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 .
Claim Status
Claims 3-5, 7-8, 10, 16-17, 19-20, 22-23, 25, 27-30, 32-33, 35-36, 39, 41-43, 46-71, 74, 76, 79, 82, 84-96, 98, 100-102, 104, 106-117 are cancelled.
Claims 97, 99 are amended.
Claims 1-2, 6, 9, 11, 15, 18, 24, 31, 34, 37-38, 40, 44-45, 72-73, 75 are examined on the merits.
Priority
The applicant’s application is a U.S. National Stage application of PCT International Patent Application Serial No. PCT/IB2021/000246, filed April 14, 2021, which itself claims the benefit of a Provisional Application Serial No. 63009736, filed April 14, 2020 is acknowledged.
Receipt is acknowledged of certified copies of papers required by 37 CFR 1.55.
Election/Restrictions
Applicant’s election without traverse of Group I corresponding to claims 1-2, 6, 9, 11, 15, 18, 21, 24, 26, 31, 34, 37-38, 40, 44-45, 72-73, and 75 in the reply filed on 12/17/2025 is acknowledged.
II. Species Election
Applicant hereby elects the following species, without traverse:
(i) let-7c target site as the microRNA target site for the first cassette;
(ii) let-7c target site as the microRNA target site for the second cassette;
(iii) PIT transactivator response element (SEQ ID NO: 139) as the transactivator response element sequence in Table 3;
(iv) HNFl transcription factor response element (SEQ ID NO: 216) as the transcription factor response element sequence in Table 4;
(v) a minimal TATA box as the promoter element sequence;
(vi) PTI::VP16 TAD-2 transactivator (SEQ ID NO: 98) as the transactivator in Table 2; and
(vii) SEQ ID NO: 286 as the nucleic acid sequence in Table 6.
Claims 77-78, 80-81, 83, 97, 99, 103, 105 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected invention, there being no allowable generic or linking claim.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 12/17/2025.
Although the reply filed 12/17/2025 indicates that claims 21 and 26 are readable upon the elected species, these claims require a microRNA target site of miR-199a-3p or miR-9-5p. These target sites are not readable upon the elected species of let-7c.
Claims 21 and 26 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to a nonelected species, there being no allowable generic or linking claim. Election was made without traverse in the reply filed on 12/17/2025.
Claims 1-2, 6, 9, 11, 15, 18, 24, 31, 34, 37-38, 40, 44-45, 72-73, 75 are under consideration.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 1, 11, 15, 18, 24, 31, 34, 37, 38, 40, 44-45, 72-73, 75 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claims 1, 11, 15, 18, 34, 44-45 recite the term “TABLE”. It is improper to claim limitations based upon a Table in the specification. It is suggested that the sequences or SEQ ID NO of the claimed sequences be inserted into the claim, rather than referring to Tables.
MPEP 2173.05(s) states "Where possible, claims are to be complete in themselves. Incorporation by reference to a specific figure or table "is permitted only in exceptional circumstances where there is no practical way to define the invention in words and where it is more concise to incorporate by reference than duplicating a drawing or table into the claim". If making the rejection, cite the MPEP and explain why it would be practical to define the invention without reference to a table or figure, such as amending the claim to list genes, compounds or nucleic acid sequences present in the referenced table or figure.
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 1-2, 6, 9, 11, 15, 18, 24, 31, 34, 37-38, 40, 44, 72-73, 75 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.
Claim 1, requires a contiguous polynucleic acid molecule comprising: a) a first cassette encoding a first RNA whose expression is operably linked to a transactivator response element, a nucleic acid sequence of an output; and a target site for a miRNA; and b) a second cassette encoding a second RNA, wherein the second RNA comprises a nucleic acid sequence of a transactivator; optionally wherein the second RNA further comprises a target site of a microRNA.
Claim 34, requires the provision of a genus of transactivators containing at least 70%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identity with a transactivator. The claim encompasses a provision of a large genus of nucleotide sequences that must function to bind a transactivator response element. In addition, it has been well known that minor structural differences even among structurally related compounds can result substantially different biology, expression and activities. The transactivators not only include the transactivators having the claimed sequences, but also include transactivators having a range of homology raging between 70% to 99%, and the number of potential transactivators is corresponding large.
To provide adequate written description and evidence of possession of a claimed genus, the specification must provide sufficient distinguishing identifying characteristics of the genus. The factors to be considered include disclosure of a complete or partial structure, physical and/or chemical properties, functional characteristics, structure/function correlation, and any combination thereof.
The specification envisions a contiguous polynucleic acid molecule comprises: a) a first cassette encoding a first RNA whose expression is operably linked to a transactivator response element, wherein the first RNA comprises: (i) a nucleic acid sequence of an output; and (ii) a target site for a miRNA listed in TABLE 1 or a combination thereof; and b) a
second cassette encoding a second RNA, wherein the second RNA comprises a nucleic acid sequence of a transactivator; wherein the transactivator of the second cassette, when expressed as a protein, binds and transactivates the transactivator response element of the first cassette (e.g., lane 2, page 2). The specifications envisions that the transactivator of the second cassette is tTA, rtTA, PITRelA, PIT-VP16, ET-VP16, ET-RelA, NarLc-VP16, or NarLc-RelA (e.g., lane 1, page 5). The specification envisions a transactivator of at least one cassette is a transactivator listed in TABLE 2 or a transactivator having a least 70%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99% identity of its amino acid sequence with one or more
transactivator listed in TABLE 2 (e.g., lane 25, page 30).
The working example discloses circuit components shown to implement the logic "SOX9/10 AND HNFlA/B" in a multi-plasmid setting, comprising a SOX9/10-driven PIT-based activator (PIT::RelA or PIT::VP16), as well as a fluorescent output protein synergistically driven by PIT and HNFlA/B, were cloned between ITRs in an adeno-associated viral (AA V) transfer vector either in a divergent or convergent orientation (e.g., lane 17, page 130; Fig. 1A). The working examples disclose a circuit variant was constructed healing miR-122 targets. The PIT::VP16 activator valiant was used due to its lower DNA payload and increased available footprint for the output gene. The circuit with mCherry output, dubbed HCC.Vl-mCherry, was packaged into DJ-pseudotyped AAV vectors and re-tested in its ability to discriminate HCC cell lines from primary murine hepatocytes. The data highlight that the full circuit generates highly specific expression in HepG2 and Hep3B cell lines compared to primary hepatocytes, while in HuH-7 the circuit generates reduced output due to intermediate activity of miR-122 in these cell lines (e.g., lane 29, page 132; Fig. 2A).
The examples described in the specification does not meet the limitation of the rejected claim having a least 70%, at least 80%, at least 85%, at least 90%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99% identity of its amino acid and/or nucleotide sequence of the transactivators listed in TABLE 2.
The specification only provides data for the transactivator VP16. This specie is not representative of the very large variations allow by the claim, there is insufficient guidance provided indicating any of the elements that are critical to the functioning of the transactivators, thus it cannot be determined which amino acids can be changed without disrupting the function of the transactivator; thus, further experimentation would be required to determine which variants of transactivator in Table 2 are functional and which are not.
The state of the art with respect to transactivators is under developed and unpredictable. Roney et al. (Scientific Reports, 2016) teaches that the rtTA system offers many advantages because it enables graded and reversible transcriptional control using a non-toxic inducer, the antibiotic doxycycline, that has few pleiotropic effects2. A disadvantage of the system is that the rtTA protein retains some affinity for its DNA binding site in the absence of inducer resulting in leaky transcription of target genes (e.g., paragraph 2nd, page 1). Roney teaches the identification of single amino acid substitutions in the widely used doxycycline-inducible transactivator (rtTA) that significantly improves dynamic range without compromising maximal expression capacity. Replacing a single glycine (G72) in the rtTA-M2 variant with residues that introduce non-polar side chains reduces its ability to activate transcription in the absence of doxycycline in a manner that depends on the size of the side chain. This suggests that the reduction in leaky target gene expression may be due to an increased rigidity of the tertiary structure of rtTA that reduces its DNA binding affinity in the absence of induction (e.g., paragraph 3rd, page 6; Fig. 2). The mutations that reduce leaky target gene expression also reduce the sensitivity to doxycycline. This loss of sensitivity depends on the size of the side chain introduced at G72, suggesting a complex interplay between the rtTA DNA binding domain and its doxycycline binding pocket. The loss of sensitivity could be a problem in applications where it is not possible, or not practicable, to use high doxycycline concentrations. We have demonstrated, however, that introducing additional mutations into the G72P M2 variant can improve the sensitivity to doxycycline without introducing leaky target gene expression. The variant with high sensitivity and undetectable leaky target gene expression carries five mutations (V9I, F67S, G72P, F86Y, R171K) in the TetR domain of rtTA-M2 and the G72P mutation appears to be critical. A G72A variant has higher doxycycline sensitivity (lower EC50) than the G72P variant, but also substantially higher activity in the absence of doxycycline. These observations suggest that the combined effect of mutations that impact rtTA DNA binding and doxycycline induction are highly nonlinear (e.g., paragraph 4th, page 6; Fig. 4). Furthermore, Milbradt et al. (Nat. Struct. Mol. Biol.,2011) teaches that VP16 possesses a potent transactivation domain (TAD) when fused to heterologous DNA-binding domains, and it has been suggested to be prototypic of ‘acidic’ TADs (e.g., paragraph 1st, page 1). Milbradt teaches evaluation of two VP16 TAD constructs for binding to MED25 VBD. A shorter, 42-residue fragment consisted of the N-terminal portion of the VP16 TAD (amino acids 411–452 termed here TADn), and a longer 80-residue fragment contained the full-length TAD (amino acids 411–490; termed here TAD). Both peptides showed tight binding to MED25 VBD as determined by isothermal titration calorimetric (ITC) assays (e.g., paragraph 3rd, right column, page 2; Supplemental Figs. 1, 5). The binding site of VP16 TADn on MED25 VBD and the binding site of MED25 VBD on VP16 TADn was evaluated by NMR spectroscopy. The N-terminal VP16 TAD region was therefore identified as the primary MED25 VBD–binding portion. Consistent with this notion, a previous study showed that MED25-dependent transcriptional activation by the VP16 TAD required an intact TAD N terminus (e.g., paragraph 2nd, left column, page 3). Milbradt teaches that residues D439, D441, F442, L444, D445, L446, M447 and G448 of bound VP16 TADn experience major chemical shift changes upon binding to MED25 VBD and may constitute a core binding segment of alternating hydrophobic and negatively charged residues (Supplementary Fig. 1b shows a conserved region in the TADn between Asp437 and Gly448). In addition, Phe442 of the VP16 TADn was shown to be of critical importance for the interaction with the MED25 VBD, as a point mutation of Phe442 to proline prevented binding of the TADn to the VBD (e.g., paragraph 2nd, right column; Fig. 4; Supplemental Fig. 1b).
Thus, the prior art does not overcome the deficiency of the specification with regard to the description of a genus of transactivators. The teachings are consistent with the prior art demonstrating the underdeveloped and unpredictable nature of the invention.
Therefore, the skilled artisan would have reasonably concluded applicants were not in possession of the claimed invention for claims 1-2, 6, 9, 11, 15, 18, 24, 31, 34, 37-38, 40, 44, 72-73, 75.
The claims listed in the statement of rejection but not otherwise discussed are rejected because they are similarly not limited to particular amino acids that are considered to be adequately described by the specification.
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.
Claims 1-2, 6, 9, 15, 18, 24, 31, 37-38, 40, 45, 72-73, 75 are rejected under 35 U.S.C. 103 as being unpatentable over Huang, et al. (“Huang”, Nat. Communications, 2019, cited as reference on IDS filed 05/22/2023) in view of Greenberg et al. (“Greenberg”, WO 2017/132552 A1, cited as reference on IDS filed o1/09/2023) and Corey et al. (“Corey”, US 8,222,221 B2).
Regarding claims 1, 2, 6, 9, 31 and 45, Huang teaches a contiguous polynucleotide molecule comprising: a) a first cassette encoding a first RNA whose expression is operably linked to a 5xUAS transactivator response element, wherein the first RNA comprises: (i) a nucleic acid sequence of an effector (output of the claim); and (ii) a target site for MiR-199a-3p and a target site for miR-142; and b) a second cassette encoding a second RNA, wherein the second RNA comprises a nucleic acid sequence of a Gal4VP16 transactivator, wherein the expressed Gal4VP16 activator is capable of transactivation from the 5xUAS transactivator response element (e.g., page 3, right column; Figs. 2c and 4a). Huang teaches that the circuit setup of the polynucleic acid allows for high levels of E1A expression to trigger adenoviral replication and oncolysis when the following conditions are met in cancer cells: (1) the AFP promoter is turned on; (2) the miR-21 level is high; and (3) the miR-199-3p and miR-142 levels are low (e.g., page 5, paragraph bridging columns; Fig. 4a).
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Regarding claims 72- 73 and 75 Huang teaches an engineered adenoviral vector comprising the contiguous polynucleic acid molecule (e.g., Fig. 4a).
Regarding claims 15 and 24, Huang teaches the contiguous polynucleic acid molecule where the expression of the first RNA comprising the effector (output of the claim) is operably linked to two tetO transcription factor response elements (e.g., Fig. 4a).
Regarding claim 18, Huang teaches the contiguous polynucleic acid molecule where the second cassette comprises an AFP promoter operably linked to the sequence encoding the RNA comprising the sequence of the GAL4VP16 transactivator (e.g., Fig. 4a).
Regarding claim 37-38, 40, Huang teaches that oncolytic adeno virus which encodes immunomodulators can exert a more robust therapeutic efficacy than combinatorial treatment with oncolytic virus and immune effector (e.g., abstract). Huang teaches that the enhanced blue fluorescent protein (EBFP) gene was served as a fluorescent reporter to evaluate the performance of the sensory switch circuit, which can be flexibly replaced with immunomodulatory genes (It reads on therapeutic output of the claim) (e.g., paragraph 1st, right column, page 3; Figs. 2c and 4a). Huang teaches that the EBFP gene in synthetic oncolytic virus with genes encoding therapeutic proteins to improve local anti-tumor efficacy. Four different virus strains were produced, expressing different immunomodulators, including IL-2, mouse GM-CSF (mGM-CSF), and two scFvs against either PD-1 (anti-PD-1-scFv) or PD-L1 (anti-PD-L1-scFv) (It reads on therapeutic output) (e.g., paragraph 2nd, right column, page 5).
Huang does not teach the contiguous polynucleic acid molecule where the first RNA comprises a let-7c target site, where the second RNA comprises a let-7c target site, or where the first and second RNA each comprise a let-7c target site. However, this is cured by Greenberg and Corey.
Greenberg teaches oncolytic viral vectors incorporate one or more of the following features: viral replication restriction by insertion of tumor-suppressive microRNA (miRNA) target sequences into the viral genome; disruption of oncogenic miRNA function; cancer microenvironment remodeling; and cancer cell targeting by incorporation of protease-activated antibodies into the viral particle (e.g., abstract). Greenberg teaches the mir-let 7c target site (e.g., paragraph 0013).
Corey teaches method of modulating expression of a target gene in a cell comprising contacting an endogenous miRNA complementary to a portion of a promoter of the target gene with a single-stranded complementary oligonucleotide that hybridizes to the miRNA (e.g., paragraph 3rd, column 3). Corey teaches SEQ ID NO: 20344 that has 100% homology with SEQ ID NO: 42 (corresponding to miR-let7c-5p) of the instant claims.
Based on these teachings, it would have been prima facie obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to modify the teachings of Huang -a contiguous polynuleic acid molecule comprising: a) a first cassette encoding a first RNA for the Effector output whose expression is operably linked to a 5xUAS transactivator response element, where the first RNA comprises (i) a nucleic acid sequence of the Effector (output of the claim) and (ii) a target site for miR-199a-3p and miR-142 and b) a second cassette encoding an RNA for the transactivator Gal4VP16 under the control of pAFP and a target site for miR-21, with the teachings of Greenberg -viral vectors comprising: viral replication restriction by insertion of tumor-suppressive miR-let-7c target site and with the teachings of Corey – the sequence corresponding to miR-let-7c target site; for someone skilled in the art would have been obvious to use these teachings and substitute the miR-199a, miR-142, miR-21 target sequence with the miR-let-7c target site to achieve the predictable result of developing an oncolytic vector comprising: a) a first cassette encoding a first RNA for a therapeutic output whose expression is operably linked to a 5xUAS transactivator response element, where the first RNA comprises (i) a nucleic acid sequence of a therapeutic output and (ii) a target site for miR-let-7c and b) a second cassette encoding an RNA for the transactivator Gal4VP16 under the control of pAFP and a target site for miR-let-7c.
One of ordinary skill in the art before the effective filing date of the invention would have been motivated to try to develop an oncolytic adenovirus programmed by synthetic gene circuit for sensing cancer-specific miRNA and delivering immune effector molecules for cancer immunotherapy.
Claims 11, 31 and 34 are rejected under 35 U.S.C. 103 as being unpatentable over Huang, et al. (“Huang”, Nat. Communications, 2019, cited as reference on IDS filed 05/22/2023), Greenberg et al. (“Greenberg”, WO 2017/132552 A1, cited as reference on IDS filed 01/09/2023) and Corey et al. (“Corey”, US 8,222,221 B2) as applied to claims 1-2, 6, 9, 15, 18, 24, 31, 37-38, 40, 45, 72-73, 75 above, and further in view of Burns et al. (“Burns”, US 7,626,010 B2), Fussenegger et al. (“Fussenegger”, US 6,287,831 B1) and Gonzalez-Nicolini et al. (“Gonzalez-Nicolini).
Huang, Greenberg and Corey, do not teach the PIT transactivator element of SEQ ID NO 139, as required by the instant claims. Huang, Greenberg and Corey do not teach wherein the first cassette and the second cassette are in a divergent orientation, a convergent orientation, or a head-to-tail orientation. Huang, Greenberg and Corey do not teach the transactivator PIT:VP16TAD-1 of SEQ ID NO 97, as required by the instant claims. However, these is cured by Burns, Fussenegger and Gonzalez-Nicolini.
Burns teaches the DNA sequence of the PIT transactivator response element of SEQ ID NO 3 [respond to transactivator PIT::V16PTAD-1], that has 100% homology with SEQ ID NO 139 of the instant claims.
Fussenegger teaches a novel system for gene regulation in eukaryotic cells, and methods of using the same for protein production, tissue engineering and gene therapy (e.g., abstract). Fussenegger teaches SEQ ID NO 4 that 100% homology to SEQ ID NO 97 (transactivator PIT::VP16TAD-1), as the instant claims (SEQ ID NO 97 is the nucleotide sequence of SEQ ID NO 98 elected by the Applicant), see alignment below.
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Gonzalez-Nicolini teaches bidirectional expression cassette form autoregulated streptogramin-responsive expression of a desired transgene. A bidirectional promoter consisting of a central PIT (pristinamycin-dependent transactivator)-specific operator (PTR) flanked by minimal versions of the human cytomegalovirus immediate-early and the Drosophila heat shock protein 70 promoter (PhCMVmin; Phsp70min) drives divergent expression of YFP and PIT, respectively (pAI-YFP ← PhCMVmin-PTR-Phsp70min → PIT-pAII (It reads on comprising a PIT transactivator and transactivator response element, as required by instant claims 11 and 34) (e.g., paragraph 4th, right column, page 576; Fig. 1A).
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Based on these teachings, it would have been prima facie obvious to one of ordinary skill in the art, before the effective filing date of the claimed invention, to modify the teachings of Huang, Greenberg and Corey -developing oncolytic vector comprising: a) a first cassette encoding a first RNA for a therapeutic output whose expression is operably linked to a 5xUAS transactivator response element, where the first RNA comprises (i) a nucleic acid sequence of a therapeutic output and (ii) a target site for miR-let-7c and b) a second cassette encoding an RNA for the transactivator Gal4VP16 under the control of pAFP and a target site for miR-let-7c and substitute the upstream activation sequence (5xUAS) (first cassette) and the pAFP promoter (second cassette) taught by Huang with the PIT transactivator response element taught by Burns that respond to transactivator PIT::V16P-TAD-1 taught by Fussenegger and the bidirectional expression cassette taught Gonzalez-Nicolini; for someone skilled in the art would have been obvious to use these teachings to achieve the predictable result of developing oncolytic vector comprising two cassettes 1) a first cassette with a transactivator responsive element [respond to PIT::VP16TAD-1], genes coding for immune effectors like cytokines and a miRNA target site (let-7c) and 2) a second cassette that comprise a transactivator responsive element [respond to PIT::V16PTAD-1], that controls the expression of the transactivator PIT::VP16TAD-1 and a miRNA target site (let-7c), where both expression cassettes may have different combinations (same or opposite orientations, upstream or downstream of each other).
One of ordinary skill in the art before the effective filing date of the invention would have been motivated to try to develop an oncolytic adenovirus programmed by synthetic gene circuit for sensing cancer-specific miRNA and delivering immune effector molecules for cancer immunotherapy.
Conclusion
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JULIO GOMEZ RODRIGUEZ whose telephone number is (571)270-0991. The examiner can normally be reached Monday - Friday 8:00 am - 5:00 pm.
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/JULIO WASHINGTON GOMEZ RODRIGUEZ/Examiner, Art Unit 1637
/Jennifer Dunston/Supervisory Patent Examiner, Art Unit 1637