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 Interpretation
Claim 1 recites, in a method of administering trichostatin A (TSA) to a cancer patient, the improvement comprising: selecting as said patient an individual identified as: overexpressing at least one gene selected from a group consisting of: TLE4, SMO, GPC2, SNTA1, YPEL1, PLEKHA2, GPR137C, CD72, ZFP36L1, PAX5, ZCCHC7, ADARBI, SMIM14, SNX22, AFF2, GJC1, RIPOR2, ARID5B, RAB9B, MIR570HG, CD79B, IKZF2, ZNF318, EBF1, SOX4, TRIB2, GRAC24, RASGRP1, MIR5195, FAM81A, IGHV5-78, LRMP, MS4A1, GPR146, CHI3L2, ZNF608, CDC25B, C12orf77, GPR18, PCDH12, SCML4, CD24, INA, TUNAR, FAM241B, TCL1B, IGLV1-44, and ENPEP; or underexpressing at least one gene selected from a group consisting of: PLA2G4A, KCNQ1, CYB561, RAB32, LTBR, MGST1. JAG1, SPART, FUCA2, PRRG4, FAM83H, IMPACT, TMEM173, EHHADH, ANTXR2, STOM, FNDC3B, DCBLD1, WDFY3, MIR4435-2HG, PSEN2, UBR5-AS1, GALNT11, LGALS1, ERVK13-1, PLSCR1, SELENOT, GALC, FZD6, NEK3, TMBIM1, LINC01814, LINC01873, TRIQK, BIN2, HCG11, AP1S3, CYTOR, SPECCI, CFLAR, CICP14, PLD3, CD151, TTC38, OXR1, ACSL1, INPP1, PLOD3, DHX32, BOLA2-SMG1P6, SIL1, ST3GAL1, TMEM150A, PLBD2, PDIA5, ZC3HAV1L, LINC01410, SLC38A5, MYDGF, BST2, IL15RA, MFSD1, EXOC6B, FAH, SLC19A2, HSP90B1, TTC12, AGAP9, MLKL, PLEC, SMPD1, P4HB, PLOD1, GALNT10, ACOT2, NBPF14, HSPA5, ZBTB7B, NBPF10, CD63, CREB3L2, RAB4A, CTSA, MFSD10, and C4orf36.
Claim 1 includes (1) a preamble comprising a general description of all the elements or steps of the claimed combination which are conventional or known, (2) a phrase such as "wherein the improvement comprises," and (3) those elements, steps and/or relationships which constitute that portion of the claimed combination which the applicant considers as the new or improved portion. See MPEP 37 CFR 1.75(e) Claim(s). Therefore, claim 1 is interpreted to be a Jepson claim. Hence the preamble for “a method of administering trichostatin A (TSA) to a cancer patient,” is taken as an implied admission that the subject matter of the preamble is the prior art work of another. In re Fout, 675 F.2d 297, 301, 213 USPQ 532, 534 (CCPA 1982). See MPEP 2129 (III). Thus for the sake of applying prior art the active step of the claim is the selecting as said patient an individual.
Claim Rejections - 35 USC § 101
35 U.S.C. 101 reads as follows:
Whoever invents or discovers any new and useful process, machine, manufacture, or composition of matter, or any new and useful improvement thereof, may obtain a patent therefor, subject to the conditions and requirements of this title.
Claims 1 – 3, and 11 – 12 are rejected under 35 U.S.C. 101 because the claimed invention is directed to an abstract idea without significantly more. The claims recite in a method of administering trichostatin A (TSA) to a cancer patient, the improvement comprising: selecting as said patient an individual identified as: overexpressing at least one gene selected from a group consisting of: TLE4, SMO, GPC2, SNTA1, YPEL1, PLEKHA2, GPR137C, CD72, ZFP36L1, PAX5, ZCCHC7, ADARBI, SMIM14, SNX22, AFF2, GJC1, RIPOR2, ARID5B, RAB9B, MIR570HG, CD79B, IKZF2, ZNF318, EBF1, SOX4, TRIB2, GRAC24, RASGRP1, MIR5195, FAM81A, IGHV5-78, LRMP, MS4A1, GPR146, CHI3L2, ZNF608, CDC25B, C12orf77, GPR18, PCDH12, SCML4, CD24, INA, TUNAR, FAM241B, TCL1B, IGLV1-44, and ENPEP; or underexpressing at least one gene selected from a group consisting of: PLA2G4A, KCNQ1, CYB561, RAB32, LTBR, MGST1. JAG1, SPART, FUCA2, PRRG4, FAM83H, IMPACT, TMEM173, EHHADH, ANTXR2, STOM, FNDC3B, DCBLD1, WDFY3, MIR4435-2HG, PSEN2, UBR5-AS1, GALNT11, LGALS1, ERVK13-1, PLSCR1, SELENOT, GALC, FZD6, NEK3, TMBIM1, LINC01814, LINC01873, TRIQK, BIN2, HCG11, AP1S3, CYTOR, SPECCI, CFLAR, CICP14, PLD3, CD151, TTC38, OXR1, ACSL1, INPP1, PLOD3, DHX32, BOLA2-SMG1P6, SIL1, ST3GAL1, TMEM150A, PLBD2, PDIA5, ZC3HAV1L, LINC01410, SLC38A5, MYDGF, BST2, IL15RA, MFSD1, EXOC6B, FAH, SLC19A2, HSP90B1, TTC12, AGAP9, MLKL, PLEC, SMPD1, P4HB, PLOD1, GALNT10, ACOT2, NBPF14, HSPA5, ZBTB7B, NBPF10, CD63, CREB3L2, RAB4A, CTSA, MFSD10, and C4orf36. The claim sets forth a mental process abstract idea judicial exception that requires the selection of a patient that is overexpressing a gene or underexpressing a gene. Additionally, the claim implies in the selecting step a comparison of the expression values of genes to some standard in order to determine if the gene is overexpressed or underexpressed. Thus the inherent comparing is also a mathematical concept.
This judicial exception is not integrated into a practical application because the claim is a Jepson claim with the selection step as the only active step of the method. Moreover, the patient is not required to have either the overexpressed or under expressed gene. Therefore, when the treatment step is not required, the claim does not apply or use the judicial exception in any way. The selection step is interpreted to mean that there are at least two distinct patient populations: (1) a population with the overexpressed genes as recited in claim 1 or a population without the overexpressed genes as recited in claim 1 (2) a population with the underexpressed genes as recited in claim 1 or a population without the underexpressed genes as recited in claim 1.
Furthermore, for either the population with the either an overexpressed or underexpressed gene are recited in claim 1, the administration of TSA is not required in the claim; since the only active step is the selection step. Thus as a whole, claim 1 does not include additional elements that are sufficient to amount to significantly more than the judicial exception because the only active step in the method as claimed by claim 1 is the judicial exception, of a mental processes step. To overcome this 101 rejection applicant may amend the claims to clearly require administering the drug in all embodiments. Therefore, given the limitation for a judicial exception without integrating the judicial exception into a practical application claim 1 is rejected under 35 U.S.C. 101. Moreover, claims 2 – 3, and 11 – 12 are included in the rejection since the claims dependent from claim 1 but do not address the deficiency.
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, 3, and 11 are rejected under 35 U.S.C. 103 as being unpatentable over International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form) in view of International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form).
Regarding claims 1, 3, and 11, Polymeropoulos‘121 teach a method of treating cancer in an individual comprising administering effective amount of trichostatin A (TSA). See page 2. Furthermore, Polymeropoulos‘121 teach an embodiment, the invention provides a method of treating a cancer in an individual, the method comprising: determining, from a tumor sample obtained from the individual's body, a level of aurora kinase A (AURKA) expression; and in the case that the level of AURKA expression is indicative of overexpression, administering to the individual an effective amount of trichostatin A (TSA). See page 2. See claim 1 limitation for a method in which a patient goes through a selection process. Moreover, Polymeropoulos‘121 teach an embodiment where treatment with TSA is combined with one or more other cancer treatments. See page 2.
Additionally, Polymeropoulos‘121 teach that cancers that may be treated according to the disclosure include breast cancer, gastric cancer, colon cancer, rectal cancer, bladder cancer, pancreatic cancer, ovarian cancer, prostate cancer, lung cancer, hematological cancer, skin cancer, and malignancies. See page 3. Furthermore, Polymeropoulos‘121 teach that while the disclosure describes in conjunction with the specific embodiments outlined above, it is evident that many alternatives, modifications and variations will be apparent to those skilled in the art or are otherwise intended to be embraced. See pages 6 – 7. Accordingly, Polymeropoulos‘121 teach that the embodiments of the invention as set forth above are intended to be illustrative, not limiting. See pages 6 – 7. Thus, Polymeropoulos‘121 suggest that modification to the method as taught could be motivated by one of ordinary skill in the art.
However, Polymeropoulos ‘121 fails to teach a method or modification where the patient is identified as having overexpressed IKZF2. See claim 1 limitation. See claim 3 limitation.
Nevertheless, Adcock‘334 teach that IKZF2 is believed to have an important role in the function and stability of regulatory T cells (Tregs). See page 1 lines 26 – 27. Moreover, Adcock’334 teach that overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers such as CD103 and GITR and the IKZF2 overexpressing cells showed increased suppression of responder T-cells. See page 1 lines 29 – 31. Thus, Adcock’334 suggest IKZF2 as a potential target especially in diseases and conditions that over express IKZF2. For example, Adcock’334 teach embodiments for a method of treating a disease or disordered that are affected by a decrease in IKZF2 protein levels which include a variety of cancers which include breast carcinoma, gastric cancer, colon cancer, pancreatic cancer, ovarian cancer, prostate cancer, and lung cancer. See page 18 lines 1 – 15. Thus, Adcock’334 teach a list of cancers that are affected by a decrease in IKZF2 protein levels which overlap with cancers that are disclosed in Polymeropoulos‘121.
Moreover, Adcock‘334 teach an embodiment where the compounds of the disclosure are used in combination with one or more HDAC inhibitors which includes trichostatin A (TSA). See page 303 lines 32 – 36. Thus, Adcock’334 suggest the administration of TSA for the treatment of diseases and conditions that over express IKZF2 which overlap with cancers that are disclosed in Polymeropoulos‘121. Moreover, while the prior art is silent about specifically selecting patients that overexpress IKZF2 given the relatively high skill level of one of ordinary skill in the pharmaceutical arts which is that of a Ph.D. and given the prior art teachings of Adcock’334 and Polymeropoulos‘121 it would have been obvious to such artisan to treat a patient with a disease or disordered that is affected by a decrease in IKZF2 protein levels there would need to be a step confirming the patient is overexpressing IKZF2.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to modify the method of Polymeropoulos ‘121 for treating cancer patients overexpressing AURKA comprising administering trichostatin A (TSA) in view of Adcock‘334, that is to select a patient that is overexpressing IKZF2. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Claim 2 is rejected under 35 U.S.C. 103 as being unpatentable over International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos‘121; cited on the ISR form) in view of Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract).
The teachings of Polymeropoulos‘121 as they relate to claim 1, from which claim 2 depends, are given previously in this office action and are fully incorporated here.
However, Polymeropoulos ‘121 fails to teach a method or modification where the patient is identified as having overexpressed CD24. See claim 2 limitation.
Nevertheless, Przychodzen teaches that histone deacetylase inhibitors (HDACi) can enhance its anti-tumor effects via the pharmacologic modulation of macrophage. See page 1. Moreover, Przychodzen teach that the HDACi such as Trichostatin A (TSA) can also affected the tumor immune microenvironment by suppressing the activity of infiltrating macrophages and inhibiting myeloid-derived suppressor cell recruitment. See page 1. Furthermore, Przychodzen teach that a high throughput screen comparing gene expression profiles in known hematological cell lines to identify transcriptional signatures associated with TSA sensitivity was obtained from GDSC. See page 1. Moreover, Przychodzen teach that 49 genes that were upregulated and 85 that were downregulated, with CD24 a small GPI linked glycoprotein expressed at the surface of most B lymphocyte precursors, neutrophils, epithelial cells and frequently found to be highly expressed in various hematological and solid neoplasms. See page 1. Additionally, Przychodzen teach that IKZF2, transcription factor regulating lymphocyte development and quiescence and which is frequently deleted in hypodiploid B-ALLs was also overexpressed. See page 1.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to modify the method of Polymeropoulos ‘121 for treating cancer patients overexpressing AURKA comprising administering trichostatin A (TSA) in view of Przychodzen, that is to select a patient that is overexpressing CD24. One of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms.
Claim 12 is rejected under 35 U.S.C. 103 as being unpatentable over International Patent Application Publication Number WO 2020012334 A1 to (‘334; cited on the ISR form) and as applied to claim 1 above, and further in view of Han et. al. ((2020), Integrin-associated CD151 is a suppressor of prostate cancer progression, Am J Transl Res, 12, 1428 – 1442).
The teachings of Polymeropoulos‘121 as they relate to claim 1, from which claim 12 depends, are given previously in this office action and are fully incorporated here.
However, Polymeropoulos ‘121 fails to teach a method or modification where the patient is identified as having overexpressed CD24. See claim 2 limitation.
Nevertheless, Han et. al. teach that despite advances in targeted therapies, prostate cancer remains one of the deadliest diseases among men world-wide. See page 1428 column 1 paragraph 1. Moreover, Han et. al. teach that multiple members of the tetraspanin family, including CD9, CD81, CD82, TSPAN1 and CD151, exhibit aberrant expression during prostate tumor progression and metastasis. See page 1429 column 1 paragraph 1. Furthermore, Han et. al. teach that an investigation into the consequences of decreased CD151 expression in advanced prostrate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line. See page 1432 column 2 paragraph 2.
Moreover, Han et. al. teach that CD151 represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. See page 1432 column 2 paragraph 2. Thus Han et. al. suggest that the decreased CD151 expression, that is under expression, at least in advanced prostate tumors markedly increased cell growth. Moreover, while the prior art is silent about specifically selecting patients that under express CD151 given the relatively high skill level of one of ordinary skill in the pharmaceutical arts which is that of a Ph.D. and given the prior art teachings of Han et. al. and Polymeropoulos‘121 it would have been within the purview of such artisan that to at least try and treat advanced prostate tumors that under express CD151.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to modify the method of Polymeropoulos ‘121 for treating cancer patients comprising administering trichostatin A (TSA) in view of Han et. al., that is to at least try and treat a patient with advanced prostate tumors underexpressing CD151. One of ordinary skill in the art would have been motivated to make this modification because represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. One of ordinary skill in the art would have a reasonable expectation of success because the consequences of decreased CD151 expression in advanced prostate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line.
Claims 5, 7 – 8, and 10, are rejected under 35 U.S.C. 103 as being unpatentable over International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form) in view of International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form) and Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226).
Regarding claims 5, 7 – 8, and 10, Polymeropoulos‘121 teach a method of treating cancer in an individual comprising administering effective amount of trichostatin A (TSA). See page 2. Furthermore, Polymeropoulos‘121 teach an embodiment, the invention provides a method of treating a cancer in an individual, the method comprising: determining, from a tumor sample obtained from the individual's body, a level of aurora kinase A (AURKA) expression; and in the case that the level of AURKA expression is indicative of overexpression, administering to the individual an effective amount of trichostatin A (TSA). See page 2. See claim 5 limitation for a method in which a patient goes through a selection process. Moreover, Polymeropoulos‘121 teach an embodiment where treatment with TSA is combined with one or more other cancer treatments. See page 2. See claim 8 limitation for a of enhancing tumor suppression therapy.
Additionally, Polymeropoulos‘121 teach that cancers that may be treated according to the disclosure include breast cancer, gastric cancer, colon cancer, rectal cancer, bladder cancer, pancreatic cancer, ovarian cancer, prostate cancer, lung cancer, hematological cancer, skin cancer, and malignancies. See page 3. Furthermore, Polymeropoulos‘121 teach that while the disclosure describes in conjunction with the specific embodiments outlined above, it is evident that many alternatives, modifications and variations will be apparent to those skilled in the art or are otherwise intended to be embraced. See pages 6 – 7. Accordingly, Polymeropoulos‘121 teach that the embodiments of the invention as set forth above are intended to be illustrative, not limiting. See pages 6 – 7. Thus, Polymeropoulos‘121 suggest that modification to the method as taught could be motivated by one of ordinary skill in the art.
However, Polymeropoulos‘121 fails to teach a method for inhibiting tumor growth in a cancer patient. See claim 5 limitation. Moreover, Polymeropoulos‘121 fails to teach a method where the patient is identified as having overexpressed IKZF2. See claim 7 limitation.
Nevertheless, Adcock‘334 teach that IKZF2 is believed to have an important role in the function and stability of regulatory T cells (Tregs). See page 1 lines 26 – 27. Moreover, Adcock’334 teach that overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers such as CD103 and GITR and the IKZF2 overexpressing cells showed increased suppression of responder T-cells. See page 1 lines 29 – 31. Thus, Adcock’334 suggest IKZF2 as a potential target especially in diseases and conditions that over express IKZF2. For example, Adcock’334 teach embodiments for a method of treating a disease or disordered that are affected by a decrease in IKZF2 protein levels which include a variety of cancers which include breast carcinoma, gastric cancer, colon cancer, pancreatic cancer, ovarian cancer, prostate cancer, and lung cancer. See page 18 lines 1 – 15. Thus, Adcock’334 teach a list of cancers that are affected by a decrease in IKZF2 protein levels which overlap with cancers that are disclosed in Polymeropoulos‘121.
Moreover, Adcock‘334 teach an embodiment where the compounds of the disclosure are used in combination with one or more HDAC inhibitors which includes trichostatin A (TSA). See page 303 lines 32 – 36. Thus, Adcock’334 suggest the administration of TSA for the treatment of diseases and conditions that over express IKZF2 which overlap with cancers that are disclosed in Polymeropoulos‘121. Moreover, while the prior art is silent about specifically selecting patients that overexpress IKZF2 given the relatively high skill level of one of ordinary skill in the pharmaceutical arts which is that of a Ph.D. and given the prior art teachings of Adcock’334 and Polymeropoulos‘121 it would have been obvious to such artisan to treat a patient with a disease or disordered that is affected by a decrease in IKZF2 protein levels there would need to be a step confirming the patient is overexpressing IKZF2. See claim 7 limitation for a method where IKZF2 is over expressed. See claim10 limitation for a method where IKZF2 is over expressed.
However, Adcock’334 fails to teach a method for inhibiting tumor growth in a cancer patient. See claim 5 limitation.
Nevertheless, Platta et. al. teach histone deacetylase inhibitors (HDACIs) are a new class of anticancer agents. See page 219 column 2 paragraph 2. Moreover, Platta et. al. teach trichostatin A (TSA), as a known HDACI, has been previously shown to exert multiple antitumor effects. See page 220 column 1 paragraph 2. Furthermore, Platta et.al. teach that TSA has been shown to inhibit tumor cell growth in a variety of cancerous cell lines in vitro. See page 221 column 2 paragraph 2. Specially, Platta et. al. teach that significant growth inhibition was evident at doses as low as 25 nM in DMS53 cells were treated with TSA for 8 d. See page 221 column 2 paragraph 2.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to modify the method of Polymeropoulos‘121 for treating cancer patients overexpressing AURKA comprising administering trichostatin A (TSA) in view of Adcock‘334, that is to select a patient that is overexpressing IKZF2 and in view of Platta et.al. that is for an inhibition of tumor growth. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Claims 6 and 9 are rejected under 35 U.S.C. 103 as being unpatentable over International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos‘121; cited on the ISR form) and Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226), in view of Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract).
The teachings of Polymeropoulos‘121 and Platta et.al. as they relate to claims 5 and 8, from which claims 6 and 9 depends, are given previously in this office action and are fully incorporated here.
However, the prior art of Polymeropoulos‘121 and Platta et. al. fail to teach a method where the patient is identified as having overexpressed CD24. See claims 6 and 9 limitation.
Nevertheless, Przychodzen teaches that histone deacetylase inhibitors (HDACi) can enhance its anti-tumor effects via the pharmacologic modulation of macrophage. See page 1. Moreover, Przychodzen teach that the HDACi such as Trichostatin A (TSA) can also affected the tumor immune microenvironment by suppressing the activity of infiltrating macrophages and inhibiting myeloid-derived suppressor cell recruitment. See page 1. Furthermore, Przychodzen teach that a high throughput screen comparing gene expression profiles in known hematological cell lines to identify transcriptional signatures associated with TSA sensitivity was obtained from GDSC. See page 1. Moreover, Przychodzen teach that 49 genes that were upregulated and 85 that were downregulated, with CD24 a small GPI linked glycoprotein expressed at the surface of most B lymphocyte precursors, neutrophils, epithelial cells and frequently found to be highly expressed in various hematological and solid neoplasms. See page 1. Additionally, Przychodzen teach that IKZF2, transcription factor regulating lymphocyte development and quiescence and which is frequently deleted in hypodiploid B-ALLs was also overexpressed. See page 1.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date of the instant application to modify the method of Polymeropoulos ‘121 for treating cancer patients overexpressing AURKA comprising administering trichostatin A (TSA) in view of Platta et. al. for a method of inhibiting tumor cell growth in further view of Przychodzen, that is to select a patient that is overexpressing CD24. One of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms.
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, and 5 – 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claim s 1 – 10 of U.S. Patent No. US 10265282 B2 to Polymeropoulos et. al. (Polymeropoulos’282) in view of International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form), International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form), Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226), Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract), and Han et. al. ((2020), Integrin-associated CD151 is a suppressor of prostate cancer progression, Am J Transl Res, 12, 1428 – 1442).
Polymeropoulos’282 recite a method of treating a patient diagnosed with cancer with trichostatin A (TSA), the improvement comprising: selecting for treatment a patient determined to have both increased histone deacetylase (HDAC) activity and aurora kinase A (AURKA) expression, wherein the cancer is selected from a group consisting of breast cancer, gastric cancer, colon cancer, bladder cancer, pancreatic cancer, ovarian cancer, prostate cancer, and lung cancer. See reference claim 1. See examined claims 5 and 8. Furthermore, Polymeropoulos’282 recites the improvement of (reference) claim 1, where the dosage and administration modes are recited. See reference claims 2 – 9. Moreover, Polymeropoulos’282 recites the improvement of (reference) claim 1 where the cancer is breast cancer. See reference claim 10.
However, Polymeropoulos’282 fails to recite a method where the patient is selected that either overexpresses or under expressed at least one gene as recited in examined claims 1, 5, and/or 8. See examined claims 2 – 3, 6 – 7, and 9 – 12. Furthermore, Polymeropoulos’282 fails to recite a method for inhibiting tumor growth in a cancer patient. See examined claim 5. Moreover, Polymeropoulos’282 fails to recite a method for enhancing a tumor suppression therapy. See examined claim 8 limitation.
Nevertheless, the prior art teachings of Polymeropoulos‘121, Adcock‘334, Platta et. al., Przychodzen, and Han et.al. as they relate to the prior art rejections of examined claims 1 – 3, and 5 – 12 are given previously in this office action and are fully incorporated here.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date modify the invention of Polymeropoulos‘282 for a method of treating cancer patients overexpressing AURKA comprising administering trichostatin A (TSA) in view of Adcock‘334, Przychodzen, and/or Han et.al. that is to select a patient that is overexpressing IKZF2 and/or CD24 or under expressing CD151. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Moreover, one of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms. Furthermore, one of ordinary skill in the art would have been motivated to make this modification because represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. One of ordinary skill in the art would have a reasonable expectation of success because the consequences of decreased CD151 expression in advanced prostate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line.
Claims 1 – 3, and 5 – 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 9 of U.S. Patent No. US 11078289 B2 Polymeropoulos et. al. (Polymeropoulos’289) in view of International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form), International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form), Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226), Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract), and Han et. al. ((2020), Integrin-associated CD151 is a suppressor of prostate cancer progression, Am J Transl Res, 12, 1428 – 1442).
Polymeropoulos’289 recite in a method of treating a patient diagnosed with cancer with trichostatin A (TSA), the improvement comprising: selecting for treatment a patient determined to have increased aurora kinase A (AURKA) expression, wherein the treating includes administering TSA to the selected patient in an amount sufficient to decrease an AURKA level in the selected patient, and wherein TSA is the only AURKA inhibitor administered to the individual. See reference claims 1. See examined claims 5 and 8. Furthermore, Polymeropoulos’289 recites the improvement of (reference) claim 1, where the cancer, the dosage and administration modes are recited. See reference claims 2 – 8. Moreover, Polymeropoulos’289 recites the improvement of (reference) claim 1 where the cancer is breast cancer. See reference claims 5 and 9.
However, Polymeropoulos’289 fails to recite a method where the patient is selected that either overexpresses or under expressed at least one gene as recited in examined claims 1, 5, and/or 8. See examined claims 2 – 3, 6 – 7, and 9 – 12. Furthermore, Polymeropoulos’289 fails to recite a method for inhibiting tumor growth in a cancer patient. See examined claim 5. Moreover, Polymeropoulos’289 fails to recite a method for enhancing a tumor suppression therapy. See examined claim 8 limitation.
Nevertheless, the prior art teachings of Polymeropoulos‘121, Adcock‘334, Platta et. al., Przychodzen, and Han et. al. as they relate to the prior art rejections of examined claims 1 – 3, and 5 – 12 are given previously in this office action and are fully incorporated here.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date modify the invention of Polymeropoulos‘289 for a method of treating cancer patients overexpressing AURKA comprising administering trichostatin A (TSA) in view of Adcock‘334, Przychodzen, and/or Han et. al. that is to select a patient that is overexpressing IKZF2 and/or CD24 or under expressing CD151. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Moreover, one of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms. Furthermore, one of ordinary skill in the art would have been motivated to make this modification because represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. One of ordinary skill in the art would have a reasonable expectation of success because the consequences of decreased CD151 expression in advanced prostate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line.
Claims 1 – 3, and 5 – 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 10 of U.S. Patent No. US 11667718 B2 to Polymeropoulos et. al. (Polymeropoulos’718) in view of International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form), International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form), Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226), Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract), and Han et. al. ((2020), Integrin-associated CD151 is a suppressor of prostate cancer progression, Am J Transl Res, 12, 1428 – 1442).
Polymeropoulos’718 recite in a method of treating a patient diagnosed with cancer with trichostatin A (TSA), the improvement comprising: selecting for treatment a patient determined to have increased aurora kinase A (AURKA) expression, wherein the treating includes administering TSA to the selected patient in an amount sufficient to decrease an AURKA level in the selected patient. See reference claims 1. See examined claims 5 and 8. Furthermore, Polymeropoulos’718 recites the improvement of (reference) claim 1, where the cancer, the dosage and administration modes are recited. See reference claims 2 – 8. Moreover, Polymeropoulos’718 recites the improvement of (reference) claim 1 where the cancer is breast cancer or a malignancy. See reference claims 5, and 9 – 10.
However, Polymeropoulos’718 fails to recite a method where the patient is selected that either overexpresses or under expressed at least one gene as recited in examined claims 1, 5, and/or 8. See examined claims 2 – 3, 6 – 7, and 9 – 12. Furthermore, Polymeropoulos’718 fails to recite a method for inhibiting tumor growth in a cancer patient. See examined claim 5. Moreover, Polymeropoulos’718 fails to recite a method for enhancing a tumor suppression therapy. See examined claim 8 limitation.
Nevertheless, the prior art teachings of Polymeropoulos‘121, Adcock‘334, Platta et. al., Przychodzen, and Han et. al. as they relate to the prior art rejections of examined claims 1 – 3, and 5 – 12 are given previously in this office action and are fully incorporated here.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date modify the invention of Polymeropoulos‘718 for a method of treating a patient diagnosed with cancer overexpressing AURKA comprising administering trichostatin A (TSA) in view of Adcock‘334, Przychodzen, and/or Han et. al. that is to select a patient that is overexpressing IKZF2 and/or CD24 or under expressing CD151. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Moreover, one of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms. Furthermore, one of ordinary skill in the art would have been motivated to make this modification because represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. One of ordinary skill in the art would have a reasonable expectation of success because the consequences of decreased CD151 expression in advanced prostate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line.
Claims 1 – 3, and 5 – 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 5 of U.S. Patent No. US 12590162 B2 to Polymeropoulos et. al. (Polymeropoulos’162) in view of International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form), International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form), Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226), Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract), and Han et. al. ((2020), Integrin-associated CD151 is a suppressor of prostate cancer progression, Am J Transl Res, 12, 1428 – 1442).
Polymeropoulos’162 recites a method of treating a patient suffering from breast cancer, the method comprising: determining, from a tumor sample of the patient, that the patient has increased aurora kinase A (AURKA) expression; and administering to the patient a dose of trichostatin A (TSA) of between about 0.1 mg/kg/day and about 10 mg/kg/ day. See reference claim 1. Furthermore, Polymeropoulos’162 recites the improvement of (reference) claim 1, where the cancer, the dosage and administration modes are recited. See reference claims 2 – 8.
However, Polymeropoulos’162 fails to recite a method where the patient is selected that either overexpresses or under expressed at least one gene as recited in examined claims 1, 5, and/or 8. See examined claims 2 – 3, 6 – 7, and 9 – 12. Furthermore, Polymeropoulos’162 fails to recite a method for inhibiting tumor growth in a cancer patient. See examined claim 5. Moreover, Polymeropoulos’162 fails to recite a method for enhancing a tumor suppression therapy. See examined claim 8 limitation.
Nevertheless, the prior art teachings of Polymeropoulos‘121, Adcock‘334, Platta et. al., Przychodzen, and Han et. al. as they relate to the prior art rejections of examined claims 1 – 3, and 5 – 12 are given previously in this office action and are fully incorporated here.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date modify the invention of Polymeropoulos‘162 for a method of treating a patient suffering from breast cancer that overexpresses AURKA comprising administering trichostatin A (TSA) in view of Adcock‘334, Przychodzen, and/or Han et.al. that is to select a patient that is overexpressing IKZF2 and/or CD24 or under expressing CD151. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Moreover, one of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms Furthermore, one of ordinary skill in the art would have been motivated to make this modification because represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. One of ordinary skill in the art would have a reasonable expectation of success because the consequences of decreased CD151 expression in advanced prostate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line.
Claims 1 – 3, and 5 – 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 2 – 13 of U.S. Patent No. US 11737993 B2 to Polymeropoulos et. al. (Polymeropoulos’993) in view of International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form), International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form), Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226), Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract), and Han et. al. ((2020), Integrin-associated CD151 is a suppressor of prostate cancer progression, Am J Transl Res, 12, 1428 – 1442).
Polymeropoulos’993 recite a method of treating a patient suffering from multiple myeloma (MM), the method comprising: determining or having determined, from a biological sample obtained from the patient's body, that a level of expression of one or more gene selected from a group consisting of: AURKB, BIRC5, KIF11, K1F2C, TOP2A, ASPM, CKS1B, and WEE1 is indicative of overexpression; and administering to the patient an effective amount of trichostatin A (TSA), wherein the effective amount is between about 0.01 mg/kg/day and about 100 mg/kg/day and effective to decrease expression of the one or more gene. See reference claim 1. Furthermore, Polymeropoulos’993 recites the method of (reference) claim 1, where the dosage, the gene and administration modes are recited. See reference claims 2 – 13.
However, Polymeropoulos’993 fails to recite a method where the patient is selected that either overexpresses or under expressed at least one gene as recited in examined claims 1, 5, and/or 8. See examined claims 2 – 3, 6 – 7, and 9 – 12. Furthermore, Polymeropoulos’993 fails to recite a method for inhibiting tumor growth in a cancer patient. See examined claim 5. Moreover, Polymeropoulos’993 fails to recite a method for enhancing a tumor suppression therapy. See examined claim 8 limitation.
Nevertheless, the prior art teachings of Polymeropoulos‘121, Adcock‘334, Platta et. al., Przychodzen, and Han et. al. as they relate to the prior art rejections of examined claims 1 – 3, and 5 – 12 are given previously in this office action and are fully incorporated here.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date modify the invention of Polymeropoulos‘993 for treating multiple myeloma patients expressing AURKB comprising administering trichostatin A (TSA) in view of Adcock‘334, Przychodzen, and/or Han et. al. that is to select a patient that is overexpressing IKZF2 and/or CD24 or under expressing CD151. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Moreover, one of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms. Furthermore, one of ordinary skill in the art would have been motivated to make this modification because represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. One of ordinary skill in the art would have a reasonable expectation of success because the consequences of decreased CD151 expression in advanced prostate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line.
Claims 1 – 3, and 5 – 12 are rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 18 of U.S. Patent No. US 12673033 B2 to Polymeropoulos et. al. (Polymeropoulos’033) in view of International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form), International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form), Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226), Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract), and Han et. al. ((2020), Integrin-associated CD151 is a suppressor of prostate cancer progression, Am J Transl Res, 12, 1428 – 1442).
Polymeropoulos’033 recite a method of treating a patient suffering from multiple myeloma (MM), the method consisting essentially of: administering to the patient an amount of trichostatin A (TSA) effective to decrease expression of at least one 15 gene in the patient, the at least one gene being selected from a group consisting of: CCNB1, AURKB, CDC2, KIF11, KIF2C, TOP2A, ASPM, CKS1B, and WEE1. See reference claim 1. Furthermore, Polymeropoulos’033 recites the method of (reference) claim 1, where the dosage, the gene and administration modes are recited. See reference claims 2 – 18.
However, Polymeropoulos’033 fails to recite a method where the patient is selected that either overexpresses or under expressed at least one gene as recited in examined claims 1, 5, and/or 8. See examined claims 2 – 3, 6 – 7, and 9 – 12. Furthermore, Polymeropoulos’033 fails to recite a method for inhibiting tumor growth in a cancer patient. See examined claim 5. Moreover, Polymeropoulos’033 fails to recite a method for enhancing a tumor suppression therapy. See examined claim 8 limitation.
Nevertheless, the prior art teachings of Polymeropoulos‘121, Adcock‘334, Platta et. al., Przychodzen, and Han et. al. as they relate to the prior art rejections of examined claims 1 – 3, and 5 – 12 are given previously in this office action and are fully incorporated here.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date modify the invention of Polymeropoulos‘033 for treating multiple myeloma patients expressing AURKB comprising administering trichostatin A (TSA) in view of Adcock‘334, Przychodzen, and/or Han et. al. that is to select a patient that is overexpressing IKZF2 and/or CD24 or under expressing CD151. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Moreover, one of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms. Furthermore, one of ordinary skill in the art would have been motivated to make this modification because represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. One of ordinary skill in the art would have a reasonable expectation of success because the consequences of decreased CD151 expression in advanced prostate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line.
Claims 1 – 3, and 5 – 12 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1 – 20 of copending Application No. 19/704558 to Polymeropoulos et. al. (Polymeropoulos’558) in view of International Patent Application Publication Number WO 2015/027121 A2 to Polymeropoulos et. al. (Polymeropoulos ‘121; cited on the ISR form), International Patent Application Publication Number WO 2020012334 A1 to (Adcock‘334; cited on the ISR form), Platta et. al. ((2007), The HDAC Inhibitor Trichostatin A Inhibits Growth of Small Cell Lung Cancer Cells, Journal of Surgical Research, 142, 219 – 226), Przychodzen ((2021), Trichostatin A sensitivity signature across hematological cell lines, Journal of Clinical Oncology, 39, abstract), and Han et. al. ((2020), Integrin-associated CD151 is a suppressor of prostate cancer progression, Am J Transl Res, 12, 1428 – 1442).
Polymeropoulos’558 recite a method of treating multiple myeloma (MM), in an individual, the method comprising administering to the individual an effective amount of trichostatin A (TSA). See reference claim 1. Furthermore, Polymeropoulos’033 recites the method of (reference) claim 1, where the dosage, genes, and administration modes are recited. See reference claims 2 – 20.
However, Polymeropoulos’558 fails to recite a method where the patient is selected that either overexpresses or under expressed at least one gene as recited in examined claims 1, 5, and/or 8. See examined claims 2 – 3, 6 – 7, and 9 – 12. Furthermore, Polymeropoulos’558 fails to recite a method for inhibiting tumor growth in a cancer patient. See examined claim 5. Moreover, Polymeropoulos’558 fails to recite a method for enhancing a tumor suppression therapy. See examined claim 8 limitation.
Nevertheless, the prior art teachings of Polymeropoulos‘121, Adcock‘334, Platta et. al., Przychodzen, and Han et.al. as they relate to the prior art rejections of examined claims 1 – 3, and 5 – 12 are given previously in this office action and are fully incorporated here.
Therefore, it would have been obvious to one of ordinary skill in the art before the effective filing date modify the copending Polymeropoulos‘558 for a method treating of treating multiple myeloma comprising administering trichostatin A (TSA) in view of Adcock‘334, Przychodzen, and/or Han et. al. that is to select a patient that is overexpressing IKZF2 and/or CD24 or under expressing CD151. One of ordinary skill in the art would have been motivated to make this modification because overexpression of IKZF2 in isolated murine Tregs has been shown to increase expression of Treg related markers. Moreover, one of ordinary skill in the art would have had a reasonable expectation of success because both prior art of Adcock’334 and Polymeropoulos’121 suggest the administration of TSA in overlapping cancers which exhibit overexpression of IKZF2 and AURKA.
Moreover, one of ordinary skill in the art would have been motivated to make this modification and have a reasonable expectation of success because CD24 is highly expressed in in various hematological and solid neoplasms. Furthermore, one of ordinary skill in the art would have been motivated to make this modification because represses tumor cell growth via promoting cell-cell contact and/or counteracting the EMT-like program. One of ordinary skill in the art would have a reasonable expectation of success because the consequences of decreased CD151 expression in advanced prostate tumors via RNAi oligo or lentiviral-mediated expression of shRNAs markedly increased cell growth in an immortalized E-cadherin-positive BPH cell line.
This is a provisional nonstatutory double patenting rejection.
Conclusion
Claims 1 –3, 5 – 12 are rejected.
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