Colon cancers can be broadly separated into those that have intact of defective DNA mismatch repair (MMR). Significant differences in the pathology, molecular alterations and prognosis of these subsets of colon cancer exist. The epidermal growth factor receptor (EGFR) is a critical cell signaling regulator that drives proliferation of multiple tumor cells. We recently identified a novel mutation in the 3'UTR of the EGFR gene in mismatch repair deficient colon cancers. Presence of this mutation results in increased EGFR mRNA stability, which in turn results in increased EGFR mRNA and protein expression. The purpose of this study is to investigate the mechanism by which mutations in EGFR increase its mRNA stability. This study will provide important insights into the molecular basis by which MMR deficient colon cancers arise, and could identify patients likely to benefit from EGFR targeting-therapies, cetuximab and panitumumab.