The validation of KRAS mutations as a negative marker of response to anti−epidermal growth factor receptor (EGFR) antibodies has meant a seminal advance towards treatment individualisation of colorectal cancer (CRC) patients. However, as a KRAS wild−type status does not guarantee a response to anti−EGFR antibodies, a current challenge is the identification of other biomarkers of response. On the basis of pre−clinical evidence, we hypothesised that mitogen−activated protein kinase phosphatase−1 (MKP−1), a phosphatase that inactivates MAPKs, could be a mediator of resistance to anti−EGFR antibodies.Methods:Tumour specimens from 48 metastatic CRC patients treated with cetuximab−based chemotherapy were evaluated for KRAS and BRAF mutational status and MKP−1 expression as assessed by immunohistochemistry.
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03/16/10