EGFR and downstream genetic alterations in KRAS/BRAF and PI3K/AKT pathways in colorectal cancer: implications for targeted therapy.
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| Abstract |
The promise of individualized treatment is gradually being fulfilled, and targeted therapy is becoming a powerful strategy to treat selected patients based on their molecular profile. For metastatic colorectal cancer (mCRC) patients anti-EGFR (epidermal growth factor receptor) targeted therapy has markedly improved disease control and survival. However, only a subgroup of patients with mCRC respond to anti-EGFR treatment, and selecting the patients with a positive effect from treatment is important for both the patient and the society. Patients with mutations in the KRAS gene are known as non-responders to anti-EGFR treatment and, consequently, KRAS testing has been employed in routine clinical practice for patient selection. However, a large number of the KRAS wildtype patients do not respond to this treatment. The molecular mechanism underlying response is not fully understood, and other members of the KRAS-BRAF pathway and PI3K-AKT pathway are investigated as predictive biomarkers. Furthermore, concordance of mutation status of primary tumors and their corresponding hepatic or pulmonary metastases, as well as treatment-induced mutations, possess another challenge for properly tailoring the appropriate therapy to this patient group. In this review, molecular biomarkers involved in prediction of response to anti-EGFR treatment are discussed.
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| Authors | Marianne Berg, Kjetil Soreide |
| Journal | Discovery medicine (Discov Med) Vol. 14 Issue 76 Pg. 207-14 (Sep 2012) ISSN: 1944-7930 [Electronic] United States |
| PMID | 23021375 (Publication Type: Journal Article, Review) |
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