抑癌基因 RUNX3 在人胃癌中的甲基化。
Methylation of the Tumor Suppressor Gene RUNX3 in Human Gastric Carcinoma.
机构信息
Department of Internal Medicine, Ewha Medical Research Institute, School of Medicine, Ewha Womans University, Seoul, Korea.
出版信息
Gut Liver. 2008 Sep;2(2):119-25. doi: 10.5009/gnl.2008.2.2.119. Epub 2008 Sep 30.
BACKGROUND/AIMS: RUNX3 (PEBP2alphaC/CBFA3/AML2) is a novel tumor suppressor gene in the human gastric carcinoma. The aims of this study were to determine the methylation of RUNX3 promoter and the association between RUNX3 methylation and the clinicopathological characteristics of patients with gastric carcinoma.
METHODS
Seventy-nine patients with gastric carcinoma were studied prospectively from April 2005 to May 2007. The methylations of RUNX3 promoter on the gastric carcinoma specimens and the corresponding nonneoplastic mucosa were evaluated by methylation-specific polymerase chain reaction.
RESULTS
Comparison of the results with the clinicopathological characteristics identified RUNX3 monoallelic methylation in 32.9% (26/79) of the gastric carcinoma patients and in 11.4% (9/79) of those with nonneoplastic mucosa (p=0.053). The monoallelic methylated gastric carcinoma specimens predominantly consisted of well- and moderately differentiated carcinomas (44.7%), with the unmethylated group constituting 22.0% of them (p=0.031). Among the 48 patients (60.8%) who underwent gastrectomy, there was no correlation between the two groups with regard to Lauren's classification (p=0.235), depth of invasion (p=0.990), nodal status (p=0.601), stage (p=0.900), lymphatic invasion (p=0.537), and vascular invasion (p=0.815).
CONCLUSIONS
Methylation of the tumor suppressor gene RUNX3 might be one of the mechanisms involved in the pathogenesis of gastric carcinoma.
背景/目的：RUNX3（PEBP2alphaC/CBFA3/AML2）是人类胃癌中的一种新型肿瘤抑制基因。本研究旨在确定 RUNX3 启动子的甲基化及其与胃癌患者临床病理特征之间的关联。
方法
前瞻性研究 2005 年 4 月至 2007 年 5 月的 79 例胃癌患者。采用甲基化特异性聚合酶链反应评估胃癌标本和相应非肿瘤黏膜中 RUNX3 启动子的甲基化情况。
结果
将结果与临床病理特征进行比较，发现 32.9%（26/79）的胃癌患者和 11.4%（9/79）的非肿瘤黏膜患者存在 RUNX3 单等位基因甲基化（p=0.053）。单等位基因甲基化的胃癌标本主要由高分化和中分化癌组成（44.7%），而未甲基化组中 22.0%为该类型（p=0.031）。在接受胃切除术的 48 例患者（60.8%）中，两组之间的 Lauren 分类（p=0.235）、浸润深度（p=0.990）、淋巴结状态（p=0.601）、分期（p=0.900）、淋巴血管侵犯（p=0.537）和血管侵犯（p=0.815）均无相关性。
结论
肿瘤抑制基因 RUNX3 的甲基化可能是胃癌发病机制中的一种机制。
Zotero 插件