Table of Contents Author Guidelines Submit a Manuscript
Journal of Oncology
Volume 2009 (2009), Article ID 831626, 9 pages
Research Article

Concordance of KRAS/BRAF Mutation Status in Metastatic Colorectal Cancer before and after Anti-EGFR Therapy

1Institute of Pathology, University of Würzburg, 97080 Würzburg, Germany
2Department of Internal Medicine II, University of Würzburg, 97080 Würzburg, Germany
3Department of Surgery, University of Würzburg, 97080 Würzburg, Germany
4Institute of Pathology, Ostalb-Klinikum Aalen, 73430 Aalen, Germany
5Department of Internal Medicine , Ostalb-Klinikum Aalen, 73430 Aalen, Germany

Received 30 August 2009; Revised 9 November 2009; Accepted 31 December 2009

Academic Editor: Francis Seow-Choen

Copyright © 2009 S. Gattenlöhner et al. 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.


Anti-EGFR targeted therapy is a potent strategy in the treatment of metastatic colorectal cancer (mCRC) but activating mutations in the KRAS gene are associated with poor response to this treatment. Therefore, KRAS mutation analysis is employed in the selection of patients for EGFR-targeted therapy and various studies have shown a high concordance between the mutation status in primary CRC and corresponding metastases. However, although development of therapy related resistance occurs also in the context of novel drugs such as tyrosine kinase-inhibitors the effect of the anti-EGFR treatment on the KRAS/BRAF mutation status itself in recurrent mCRC has not yet been clarified. Therefore, we analyzed 21 mCRCs before/after anti-EGFR therapy and found a pre-/posttherapeutic concordance of the KRAS/BRAF mutation status in 20 of the 21 cases examined. In the one discordant case, further analyses revealed that a tumor mosaicism or multiple primary tumors were present, indicating that anti-EGFR therapy has no influence on KRAS/BRAF mutation status in mCRC. Moreover, as the preselection of patients with a genotype for anti-EGFR therapy has become a standard procedure, sample sets such ours might be the basis for future studies addressing the identification of potential anti-EGFR therapy induced genetic alterations apart from KRAS/BRAF mutations.