Department of Gastroenterology, Fujita Health University School of Medicine, Toyoake, 1-98 Dengakugakubo Kutsukake-cho, Toyoake, Aichi, 470-1192, Japan.
Expert Rev Mol Diagn. 2012 Jun;12(5):489-97. doi: 10.1586/erm.12.38.
DNA methylation has been deeply involved in the development and progression of digestive cancer, while aberrant DNA methylation has also often been observed in aged and inflammatory digestive tissues. Helicobacter pylori-related chronic gastritis, ulcerative colitis, and hepatitis B virus- and hepatitis C virus-related chronic hepatitis, are significant risk factors for developing cancer. A number of studies have revealed the specific methylation patterns for specific tissue types. DNA methylation status is stably transmitted to daughter cells. Also, unlike genetic mutations, it is possible to detect very tiny amounts of methylated DNA among tissues. Therefore, the use of aberrant methylation as a marker could be applicable to risk estimation of cancer development. We discuss the potential usefulness of DNA methylation as a risk marker for inflammation-associated digestive cancer, especially with attempts on gastric cancer, ulcerative colitis-associated cancer, and hepatitis B virus- and hepatitis C virus-related hepatocellular carcinoma.
DNA 甲基化在消化道癌症的发生和发展中起着重要作用，而异常的 DNA 甲基化在衰老和炎症性消化道组织中也经常被观察到。幽门螺杆菌相关的慢性胃炎、溃疡性结肠炎、乙型肝炎病毒和丙型肝炎病毒相关的慢性肝炎，是发展为癌症的重要危险因素。许多研究已经揭示了特定组织类型的特定甲基化模式。DNA 甲基化状态稳定地传递给子细胞。此外，与基因突变不同，在组织中可以检测到非常微量的甲基化 DNA。因此，将异常甲基化作为标志物可用于癌症发展的风险估计。我们讨论了 DNA 甲基化作为炎症相关消化道癌风险标志物的潜在用途，特别是在胃癌、溃疡性结肠炎相关癌以及乙型肝炎病毒和丙型肝炎病毒相关肝细胞癌方面的尝试。
