By Kevin E. Noonan --
The latest company targeted by Myriad Genetics for offering a genetic diagnostic test encompassing the human BRCA 1 and BRCA 2 genes is Invitae Corp. located in San Francisco. Myriad sued Invitae on Monday in the District of Utah, Central Divisions (Case No. 2:13-CV-01049-EJF; complaint), and the next day Invitae filed its own lawsuit, seeking a declaratory judgment, in the Northern District of California (Case No. 3-13-cv-05495; complaint). Myriad's complaint is similar to Myriad's complaints against other defendants, and includes infringement allegations relating to its mutY homolog (MUTYH) test for hereditary colon cancer in addition to its BRCA gene patent-based claims. Once again, Myriad is joined by the University of Utah Research Foundation, the Trustees of the University of Pennsylvania, HSC Research and Development Limited Partnership, and Endorecherche Inc.
This Complaint alleges that:
On September 10, 2013, Defendant announced that it would "add BRCA1 and BRCA2 testing in future product releases." At the 2013 Annual Meeting of the Association for Molecular Pathology held in Phoenix, Arizona from November 12-16, 2013, Defendant announced that it would begin offering its BRCA1 and BRCA2 analysis as part of its cancer-testing menu during the week of November 18, 2013. Defendant added BRCA1 and BRCA2 gene testing into the offered panel testing services promoted on its website on November 19, 2013. On information and belief, Defendant offers full gene sequencing and deletion/duplication analyses for the BRCA 1, BRCA 2, and MUTYH genes as part of multiple hereditary cancer panels that test cancer susceptibility using next-generation sequencing technology.
Myriad alleges infringement by Invitae's "making, manufacturing, promoting, marketing, advertising, distributing, offering for sale and selling and/or causing to be offered or sold certain "Hereditary Breast and Ovarian Cancer Syndrome," "High-Risk Hereditary Breast Cancers," "Women's Hereditary Cancers," and "Hereditary Cancer Syndromes" panel products." The specific claims Myriad alleges are infringed include the following: claim 6 of U.S. Patent No. 5,747,282; claims 7, 8, 12, 23, and 26 of U.S. Patent No. 5,753,441; claim 4 of U.S. Patent No. 6,033,857; claims 32 and 33 of U.S. Patent No. 6,051,379; claim 5 of U.S. Patent No. 6,951,721; claims 3, 4, 5, 6, 7, 8, 11, 14, 17, 18, 19 of U.S. Patent No. 7,250,497; claims 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17 and 18 of U.S. Patent No. 7,470,510; claims 10, 11, 15, 16, 17 and 19 of U.S. Patent No. 7,622,258; claims 2, 8 and 16 of U.S. Patent No. 7,838,237; claims 2, 3, 5, 9, 10 and 12 of U.S. Patent No. 7,670,776; and claims 2 and 7 of U.S. Patent No. 7,563,571.
This complaint is unlike several of Myriad's earlier complaints, insofar as Myriad is not asserting certain patents or claims that it has asserted in past complaints. These non-asserted patents and claims include:
This claim from U.S. Patent No. 5,709,999:
Claim 6: A method for detecting a germline alteration in a BRCA1 gene, said alteration selected from the group consisting of the alterations set forth in Tables 12A, 14, 18 or 19 in a human which comprises analyzing a sequence of a BRCA1 gene or BRCA1 RNA from a human sample or analyzing a sequence of BRCA1 cDNA made from mRNA from said human sample with the proviso that said germline alteration is not a deletion of 4 nucleotides corresponding to base numbers 4184-4187 of SEQ ID NO:1, wherein a germline alteration is detected by amplifying all or part of a BRCA1 gene in said sample using a set of primers specific for a wild-type BRCA1 gene to produce amplified BRCA1 nucleic acids and sequencing the amplified BRCA1 nucleic acids.
These claims of U.S. Patent No. 5,747,282:
Claim 16: A pair of single-stranded DNA primers for determination of a nucleotide sequence of a BRCA1 gene by a polymerase chin reaction, the sequence of said primers being derived from human chromosome 17q, wherein the use of said primers in a polymerase chain reaction results in the synthesis of DNA having all or part of the sequence of the BRCA1 gene.
Claim 17: The pair of primers of claim 16 wherein said BRCA1 gene has the nucleotide sequence set forth in SEQ ID NO:1.
These claims of U.S. Patent No. 5,837,492:
Claim 29. A pair of single-stranded DNA primers of at least 15 nucleotides in length for determination of the nucleotide sequence of a BRCA2 gene by a polymerase chain reaction, the sequence of said primers being isolated from human chromosome 13, wherein the use of said primers in a polymerase chain reaction results in the synthesis of DNA comprising all or at least 15 contiguous nucleotides of the BRCA2 gene.
Claim 30. The pair of primers of claim 29 wherein said BRCA2 gene has the nucleotide sequence set forth in SEQ ID NO:1.
These claims of U.S. Patent No. 5,654,155:
Claim 2. A method of identifying individuals having a BRCA1 gene with a BRCA1 coding sequence not associated with breast or ovarian cancer comprising:
a) amplifying a DNA fragment of an individual's BRCA1 coding sequence using an oligonucleotide primer which specifically hybridizes to sequences within the gene;
b) sequencing said amplified fragment by dideoxy sequencing;
c) repeating steps (a) and (b) until said individual's BRCA1 coding sequence is completely sequenced;
d) comparing the sequence of said amplified DNA to the sequence of SEQ. ID. NO: 1;
e) determining the presence or absence of each of the following polymorphic variations in said individual's BRCA1 coding sequence:
AGC and ACT at position 2201, TTG and CTG at position 2430, CCG and CTG at position 2731, GAA and GGA at position 3232, AAA and AGA at position 3667, TCT and TCC at position 4427, and ACT and GGT at position 4956;
f) determining any sequence differences between said individual's BRCA1 coding sequences and SEQ. ID. NO: 1 wherein the presence of any of the said polymorphic variations and the absence of a polymorphism outside of positions 2201, 2430, 2731, 3232, 3667, 4427, and 4956, is correlated with an absence of increased genetic susceptibility to breast or ovarian cancer resulting from a BRCA1 mutation in the BRCA1 coding sequence.
Claim 3. A method according to claim 2 wherein said oligonucleotide primer is labeled with a radiolabel, a fluorescent label, a bioluminescent label, a chemiluminescent label or an enzyme label.
Claim 4. A method of detecting an increased genetic susceptibility to breast and ovarian cancer in an individual resulting from the presence of a mutation in the BRCA1 coding sequence, comprising:
a) amplifying a DNA fragment of an individual's BRCA1 coding sequence using an oligonucleotide primer which specifically hybridizes to sequences within the gene;
b) sequencing said amplified fragment by dideoxy sequencing;
c) repeating steps (a) and (b) until said individual's BRCA1 coding sequence is completely sequenced;
d) comparing the sequence of said amplified DNA to the sequence of SEQ. ID. NO: 1;
e) determining any sequence differences between said individual's BRCA1 coding sequences and SEQ. ID. NO: 1 to determine the presence or absence of polymorphisms in said individual's BRCA coding sequences wherein a polymorphism which is not any of the following:
AGC or AGT at position 2201, TTG or CTG at position 2430, CCG or CTG at position 2731, GAA or GGA at position 3232, AAA or AGA at position 3667, TCT or TCC at position 4427, and AGT or GGT at position 4956;
is correlated with the potential of increased genetic susceptibility to breast or ovarian cancer resulting from a BRCA1 mutation in the BRCA1 coding sequence.
These claims of U.S. Patent No. 5,750,400:
Claim 2. A method of identifying individuals having a BRCA1 gene with a BRCA1 coding sequence not associated with ovarian or breast cancer disease, comprising:
(a) amplifying a DNA fragment of an individual's BRCA1 coding sequence using an oligonucleotide primer which specifically hybridizes to sequences within the gene;
(b) sequencing said amplified DNA fragment by dideoxy sequencing;
(c) repeating steps (a) and (b) until said individual's BRCA1 coding sequence is completely sequenced;
(d) comparing the sequence of said amplified DNA fragment to a BRCA1(omi) DNA sequence selected from the group consisting of: SEQ ID NO: 1 together with SEQ ID NO: 3, SEQ ID NO: 1 together with SEQ ID NO: 5, SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 1 together with SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 3 and SEQ ID NO: 5;
(e) determining the presence or absence of each of the following polymorphic variations in said individual's BRCA1 coding sequence:
(i) C and T at position 2201,
(ii) T and C at position 2430,
(iii) C and T at position 2731,
(iv) A and G at position 3232,
(v) A and G at position 3667,
(vi) T and C at position 4427, and
(vii) A and G at position 4956;
(f) determining any sequence differences between said individual's BRCA1 coding sequences and a BRCA1(omi) DNA sequence selected from the group consisting of: SEQ ID NO: 1 together with SEQ ID NO: 3, SEQ ID NO: 1 together with SEQ ID NO: 5, SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 1 together with SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 3 and SEQ ID NO: 5, wherein the presence of said polymorphic variations and the absence of a variation outside of positions 2201, 2430, 2731, 3232, 3667, 4427 and 4956 is correlated with an absence of increased genetic susceptibility to breast or ovarian cancer resulting from a BRCA1 mutation in the BRCA1 coding sequence.
Claim 3. A method of identifying individuals having a BRCA1 gene with a BRCA1 coding sequence not associated with ovarian or breast cancer disease, comprising:
(a) amplifying a DNA fragment of an individual's BRCA1 coding sequence using an oligonucleotide primer which specifically hybridizes to sequences within the gene;
(b) sequencing said amplified DNA fragment by dideoxy sequencing;
(c) repeating steps (a) and (b) until said individual's BRCA1 coding sequence is completely sequenced;
(d) comparing the sequence of said amplified DNA fragment to a BRCA1(omi)) DNA sequence selected from the group consisting of: SEQ ID NO: 1 together with SEQ ID NO: 3, SEQ ID NO: 1 together with SEQ ID NO: 5, SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 1 together with SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 3 and SEQ ID NO: 5;
(e) determining the presence or absence of each of the following polymorphic variations in said individual's BRCA1 coding sequence:
(i) C and T at position 2201,
(ii) T and C at position 2430,
(iii) C an d T at position 2731,
(iv) A and G at position 3232,
(v) A and G at position 3667,
(vi) T and C at position 4427, and
(vii) A and G at position 4956; and
(f) determining any sequence differences between said individual's BRCA1 coding sequences and a BRCA1(omi) DNA sequence selected from the group consisting of: SEQ ID NO: 1 together with SEQ ID NO: 3, SEQ ID NO: 1 together with SEQ ID NO: 5, SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 1 together with SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 3 and SEQ ID NO: 5, wherein the presence of said polymorphic variations and the absence of a variation outside of positions 2201, 2430, 2731, 3232, 3667, 4427 and 4956 is correlated with an absence of increased genetic susceptibility to breast or ovarian cancer resulting from a BRCA1 mutation in the BRCA1 coding sequence;
wherein codon variations occur at the following frequencies, respectively, in a Caucasian population of individuals with no family history of breast or ovarian cancer:
(i) at position 2201, C and T occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively;
(ii) at position 2430, T and C occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively;
(iii) at position 2731, C and T occur at frequencies from about 25 to about 35%, and from about 65 to about 75%, respectively;
(iv) at position 3232, A and G occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively;
(v) at position 3667, A and G occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively;
(vi) at position 4427, T and C occur at frequencies from about 45 to about 55%, and from about 45 to about 55%, respectively; and
(vii) at position 4956, A and G occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively.
Claim 4. A method according to claims 2 or 3, wherein said oligonucleotide primer is labeled with a radiolabel, a fluorescent label, a bioluminescent label, a chemiluminescent label, or an enzyme label.
Claim 5. A method of detecting an increased genetic susceptibility to breast and ovarian cancer in an individual resulting from the presence of a mutation in the BRCA1 coding sequence, comprising:
(a) amplifying a DNA fragment of an individual's BRCA1 coding sequence using an oligonucleotide primer which specifically hybridizes to sequences within the gene;
(b) sequencing said amplified DNA fragment by dideoxy sequencing;
(c) repeating steps (a) and (b) until said individual's BRCA1 coding sequence is completely sequenced;
(d) comparing the sequence of said amplified DNA fragment to a BRCA1(omi) DNA sequence selected from the group consisting of: SEQ ID NO: 1 together with SEQ ID NO: 3, SEQ ID NO: 1 together with SEQ ID NO: 5, SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 1 together with SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 3 and SEQ ID NO: 5;
(e) determining any sequence differences between said individual's BRCA1 coding sequences and a BRCA1(omi) DNA sequence selected from the group consisting of: SEQ. ID. NO.: 1 together with SEQ ID NO: 3, SEQ ID NO: 1 together with SEQ ID NO: 5, SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 1 together with SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 3 and SEQ ID NO: 5 in order to determine the presence or absence of base changes in said individual's BRCA1 coding sequence wherein a base change which is not any one of the following:
(i) C and T at position 2201,
(ii) T and C at position 2430,
(iii) C and T at position 2731,
(iv) A and G at position 3232,
(v) A and G at position 3667,
(vi) T and C at position 4427, and
(vii) A and G at position 4956, is correlated with the potential of increased genetic susceptibility to breast or ovarian cancer resulting from a BRCA1 mutation in the BRCA1 coding sequence.
Claim 6. A method of detecting an increased genetic susceptibility to breast and ovarian cancer in an individual resulting from the presence of a mutation in the BRCA1 coding sequence, comprising:
(a) amplifying a DNA fragment of an individual's BRCA1 coding sequence using an oligonucleotide primer which specifically hybridizes to sequences within the gene;
(b) sequencing said amplified DNA fragment by dideoxy sequencing;
(c) repeating steps (a) and (b) until said individual's BRCA1 coding sequence is completely sequenced;
(d) comparing the sequence of said amplified DNA fragment to a BRCA1(omi) DNA sequence selected from the group consisting of: SEQ ID NO: 1 together with SEQ ID NO: 3, SEQ ID NO: 1 together with SEQ ID NO: 5, SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 1 together with SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 3 and SEQ ID NO: 5;
(e) determining any sequence differences between said individual's BRCA1 coding sequences and a BRCA1(omi) DNA sequence selected from the group consisting of: SEQ ID NO: 1 together with SEQ ID NO: 3, SEQ ID NO: 1 together with SEQ ID NO: 5, SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 1 together with SEQ ID NO: 3 together with SEQ ID NO: 5, SEQ ID NO: 3 and SEQ ID NO: 5 in order to determine the presence or absence of base changes in said individual's BRCA1 coding sequence wherein a base change which is not any one of the following:
(i) C and T at position 2201,
(ii) T and C at position 2430,
(iii) C and T at position 2731,
(iv) A and G at position 3232,
(v) A and G at position 3667,
(vi) T and C at position 4427, and
(vii) A and G at position 4956, is correlated with the potential of increased genetic susceptibility to breast or ovarian cancer resulting from a BRCA1 mutation in the BRCA1 coding sequence, wherein codon variations occur at the following frequencies, respectively, in a Caucasian population of individuals with no family history of breast or ovarian cancer:
(i) at position 2201, C and T occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively;
(ii) at position 2430, T and C occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively;
(iii) at position 2731, C and T occur at frequencies from about 25 to about 35%, and from about 65 to about 75%, respectively;
(iv) at position 3232, A and G occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively;
(v) at position 3667, A and G occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively;
(vi) at position 4427, T and C occur at frequencies from about 45 to about 55%, and from about 45 to about 55%, respectively; and
(vii) at position 4956, A and G occur at frequencies from about 35 to about 45%, and from about 55 to about 65%, respectively.
Claim 7. A method according to claims 5 or 6, wherein said oligonucleotide primer is labeled with a radiolabel, a fluorescent label, a bioluminescent label, a chemiluminescent label, or an enzyme label.
This claim from U.S. Patent No. 6,083,698:
Claim 73. A chip array having "n" elements for performing allele specific sequence-based techniques comprising:
a solid phase chip and
oligonucleotides having "n" different nucleotide sequences,
wherein "n" is an integer greater than one, p1 wherein said oligonucleotides are bound to said solid phase chip in a manner which permits said oligonucleotides to effectively hybridize to complementary oligonucleotides or polynucleotides,
wherein oligonucleotides having different nucleotide sequence are bound to said solid phase chip at different locations so that a particular location on said solid phase chip exclusively binds oligonucleotides having a specific nucleotide sequence, and
wherein at least one oligonucleotide is an oligonucleotide that is an isolated nucleotide that hybridizes to either a normal or a mutant BRCA1 gene selected from the group consisting of:
a first oligonucleotide for detecting a deletion of a nucleotide in intron 6 at nucleotide number 421-2 of a BRCA1 gene sequence, wherein said first oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 421-2 of the BRCA1 gene,
a second oligonucleotide for detecting a deletion of two nucleotides at nucleotide number 815 of a BRCA1 gene sequence, wherein said second oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 815 of the BRCA1 gene,
a third oligonucleotide for detecting an insertion of 10 nucleotides at nucleotide number 926 of a BRCA1 gene sequence, wherein said third oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 926 of the BRCA1 gene,
a fourth oligonucleotide for detecting a deletion of one nucleotide at nucleotide number 1506 of a BRCA1 gene sequence, wherein said fourth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 1506 of the BRCA1 gene,
a fifth oligonucleotide for detecting a mutation of one nucleotide at nucleotide number 2034 of a BRCA1 gene sequence, wherein said fifth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 2034 of the BRCA1 gene,
a sixth oligonucleotide for detecting an amino acid change from serine to a stop codon at codon 770 of a BRCA1 gene sequence, wherein said sixth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 2428 of the BRCA1 gene,
a seventh oligonucleotide for detecting an amino acid change from tryptophan to a stop codon at codon 1508 of a BRCA1 gene sequence, wherein said seventh oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 4643 of the BRCA1 gene,
an eighth oligonucleotide for detecting a deletion of one nucleotide at nucleotide number 5053 of a BRCA1 gene sequence, wherein said eighth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 5053 of the BRCA1 gene,
an ninth oligonucleotide for detecting a deletion of one nucleotide at nucleotide number 5210 of a BRCA1 gene sequence, wherein said ninth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 5210 of the BRCA1 gene,
a tenth oligonucleotide for detecting an insertion of 12 nucleotides at nucleotide number 5396+40 in intron 20 of a BRCA1 gene sequence, wherein said tenth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 5396+40 of the BRCA1 gene,
an eleventh oligonucleotide for detecting a deletion of one nucleotide at nucleotide number 5150 of a BRCA1 gene sequence, wherein said eleventh oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 5150 of the BRCA1 gene,
a twelfth oligonucleotide for detecting an amino acid change from serine to a stop codon at codon 1262 of a BRCA1 gene sequence, wherein said twelfth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 3904 of the BRCA1 gene,
a thirteenth oligonucleotide for detecting an amino acid change from tyrosine to stop at nucleotide number 903 of a BRCA1 gene sequence, wherein said thirteenth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 903 of the BRCA1 gene, and
a fourteenth oligonucleotide for detecting a detecting an amino acid change from threonine to proline at nucleotide number 4164 of a BRCA1 gene sequence, wherein said fourteenth oligonucleotide specifically hybridizes to a region encompassing the nucleotide number 4164 of the BRCA1 gene.
It is unclear from the complaint whether Myriad has not asserted these claims because Invitae's genetic diagnostic methods are substantially different from the other Defendants sued in other lawsuits, or if Myriad is changing its litigation strategies at least with regard to whether it can assert claims to oligonucleotide primers and probes.
Myriad and its co-plaintiffs demand a jury trial, and request judgment of patent infringement, a preliminary and permanent injunction, an accounting and damages, delivery for destruction of all "products" that infringe any of the asserted claims, a finding of willful infringement, and a request for attorneys' fees, enhanced damages, and costs of suit.
Invitae's lawsuit seeks a declaratory judgment that its genetic diagnostic tests do not infringe any of Myriad's asserted patents and (or) that these patents are invalid. In its General Allegations, Invitae asserts that it is a CLIA-certified lab "that offers customizable, clinically-relevant next-generation sequencing-based genetic testing services." Among those services are "state of the art" genetic sequencing and testing methodologies that provide "a single test for numerous genes of interest at less than the cost of most single gene tests" currently available. These tests encompass "over 200 human genes," including the human BRCA 1 and BRCA 2 as well as the MUTYH genes that are the subject of Myriad's patents. Importantly, like Quest in its declaratory judgment action, Invitae alleges that it "performs its sequencing using a very different approach" than the ways claimed in Myriad's asserted patents.
Invitae's complaint acknowledges Myriad's complaint filed in Utah, and the company asserts that it intends to file a motion to dismiss in that action. Invitae asserts that "Myriad's filing of the Utah Action, however, makes it inescapably clear that an actual and justiciable controversy has arisen and presently exists between the parties with respect to the validity and infringement by Invitae of the Myriad Patents," justifying Invitae's attempt to have the California court grant judgment of non-infringement and/or invalidity. Invitae claims that it does not use BRCA gene-specific primers, and thus that it does not infringe any of Myriad's claims reciting primer-based hybridization or sequencing methods. In addition, like other defendants, Invitae invokes the Supreme Court (and Federal Circuit) decisions in AMP v. Myriad and the Supreme Court's Mayo v. Prometheus decision for its invalidity contentions ("A vast portion of the landscape purportedly claimed by the Myriad Patents has been washed away in the wake of the Federal Circuit and Supreme Court’s decisions" in those cases, according to Invitae).
Invitae also demands a jury trial, a declaration of non-infringement and invalidity and a finding that this is an exceptional case entitling Invitae to attorneys' fees and costs.
For those keeping score, there are now five patent infringement lawsuits pending in the District of Utah, against Ambry Genetics, Gene-by-Gene, Quest, GeneDx, and Invitae, and three declaratory judgment actions by Quest, Invitae, and Counsyl, pending in various California district courts.
For additional information regarding this and other related topics, please see:
• "Where Do We Stand?" October 31, 2013
• "Defendants' Oppose Myriad's Motions to Dismiss Antitrust Counterclaims," October 28, 2013
• "Myriad Genetics Files Amended Complaint Relating to Colon Cancer Genetic Diagnostic Testing," October 23, 2013
• "Myriad Genetics Sues Quest for Patent Infringement," October 22, 2013
• "Myriad Sues GeneDx on BRCA and Other Genetic Diagnostic Patents," October 21, 2013
• "Diagnostics Giant Quest Files Declaratory Judgment Action against Myriad Genetics," October 13, 2013
• "Bay Area Genetic Diagnostics Company Files Declaratory Judgment Action against Myriad Genetics," October 10, 2013
• "Preliminary Injunction in Myriad v. Ambry and Gene-by Gene: Myriad Replies," October 9, 2013
• "Defendants' Response to Myriad's Preliminary Injunction Motions," September 19, 2013
• "Myriad Moves to Dismiss Ambry's Antitrust Counterclaims on Noerr-Pennington Doctrine," August 28, 2013
• "Amici Submit Brief in Support of Ambry Genetics and Gene by Gene," August 27, 2013
• "Ambry Responds to Myriad Lawsuit," August 7, 2013
• "Why Does Myriad Think It Can Win BRCA Gene Lawsuits?" July 30, 2013
• "Senator Leahy Urges NIH to Use March-In Rights on Myriad BRCA Test," July 17, 2013
• "Myriad Genetics Files Infringement Suit Against Gene by Gene for Genetic Diagnostic Testing of BRCA Genes," July 10, 2013
• "Myriad Genetics Files Suit Against Ambry Genetics for Genetic Diagnostic Testing of BRCA Genes," July 9, 2013
More Misinformation Regarding the Patent System and Non-Practicing Entities
By Michael Borella and Andrew Williams --
The need for patent reform has arguably diminished. Three decisions handed down by the Supreme Court last year, Alice, Octane Fitness, LLC v. Icon Health & Fitness, Inc., and Nautilus, Inc. v. Biosig Instruments, Inc., each addressed one of the alleged weakness in the patent system that so-called trolls are thought to exploit. These cases have been credited for the drop in patent litigation seen since the end of the Court's last term. Moreover, the Patent Trial and Appeals Board ("PTAB") has been accused of becoming a patent "death squad" because of the large number of inventions that it has recently found to be unpatentable.
These articles, therefore, appear to be desperate attempts to flame the anti-patent fervor that existed last year. As we have come to expect, both articles present only one side of the story, and do not consider the negative consequences that further anti-NPE legislation could bring about, and that the Alice decision has already produced. Further, the authors make unsupported assertions, draw questionable conclusions, and exhibit a profoundly flawed understanding of patent law.
For example, as with similar articles, the Potter and Samuels's article starts from the presupposition that "our patent system is out of balance," citing the Alice decision for support. The unsuspecting reader will assume that this is a forgone conclusion. Nevertheless, it is through their explanation of how this decision and proposed legislation are meant to "solve" the supposed crisis, the authors reveal a lack of understanding of the historical and philosophical basis of the patent system.
To that point, the authors equate "trolls" with NPEs (non-practicing entities). The term NPE, however, encompasses all entities that do not manufacture products, including most universities, research institutions, and individual inventors. Interestingly, Ms. Samuels's previous organization, the EFF, accused universities of fueling the patent troll problem. Patent asserting organizations have been acknowledged by most, including the White House, to serve an important role as mediator between such NPEs and operating companies often necessary to commercialize inventions. In fact, the United States' patent system purposefully encourages such actions by making patent property rights freely assignable and eschewing a "working" requirement. This philosophy goes back to the framers of the Constitution, and allows the patent system to be accessible to everyone, not just those with abundant resources.
Potter and Samuels go on to assert, without citing any support, that NPEs "grievously injure innovators, bankrupt small companies, and waste judicial resources." Yet, the current functioning patent system is essential to the business models of these same innovators and small companies. Without patents, the innovations of a small software company can be easily reverse engineered and copied by larger players with more market clout, or foreign companies with lower overheads. Trademarks, copyrights, and trade secrets do little to help in these situations.
In addition, the authors fail to consider the fact that these "innovators" and "small companies" (or any defendant in a patent litigation case for that matter), might actually infringe a valid patent. If so, should they be allowed to freeload off the labor of others without penalty just because the patent at issue encompasses a business method or software, or happens to be owned by an NPE?
Bessen states that a recent the Government Accountability Office ("GAO") report "attributed 89 percent of the increase in patent litigation [in the 2007-2011 time frame] to software patents." This report, however, conflated actual software patents and business method patents, collectively referring to both as "software patents." In fact, the GAO found that "operating companies brought most of the patent infringement lawsuits from 2007 to 2011." Additionally, the report indicated that the number of defendants in software and business method patent litigation increased 89 percent, but the number of lawsuits increased more modestly. According to the report, the increase in the number of patent lawsuits in 2011 "was most likely influenced by the anticipation of changes in the 2011 Leahy-Smith America Invents Act (AIA), which made several significant changes to the U.S. patent system, including limiting the number of defendants in a lawsuit, causing some plaintiffs that would have previously filed a single lawsuit with multiple defendants to break the lawsuit into multiple lawsuits."
Of course, even if there was an increase in software patent litigation, it would have likely been a reflection of the increased importance of software in our everyday lives. The 2007-2011 time frame tracks the rise of the smartphone and always-on computing, dramatic growth in social media, and a multimedia streaming revolution led by Netflix and YouTube, among other factors. Like it or not, software is now an integral part of our personal and professional lives, as we carry our laptops, tablets, phones, e-readers, and digital fitness trackers with us whether we are going to work or on vacation. An increase in the number of software patents granted, as well as an increase in software patent litigation, is a natural consequence of the ubiquity of software.
Certainly, no one is denying that there are bad actors that abuse the litigation system both with regard to intellectual property rights and otherwise. However, elevating this minority of cases to be representative of the norm is not a reason to dispense with the entire system. In fact, Bessen's methodologies for assessing the cost of so-called patent trolls have been called into question. See, e.g., Schwartz & Kesan, Analyzing the Role of Non-Practicing Entities in the Patent System, Cornell Law Review, Vol. 99:2, pp. 425-56 (2014). As a result, the implications that can be drawn from the data with regard to the impact of NPEs on the system are dubious at best.
With respect to the Alice decision, both sets of authors ignore the damage that this case has already caused to the patent system. Under Alice, when determining whether a patent claim meets the statutory requirements for patent-eligibility, one must determine whether the claim is directed to a patent-ineligible law of nature, natural phenomenon, or abstract idea. If so, then one determines whether any additional claim elements transform the claim into a patent-eligible application that amounts to significantly more than the ineligible concept itself.
This two-prong test has been widely criticized for its vagueness and subjectivity. The Supreme Court refused to define what it meant by the term "abstract idea," leading to consternation among patentees, patent attorneys, and even federal judges. For instance, Judge Wu of the United States District Court for the Central District of California criticized Alice for setting forth an "I know it when I see it" test. Judge Pfaelzer, a colleague of Judge Wu, wrote that the Supreme Court's patent-eligibility cases "often confuse more than they clarify [and] appear to contradict each other on important issues."
The Supreme Court also blurred the lines between the assessment of patent-eligibility and other patentability requirements. The patent law requires that, among other things, claims must be novel and non-obvious, as well as encompassing patent-eligible subject matter. In 1981, the Supreme Court clarified that each of these inquiries were separate and distinct, and that it was "inappropriate to dissect the claims into old and new elements and then to ignore the presence of the old elements in the analysis." Alice, as well as its 2012 predecessor case Mayo Collaborative Servs. v. Prometheus Labs., Inc., turned this notion around. Now, when conducting a patentable subject matter review, claims can be analyzed element by element and compared to prior art.
As many commentators have articulated since the Mayo opinion was handed down, determining whether the breadth of a claim is appropriate is better served by conducting the well-understood and more objective and established analyses of novelty and obviousness. Despite the lack of any suggestion from Congress that patent-eligibility is to be used for these purposes, the Supreme Court, now followed by the Federal Circuit, has made patentable subject matter a perverse weapon for the unsupported rejection and invalidation of claims.
The well-understood obviousness analysis asks whether the differences between the claimed invention and the prior art would have been obvious to one of ordinary skill in the art. The Alice test, for a claim that incorporates a preexisting algorithm or a longstanding practice, inquires if the claim adds "significantly more" to that algorithm or practice. The substantive difference between the two is that the obviousness test is grounded using prior art as a reference point for what is known, while the Alice test is not. This eliminates much of the objectivity from the Alice analysis, putting thousands of patents in a state of legal uncertainty. The "validity" of such patents may depend on which judge or panel conducts the test.
Bessen goes as far as to suggest that while the Alice decision is limiting the number of granted business method patents, it hasn't gone far enough to similarly limit software patents. But why should we view patents in such sweeping terms, with the connotation that business method and software patents are inherently bad? Patents are either valid or invalid, regardless of the technology claimed therein.
Furthermore, the implication that software should not warrant patent protection unfairly singles out one of the greatest drivers of the U.S. economy over the last forty years. A major aspect of innovation is to make products and services faster, cheaper, and better. The patent system is intended to incentivize individuals and organizations to publicly disclose such inventions, and as a result receive a limited exclusive-use property right thereover. Despite contentions of the deleterious impact of a "broken" patent system on the software industry, the computer and information industry as a whole continues to grow, as evidenced by recent record-breaking stock values, billion-dollar acquisitions, and successful initial public offerings. A broad exclusion of computer-implemented inventions is illogical and disregards the fundamental tradeoff on which the system is based.
Graphic of troll (above) by JNL was modified (cropped) from a graphic available at the Wikipedia Commons, pursuant to the Free Art License. Any use of the modified graphic is subject to the same license.
Posted at 11:47 PM in Media Commentary, Patent Litigation | Permalink | Comments (8)