DNA methylation defects in sporadic and hereditary colorectal cancer

被引：4

作者：

Xicola, Rosa M. ^{[1
]}

Llor, Xavier ^{[1
]}

机构：

[1] Univ Illinois, Chicago, IL 60680 USA

来源：

GASTROENTEROLOGIA Y HEPATOLOGIA | 2012年 / 35卷 / 07期

关键词：

Methylation; Colorectal cancer; LYNCH-SYNDROME; RISK; HYPERMETHYLATION; INSTABILITY; MUTATIONS; PHENOTYPE; MSH2; INACTIVATION; EPIGENETICS; ADENOMAS;

D O I：

10.1016/j.gastrohep.2012.01.010

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

DNA methylation is a fundamental epigenetic mechanism in regulating the expression of genes controlling crucial cell functions in cancer development. Methylation defects (both global hypomethylation and hypermethylation of CpG islands) are implicated in colorectal carcinogenesis. Some nutrients have a clear effect on methylation, suggesting that some dietary-associated differences in the incidence of colorectal cancer could be due to the effect of diet on methylation. The presence of methylation defects has clear diagnostic and prognostic implications. Thus, several tests are being used for colorectal cancer screening based on methylated gene analysis, whether in feces or blood. In addition, the reversibility of methylation processes allows the development of chemotherapies that regulate this process through their antineoplastic activity. (C) 2012 Elsevier Espana, S.L. and AEEH y AEG. All rights reserved.

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收藏

页码：480 / 487

页数：8

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