph [0445], Table A, p48, table C, p52; paragraph [0450]) (of which Sézary syndrome is a known type). A person of ordinary skill in the art would have been motivated to further target PTEN in order to study interactions the context of this disease state. Furthermore, since Zhang teaches that PTEN can be a target for inhibition for neoplastic diseases, it could have been done with predictable results and a reasonable expectation of success.
In regards to claims 7 and 8 specifically, Zhang teaches that genes may be targeted by CRISPR-induced modification of target sequences within a genome (claim 1; paragraph [0476]). As this engineered gene is synthetic, it is not found in nature, and is therefore, a heterologous polynucleotide.
In regards to whether expression of CTLA4 (claim 3) is decreased, IL2 (claim 6) is increased, IL2 (claim 7) is decreased, expression of IL2RA is increase (claim 8), or if expression of IL2RA is decreased (claim 9) in the T cell relative the expression of CTLA4/IL2/IL2RA in a T cell not comprising the genetic modification or heterologous nucleotide as in claims 3 and 6-9, Applicant should note that these are natural properties of the cells themselves (see MPEP 2112).
In the instant case, the claims suggest that genetic modification of T cell in regards to MED12 and PTEN is sufficient to cause both subsequent decreases or increases in CTLA1, IL2, or IL2RA (different genes from PTEN). Thus, since the T cell as taught above, comprises genetic modification of T cell in regards to MED12 and PTEN it would be expected to naturally possess the property of exhibiting respective decreased/increased CTLA4, IL2, or IL2RA expression.
Furthermore, as evidenced by Arce et al. (Nature, 2025), perturbance (knockout) of MED12 results in both increases and decreases in CTLA4, IL2, and IL2RA over time (Extended Data Fig. 2g; Extended Data Figs. 4c and 4d; Fig. 2b, p932).
Thus, inhibition of MED12 in T cells itself is sufficient to cause subsequent respective decreases or increases in CTLA4 or IL2 in T cells.
In regards to claim 5, Zhang teaches that FOXP3 can also be a target (paragraphs [0443-0445]; Table 2, p49).
Additionally, person of ordinary skill in the art would have been motivated to also target FOXP3 for inhibitor because Krejsgaard teaches that FOXP3 is abnormally spliced in Sézary syndrome, making it functionally different from wild-type FOXP3, and that it may be involved in the differentiation of Tregs (Title, Abstract, p2230; Discussion, p2237). Thus, a person of ordinary skill in the art would have been motivated to inhibit expression of FOXP3 in order to study Treg disfunction in Sézary syndrome. Furthermore, because as above, Zhang explicitly teaches that FOXP3 can also be a target, it could have been done with predictable results and a reasonable expectation of success.
In regards to decreased expression of FOXP3 it is noted that inhibition of this gene would naturally result in decreased relative expression compared to a T cell without this modification. Indeed, as taught by Krejsgaard above, FOXP3 is mis-spliced in malignant T cells.
In regards to claim 12, Zhang teaches that the genetically modified cells may be a population of cells (paragraph [0047]).
Therefore, the combined teachings of Zhang and Krejsgaard render obvious the invention as claimed.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 1-3, 5-9 and 12 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 42-61 of copending Application No. 18/251696 in view of over Zhang et al. (US20190106710A1, previously cited) as evidenced by Arce et al. (Nature, 2025, previously cited).
Although the conflicting claims of copending Application No. 18/251696 are not identical to the currently prosecuted claims, they are not patentably distinct from each other because the claims of both inventions are drawn to a modified (engineered) T cell, that can be an effector T cell comprising a heterologous polynucleotide that that inhibits MED12 (claims 42, 44, 46-48, 51-56).
In regards to the embodiments as in claims these, genetic modifications directed towards these genes were known in the art before the effective filing date.
As discussed above, Zhang teaches genetically modified cells (claim 12) that can be derived from T-cell lymphoma (and thus T cells) (paragraph [0048]). Zhang teaches that the MED12 (which is a nuclear factor) gene can be specifically targeted for modification (paragraphs [0501, 0509]). Zhang teaches that these cells may be engineered with multiple regulatory elements (claim 1), and therefore, can be directed towards multiple factors (genes). As above, Zhang teaches that modifications can be directed towards either MYB or PTEN (claim 1; paragraph [0044]; paragraphs [0504, 507]; paragraph [0445], Table A, p48, table C, p52; paragraph [0450]) and FOXP3 (paragraphs [0443-0445]; Table 2, p49).
A person of ordinary skill in the art would have been motivated to further target these genes in order to study their effect on T cells. Furthermore, because Zhang teaches that they may be targets for T cell genetic modification, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various properties in regards to increases/decreases in expression of CTLA4, IL2, IL2RA, as above, Applicant should note that these are natural properties of the cells themselves (see MPEP 2112).
In the instant case, the claims suggest that genetic modification of T cell in regards to MED12 and MYB/PTEN is sufficient to cause both subsequent decreases or increases in CTLA1, IL2, or IL2RA (which are different genes from MYB of PTEN). Thus, since the T cell as taught above, comprises that genetic modification of T cell in regards to MED12 and PTEN it would be expected to naturally possess the property of exhibiting respective decreased/increased CTLA4, IL2, or IL2RA expression.
Furthermore, as evidenced by Arce et al. (Nature, 2025), perturbance (knockout) of MED12 results in both increases and decreases in CTLA4, IL2, and IL2RA over time (Extended Data Fig. 2g; Extended Data Figs. 4c and 4d; Fig. 2b, p932).
Claims 1-3, 5-9 and 12 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-19 and 25 of copending Application No. 19/120,196 in view of over Zhang et al. (US20190106710A1, previously cited) and Krejsgaard et al. (Leukemia, 2008) as evidenced by Arce et al. (Nature, 2025, previously cited).
Although the conflicting claims of copending Application No. 19/120,196 are not identical to the currently prosecuted claims, they are not patentably distinct from each other because the claims of both inventions are drawn to a modified (engineered) T cell, comprising a modification to MED12 (claims 5 and 25) (which results in a heterologous polypeptide).
In regards to the embodiments as in claims these, genetic modifications directed towards these genes were known in the art before the effective filing date.
As discussed above, Zhang teaches genetically modified cells (claim 12) that can be derived from T-cell lymphoma (and thus T cells) (paragraph [0048]). Zhang teaches that the MED12 (which is a nuclear factor) gene can be specifically targeted for modification (paragraphs [0501, 0509]). Zhang teaches that these cells may be engineered with multiple regulatory elements (claim 1), and therefore, can be directed towards multiple factors (genes). As above, Zhang teaches that modifications can be directed towards either MYB or PTEN (claim 1; paragraph [0044]; paragraphs [0504, 507]; paragraph [0445], Table A, p48, table C, p52; paragraph [0450]) and FOXP3 (paragraphs [0443-0445]; Table 2, p49).
A person of ordinary skill in the art would have been motivated to further target these genes in order to study their effect on T cells. Furthermore, because Zhang teaches that they may be targets for T cell genetic modification, it could have been done with predictable results and a reasonable expectation of success.
In regards to the various properties in regards to increases/decreases in expression of CTLA4, IL2, IL2RA, as above, Applicant should note that these are natural properties of the cells themselves (see MPEP 2112).
In the instant case, the claims suggest that genetic modification of T cells in regards to MED12 and MYB/PTEN is sufficient to cause both subsequent decreases or increases in CTLA1, IL2, or IL2RA (which are different genes from MYB of PTEN). Thus, since the T cell as taught above, comprises this genetic modification of T cell in regards to MED12 and PTEN it would naturally possess the property of exhibiting respective decreased/increased CTLA4, IL2, or IL2RA expression.
Furthermore, as evidenced by Arce et al. (Nature, 2025), perturbance (knockout) of MED12 results in both increases and decreases in CTLA4, IL2, and IL2RA over time (Extended Data Fig. 2g; Extended Data Figs. 4c and 4d; Fig. 2b, p932).
Thus, inhibition of MED12 in T cells itself is sufficient to cause subsequent respective decreases or increases in CTLA4 or IL2 in T cells.
In regards to the cell type, Krejsgaard teaches that Sézary syndrome (SS) is an aggressive variant of cutaneous T cell lymphoma characterized by malignant Tregs (Title, Abstract, p2231). Therefore, a person of ordinary skill in the art would have been motivated to choose Tregs in order to study Treg function in this form of T cell lymphoma. Furthermore, because Zhang teaches that an object the invention is to provide compositions related to generating models to study proliferative disorders and can be used to study T-cell lymphomas (paragraphs [0048-0049]), and because malignant Tregs are known to be involved in T-cell lymphomas, it could have been done with predictable results and a reasonable expectation of success
In regards to decreased expression of FOXP3 it is noted that inhibition of this gene would naturally result in decreased relative expression compared to a T cell without this modification. Indeed, as taught by Krejsgaard above, FOXP3 is mis-spliced in malignant T cells.
Response to Arguments
Applicant argues that the claims as amended are not prima facie obvious under 35 USC 103 (p15-19). In particular, Applicant argues that Zhang only discusses MED12 in the context of compositions and methods related to generating models to study cancer, but does not teach that cells are derived from T cell lymphoma are Treg or effector T cells (Remarks, p16). Instead, Applicant argues T cell lymphomas, such as acute lymphoblastic leukemia involve T cell precursors not post-thymic T cell phenotypes such as Treg or effector T cells (citing Fattizzo et al. (2020); Remarks, p16).
Applicant’s arguments filed 06/24/2026 have been fully considered but are moot because of the new grounds of rejection in view of the claims as amended as discussed above.
Additionally, in regards to Fattizzo if Applicant would like this reference to be considered then it needs to be filed on an IDS.
However, in regards to the rejections under 35 USC 103 specifically, Applicant’s arguments filed 06/24/2026 have been fully considered but are not persuasive.
As discussed above, Zhang teaches genetically modified cells (claim 12). Zhang teaches that the cells can be derived from T-cell lymphoma (paragraph [0048]), and are therefore, T cells.
Zhang teaches that the MED12 (which is a nuclear factor) gene can be specifically targeted for modification (paragraphs [0501, 0509]). Zhang teaches that these cells may be engineered with multiple regulatory elements (claim 1), and therefore, can comprise at least one factor.
A person of ordinary skill in the art would have been motivated to choose MED12 as a target in order to study its effects on T-cell lymphoma. Furthermore, because Zhang explicitly teaches MED12 as a target, it could have been done with predictable results and a reasonable expectation of success.
In regards to the cell type, Zhang is silent as to the specific T cell type.
However, Krejsgaard teaches that Sézary syndrome (SS) is an aggressive variant of cutaneous T cell lymphoma characterized by malignant Tregs (Title, Abstract, p2231). Therefore, a person of ordinary skill in the art would have been motivated to choose Tregs in order to study Treg function in this form of T cell lymphoma. Furthermore, because Zhang teaches that an object the invention is to provide compositions related to generating models to study proliferative disorders that can be used to study T-cell lymphomas (paragraphs [0048-0049]), and because malignant Tregs are known to be involved in T-cell lymphomas, it could have been done with predictable results and a reasonable expectation of success
Applicant request withdrawal of the double-patenting rejections (Remarks, p18).
Applicant’s request is noted however, because the claims as still prima facie obvious the double-patenting rejections and therefore cannot be withdrawn at this time. Thus, Applicant’s arguments filed 06/24/2026 have been fully considered bur are not found persuasive.
Applicant request withdrawal of the election requirement (p14-15).
Applicant’s request is noted however, because the claims as still prima facie obvious the election requirement is maintained. Therefore, Applicant’s arguments filed 06/24/2026 have been fully considered bur are not found persuasive.
Conclusion
No claims are allowed.
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/JOSEPH PAUL MIANO/Examiner, Art Unit 1631
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