Abstract: The disclosure provides compositions and methods for detecting and predicting acquired resistance to anti-EGFR treatment in colorectal cancers. Also provided are compositions and methods of preventing, reversing or delaying the acquired resistance. The present disclosure also provides kits for use in the methods described herein.

Abstract: The disclosure provides compositions and methods for detecting and predicting acquired resistance to anti-EGFR treatment in colorectal cancers. Also provided are compositions and methods of preventing, reversing or delaying the acquired resistance. The present disclosure also provides kits for use in the methods described herein.

Abstract: The disclosure provides compositions and methods for detecting and predicting acquired resistance to anti-EGFR treatment in colorectal cancers. Also provided are compositions and methods of preventing, reversing or delaying the acquired resistance. The present disclosure also provides kits for use in the methods described herein.

Abstract: The present application relates to K-ras mutations, to polynucleotides encoding mutant K-ras polypeptides, and to methods of identifying K-ras mutations. The present application also relates to B-raf mutations, to polynucleotides encoding mutant B-raf polypeptides, to vectors containing those polynucleotides, and to methods of identifying B-raf mutations. The present application also relates to methods of diagnosing cancer; and methods and kits for predicting the usefulness of anti-EGFr specific binding agents in the treatment of tumors.

Abstract: Methods of predicting whether an anti-epidermal growth factor receptor (“EGFr”)-specific binding agent treatment will be efficacious in treating cancer, and methods of treating patients with anti-EGFr-specific binding agents, are provided.

Abstract: The invention relates to an indidualized and personalized diagnosis and therapy of cancer based on specific molecular alterations which occur in specific tumor tissue of specific tumor patient populations. The therapy and diagnostic is based on the findings that proliferation and tumor growth of specific EGFR bearing tumor tissue expressing an amplified EGFR gene copy number may be abolished by anti-EGFR antibodies, while other individual molecular alterations such as mutations occurring in tumor tissues are unaffected by the same anti-EGFR antibody treatment.

Abstract: The present application relates to K-ras mutations, to polynucleotides encoding mutant K-ras polypeptides, and to methods of identifying K-ras mutations. The present application also relates to B-raf mutations, to polynucleotides encoding mutant B-raf polypeptides, to vectors containing those polynucleotides, and to methods of identifying B-raf mutations. The present application also relates to methods of diagnosing cancer; and methods and kits for predicting the usefulness of anti-EGFr specific binding agents in the treatment of tumors.

Abstract: Methods of predicting whether an anti-epidermal growth factor receptor (“EGFr”)-specific binding agent treatment will be efficacious in treating cancer, and methods of treating patients with anti-EGFr-specific binding agents, are provided.