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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 06/02/2026 has been entered.
Priority
Applicant’s claim to priority from Provisional Application No. 62/952,725 filed 12/23/2019 and PCT/US2020/066557 filed 12/22/2020 is hereby acknowledged.
Election/Restrictions
Applicant's election of Species consisting of the combination of
transdifferentiation determinants SP1 and IKZF1 in the reply filed on 08/18/2025 was
acknowledged. Because applicant did not distinctly and specifically point out a
supposed error in the restriction requirement, the election has been treated as an
election without traverse (MPEP § 818.01 (a)).
Applicant also elected "increased" for the expression of the determinants.
However, in the response dated 08/18/2025, Applicant indicated that claim 25(a)-(k) also reads on the elected species. Therefore, Examiner interprets the election of
Species includes combination of determinants comprising both Spl1 and IKZF1. Therefore, claims 11 and 21 are being examined as well.
The restriction requirement dated 06/16/2025 and the election/response filed 08/18/2025 are still valid and in effect in this Office Action.
Application Status
This Application is a National Stage entry application under 35 U.S.C. §371 of PCT/US2020/066557 filed 12/22/2020.
This Office Action is in response to the amendments and Remarks filed 06/02/2026.
Amendments to claims filed 06/02/2026 are hereby acknowledged.
Claims 6, 8, 16, 18 and 23 are still cancelled.
Claims 1, 3-5, 12, 15 and 24-25 are currently amended.
Claims 1-5, 7, 9-15, 17, 19-22 and 24-25 are currently pending.
Therefore, claims 1-5, 7, 9-15, 17, 19-22 and 24-25 are under consideration in this office action.
Any objection or rejection not reiterated herein has been overcome by Applicant’s amendments and is withdrawn. Applicant’s amendments and arguments have been thoroughly reviewed but are not persuasive to place the claims in condition for allowance for the reasons that follow.
Information Disclosure Statement
The listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, or have been submitted on an IDS, they have not been considered.
Claim Rejections - 35 USC § 112(d)
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
Claims 3 and 4 are rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Regarding claim 3, it recites “The method of claim 1, wherein increasing
expression of the transdifferentiation determinants in the glioblastoma cells results in transdifferentiation of one or more of the glioblastoma cells into antigen presenting cells.” The claim recites an end-result, without adding specific method step.
Regarding claim 4, it recites “The method of claim 1, wherein increasing expression of the one or more transdifferentiation determinants in cells of the glioblastoma cells results in reduced growth rate of the glioblastoma cells”.
The claim recites an end-result. There is no additional limitation on elements of claim 1, since there is no additional active step for the method of treating glioblastoma.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
Response to Arguments
Applicant's arguments filed 06/02/2026 have been fully considered but they are not persuasive.
Applicant’s Remarks, on page 8, state that “It is not clear why the Examiner is of the opinion that (a) the “inducing an immune response against the glioblastoma” and “reducing growth of the glioblastoma cells” need to be explicitly recited in claim 1 in order for claim 4 to further limit claim 1. It is also not clear why the Examiner is of the opinion that the treating of claim 1 includes only “reducing growth of the glioblastoma cells,” or, alternatively, why “inducing an immune response against the glioblastoma” is not encompassed by claim 1”.
In response, Applicant recites a method of transdifferentiating a cancer cell into
an antigen presenting cell in vivo. This step implies that more cancer cells are transdifferentiated, less cancer cells will remain, which is consistent with a decrease in cancer growth, which is also an end-result. However, the act of inducing an immune response against a cancer cell is a broader limitation that encompasses injecting an immune activating compound such as an interleukin, an interferon, a vaccine, antibodies, or conditioned immune cells via adoptive transfer, to the subject in vivo. Therefore, “ a method of inducing an immune response” is vague and broad, while claim 1 is restricted to converting cancer cells into antigen presenting cells, which is a more detailed focus, a Species of a broader genus.
Amending claim 1 to “A method of treating glioblastoma and inducing antigen
presenting cells population and activity in glioblastoma comprising:
administering to the glioblastoma in a subject one or more nucleic acids
that increase expression of glioblastoma to antigen presenting cell transdifferentiation determinants thereby increasing expression of the transdifferentiation determinants in
glioblastoma cells of the glioblastoma, wherein the transdifferentiation determinants comprise SPI1, IKZF1, and PRKCB”, for example, would be clearer and specific.
The dependent claim 4 is supposed to add further limitation to the claim upon which it depends. Claim 4 is drawn to an end-result, and not to a method step.
Applicant may delete claims 3 and 4 or amend to add a specific method step.
For example, for claim 4, it could recite : “The method of claim 1, wherein the increasing expression of the transdifferentiation determinants in cells of the glioblastoma consists in sequential administration of two or more nucleic acids 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13 or 14 days apart, resulting in reduced growth rate of the glioblastoma cells”. (taken from Specification filed 12/18/2025, page 4, [0012] as an example of concrete method step). In another example of amendment, Applicant could add specific SEQ ID Nos to refer to said nucleic acids, thereby further limiting the method steps, restricting them to the use of specific sequences.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
The following rejections are maintained from the previous Office Action dated 03/06/2026, but are modified as necessitated by Applicant’s amendments filed 06/02/2026:
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 1-5, 7, 9, 11-15, 17, 19, 21-22 and 24 are rejected under 35 U.S.C. §103 as being unpatentable over Ribeiro Lemos Pereira (Ribeiro Lemos Pereira, C.F. et al. WO 2018/185709 A1, published October 11, 2018; previously cited), in view of Zhang ( Zhang, Y. et al. "A 63 signature genes prediction system is effective for glioblastoma prognosis". International Journal of Molecular Medicine, Vol. 41 (2018), pp: 2070-2078; previously cited) and Tsui (Tsui, C. et al. "Protein kinase C-B dictates B cell fate by regulating mitochondrial remodeling, metabolic reprogramming, and heme biosynthesis". Immunity, Vol. 48 (2018), pp: 1144-1159; previously cited).
Regarding claims 1 and 12, Ribeiro Lemos Pereira teaches a method of treating a subject in need of treatment using a composition for reprogramming cells into dendritic cells or antigen presenting cells (see title and abstract). Ribeiro Lemos Pereira teaches the isolation of transcription factors that can reprogram or induce differentiated cells into dendritic cells, i.e. transdifferentiation determinants (see [0008]). Ribeiro Lemos Pereira teaches the transdifferentiation of cancer cells, among other cancers, glioblastoma (see [0071], [0084], [00229], [00240]). Ribeiro Lemos Pereira teaches Spi-1 proto-oncogene (PU.1) as one determinant among others, used in composition to transdifferentiate cancer cells into antigen presenting cells (see [00198] and page 92, claims 1-5).
Ribeiro Lemos Pereira also teaches that IKZF1 negatively impact the number of induced dendritic cells generated (see [00163]).
Ribeiro Lemos Pereira teaches that one, two, three, four, five, six, seven, eight or more dendritic cells-inducing factor genes, SPI1 (PU.1), IRF8 and IKZF1 among others, can be encoded and expressed in one or more expression vectors to prepare the induced dendritic cells (see [00251]).
Ribeiro Lemos Pereira teaches the expression of PRKCB as one of the top 500 genes that are differentially expressed in induced dendritic cells. Ribeiro Lemos Pereira teaches that the expression of PRKCB is down regulated in induced dendritic cells at day 9 (see Table 5, [00183], page 54).
Regarding claims 1 and 12, Ribeiro Lemos Pereira does teach PRKCB as a gene with a difference in expression when comparing naïve dendritic cells to the induced dendritic cells (see page 54, Table 5, [00182]). However, Ribeiro Lemos Pereira does not teach PRKCB as one of the determinant of transdifferentiation, which expression needs to be modulated, either increased or decreased by contacting the glioblastoma cells with specific nucleic acid for said effect.
However, Zhang established an effective prognostic prediction system and validated its performance for glioblastoma multiforme using PRKCG, PRKCB and CAMK2A as prognostic factors (see page 2077, right column, last paragraph). Zhang teaches that PRKCB is a tumor promoter gene that modulates the rate of autophagy, which serves as a pro-death or pro-survival mechanism. Therefore, Zhang teaches that PRKCB participates in the regulation of cell survival and apoptosis and is aberrantly expressed in Glioblastoma multiforme, its upregulation being beneficial for patient survival (see page 2077, right column, second paragraph).
Tsui teaches that PRKCB dictates B cell fate (see title) and that lack of PRKCB undermined antibody production and antigen presentation (see abstract). Tsui teaches that transgenic PRKCB-/- mice are severely immunodeficient, with less germinal center B cells, less splenic T cells and plasma cells, compared to wild type mice (see abstract and Figure 1). Tsui teaches that PRKCB instructs plasma cell differentiation in B cells (see page 1147, right column, and Figure 3).
Therefore, it would have been obvious to one with ordinary skills in the art before the effective filing date of the claimed invention to have combined the teachings of Ribeiro Lemos Pereira with the teachings of Zhang and Tsui, and combined SPI1 or (PU.1) and IKZF1 as taught by Ribeiro Lemos Pereira, with PRKCB as taught by Zhang and Tsui, as transdifferentiation determinants necessary to transform glioblastoma multiforme cells into immune cells/antigen presenting cells. One with ordinary skills in the art, motivated in ensuring that the glioblastoma cells dedifferentiate and enter an immune cell differentiation program, could have performed this modification with a reasonable expectation of success and arrived at the claimed invention.
Regarding claim 2, Ribeiro Lemos Pereira teaches glioma and glioblastoma (see [0071], [0084], [00240] and Table 2). However, Ribeiro Lemos Pereira does not specify which glioma/glioblastoma.
Examiner interprets that Ribeiro Lemos Pereira teaches all species in the larger genus “Glioblastoma”.
Regarding claims 3 and 4, Ribeiro Lemos Pereira teaches overexpression of transdifferentiation determinants such as SPI1 (PU.1) (see [00155], [00160], [00162], [00261]).
The claims are directed to end-result of the method step which is not different from the method of expressing the transdifferentiation determinants taught by Ribeiro Lemos Pereira.
Regarding claims 5, 7, 9 and 11, Ribeiro Lemos Pereira teaches one, two, three, four, five, six, seven, eight or more dendritic cells-inducing factor genes, SPI1 (PU.1), IRF8 and IKZF1 among others, encoded and expressed in one or more expression vectors to prepare the induced dendritic cells (see [00251]).
Ribeiro Lemos Pereira teaches BATF3 as one of the determinants encoded by nucleic acids of the invention ([00197], [00251]). Ribeiro Lemos Pereira teaches BCL11A , ID2 , RUNX3, as genes to be expressed in induced dendritic cells ([00251]).
Ribeiro Lemos Pereira teaches a change in expression of some genes such as STAT6 (see [00174], [00180], and Figure 23).
Regarding claim 14, Ribeiro Lemos Pereira teaches a method of transdifferentiating cancer cells into antigen presenting cell that are dendritic cell-like cells, comprising administering to the cancer cells one or more nucleic acids, i.e. constructs, that increase or decrease expression of one or more cancer determinant of transdifferentiation ( see [00193]-[00195], [00197]-[00200]).
Regarding claim 13, Ribeiro Lemos Pereira teaches glioma and glioblastoma (see [0071], [0084], [00240] and Table 2). However, Ribeiro Lemos Pereira does not specify which glioma/glioblastoma.
Examiner interprets that Ribeiro Lemos Pereira teaches all species in the larger genus “Glioblastoma” and “glioma”.
Regarding claim 15, 17, 19 and 21, Ribeiro Lemos Pereira teaches one, two, three, four, five, six, seven, eight or more dendritic cells-inducing factor genes, such as IRF8 among others, encoded and expressed in one or more expression vectors to prepare the induced dendritic cells (see [00251]).
Ribeiro Lemos Pereira teaches BATF3, BCL11A , ID2 , RUNX3, as genes to be expressed in induced dendritic cells ([00251]).
Ribeiro Lemos Pereira teaches a change in expression of some genes such as STAT6 (see [00174], [00180], and Figure 23).
Regarding claim 22, Ribeiro Lemos Pereira teaches viral vectors, including lentiviral vector (see page 94, Ribeiro Lemos Pereira’s claim 14; [0024]). Ribeiro Lemos Pereira also teaches plasmids (see [00195], [00203]).
Regarding claim 24, Ribeiro Lemos Pereira teaches a method increasing expression of one or more transdifferentiation determinants in cancer cells, which include glioma and glioblastoma cells, resulting in induction of an immune response against the cancer cells (see [0057]-[0062], [0084], [00240], [00249]-[00252] and claims 1-6).
The obviousness of the combination of references Ribeiro Lemos Pereira, Zhang and Tsui is described above; therefore the combination of references also renders elements of the depending claims 2-3, 5, 7, 9, 11, 13-15, 17, 19, 21-22 and 24 obvious.
Claims 10, 20 and 25 are rejected under 35 U.S.C. § 103 as being unpatentable over Ribeiro Lemos Pereira (Ribeiro Lemos Pereira, C.F. et al. WO 2018/185709 A1, published October 11, 2018; previously cited), Zhang ( Zhang, Y. et al. "A 63 signature genes prediction system is effective for glioblastoma prognosis". International Journal of Molecular Medicine, Vol. 41 (2018), pp: 2070-2078; previously cited) and Tsui (Tsui, C. et al. "Protein kinase C-B dictates B cell fate by regulating mitochondrial remodeling, metabolic reprogramming, and heme biosynthesis". Immunity, Vol. 48 (2018), pp: 1144-1159; previously cited), as applied to claims 1-5, 7, 9, 11-15, 17, 19, 21-22 and 24 above and in further view of Collombet (Collombet, S. et al. “Logical modeling of lymphoid and myeloid cell specification and transdifferentiation”. PNAS, Vol. 114, No. 23 (2017), pp: 5792-5799; previously cited), Xu (Xu, W. et al. “E2A transcription factors limit expression of GATA3 to facilitate T lymphocyte lineage commitment”. Blood, Vol. 121, No. 9 (2013), pp: 1534-1542; previously cited), Rehli-1 (Rehli, M. et al. “Transcriptional regulation of CHI3L1, a marker gene for late stage of macrophage differentiation”. The Journal of Biochemical Chemistry, Vol. 278, No. 45 (2003), pp: 44058-44067; previously cited) and Rehli-2 (Rehli, M. et al. “TFEC is a macrophage-restricted member of the Microphthalmia-TFE subfamily of Basic Helix-Loop-Helix Leucine Zipper transcription factors”. The Journal of Immunology,Vol.162 (1999), pp: 1559-1565; previously cited).
The rejections of claims 1-5, 7, 9, 11-15, 17, 19, 21-22 and 24 are described above. It is noted that claims 5, 9 and 19 are rendered obvious by the combination of Ribeiro Lemos Pereira, Zhang and Tsui.
Regarding claims 10 and 20, they recite “ wherein the one or more additional transdifferentiation determinants are selected from the group consisting of: CTSZ, TFEC, USF1, GATA3, RBFOX2, and SALL2.”
Regarding claim 25, it recites specific combinations of determinants:
CTSZ, TFEC, USF1, GATA3, or RBFOX2;
CTSZ and TFEC, CTSZ and USF1, CTSZ and GATA3, or CTSZ and RBFOX2;
TFEC and USF1, TFEC and GATA3, TFEC and RBFOX2, or TFEC and SALL2;
USF1 and GATA3, USF1 and RBFOX2, or USF1 and SALL2; or
GATA3 and RBFOX2, or GATA3 and SALL2.
The combination of references Ribeiro Lemos Pereira, Zhang and Tsui does not render obvious the specific transdifferentation determinants CTSZ, TFEC, USF1, GATA3, RBFOX2, and SALL2.
However, regarding claims 10, 20 and 25 (a)-(c), Rehli-1 teaches that several known transcription factors are needed and specifically bind the promoter of a specific late-stage marker of macrophage differentiation, CHI3L1 (see title and abstract). Rehli-1 teaches that these transcription factors are PU.1 (i.e. SPI1), Sp1, Sp3 and USF (see abstract). Rehli-1 teaches that complexes containing SP1, Sp3, USF1 and USF2a were detectable in super-shift analysis (see Figure 5C and page 44063, left column).
Therefore, Rehli-1’s teachings indicate that transcription factors associated with terminal differentiation in antigen presenting cells such as macrophages include USF1.
Regarding claims 10, 20 and 25 (a), (c) and (d), Collombet teaches about factors important in myeloid cell specification and transdifferentiation (see title and abstract). Collombet teaches the transcription factors needed for different stages of cell lineage commitment as seen in Figure 1 and below:
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Collombet teaches that Spi1 (PU.1) and IKZF1 (Ikaros) are important determining transcription factors that are active in cell commitment towards common lymphoid progenitor cells and monocyte lineages (see above, and Figure 1A).
Collombet teaches that E2a is as important as Ikaros for commitment into common lymphoid progenitor lineage (see Figure 1A and Figure 3). Collombet teaches that E2a is known to be a master regulator of lymphoid and myeloid cell specification (see page 5798, right column, second paragraph). Collombet refers to reference #38 for this teaching; reference #38 is Xu.
Xu teaches that E2a targets GATA3 gene expression (see title). Xu teaches that overexpression of GATA3 extends the self-renewal capacity of thymocytes (DN2 cells) and increases the propensity to inhibits a T-cell lineage commitment ( see page 1535, left column, first paragraph).
Therefore, according to Collombet and Xu’s teachings, overexpression of GATA3 together with Ikaros (IKZF1) will likely block the common lymphoid progenitor (see Figure 1A) commitment towards T cell differentiation and favor the commitment towards pre-B lineages capable of transdifferentiating into antigen presenting cells.
Collombet and Xu’s teachings also suggest that overexpression of GATA3 and Ikaros together with SPI1 will certainly redirect any transdifferentiation towards antigen presenting cells.
Regarding claims 10, 20 and 25 (a), (c),(d), Rehli-2 teaches that TFEC is a macrophage-restricted transcription factor (see title and abstract). Rehli-2 teaches that PU.1 (SPI1) is necessary for gene expression regulation of TFEC gene in macrophages. Rehli-2 teaches that TFEC might itself individually or in concert with other transcription factors in the same family play a role in macrophage-specific gene regulation (see abstract; see page 1560, left column, 4th paragraph).
Therefore, it would have been obvious to one with ordinary skills in the art before the effective filing date of the claimed invention to have combined the transcription factors Spi1 (PU.1) and Ikaros (IKZF1) as taught by Ribeiro Lemos Pereira, with PRKCB as taught by Zhang and Tsui, with an additional gene such as USF1 as taught by Rehli-1, or GATA3 gene as taught by Collombet/Xu, or TFEC gene as taught by Rehli-2. One with ordinary skills in the art, motivated in insuring that the cells commit to an antigen presenting cells lineage to enhance the chances of producing cells that are effective for adoptive cell transfer and immunotherapy for glioma or glioblastoma could have performed this modification with a reasonable expectation of success based on the teachings of Rehli-1, Collombet/Xu and Rehli-2. One motivated in a high rate of cell transdifferentiation into macrophages could have combined the teachings of Ribeiro Lemos Pereira modified with Zhang and Tsui, with the teachings of Rehli-1, Collombet, Xu and Rehli-2 since all the references are drawn to markers specific for cell lineage commitment and/or transdifferentiation. One with ordinary skills in the art could have used Spi1, Ikaros, PRKCB, USF1, GATA3, and TFEC genes in one or more expression vector and transformed the cancer cells into antigen presenting cells and arrived at the claimed invention.
Response to Arguments
Applicant's arguments filed 06/02/2026 have been fully considered but they are not persuasive.
In response to Applicant’s argument on page 9 of Remarks, stating
“Further, do Carmo et al. (in "PKC signaling in glioblastoma" Cancer Biology & Therapy
(2013) 14(4):287-294) teaches that PRKB is a tumor promoter in glioma tumor cells (Table 3), contributes to increasing proliferation and resistance to apoptosis of glioma cells, and contributes to angiogenesis, proliferation and survival of glioma cells (p. 291, col. 1, para. 3)”, the reference cited here is nowhere found in the IDS that Applicant provided. Examiner did not cite this reference in any rejection. If Applicant had wished for this specific reference to be officially part of the Examiner to consider, it should have been added to a submitted IDS for consideration.
This said, the Do Carmo reference seems to be contrary to Applicant’s position regarding PRKB being a viable option for the transdifferentiation of the glioblastoma cells into antigen presentation.
If Examiner had to consider this reference as submitted on an IDS prior making the rejections, it could have contributed to additional rejections under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, since while being enabling for “PRKCB’s expression as a transdifferentiation determinant”, the Specification may not have reasonably provided enablement for “increase of PRKCB expression for transdifferentiation of glioblastoma cells and reduction of tumor growth” according to the “Do Carmo” reference.
Instead, Examiner has considered PKRCB as a more nuanced, “positive” factor enabling the claim as written. Therefore, the examination and search were directed toward a positive effect of this tumor promoter gene although capable of pro-death or pro-survival regulation, as suggested by Zhang (page 2077, right column, second paragraph). In view of Tsui teaching PKCβ-null (Prkcb -/-) mice are severely immunodeficient with impaired antigen presentation (see abstract), Examiner’s conclusion was that this gene has potentially a different effect on cells according to their cell type, cell cycle stage and microenvironment.
In response to applicant's arguments, pages 8-10, 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
No claim is allowed.
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/A.D./Examiner, Art Unit 1636
/NANCY J LEITH/Primary Examiner, Art Unit 1636
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