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. Author manuscript; available in PMC: 2012 Jan 1.
Published in final edited form as: Gut. 2010 Oct 4;60(1):116–129. doi: 10.1136/gut.2009.206250

Figure 1. The adenoma-to-carcinoma progression sequence.

Figure 1

Colorectal carcinogenesis progresses by at least two well-recognized pathways. The chromosome instability (CIN) pathway is characterized by classic tubular adenoma histology and the early acquisition of APC mutations that lead to deregulated WNT signaling, frequent activating mutations of the KRAS oncogene at the early adenoma stage, loss of heterozygosity at chromosome 18q (18qLOH) in late adenomas, and TP53 mutations that facilitate the transition to frank malignancy. By contrast, tumors that harbor microsatellite instability (MSI) frequently acquire BRAF mutations and are not associated with 18qLOH or TP53 mutations. Sporadic MSI cancers appear to commonly arise via the serrated neoplasia pathway, in which sessile serrated adenomas are the most frequently observed pre-cancerous lesions.