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            <funder>We thank Stéphane Liva and Patrick Poullet for bioinformatics support. This work was financed by the Institut Curie Evaluation Committee of Translational Research (CEST) and Institut Carnot Curie-Cancer 2013</funder>
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                <title level="j">British Journal of Cancer</title>
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                  <biblScope unit="volume">117</biblScope>
                  <biblScope unit="issue">12</biblScope>
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                <term xml:lang="en">Male</term>
                <term xml:lang="en">Cetuximab</term>
                <term xml:lang="en">Class I Phosphatidylinositol 3-Kinases</term>
                <term xml:lang="en">Colorectal Neoplasms</term>
                <term xml:lang="en">Drug Resistance</term>
                <term xml:lang="en">Neoplasm</term>
                <term xml:lang="en">Epigenesis</term>
                <term xml:lang="en">Genetic</term>
                <term xml:lang="en">Middle Aged</term>
                <term xml:lang="en">MAP Kinase Signaling System</term>
                <term xml:lang="en">Carcinoma</term>
                <term xml:lang="en">Leucovorin</term>
                <term xml:lang="en">Humans</term>
                <term xml:lang="en">ras</term>
                <term xml:lang="en">Genes</term>
                <term xml:lang="en">Fluorouracil</term>
                <term xml:lang="en">Epidermal Growth Factor</term>
                <term xml:lang="en">Organoplatinum Compounds</term>
                <term xml:lang="en">Monoclonal</term>
                <term xml:lang="en">Antibodies</term>
                <term xml:lang="en">Wnt Signaling Pathway</term>
                <term xml:lang="en">Retrospective Studies</term>
                <term xml:lang="en">ErbB-2</term>
                <term xml:lang="en">ErbB-3</term>
                <term xml:lang="en">Response Evaluation Criteria in Solid Tumors</term>
                <term xml:lang="en">Receptor</term>
                <term xml:lang="en">Mutation</term>
                <term xml:lang="en">Female</term>
                <term xml:lang="en">Protein Kinase Inhibitors</term>
                <term xml:lang="en">Proto-Oncogene Proteins B-raf</term>
                <term xml:lang="en">Phosphorylation</term>
                <term xml:lang="en">Antineoplastic Combined Chemotherapy Protocols</term>
                <term xml:lang="en">Biomarkers</term>
                <term xml:lang="en">Tumor</term>
                <term xml:lang="en">Camptothecin</term>
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              <p>Background: Metastatic colorectal cancer (mCRC) patients with mutant KRAS or NRAS are ineligible for anti-epidermal growth factor receptor (anti-EGFR) therapy, as RAS mutations activate downstream pathways independently of EGFR and induce primary resistance. However, even among RAS wild-type (WT) patients, only a fraction responds to anti-EGFR therapy, suggesting that other mechanisms of resistance exist. We hypothesise that different (epi)genetic alterations can lead to primary anti-EGFR resistance and that the crucial end point is the activation of protein signalling pathways.Methods: We analysed the expression and activation of proteins involved in cell signalling, using reverse phase protein arrays, on a multicentre French cohort of RAS WT mCRC treated with anti-EGFR treatment.Results: We identify activated EGFR and HER3 as protein biomarkers predictive for better overall survival. Active EGFR signalling and downstream PI3K, but not MAPK, pathway activation are associated with response to anti-EGFR treatment. Left-sided mCRC displays active ErbB2/3 and Wnt pathways and a better response to anti-EGFR therapy compared to right-sided mCRC.Conclusions: We identify active EGFR and PI3K signalling as a key factor for response to anti-EGFR treatment in mCRC and highlight the importance of developing these biomarkers in clinical practice for the selection of RAS WT mCRC patients that would benefit from anti-EGFR treatment.</p>
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