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Molecular Alterations in Inflammatory Colonic Carcinogenesis and Markers for Detecting Colitis-Associated Cancer

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Book cover Colitis-Associated Cancer

Abstract

The incidence of colorectal neoplasia is higher among patients with long-standing and extensive ulcerative colitis (UC) and Crohn’s disease (CD), such as that for these patients surveillance colonoscopy is widely recommended. However, colitis-associated cancer (CAC) is often difficult to detect endoscopically and histologically because of modifications of the mucosal structure by inflammation. Repeated flare-ups of inflammation are believed to promote oncogenic insults to the colonic epithelium. Chronic inflammation and thus the increased turnover of epithelial cells contribute to the development of low-grade and high-grade dysplasia and therefore, over time, CAC. This is a different sequence of tumorigenic events that occurs in the development of sporadic CRC. Although the genetic and epigenetic features that lead to sporadic CRC (chromosomal instability, microsatellite instability, DNA methylation, and microRNAs) also occur in CAC, in the inflamed colonic mucosa, unlike the normal mucosa, these molecular alterations take place before there is any histopathologic evidence of dysplasia and cancer. Recently, several molecular alterations of the nonneoplastic epithelium have been identified in UC patients with neoplasia. These alterations may be promising as markers for identifying patients at high risk of developing CAC.

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Toiyama, Y., Araki, T., Tanaka, K., Mohri, Y., Kusunoki, M. (2016). Molecular Alterations in Inflammatory Colonic Carcinogenesis and Markers for Detecting Colitis-Associated Cancer. In: Kusunoki, M. (eds) Colitis-Associated Cancer. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55522-3_5

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