Claims for Patent: 8,232,053

Summary for Patent: 8,232,053

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:	13/095,342
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) determining the presence of a wild-type KRAS protein or a nucleic acid encoding a wild-type KRAS protein in a sample of said tumor or (ii) determining the presence of a KRAS protein with a mutation in codon 12 or 13 or a nucleic acid encoding a KRAS protein in a sample of said tumor with a mutation in codon 12 or 13; wherein (a) the presence of a wild-type KRAS protein or a nucleic acid encoding a wild-type KRAS protein indicates that the tumor in a human subject is responsive to treatment with cetuximab or panitumumab and (b) the presence of a KRAS protein with a mutation in codon 12 or 13 or a nucleic acid encoding a KRAS protein with a mutation in codon 12 or 13 indicates that the tumor in a human subject is resistant to treatment with cetuximab or panitumumab. 2. A method for determining whether a colorectal tumor in a human subject is not responsive to therapy with cetuximab comprising determining the presence of a KRAS protein with a mutation in codon 12 or 13 or a nucleic acid encoding a KRAS protein with a mutation in codon 12 or 13 in a sample of said tumor, wherein the presence of said mutation in codon 12 or 13 indicates that the tumor is resistant to treatment with cetuximab. 3. A method for determining whether a colorectal tumor in a human subject is not responsive to therapy with panitumumab comprising determining the presence of a KRAS protein with a mutation in codon 12 or 13 or a nucleic acid encoding KRAS protein with a mutation in codon 12 or 13 in a sample of said tumor, wherein the presence of said mutation in codon 12 or 13 indicates that the tumor is resistant to treatment with panitumumab. 4. A method for determining whether a colorectal tumor in a human subject is responsive to treatment with cetuximab, comprising determining the presence of a wild-type KRAS protein or a nucleic acid encoding a wild-type KRAS protein indicates that the tumor in a human subject is responsive to treatment with cetuximab. 5. A method for determining whether a colorectal tumor in a human subject is responsive to treatment with panitumumab, comprising determining the presence of a wild-type KRAS protein or a nucleic acid encoding a wild-type KRAS protein indicates that the tumor in a human subject is responsive to treatment with panitumumab. 6. The method of claim 1, 2, or 3, wherein said mutation in codon 12 or 13 comprises a G12A, G12C, G12D, G12R, G12S, G12V, G13C, or G13D mutation. 7. The method of claim 1, 2, or 3, wherein determination of the presence of said mutation in codon 12 or 13 in said tumor sample comprises contacting nucleic acid from said tumor sample with a nucleic acid probe that is capable of hybridizing to nucleic acid comprising a nucleic acid encoding a KRAS protein or fragment thereof, and detecting said hybridization. 8. The method of claim 1, 4, or 5, wherein determination of the presence of a nucleic acid encoding a wild-type KRAS gene protein in said tumor sample comprises contacting nucleic acid from said tumor sample with a nucleic acid probe that is capable of hybridizing to nucleic acid comprising a nucleic acid encoding a KRAS protein or fragment thereof, and detecting said hybridization. 9. The method of claim 1, 2, or 3, wherein determination of the presence of said mutation in codon 12 or 13 in said tumor sample comprises sequencing the nucleic acid encoding the KRAS protein or a fragment thereof. 10. The method of claim 1, 4, or 5, wherein determination of the presence of a nucleic acid encoding a wild-type KRAS protein in said tumor sample comprises sequencing the nucleic acid encoding the KRAS protein or a fragment thereof.

Details for Patent 8,232,053

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