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lüll KRAS mutation in colon cancer: a marker of resistance to EGFR-I therapy Siddiqui AD; Piperdi BAnn Surg Oncol 2010[Apr]; 17 (4): 1168-76INTRODUCTION AND DESIGN: The introduction of the epidermal growth factor receptor inhibitors (EGFR-I) has increased the treatment options available for patients with metastatic colorectal cancer (mCRC). Two EGFR-I agents currently approved for the treatment of mCRC are the fully human monoclonal antibody panitumumab and the mouse-human chimeric monoclonal antibody cetuximab. While these agents have demonstrated activity across multiple lines of therapy, early studies suggested that clinical benefit was confined to a subset of patients treated. Mutation of the KRAS oncogene has emerged as a powerful negative predictive biomarker to identify patients with mCRC who do not benefit from EGFR-I therapy. Multiple retrospective analyses have demonstrated that clinical benefit from treatment with EGFR-I is limited to patients with tumors harboring the wild-type KRAS gene. In this review, the KRAS pathway and studies evaluating KRAS as a prognostic marker in CRC are discussed along with advances in KRAS gene mutation testing. Clinical trials evaluating the role of KRAS status in response to EGFR-I monotherapy or in combination with chemotherapy are also highlighted along with ongoing studies evaluating the role of EGFR-I treatment on curative resections rates. RESULTS AND CONCLUSION: Future studies investigating EGFR-I therapy in mCRC should incorporate KRAS mutation testing into the study protocol in order to more accurately determine the patient population that will obtain clinical benefit from these novel agents.|*Drug Resistance, Neoplasm[MESH]|Antineoplastic Agents/*therapeutic use[MESH]|Biomarkers, Tumor/*genetics[MESH]|Clinical Trials as Topic[MESH]|Colonic Neoplasms/drug therapy/*genetics/metabolism[MESH]|ErbB Receptors/*antagonists & inhibitors/metabolism[MESH]|Humans[MESH]|Mutation/*genetics[MESH]|Proto-Oncogene Proteins p21(ras)[MESH]|Proto-Oncogene Proteins/*genetics/metabolism[MESH]|ras Proteins/*genetics/metabolism[MESH] |