The molecular understanding of this sequence has had a profound impact on our understanding of the process(s) of colonic carcinogenesis and this understanding has begun to change the clinical care of patients with colonic polyps and cancer including changes in therapy of established CRCs (anti-epidermal growth factor receptor antibody therapy is no longer offered to patients with mutant KRAS CRCs), identification of high-risk groups (diagnosis of Lynch syndrome by molecular analysis of CRCs) and the management of precursor lesions (identification of the serrated polyp pathway to CRC).
Conversely, KRAS mutations were most frequent in goblet cell serrated polyp (46.2%) and less frequent in microvesicular serrated polyp (13.2%) and serrated polyp with abnormal proliferation (7.1%).