Claims for Patent: 7,932,026

Summary for Patent: 7,932,026

Title:	EGFR mutations
Abstract:	The present invention relates to mutations in Epidermal Growth Factor Receptor (EGFR) and methods of detecting such mutations as well as prognostic methods method for identifying a tumors that are susceptible to anticancer therapy such as chemotherapy and/or kinase inhibitor treatment. The methods involve determining the presence of a mutated EGFR gene or mutated EGFR protein in a tumor sample whereby the presence of a mutated EGFR gene or protein indicates the tumor is susceptible to treatment.
Inventor(s):	Seshagiri; Somasekar (San Carlos, CA)
Assignee:	Genentech, Inc. (South San Francisco, CA)
Application Number:	11/145,566
Patent Claims:	1. A method for determining whether a colorectal tumor in a human subject is responsive to treatment with cetuximab or panitumumab, comprising (i) assaying for the presence of a wild-type KRAS gene encoding a glycine residue at codon 12 and 13 in a sample of said tumor or for the presence of a mutated KRAS gene in a sample of said tumor, wherein said mutated KRAS gene encodes a G12C; G12A; G12D; G12R; G12S; G12V; or G13C mutation and (ii) identifying the tumor in the human subject as responsive to treatment with cetuximab or panitumumab when the wild-type KRAS gene is present, or identifying the tumor in a human subject as not responsive to treatment with cetuximab or panitumumab when said mutated KRAS gene is present. 2. A method for determining whether a colorectal tumor in a human subject is not responsive to therapy with cetuximab or panitumumab, comprising: assaying for the presence of a KRAS gene having a mutation in a sample of said tumor, wherein said KRAS gene encodes a G12C; G12A; G12D; G12R; G12S; G12V; or G13C mutation and identifying the presence of the KRAS gene mutation indicates that the tumor is not responsive to treatment with cetuximab or panitumumab. 3. A method for identifying a colorectal tumor in a human subject that is responsive to treatment with cetuximab or panitumumab comprising (i) assaying for the presence of a wild-type KRAS gene encoding a glycine residue at codon 12 and 13 in a sample of said tumor or for the presence of a mutated KRAS gene in a sample of said tumor, wherein said mutated KRAS gene encodes a G12C; G12A; G12D); G12R; G12S; G12V; or G13C mutation and (ii) identifying the tumor in the human subject as responsive to treatment with cetuximab or panitumumab when the wild-type KRAS gene is present, or identifying the tumor in a human subject as not responsive to treatment with cetuximab or panitumumab when said mutated KRAS gene is present. 4. A method for determining whether a colorectal tumor in a human subject is responsive to treatment with panitumumab, comprising (i) assaying for the presence of a wild-type KRAS gene encoding a glycine residue at codon 12 and 13 in a sample of said tumor or for the presence of a mutated KRAS gene in a sample of said tumor, wherein said mutated KRAS gene encodes a G12C; G12A; G12D; G12R; G12S; G12V; or G13C mutation and (ii) identifying the tumor in a human subject as responsive to treatment with panitumumab when the wild-type KRAS gene is present or identifying the tumor in the human subject as not responsive to treatment with panitumumab when said mutated KRAS gene is present. 5. A method for determining whether a colorectal tumor in a human subject is responsive to treatment with cetuximab, comprising (i) assaying for the presence of a wild-type KRAS gene encoding a glycine residue at codon 12 and 13 in a sample of said tumor or for the presence of a mutated KRAS gene in a sample of said tumor, wherein said mutated KRAS gene encodes a G12C; G12A; G12D; G12R; G12S; G12V; or G13C mutation and (ii) identifying the tumor in the human subject as responsive to treatment with cetuximab when the wild-type KRAS is present or identifying the tumor in a human subject as not responsive to treatment with cetuximab when the mutated KRAS is present. 6. The method of claim 1, 2, 3, 4, or 5 wherein said KRAS gene mutation encodes a G12C mutation. 7. The method of claim 6 wherein the G12C mutation is detected using an amplification assay, a hybridization assay or by molecular cloning and sequencing. 8. The method of claim 1, 2, 3, 4, or 5 wherein said KRAS gene mutation encodes a G12A mutation. 9. The method of claim 8 wherein the G12A mutation is detected using an amplification assay, a hybridization assay or by molecular cloning and sequencing. 10. The method of claim 1, 2, 3, 4, or 5 wherein said KRAS gene mutation encodes a G12D mutation. 11. The method of claim 10 wherein the G12D mutation is detected using an amplification assay, a hybridization assay or by molecular cloning and sequencing. 12. The method of claim 1,2,3,4, or 5 wherein said KRAS gene mutation encodes a G12R mutation. 13. The method of claim 12 wherein the G12R mutation is detected using an amplification assay, a hybridization assay or by molecular cloning and sequencing. 14. The method of claim 1,2,3,4, or 5 wherein said KRAS gene mutation encodes a G12S mutation. 15. The method of claim 14 wherein the G12S mutation is detected using an amplification assay, a hybridization assay or by molecular cloning and sequencing. 16. The method of claim 1,2,3,4, or 5 wherein said KRAS gene mutation encodes a G12V mutation. 17. The method of claim 16 wherein the G12V mutation is detected using an amplification assay, a hybridization assay or by molecular cloning and sequencing. 18. The method of claim 1,2,3,4, or 5 wherein said KRAS gene mutation encodes a G13C mutation. 19. The method of claim 18 wherein the G13C mutation is detected using an amplification assay, a hybridization assay or by molecular cloning and sequencing. 20. The method of claim 1,2,3,4, or 5 in which the KRAS gene in the tumor sample is detected using a DNA amplification assay. 21. The method of claim 13 in which a polymerase chain reaction is used to amplify the KRAS gene in the tumor sample. 22. The method of claim 13 in which a ligase chain reaction is used to amplify the KRAS gene in the tumor sample. 23. The method of claim 1,2,3,4, or 5 in which a DNA hydridization assay is used to detect the KRAS gene in the tumor sample. 24. The method of claim 1,2,3,4, or 5 in which the KRAS gene in the tumor sample is molecularly cloned and sequenced.

Details for Patent 7,932,026

Applicant	Tradename	Biologic Ingredient	Dosage Form	BLA	Approval Date	Patent No.	Expiredate
Eli Lilly And Company	ERBITUX	cetuximab	Injection	125084	02/12/2004		2024-06-04
Eli Lilly And Company	ERBITUX	cetuximab	Injection	125084	03/28/2007		2024-06-04
Amgen, Inc.	VECTIBIX	panitumumab	Injection	125147	09/27/2006		2024-06-04