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. 2015 Mar 31;6(2):185–205. doi: 10.3390/genes6020185

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© 2015 by the authors; licensee MDPI, Basel, Switzerland.

This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/).

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Summary diagram relating colorectal pathogenesis that may be modulated by EMAST, affecting patient outcome. Colorectal cancers can be dichotomized into MSI-H and MSS, and previously MSI-L was lumped in with MSS cancers. EMAST, the biomarker for loss of MSH3 (MutSβ function), may modify the behavior of colorectal cancer, worsening patient survival. This is in contrast to patients with MSI-H colorectal cancers with the dominant genotype of loss of DNA mismatch repair and who have good survival outcome. Among EMAST cancers, a more balanced defect between moderate loss of mismatch repair and moderate loss of repair of double strand breaks may drive the overall worse behavior. Data indicates that there are racial differences for the prevalence of MSI-H and EMAST, as well as the type of inflammation associated with each biomarker.