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 .
Claims 1-10 are the current claims hereby under examination.
Claim Objections
Claims 3-7 are objected to as each of the claims recites a reference to a Table 2 or Table 3. Claim 1 properly references the tables as Table S2 or Table S3. It is understood claims 3-7 are referencing the same tables, but indicate different identifiers. Appropriate corrections are required.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1-10 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. The claims recite a method of using at least a gene or CpG selected from Tables S2, S3 or S4 for use in a method for comparing methylation to a baseline level as an indication a subject will respond to a VLCKD. However, the tables S2-S4 comprise 44 pages in the specification of hundreds of genes and CpG sites, which results in millions of possible different combinations of at least a gene or CpG to select. The specification does not provide the requisite blaze marks for one of ordinary skill in the art to select any specific combination of at least a gene or CpG site for use in the method of methylation comparison. Without sufficient blaze marks, the specification does not appear to support the specific claimed requirement of selecting some specific combination of at least a gene or CpG site for which to perform the methylation comparison.
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.
Claim(s) 1, 4-5, and 8-10 is/are rejected under 35 U.S.C. 103 as being unpatentable over Milagro et al. (A dual epigenomic approach for the search of obesity biomarkers: DNA methylation in relation to diet-induced weight loss, FASEB Journal, vol 25, 2011, pages 1378-1389) in view of Jacobsen et al. (Effects of short-term high-fat overfeeding on genome-wide DNA methylation in the skeletal muscle of healthy young men, Diabetologia (2012) vol 55, pages 3341-3349) and further in view of Larkin et al. (Epigenetic regulation of ILDR2 in the cord blood of obese mothers, Translational Metabolic Syndrome Research, vol. 3, 2020, pages 6-8).
Milargo et al. teach a correlation via comparison of DNA methylation patterns in specific CpG genomic sites to high and low responders from a hypocaloric diet. Milargo et al. Milargo et al. teach that baseline DNA methylation patterns may be used for comparison against altered DNA methylation status of specific genes as epigenetic markers that could help predict weigh loss.
Milargo et al. suggest but do not explicitly teach looking at the level of DNA methylation for comparison of least one gene from one of the tables in claim 1. Milargo et al. suggests this because they teach the same methodology as claimed with regards to evaluating the DNA methylation of particular genes by comparing it to a baseline level for significance in order to predict weight loss from a low calorie diet.
Jacobsen et al. establishes that it is known where diet impacts the DNA methylation across the genome. Jacobsen et al. establishes this via a high-fat overfeeding diet on genome-wide DNA methylation, see abstract. Jacobsen et al. teach that diet can induce transient genome-wide DNA methylation that impacts metabolic disease. They teach this by demonstrating that a high-fat overfeeding diet introduced widespread DNA methylation affecting 45% of genes wherein the expression levels of said genes were little changed but the DNA methylation across the genome was a useful marker. As such, Jacobsen et al. teach that looking at genome-wide DNA methylation in light of diet may be an indicator for various things, such as metabolic disease. As such, they suggest that when looking at DNA methylation, looking at anywhere in the genome for evaluating levels of DNA methylation in light of diet can be helpful. Therefore, the genome-wide DNA methylation level evaluation encompasses the genes of the claimed tables wherein at least one or more genes are evaluated for its DNA methylation.
Jacobsen et al. suggests but do not explicitly teach evaluating the methylation level of at least one of the specific genes from one of the tables claimed.
Jacobsen et al. suggests this because they take a genome-wide DNA methylation approach to look at indicators associated with diet. They found that diet plays a transient role in the genome-wide DNA methylation which can be an indicator for various things. As such, they suggest that when looking at DNA methylation, looking at anywhere in the genome for evaluating levels of DNA methylation in light of diet can be helpful. Therefore, the genome-wide DNA methylation level evaluation encompasses the genes of the claimed tables wherein at least one or more genes are evaluated for its DNA methylation.
Larkin et al. teach DNA methylation found in blood of specific genes may be an indicator for things such as metabolic disease in children from in obese mothers. Larkin et al. teach wherein DNA methylation patterns may have clinical utility as a predictor, see introduction. Larkin et al. specifically teach wherein ILDR2 (one of the genes evaluated from one of the tables) and its level of DNA methylation in obese mothers was a top target for evaluation as a predictor, see results and discussion.
Milargo et al. establishes the primary framework for evaluating DNA methylation levels compared to baseline levels for predicting a response of individuals to a low calorie diet, but fails to teach measuring these levels in at least one gene from one of the tables claimed. Jacobsen et al. makes it obvious to look at genome-wide DNA methylation levels when evaluating them as predictors in light of diets. The genome-wide DNA methylation approach encompasses the genes of the claimed table, but appears to not focus on at least one specific gene from the tables of claim 1. Larkin et al. finalizes the established connection between at least one of the specific genes from one of the tables claimed (i.e. ILDR2) for evaluating DNA methylation levels in light of obesity. Therefore it would have been obvious to one of ordinary skill in the art at the time of the instant invention to have evaluated at least the ILDR2 gene DNA methylation level as taught by Larkin et al. and suggested by Jacobsen et al. for use in the method of comparing DNA methylation levels of genes to baseline levels for use as predictor for a response to a low calorie diet taught by Milargo et al. Milargo et al. established a baseline framework from which to evaluate the DNA methylation level of genes against baseline levels as a predictor for a response to a low calorie diet. The combination of Jacobsen et al. and Larkin et al. demonstrate that many genes across the genome would be good candidates for evaluating DNA methylation and specifically ILDR2 may be a highly valuable target. As such a person of ordinary skill in the art would have been motivated to combine the prior art to achieve the claimed invention and there would have been a reasonable expectation of success.
Milargo et al. at page 1386 describe hypomethylation being significant in the responding group, which reads on claim 8.
Milargo et al. teach using PCR on peripheral blood mononuclear cells, which encompasses leucocytes as in claims 9-10.
Conclusion
No claim is allowed
Any inquiry concerning this communication or earlier communications from the examiner should be directed to Jason Sims, whose telephone number is (571)-272-7540.
If attempts to reach the Examiner by telephone are unsuccessful, the Examiner’s supervisor, Jonathan Moffat can be reached via telephone (571)-272-4390.
Papers related to this application may be submitted to Technical Center 1600 by facsimile transmission. Papers should be faxed to Technical Center 1600 via the Central PTO Fax Center. The faxing of such papers must conform with the notices published in the Official Gazette, 1096 OG 30 (November 15, 1988), 1156 OG 61 (November 16, 1993), and 1157 OG 94 (December 28, 1993) (See 37 CFR § 1.6(d)). The Central PTO Fax Center number is (571)-273-8300.
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/JASON M SIMS/Supervisory Patent Examiner, Art Unit 3791
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