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Pathology Research International
Volume 2011, Article ID 219309, 11 pages
Review Article

Impact of KRAS Mutations on Management of Colorectal Carcinoma

Department of Medicine, Section of Hematology/Oncology, Albert Einstein College of Medicine, Beth Israel Medical Center, Phillips Ambulatory Care Center, 10 Union Square East, Suite 4C, NY 10003, USA

Received 28 September 2010; Revised 2 January 2011; Accepted 10 January 2011

Academic Editor: Wade Samowitz

Copyright © 2011 Kevin M. Sullivan and Peter S. Kozuch. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The epidermal growth factor receptor (EGFR) pathway is a therapeutic target in the management of colorectal cancer (CRC). EGFR antagonists are active in this disease; however, only a subset of patients respond to such therapy. A Kirsten ras sarcoma viral oncogene (KRAS) wild-type (WT) status of the tumor is necessary, but possibly not sufficient, for a response to anti-EGFR monoclonal antibody therapy. Mechanisms of primary resistance to such therapy in patients harboring KRAS WT tumors are discussed. Strategies to overcome resistance to anti-EGFR monoclonal antibody therapy, including novel agents and combinations of novel therapies, are explored. Also, the use of anti-EGFR monoclonal antibodies in the adjuvant and neoadjuvant setting is reviewed.