Checkpoint with forkhead-associated and ring finger promoter hypermethylation correlates with microsatellite instability in gastric cancer
Checkpoint with forkhead-associated and ring finger promoter hypermethylation correlates with microsatellite instability in gastric cancer作者机构：Department of Surgery and Science Graduate School of Medical Sciences Kyushu University 3-1-1 Maidashi Higashi-ku Fukuoka 812-8582 Japan Department of Gastroenterology National Kyushu Cancer Center 3-1-1 Notame Minarni-ku Fukuoka 811-1395 Japan
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2009年第15卷第20期
页 面：2520-2525页
核心收录：
学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学]
主 题：Checkpoint with forkhead-associated and ring finger Methylation Microsatellite instability Gastric cancer p53
摘 要：AIM:To examine the methylation status of the promoter region of the checkpoint with forkhead-associated and ring fi nger(CHFR) and microsatellite mutator status in 59 primary gastric ***:We investigated the promoter methylation of CHFR in 59 cases of gastric cancer using methylation-specifi c *** microsatellite loci were analyzed using high-intensity microsatellite analysis reported previously, and p53 gene mutations were investigated by direct ***:Twenty cases(33.9%) showed promoter methylation and no relation was observed with the clinicopathological *** found that the promoter methylation of CHFR was frequently accompanied with microsatellite instability(MIN).Seven of 20(35.0%) cases showed MIN in hypermethylation of the CHFR tumor, while three of 39(7.7%) cases showed MIN in the non-methylated CHFR tumor(P 0.01).However, we failed to fi nd any relationship between CHFR methylation and p53 mutation ***:The coordinated loss of both the mitotic check point function and mismatch repair system suggests the potential to overcome the cell cycle check point, which may lead to an accumulation of ***, the p53 mutation was not related to hypermethylation of the CHFR promoter and MIN, which indicates that an abnormality in p53 occurs as an independent process from the mismatch repair deficiency in carcinogenesis.
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