DOI: 10.1038/nature10868
The reason why a subset of colon cancers responds less favorably than melanomas to a treatment that targets a mutation both cancers share is proposed in Nature this week. The work suggests that combining vemurafenib, an approved melanoma treatment, with drugs that target a second oncoprotein could overcome treatment resistance in colon cancer.
Activating mutations in the BRAF oncogene, BRAF(V600E), are seen in around 70% of melanomas and 10% of colon cancers. Vemurafenib inhibits the BRAF(V600E) oncoprotein and is highly effective in the treatment of melanomas with activating BRAF(V600E) mutations, but not in colon cancers sharing the same mutation. René Bernards and colleagues investigate the cause of this discrepancy. They find that BRAF inhibition activates the epidermal growth factor receptor (EGFR, a protein expressed in colon cancer), which interferes with the response to BRAF inhibition. In contrast to colon cancers, EGFR is not expressed in melanomas and therefore not activated following vemurafenib treatment.
The authors demonstrate that EGFR inhibition is required to overcome resistance to BRAF inhibition. They propose that combinations of EGFR and BRAF inhibitors should be assessed in clinical trials for colon cancers carrying activating BRAF mutations.
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René Bernards (The Netherlands Cancer Institute, Amsterdam, Netherlands)
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