DETAILED ACTION
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
The claim listing filed December 22, 2025 is pending.
Claims 1-20 are pending.
Election/Restriction
Applicant’s election of Invention I (claims 1-8, drawn to a method of treating a subject having a HER2 non-amplified (HER2- negative) cancer or low HER2 expressing (HER2-low) cancer); and the species of HER2 non-amplified (HER2-negative) breast cancer, luminal A breast cancer, a HER2-targeted cancer treatment, lapatinib, LITAF, SEQ ID NO: 1, and the wild type exon 4 of BCAR4 in the reply filed on December 22, 2025 is acknowledged.
Because the Applicant did not distinctly and specifically point out the supposed errors in the restriction requirement, the election has been treated as an election without traverse (MPEP § 818.01(a)).
Claims 9-20 have been withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions.
Claims 1-8 are currently under consideration.
Claim 1 is an independent claim.
Priority
The present application claims domestic benefit PRO 63/342,274 filed 05/16/2022.
Claim Rejections - 35 USC § 112
Enablement
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 1-8 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specification, while being enabling for a method of treating a subject having a HER2 non-amplified (HER2-negative) cancer, the method comprising: (1) providing a biological sample from the subject; (2) detecting expression of a BCAR4 gene fusion comprising a 5’ untranslated regulatory exon and the 4th exon of BCAR4 comprising an ORF in the biological sample; and (3) administering lapatinib or trastuzumab to the subject if expression of the BCAR4 gene fusion is detected; does not reasonably provide enablement for a method of treating a subject having a HER2 non-amplified (HER2-negative) cancer, the method comprising: (1) providing a biological sample from the subject; (2) detecting expression of any BCAR4 gene fusion in the biological sample; and (3) administering any HER2-targeted cancer treatment to the subject if expression of the BCAR4 gene fusion is detected.
The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
The factors considered in determining whether a disclosure would require undue experimentation include:
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure.
In re Wands, 8 USPQ2d, 1400 (CAFC 1988) and MPEP § 2164.01.
Nature of the invention/Breadth of the claims
The instant claims are drawn to method of treating a subject having a HER2 non-amplified (HER2-negative) cancer, the method comprising: (1) providing a biological sample from the subject; (2) detecting expression of any BCAR4 gene fusion in the biological sample; and (3) administering any HER2-targeted cancer treatment to the subject if expression of the BCAR4 gene fusion is detected.
Claim 2 limits the genus of BCAR4 gene fusions to those that comprise a nucleotide sequence derived from LITAF.
Claim 3 limits the genus of BCAR4 gene fusions to those that comprise wildtype exon 4 of the BCAR4 gene.
Claim 4 limits the genus of BCAR4 gene fusions to those that comprise a nucleotide sequence encoding a peptide comprising SEQ ID NO: 1.
Claim 8 limit the genus of HER2-targeted cancer treatments to lapatinib.
State of the prior art/Predictability of the art
Regarding the claimed genus of HER2-targeted cancer treatments, as noted above, the Applicant has disclosed that this includes monoclonal antibodies and antibody-drug conjugates. Regarding anti-HER2 antibodies, specifically, artisans are well aware that knowledge of a given antigen (for instance HER2) provides no information concerning the sequence/structure of antibodies that bind the given antigen. For example, Edwards et al. (J. Mol. Biol., 2003, 334:103-118) teach that over 1,000 different antibodies to a single protein can be generated, all with different sequences spanning almost the entire heavy and light chain germline repertoire (42/49 functional heavy chain germlines and 33 of 70 V-lambda and V-kappa light chain germlines, and with extensive diversity in the HCDR3 region sequences (that are generated by VDJ germline segment recombination) as well, see entire document).
As such, it does not seem possible to predict the sequence/structure of an antibody that binds a given antigen, as there does not appear to be any common or core structure present within all antibodies that gives rise to the function of antigen binding. Further, given data, such as that of Edwards et al., indicating the diversity of sequences in a population of antibodies that bind to a given antigen, no number of species appears to reasonably representative of the breadth of the genus of antibodies that bind the given antigen.
It should be pointed out that it is well established in the art that the formation of an intact antigen-binding site requires the association of the complete heavy and light chain variable regions of a given antibody, each of which consists of three different complementarity determining regions, CDR1, 2 and 3, which provide the majority of the contact residues for the binding of the antibody to its target epitope. The amino acid sequences and conformations of each of the heavy and light chain CDRs are critical in maintaining the antigen binding specificity and affinity which is characteristic of the parent immunoglobulin (Janeway Jr et al., Immunology, 3rd Edition, 1997 Garland Publishing Inc., pages 3:1-3:11.see entire selection).
Thus, based upon the prior art, skilled artisans would reasonably understand that it is the structure of the CDRs within an antibody which gives rise to the functional property of antigen binding, the epitope to which said CDRs bind is an inherent property which appears to necessarily be present due to conservation of critical structural elements, namely the CDR sequences themselves.
This applies to the instant invention that is drawn to a subgenus of HER2-targeted cancer treatments that encompass anti-HER2 antibodies.
Regarding the subgenera of HER2-targeted cancer treatments that encompass small molecule inhibitors, shRNA, siRNA, and sgRNA, the same logic applies. HER2-targeted cancer treatments comprising small molecule inhibitors, shRNA, siRNA, or sgRNA as the HER2-binding component still require very precise structure in order confer binding function.
Regarding the claimed genus of BCAR4 gene fusions, Nickless et al. 2022 (Mol Cancer Res. 20 (10): 1481–1488) teach that chromosomal rearrangements often result in active regulatory regions juxtaposed upstream of an oncogene to generate an expressed gene fusion (e.g. see Abstract). Repeated activation of a common downstream partner–with differing upstream regions across a patient cohort–suggests a conserved oncogenic role. Analysis of 9,638 patients across 32 solid tumor types revealed an annotated long noncoding RNA (lncRNA), Breast Cancer Anti-Estrogen Resistance 4 (BCAR4), a known oncogene (e.g. see page 1486, paragraph spanning left and right columns), was the most prevalent, uncharacterized, downstream gene fusion partner occurring in 11 cancers. Its oncogenic role was confirmed using multiple cell lines with endogenous BCAR4 gene fusions. Furthermore, overexpressing clinically prevalent BCAR4 gene fusions in untransformed cell lines was sufficient to induce an oncogenic phenotype. Nickless et al. teach that the minimum common region to all gene fusions harbors an open reading frame (ORF) that is necessary to drive proliferation (e.g. see Abstract).
All of the functional oncogenic BCAR4 gene fusions taught by Nickless et al. comprise a 5′ partner (mostly involving only the first untranslated regulatory exon of the 5′ gene) and exon 4 of BCAR4 which comprises an ORF (e.g. see paragraph spanning pages 1486 and 1487; and page 1487, left column, second paragraph).
This applies to the instant invention that is drawn to a genus of BCAR4 gene fusions which encompass species that do not comprise a 5′ partner and exon 4 of BCAR4 comprising an ORF. The art teaches that BCAR4 gene fusions lacking these elements would not have oncogenic function.
Working examples/Guidance in the specification
Regarding the claimed genus of BCAR4 gene fusions, the Applicant has disclosed that most expressed BCAR4 gene fusion transcripts include early exons of 5' partners spliced upstream of exon 4 of BCAR4 (e.g. see page 53, lines 19-20). This suggests that exon 4 of BCAR4, which harbors an open reading frame (ORF), is the minimum region necessary to drive its function (e.g. see page 53, lines 20-22, and page 106, lines 8 and 9).
The two most common 5' partners are the first untranslated exons of ZC3H7A and LITAF juxtaposed to the 4th BCAR4 exon (e.g. see page 117, lines 23-25). This results in the regulatory regions (5’ partners) serving as a switch to activate the 4th BCAR4 exon (e.g. see page 117, lines 25 and 26). The 4th BCAR4 exon contains a predicted ORF, which is common to both LITAF-BCAR4 and ZC3H7A-BCAR4 fusions (e.g. see page 118, lines 12-14). A mutant gene fusion construct was made disrupting the ATG start site of the ORF to determine if the protein function was necessary for oncogenesis (e.g. see page 118, lines 14-16). Benign epithelia cells expressing mut LITAF-BCAR4 had fewer S-phase cells than cells expressing wild-type fusions which suggests that the truncated BCAR4 protein, and therefore the ORF-containing 4th exon, is important for observed oncogenic phenotypes (e.g. see page 118, lines 16-19).
Ultimately, the Applicant discloses that truncated BCAR4 proteins behave similar to full length BCAR4 in promoting oncogenesis (e.g. see page 118, lines 29 and 30). Therefore, BCAR4-encoding gene fusions (comprising a 5’ untranslated regulatory exon and the 4th exon of BCAR4 comprising an ORF) are functional, activate HER2, sensitize cells to lapatinib (a HER2-targeted small molecule inhibitor), and promote aggressive disease in breast cancer (e.g. see page 118, lines 30-33).
The Applicant discloses that BCAR4 protein is localized to the plasma membrane and directly interacts with HER2 receptor to activate it (e.g. see page 126, lines 17 and 18). Furthermore, the BCAR4 protein causes otherwise HER2-negative/low cells to respond to HER2-targeted therapies (e.g. see page 126, line 32). It has been shown that full length BCAR4-expressing HER2-negative/low cells respond to lapatinib treatment (e.g. see page 126, lines 32 and 33). The Applicant also discloses that BCAR4 gene fusion-expressing HER2-negative/low cells also respond to lapatinib and trastuzumab which is dependent on the encoded peptide of the 4th exon of BCAR4 (e.g. see page 127, lines 1-5).
Regarding the claimed genus of HER2-targeted cancer treatments, the Applicant has disclosed many HER-targeted cancer treatments including nine specific monoclonal antibodies, three specific antibody-drug conjugates, and five specific small molecule inhibitors (e.g. see page 26, lines 16-25). The Applicant has also disclosed that the HER-targeted cancer treatment may be a short hairpin RNA (shRNA), a short interfering RNA (siRNA), or a single guide RNA (sgRNA) (e.g. see page 26, lines 26-29).
It is noted that the Applicant has disclosed two working examples of treating HER2-negative breast cancer by detecting a LITAF-BCAR4 gene fusion and administering lapatinib (small molecule inhibitor) and trastuzumab (monoclonal antibody) as the HER-targeted cancer treatments (e.g. see page 18, lines 24-29; and page 127, lines 6-20).
Amount of experimentation necessary
The instant specification discloses two working examples of treating HER2-negative breast cancer by detecting a LITAF-BCAR4 gene fusion and administering lapatinib (small molecule inhibitor) or trastuzumab (monoclonal antibody) as the HER-targeted cancer treatments. The Applicant also discloses that BCAR4-encoding gene fusions comprising a 5’ untranslated regulatory exon and the 4th exon of BCAR4 (which comprises an ORF) behave similarly to full length BCAR4 in promoting oncogenesis and sensitize HER2-negative cancer cells to the HER2-targeted treatments lapatinib and trastuzumab. The Applicant further discloses many HER-targeted cancer treatments which include nine specific monoclonal antibodies, three specific antibody-drug conjugates, and five specific small molecule inhibitors (e.g. see page 26, lines 16-25), including lapatinib and trastuzumab.
The claimed method encompass a method of treating a subject having a HER2 non-amplified (HER2-negative) cancer, the method comprising: (1) providing a biological sample from the subject; (2) detecting expression of any gene fusion that comprises any part of the BCAR4 gene and that expresses BCAR4; and (3) administering any cancer treatment that targets HER2 to the subject if expression of the BCAR4 gene fusion is detected. There is insufficient objective evidence that the disclosed methods of treating HER2-negative cancer by detecting a LITAF-BCAR4 gene fusion that comprises a 5’ untranslated regulatory exon and the 4th exon of BCAR4 (which comprises an ORF) and administering lapatinib or trastuzumab can be extrapolated to provide guidance and direction for the claimed method of treating a subject having a HER2 non-amplified (HER2-negative) cancer, the method comprising: (1) providing a biological sample from the subject; (2) detecting expression of any BCAR4 gene fusion in the biological sample; and (3) administering any HER2-targeted cancer treatment to the subject if expression of the BCAR4 gene fusion is detected.
Thus, based on the content of the disclosure in view of the prior art regarding the unpredictability of identifying a HER2-targeted cancer treatment simply on the basis of what it targets rather than by identifying the sequence/structure, namely the CDRs or molecular structure, of the HER2-targeted cancer treatment in question; and BCAR4 gene fusions lacking a 5′ partner and exon 4 of BCAR4 comprising an ORF not having oncogenic function, a skilled artisan, through extensive trial-and-error experimentation, would have to identify BCAR4 gene fusions and HER2-targeted cancer treatments and then use them in the claimed method of treating HER2-negative cancer with a reasonable expectation of success. This quantity of experimentation goes beyond what is considered “a reasonable degree of experimentation” and constitutes undue further experimentation in order to enable the method for the breadth of what is claimed. A person of ordinary skill in the art would have to perform undue experimentation in order to use any BCAR4 gene fusion to identify HER2-negative cells that are sensitive to any HER2-tartgeted treatment commensurate in scope with the breadth of the claims.
Thus, the specification does not enable one of ordinary skill in the art to use what is claimed and therefore claims 1-8 are rejected under 35 U.S.C. 112(a).
Amending claim 1 to recite that the BCAR4 gene fusion comprises a 5’ untranslated regulatory exon and the 4th exon of BCAR4 comprising an ORF; and that the HER2-targeted cancer treatment is lapatinib or trastuzumab would obviate this part of the rejection.
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.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 1, 2, and 5-7 are rejected under 35 U.S.C. 103 as being unpatentable over Godinho et al. 2012 (Br J Cancer. 107, 947–955, an IDS reference filed 04/03/2024) in view of Vasmatzis et al. 2020 (Mayo Clin Proc. 95(2):306-318).
In view of the Applicant’s species election filed 12/22/2025, independent claim 1 is drawn to method of treating a subject having a HER2 non-amplified (HER2- negative) cancer the method comprising: (1) providing a biological sample from the subject; (2) detecting expression of a BCAR4 gene fusion in the biological sample; and (3) administering a HER2-targeted cancer treatment to the subject if expression of the BCAR4 gene fusion is detected.
Dependent claim 2 limits the BCAR4 gene fusion to that which comprises a nucleotide sequence derived from LITAF.
Dependent claims 5-7 limit the cancer to breast cancer and claim 7 further limits the breast cancer to luminal A breast cancer.
Dependent claim 8 limits the HER-targeted cancer treatment to lapatinib.
Godinho et al. teach that BCAR4 expression sensitizes two luminal A HER2-negative/low breast cancer cell lines (ZR-75-1 and MCF7) to lapatinib, a HER2-targeted small molecule inhibitor, by activating HER2 receptors (e.g. see page 952, left column, second paragraph, and page 953, left column, second paragraph). HER2 is present but not overexpressed nor amplified in ZR-75-1 and MCF7 cell lines (e.g. see page 953, paragraph spanning left and right columns). BCAR4 activates HER2 signaling in these cells thereby sensitizing the otherwise HER2-treatment resistant cells to HER2-targeted therapy, such as lapatinib (e.g. see page 953, paragraph spanning left and right columns).
Godinho et al. further teach that activated HER2 has been found in oestrogen receptor-α (ER)-positive tumors classified as negative for HER2 expression according to the standard criteria (e.g. see page 953, right column, second paragraph). Moreover, evidence shows that some tumors scoring negative for HER2 expression benefit from trastuzumab therapy (an anti-HER2 antibody). Godinho et al. also teach that treatment with HER2-targeted therapies is restricted to patients with breast cancers overexpressing HER2 (i.e. HER2-positive cancers). Godinho et al. teach that until their study, there were no biomarkers to select patients with ER-positive/HER2-negative tumors, which are dependent on HER2 signaling, and may benefit from HER2-targeted therapies (e.g. see page 953, right column, second paragraph).
Godinho et al. teach that co-expression of BCAR4 and low level of HER2 occurs frequently and that these patients may benefit from a treatment comprising a HER2-targeted therapeutic (e.g. see paragraph spanning pages 953 and 954).
Godinho et al. do not teach a method of treating a subject having HER2 non-amplified (HER2-negative) cancer with a HER2-targeted cancer treatment after the detection of a BCAR4 gene fusion in a biological sample from the subject.
Vasmatzis et al. teach the BCAR4 gene fusion LITAF-BCAR4 which triggers BCAR4 overexpression (e.g. see page 306, right column, second paragraph).
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified Godinho et al. to incorporate the teachings of Vasmatzis et al. to include a method of treating a subject having HER2 non-amplified (HER2-negative) cancer with a HER2-targeted cancer treatment after the detection of a BCAR4 gene fusion in a biological sample from the subject. This is because expression of the BCAR4 protein is known sensitize traditionally resistant HER2-negative/low cancers cells to HER2-targeted therapies (Godinho et al.) and the LITAF-BCAR4 gene fusion is known to trigger the overexpression of the BCAR4 protein (Vasmatzis et al.).
Given that BCAR4 sensitizes traditionally resistant HER2-negative/low cancers cells to HER2-targeted therapies (Godinho et al.), BCAR4 is a good biomarker for identifying HER2-negative cancer patients, which are dependent on HER2 signaling, that may benefit from HER2-targeted therapies (Godinho et al.), and the LITAF-BCAR4 gene fusion is known to trigger the overexpression of the BCAR4 protein (Vasmatzis et al.); it would have been obvious to a skilled artisan, with the goal of treating patients with HER2-negative tumors, which are dependent on HER2 signaling, with HER2-targeted therapies, to test a biological sample from the HER2-negative cancer patients for the expression of a LITAF-BCAR4 gene fusion in order to select those HER2-negative cancer patients that would benefit from a HER2-targeted cancer treatment with a reasonable expectation of success. It is known that patients expressing both BCAR4 and a low level of HER2 may benefit from a treatment comprising a HER2-targeted therapeutic (Godinho et al.).
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
Claims 1, 3, and 4 are rejected under 35 U.S.C. 103 as being unpatentable over Godinho et al. 2012 (Br J Cancer. 107, 947–955, an IDS reference filed 04/03/2024) in view of Vasmatzis et al. 2020 (Mayo Clin Proc. 95(2):306-318), as applied to claim 1, and further in view of Godinho et al. 2010 (J. Cell. Physiol. 226: 1741–1749, an IDS reference filed 04/03/2024).
In view of the Applicant’s species election filed 12/22/2025, independent claim 1 is drawn to method of treating a subject having a HER2 non-amplified (HER2- negative) cancer the method comprising: (1) providing a biological sample from the subject; (2) detecting expression of a BCAR4 gene fusion in the biological sample; and (3) administering a HER2-targeted cancer treatment to the subject if expression of the BCAR4 gene fusion is detected.
Dependent claim 3 limits the BCAR4 gene fusion to that which comprises exon 4 of the BCAR4 gene.
Dependent claim 4 limits the BCAR4 gene fusion to that which comprises a nucleotide sequence encoding a peptide comprising SEQ ID NO: 1.
The combined teachings of Godinho et al. 2012 in view of Vasmatzis et al. pertaining to claim 1 and the rationale for combining them are outlined in the 103 rejection above.
The combined reference teachings do not teach that the BCAR4 gene fusion specifically comprises exon 4 of the BCAR4 gene or specifically comprises a nucleotide sequence encoding a peptide comprising SEQ ID NO: 1.
Godinho et al. 2010 teach that BCAR4 genes contain four exons and the coding region is entirely located on exon 4 (e.g. see page 1743, paragraph spanning left and right columns). Godinho et al. 2010 also teach that nucleotide sequence of the BCAR4 ORF encodes a protein that comprises instant SEQ ID NO: 1. (e.g. see page 1743, paragraph spanning left and right columns, and Figure 1). See sequence alignment below.
Query Match 14.3%; Score 87; DB 1; Length 15;
Best Local Similarity 100.0%;
Matches 15; Conservative 0; Mismatches 0; Indels 0; Gaps 0;
Qy 1 MYQPIQTYPWMNLSR 15
|||||||||||||||
Db 1 MYQPIQTYPWMNLSR 15
It would have been prima facie obvious to one of ordinary skill in the art before the effective filing date of the claimed invention to have modified the combined teachings of Godinho et al. 2012 in view of Vasmatzis et al. as applied to claim 1 and incorporate the teachings of Godinho et al. 2010 to include that the BCAR4 gene fusion specifically comprises exon 4 of the BCAR4 gene and specifically comprises a nucleotide sequence encoding a peptide comprising SEQ ID NO: 1. This is because the coding region of BCAR4 is entirely located on exon 4.
Given that BCAR4 coding region is entirely located on exon 4 of the BCAR4 gene and the nucleotide sequence of the BCAR4 ORF encodes a protein that comprises instant SEQ ID NO: 1; it would have been obvious to a skilled artisan, with the goal of selecting a BCAR4 gene fusion that expresses the BCAR4 protein, to specifically select a BCAR4 gene fusion that comprises exon 4 of BCAR gene and that comprises a nucleotide sequence encoding a peptide comprising SEQ ID NO: 1 with a reasonable expectation of success.
Combining prior art elements according to known methods to yield predictable results is obvious to one of ordinary skill in the art (see MPEP § 2143(A)). From the combined teachings of the references, it is apparent that one of ordinary skill in the art would have had a reasonable expectation of success in producing the claimed invention.
Therefore, the invention as a whole was prima facie obvious to one of ordinary skill in the art at the time the invention was made, as evidenced by the references, especially in the absence of evidence to the contrary.
Conclusion
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/GRACE H LUNDE/Examiner, Art Unit 1641
/MISOOK YU/Supervisory Patent Examiner, Art Unit 1641