Colon carcinogenesis is associated with all of the following genetic mutations, EXCEPT:

Amplification of the HER2 gene and overexpression of the HER2 protein are common in preinvasive and invasive breast cancers. The earliest molecular defect in the pathogenesis of colon cancer is the acquisition of somatic mutations in the APC gene in the normal colonic mucosa. This defect causes abnormal regulation of -catenin, which leads to abnormal cell proliferation and the initial steps in tumor formation. Mutational activation of the K-ras gene leads to constitutive activation of an impoant proliferative signaling pathway, is common at these stages, and fuher increases the proliferative potential of the adenomatous tumor cells. Ref: Moasser M.M. (2010). Chapter 5. Neoplasia. In S.J. McPhee, G.D. Hammer (Eds), Pathophysiology of Disease, 6e.