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 .
Application Status
The Amendments and Remarks filed 13 February 2026. Claims 60 and 74 are amended. Claims 1-38, 40-59, 73 and 75 are cancelled. Claims 39 and 60-72 and 74 are pending and being examined on the merits.
This rejection contains rejections not necessitated by applicant’s claim amendments and is thereby non-final.
Priority
This application is a 371 PCT of application US2016/042367 filed 7/14/2016 which claims priority to application has PRO 62/252,393 filed 11/06/2015 and applications 62/192,561 and 62/192,559 filed 7/14/2015.
Claim Rejections - 35 USC § 112
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.
Claim 39 is 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.
Claim 39 is directed to a method of identifying an agent that stabilizes an insulated neighborhood having a disrupted boundary. The claim requires that the agent performs the active step of stabilizing the boundary of an insulated neighborhood.
The specification does not adequately describe an actual reduction to practice of a method of identifying an agent that stabilizes an insulated neighborhood. The specification also does not describe a specific way to stabilize the boundary of the insulated neighborhood nor a complete structure of an agent or compound that selectively stabilizes the boundary an insulated neighborhood. Further, the specification does not describe the partial structures, or physical properties, or chemical properties of a compound that selectively stabilizes the boundary an insulated neighborhood. Nor does the specification identify any representative species of stabilizing agents, any structural class of stabilizing agents, any common structural characteristics shared by such agents, or any correlation between particular molecular features and the ability to stabilize an insulated neighborhood boundary. Rather, the disclosure states only that a test agent may be screened and that decreased proto-oncogene expression indicates that the agent stabilizes the insulated neighborhood.
The specification does describe a method of identifying an agent that stabilizes an insulated neighborhood [pg. 4, last paragraph - pg. 5 para 1; pg. 31, para 4], and a method where disruption of the insulated neighborhood leads to activation of a proto-oncogene [Example 2]. However, these disclosures do not describe the structure of such agent nor provides a correlation between how the insulated neighborhood can be stabilized to prevent activation of a proto-oncogene. Additionally, the need for a method of identifying an agent that stabilizes an insulated neighborhood weighs in favor of the conclusion that such agents were unknown. The claim encompasses any agent capable of stabilizing an insulated neighborhood, including but not limited to small molecules, peptides, proteins, nucleic acids, genome-editing reagents, epigenetic modifiers, and other compounds having unknown mechanisms of action. The specification provides no description sufficient to distinguish members of this broad genus from compounds that do not possess the claimed activity.
The level of skill and knowledge in the art is that there are no known agents that selectively stabilize the boundaries of an insulated neighborhood and no known correlation between any structural component and the ability to selectively stabilize the boundaries of an insulated neighborhood. Didych (Didych et. al. 2015 Molecular Biology Vol. 49, No. 6, 818-824) teaches that domain boundaries, i.e. insulated neighborhood boundaries, are spatially brought together, and their formation is mediated by CCCTC-binding factor (CTCF) and components of the cohesin complex. Didych teaches that the deletion of CTCF-binding regions disturbs the spatial organization of the domain, alters the transcriptional activity of the genes within, and quite frequently activates neighboring genes [pg. 820, col. 1, para 1]. However, Didych does not provide any guidance of what is needed to stabilize disruption the boundaries of those domains. Thus, the disclosure does not allow one of skill in the art to visualize or recognize the structure of any compound required to practice the claimed method. Therefore, it is highly unpredictable what is necessarily needed to stabilize the boundary of an insulated neighborhood.
Although the specification discusses insulated neighborhoods, CTCF-mediated boundaries, disrupted boundaries, proto-oncogene activation, and screening methodologies, these disclosures do not reasonably convey to one of ordinary skill in the art that the inventors were in possession of the claimed genus of agents that stabilize insulated neighborhoods as of the filing date. Instead, the disclosure merely provides a methodology for searching for such agents.
Accordingly, in view of the limited amount of guidance provided by the specification and in the art, one of ordinary skill in the art would conclude that applicant was not in possession of the claimed method of identifying an agent that stabilizes an insulated neighborhood because an agent or compound possessing the desired activity required to practice the method is not adequately described and was not known in the art.
Response to Arguments
Applicant's arguments filed 02/13/2026 have been fully considered but they are not persuasive.
Applicant argues that the specification describes a method of identifying an agent that stabilizes an insulated neighborhood and therefore provides adequate written description support for claim 39. Applicant points to the disclosure describing transfecting a cell with a super-enhancer and insulated neighborhood, contacting the cell with a test agent, and measuring proto-oncogene expression, and further argues that one of ordinary skill in the art could perform the recited method. These arguments have been considered but are not persuasive.
The issue presented by claim 39 is not whether the specification describes a screening assay. Rather, the issue is whether the specification reasonably conveys to one of ordinary skill in the art that the inventors were in possession of the claimed invention, namely a method of identifying an agent that stabilizes an insulated neighborhood. The specification discloses that a test agent may be screened and that decreased proto-oncogene expression may indicate stabilization of an insulated neighborhood boundary. However, the specification does not identify any actual agent that stabilizes an insulated neighborhood. The specification further fails to disclose any representative species of stabilizing agents, any structural class of stabilizing agents, any common structural characteristics shared by stabilizing agents, or any correlation between particular molecular features and the ability to stabilize an insulated neighborhood boundary. Instead, the disclosure merely provides a methodology for searching for compounds that may possess the claimed activity.
Applicant further relies on the disclosure describing disrupted insulated neighborhood boundaries, proto-oncogene activation, and the potential repair of such disruptions. However, describing a biological phenomenon or a desired functional result does not establish possession of the claimed genus. Although the specification discusses insulated neighborhoods, CTCF-mediated boundaries, super-enhancers, proto-oncogene activation, and screening methodologies, these disclosures do not reasonably convey possession of the broad genus of agents encompassed by the claim.
Claim 39 encompasses any agent capable of stabilizing an insulated neighborhood boundary. Such agents may include numerous structurally distinct classes of compounds having different mechanisms of action. The specification provides no representative examples of such agents and no description sufficient to distinguish members of the claimed genus from compounds that do not possess the claimed activity. As a result, the disclosure amounts to a research plan for discovering agents that stabilize insulated neighborhoods rather than a description demonstrating possession of the claimed genus itself.
Accordingly, the specification does not reasonably convey to one of ordinary skill in the art that the inventors were in possession of the full scope of the claimed invention as of the filing date. Therefore, the rejection of claim 39 under 35 U.S.C. 112(a) for lack of adequate written description is maintained.
Claim 39 is rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, a method of screening a candidate compound for an effect on proto-oncogene expression in a cell comprising a disrupted insulated neighborhood, does not reasonably provide enablement for a method of identifying an agent that stabilizes an insulated neighborhood, wherein the insulated neighborhood has a disrupted boundary as claimed. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the invention commensurate in scope with these claims.
Nature of the Invention and Breadth of the claims
Claim 39 is directed to a method of identifying an agent that stabilizes an insulated neighborhood having a disrupted boundary. The claim encompasses any agent capable of stabilizing an insulated neighborhood, regardless of the agent’s structure, mechanism of action, molecular target, or chemical class.
State of the Art
The art further recognizes that insulated neighborhoods are complex chromatin structures involving CTCF-mediated boundaries, chromatin looping, enhancer-promoter interactions, and higher-order chromosomal architecture. Didych (Didych et. al. 2015 Molecular Biology Vol. 49, No. 6, 818-824) teaches that domain boundaries, i.e. insulated neighborhood boundaries, are spatially brought together, and their formation is mediated by CCCTC-binding factor (CTCF) and components of the cohesin complex. Didych teaches that the deletion of CTCF-binding regions disturbs the spatial organization of the domain, alters the transcriptional activity of the genes within, and quite frequently activates neighboring genes [pg. 820, col. 1, para 1]. However, Didych does not provide any guidance of what is needed to stabilize disruption the boundaries of those domains.
Guidance of the Specification
The specification discloses a screening assay in which a cell containing a super-enhancer and insulated neighborhood is contacted with a test agent and proto-oncogene expression is measured. The specification further states that a test agent may repair a disruption in an insulated neighborhood boundary. However, the specification does not disclose any actual agent that stabilizes an insulated neighborhood boundary, any representative species of stabilizing agents, any structural features common to stabilizing agents, any molecular targets whose modulation results in stabilization of insulated neighborhoods, or any predictive guidance that would permit one of ordinary skill in the art to identify stabilizing agents without extensive experimentation.
Experimentation Required
Since the specification provides only a screening methodology and no representative stabilizing agents, a person of ordinary skill in the art would be required to engage in extensive screening and experimentation across a vast number of candidate compounds in order to practice the full scope of the claimed invention.
Accordingly, undue experimentation would have been required to identify substantially all agents encompassed by the claim, and the specification does not enable the full scope of the claim.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Claims 60-61, 66, 69-71 are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Fanucchi (US 2016/0215280 A1). This rejection is maintainted.
Regarding claims 60-61, and 66, Fanucchi teaches methods of silencing gene expression in a cell by way of perturbing gene regulatory elements which are engaged in chromosomal contact [abstract]. Fanucchi teaches that within topologically associating domains (TADs) boundaries are loop mediated structures that are enriched in binding sites for CTCF and cohesin complex (i.e., insulated neighborhoods), which implicates TADs importance in maintaining domain integrity and loop-mediated transcription [0012, 0015]. Fanucchi teaches that depletion of CTCF and cohesin has revealed that these factors contribute differentially to domain organization and transcriptional regulation [0012]. Fanucchi teaches that the disruption of the CTCF site 3’ of the TNFAIP2 gene, an about 11 Kb gene on chromosome 14 flanked by CTCF consensus binding sites, using CRISPR-Cas9 (and sgRNA) to induce a DSB that results in the silenced expression of TNFAIP2 [0179, 0087, Example 4 and Figure 53]. Fanucchi teaches that the region targeted is upstream of the boundary [Fig. 53]. Fanucchi teaches that the loss of boundary led to the to the partial fusion of the adjacent TADs (i.e., altering the size of an insulated neighborhood) and the formation of new and ectopic contacts, causing long range transcriptional misregulation (Dixon et al., 2012) [0012]. Fanucchi teaches that enhancer-promoter interactions are the primary means in which cell-specific gene expression is achieved and that the prevention of the loop-mediated contacts separates enhancers from the genes they regulate, thereby silencing their expression, by teaching that when TNFAIP2 cannot engage in chromosomal contact, its ability to access the focus of Pol II is limited. [0183].
Regarding claims 69-71, Fanucchi teaches that the boundary comprises a deletion in a CTCT-CTCT loop binding cite [Fig. 53, 0179].
Response to Arguments
Applicant's arguments filed 02/13/2026 have been fully considered but they are not persuasive. The applicant did not present substantive arguments addressing the examiner’s findings regarding Fanucchi. Rather, applicant amended claim 60 to incorporate limitations from former claim 73.
The amendment has been fully considered but is not persuasive of patentability. Claim 60 now recites that the gene is a proto-oncogene. However, the newly added limitation merely identifies a species of gene and does not alter the underlying editing methodology recited in the claim. The rejection was based on Fanucchi’s teachings regarding editing chromatin-loop regulatory elements and altering gene expression through disruption of chromosomal contacts and loop architecture. The newly added proto-oncogene limitation does not distinguish the claimed editing method from the teachings relied upon in the rejection.
Accordingly, the rejection is maintained.
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.
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 60-61, 66-67, 69-71, and 74 are rejected under rejected under 35 U.S.C. 103 as being unpatentable over Narendra (Narendra et. al 2/27/2015. Science Vol 347, Issue 6225, 1017-1021) in view of Didych (Didych et. al, 5/13/2015 Molecular Biology, Vol. 49, No. 6, pp. 818–824) and Dowen (Dowen et al. Cell 159, 374–387, October 9, 2014). This rejection has been modified to add the rejection of claim 67 and respond to the amendments.
Narendra teaches that CTCF function to insulate repressive and active chromatin domains within HOX clusters, creating an insulated neighborhood, by organizing Hox clusters into spatially disjoint domains. Narendra teaches that deletion of the CTCF binding sites, ablating CTCF binding, disrupts topological boundaries such that caudal Hox genes leave the repressed domain (where the gene is not expressed in the absence of disruption) and become subject to transcriptional activation [abstract]. Narendra teaches the use of CRISPR genome editing to disrupt CTCF binding sites that localize to chromatin boundaries within Hox clusters [pg 1010, col. 3, para 2]. Disruption or deletion of a chromatin boundary necessarily alters the spatial extent and limits of the insulated chromatin domain defined by that boundary. Therefore, deletion or disruption of the CTCF boundary alters the size of the insulated neighborhood by changing the genomic region encompassed by the insulated domain.
Although Narendra teaches the expansion of H3K4me3 activity that we observe in the Hox clusters is the result of aberrant enhancer contacts with caudal genes or remains to be tested, Narendra does not explicitly teach that increasing expression of a gene by altering interaction of the enhancer with the gene. Narendra does not teach where the gene is the MYC proto-oncogene.
Didych teaches that although enhancers can regulate genes that lie (in genomic coordinates) at considerable distances and even on other chromosomes, in many cases, they activate neighboring genes. Didych teaches that many of these super-enhancer–gene pairs are located in independent topological domains (i.e. insulated neighborhood) formed by looping out of long chromosome regions. Didych teaches that these domains are characterized by cohesion dependent spatial and functional interactions between super-enhancer elements and associated gene promoters. Didych teaches that the domain boundaries are spatially brought together, and their formation is mediated by CCCTC-binding factor (CTCF) and components of the cohesin complex. The deletion of CTCF-binding regions disturbs the spatial organization of the domain, alters the transcriptional activity of the genes within, and quite frequently activates neighboring genes [pg. 820, col.1, para 1].
Regarding claim 60, it would have been obvious to one ordinary skilled in the art before the effective filing date of the claimed invention that the increase in expression seen in the method of Narendra was the result of enhancer contacts with caudal genes given the teaching of Didych that super-enhancer–gene pairs are located in independent topological domains where the enhancers can regulate the genes within and on other chromosomes. Accordingly, one of ordinary skill in the art would have reasonably expected that alteration of the insulated-neighborhood boundary taught by Narendra would modify enhancer access to genes located within or adjacent to the altered insulated neighborhood, thereby altering gene expression as claimed.
Regarding claim 60 and 74, selection of a proto-oncogene as the target gene would have been an obvious matter of design choice because proto-oncogenes were known to be regulated by chromatin architecture, enhancer interactions, and insulated-neighborhood boundaries, and such genes provide clinically relevant targets for studying the effects of boundary disruption on gene expression. However, Dowen teaches that super-enhancer-driven genes generally occur within chromosome structures that are formed by the looping of two interacting CTCF sites co-occupied by cohesin [abstract]. Dowen teaches that these looped structures form insulated neighborhoods whose integrity is important for proper expression of local genes such as Myc [abstract; Fig. 1]. It would have been obvious to one ordinary skilled in the art before the effective filing date of the claimed invention to modify the method of Fanucchi where the gene is the Myc gene. One of ordinary skill would be motivated to make the modification for the advantage of reducing oncogene expression and reducing tumor cells. The combination of prior art elements according to known methods to yield predictable results supports can support a conclusion of obviousness. See MPEP 2143(I). One of ordinary skill in the art would have a reasonable expectation of success since Fanucchi, Didych, and Dowen all teach the control of gene expression in insulated neighborhoods involving enhancers.
Regarding claim 67, although Narendra does not expressly state that the gene is “not expressed” prior to deletion or disruption, Narendra teaches that the affected genes are maintained in a repressed transcriptional state prior to disruption of the chromatin boundary and become activated after disruption. A person of ordinary skill in the art would have understood that genes selected for activation through boundary disruption would include genes that are transcriptionally silent or not detectably expressed prior to disruption because such genes provide a direct and measurable indication of the effect of boundary deletion. Therefore, it would have been obvious to one of ordinary skill in the art at the time of the invention to perform the method as taught and suggested by Narendra and Didych wherein the gene is not expressed in the absence of the deletion or disruption.
Claims 62-65 and 68 are rejected under 35 U.S.C. 103 as being unpatentable over Fanucchi (US 2016/0215280 A1) in view of Didych (Didych et. al, 5/13/2015 Molecular Biology, Vol. 49, No. 6, pp. 818–824).
The teachings of Fanucchi are discussed above as applied to claim 60.
Didych teaches that although enhancers can regulate genes that lie (in genomic coordinates) at considerable distances and even on other chromosomes, in many cases, they activate neighboring genes. Didych teaches that many of these super-enhancer–gene pairs are located in independent topological domains (i.e. insulated neighborhood) formed by looping out of long chromosome regions. Didych teaches that these domains are characterized by cohesion dependent spatial and functional interactions between super-enhancer elements and associated gene promoters. Didych teaches that the domain boundaries are spatially brought together, and their formation is mediated by CCCTC-binding factor (CTCF) and components of the cohesin complex. The deletion of CTCF-binding regions disturbs the spatial organization of the domain, alters the transcriptional activity of the genes within, and quite frequently activates neighboring genes [pg. 820, col.1, para 1]. Didych teaches that MM1.S cells carry an IgH–MYC chromosomal rearrangement, and MYC, an oncogene in tumor cells, expression is controlled by the IgH super-enhancer IgH or other super-enhancers [pg. 821, col. 1, last paragraph; pg. 822, col. 1, para 2].
Regarding claims 62-64, Fanucchi teaches that the chromosomal contact may be between chromatin and/or DNA located either inter-chromosomally, intra-chromosomally or both inter-chromosomally and inter-chromosomally [0020]. Fanucchi does not explicitly teach that wherein the enhancer is located within the insulated neighborhood or wherein the enhancer and the proto-oncogene are each located within an insulated neighborhood that are different from one another. It would have been obvious to one ordinary skilled in the art before the effective filing date of the claimed invention to modify the method of Fanucchi wherein the enhancer is located within the insulated neighborhood given Didych’s disclosure that enhancers are located in insulated neighborhoods. It also would have been obvious to one ordinary skilled in the art before the effective filing date of the claimed invention to modify the method of Fanucchi where the enhancer and the gene are each located in insulated neighborhoods that are different from one another given Didych’s disclosure that both proto-oncogenes and enhancers can be found in insulated neighborhoods and that enhancers can regulate genes that lie (in genomic coordinates) at considerable distances and even on other chromosomes as discussed above. This modification would amount to a combination of prior art elements according to known methods to yield predictable results gene regulation.
Regarding claim 65 and 68, Fanucchi does not teach that the method comprises repairing a deletion or disruption of the boundary of the insulated neighborhood. Fanucchi does not teach where the method comprises editing the boundary of the insulated neighborhood with the Cas9, the sgRNA, and a template. Fanucchi teaches that perturbation of chromatin regulatory elements resulting in the abrogation of transcription is induced by TALE or CRISPR systems [0121]. Fanucchi teaches that if the integrity of the gene loop topology and chromosomal contacts were essential for co-transcription, then we hypothesized that restoring the chromosomal contacts, by restoring double stranded breaks, would restore transcription of interacting genes in the multigene complex [0168]. Fanucchi teach the design of a repair construct (i.e., template) to exploit HDR to restore genes altered by gene loop disruption using TALEN gene editing nuclease systems [0168]. It would have been obvious to one ordinary skilled in the art before the effective filing date of the claimed invention to use a template repair construct in the method of Fanucchi to exploit HDR to restore genes altered by gene loop disruption using the CRISPR gene editing nuclease systems. One of ordinary skill would be motivated to make the modification because Fanucchi teaches that perturbation of chromatin regulatory elements resulting in the abrogation of transcription is induced by TALE or CRISPR systems double stranded breaks [0121].
Claims 72 is rejected under 35 U.S.C. 103 as being unpatentable over Fanucchi (US 2016/0215280 A1) in view Lawhorn (Lawhorn et al. 2014. PLoS ONE 9(11): e113232).
The teachings of Fanucchi are discussed above as applied to claim 60 and 71.
Fanucchi do not teach where wherein the sgRNA targets a region within 200 bp up-stream or down-stream the center of the CTCF loop binding site.
Lawhorn teaches that evaluated different genomic sgRNA targeting sites for repression of TP53 [abstract]. Lawhorn teaches that the sites spanned a 200-kb distance, which included the promoter, transcript sequence, and regions flanking the endogenous human TP53 gene showed up to 86% repression.
It would have been obvious to one ordinary skilled in the art before the effective filing date of the claimed invention to modify the method of Fanucchi where the sgRNA targets a region within 200 bp up-stream or down-stream the center of the CTCF loop binding site. One or ordinary skill would be motivated to make the modification since Lawhorn teaches that sites that span 200kb distance from the transcript sequence can mediate genome modification.
Response to Arguments
Applicant's arguments filed 02/13/2026 have been fully considered but they are not persuasive.
Applicant did not present substantive arguments traversing the combination of Narendra and Didych, Fanucchi or Didych, or Fanucchi or Didych. Rather, applicant amended claim 60 to incorporate the limitation from former claim 73. The amendment has been considered but is not persuasive.
Narendra teaches CRISPR-mediated disruption of CTCF boundary elements resulting in disruption of insulated chromatin domains and activation of genes previously insulated from regulatory influence. Didych teaches enhancer-mediated regulation of genes and the role of chromatin domain organization in controlling enhancer-gene interactions. Together, the references teach that modification of chromatin boundaries alters enhancer access and gene expression.
The addition of the limitation that the gene is a proto-oncogene does not patentably distinguish the claimed method. The type of gene whose expression is altered would have been an obvious matter of target selection because the cited art teaches that disruption of insulated domains affects gene regulation generally, and the specification itself identifies proto-oncogenes as genes affected by insulated-neighborhood disruption.
Additionally, the amendment does not overcome the rejection because the added proto-oncogene limitation merely narrows the identity of the gene being regulated and does not alter the editing steps relied upon in the rejection. Fanucchi’s teachings regarding disruption and restoration of chromatin-loop architecture remain applicable.
Furthermore, the newly added proto-oncogene limitation does not modify the sgRNA-targeting limitation relied upon in the rejection of claim 72. Lawhorn was cited for the teaching of selecting genomic targeting sites in the vicinity of a target locus, while Fanucchi provides the chromatin-boundary editing framework.
Because applicant has not identified any deficiency in the cited teachings and because the amendment does not address the basis of the rejection, the rejection is maintained.
Conclusion
No claims allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to TIFFANY N GROOMS whose telephone number is (571)272-3771. The examiner can normally be reached on M-F 830-530.
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/TIFFANY NICOLE GROOMS/Examiner, Art Unit 1637
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