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Gastrointestinal Cancer

Predicting Response to EGFR Inhibitors in Metastatic Colorectal Cancer: Current Practice and Future Directions

^aSeattle Cancer Care Alliance, Fred Hutchinson Cancer Research Center, Seattle, Washington, USA; ^bNorthshore University Healthcare System, Chicago, Illinois, USA; ^cNorthwestern University Feinberg School of Medicine and Robert H. Lurie Comprehensive Cancer Center, Chicago, Illinois, USA

Correspondence: Al B. Benson III, M.D., F.A.C.P., Division of Hematology-Oncology, Northwestern University Feinberg School of Medicine, 676 North Saint Clair, Suite 850, Chicago, Illinois 60611, USA. Telephone:312-695-6180; Fax:312-695-6189; e-mail: a-benson{at}northwestern.edu

Received September 15, 2009; accepted for publication December 28, 2009; first published online in THE ONCOLOGIST Express on February 4, 2010.

Disclosures: Veena Shankaran: None; Jennifer Obel: None; Al B. Benson III: None.

The content of this article has been reviewed by independent peer reviewers to ensure that it is balanced, objective, and free from commercial bias. No financial relationships relevant to the content of this article have been disclosed by the authors or independent peer reviewers.

The identification of KRAS mutational status as a predictive marker of response to antibodies against the epidermal growth factor receptor (EGFR) has been one of the most significant and practice-changing recent advances in colorectal cancer research. Recently, data suggesting a potential role for other markers (including BRAF mutations, loss of phosphatase and tensin homologue deleted on chromosome ten expression, and phosphatidylinositol-3-kinase–AKT pathway mutations) in predicting response to anti-EGFR therapy have emerged. Ongoing clinical trials and correlative analyses are essential to definitively identify predictive markers and develop therapeutic strategies for patients who may not derive benefit from anti-EGFR therapy. This article reviews recent clinical trials supporting the predictive role of KRAS, recent changes to clinical guidelines and pharmaceutical labeling, investigational predictive molecular markers, and newer clinical trials targeting patients with mutated KRAS.