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The therapeutic activity of the epidermal growth factor receptor (EGFR)-directedmonoclonal antibody cetuximab in gastric cancer is currently being investigatedin clinical studies. Reliable biomarkers for the identification of patients whoare likely to benefit from this treatment are not available. In this study, weassessed the activity of cetuximab in five gastric cancer cell lines (AGS, AZ521,Hs746T, LMSU and MKN1). The viability of two of these cell lines, AZ521 and MKN1,was significantly reduced by cetuximab treatment. High expression and secretionlevels of the EGFR-binding ligand, amphiregulin (AREG), were associated with cetuximabresponsiveness. MET activation and mutations in Kirsten-Ras gene (KRAS) were associatedwith cetuximab resistance. By introducing a hierarchy between these markers, weestablished a model that facilitated the correct classification of all five gastriccancer cell lines as cetuximab responsive or non-responsive. The highest prioritywas allocated to activating KRAS mutations, followed by MET activation and finallyby the levels of secreted AREG. In order to validate these results, we used threeadditional human gastric cancer cell lines (KATOIII, MKN28 and MKN45). In conclusion,we propose that our model allows the response of gastric cancer cell lines tocetuximab treatment to be predicted.

Association of amphiregulin with the cetuximab sensitivity of gastric cancer cell lines