Dissecting DNA hypermethylation in cancer

被引：62

作者：

Estecio, Marcos R. H. ^{[1
]}

Issa, Jean-Pierre J. ^{[1
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Houston, TX 77030 USA

来源：

FEBS LETTERS | 2011年 / 585卷 / 13期

关键词：

DNA methylation; Cancer; ISLAND METHYLATOR PHENOTYPE; ACUTE MYELOID-LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; GENOMIC SCANNING METHOD; TUMOR-SUPPRESSOR GENES; EMBRYONIC STEM-CELLS; NON-CPG METHYLATION; COLORECTAL-CANCER; LUNG-CANCER; HUMAN BREAST;

D O I：

10.1016/j.febslet.2010.12.001

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

There is compelling evidence to support the importance of DNA methylation alterations in cancer development. Both losses and gains of DNA methylation are observed, thought to contribute pathophysiologically by inactivating tumor suppressor genes, inducing chromosomal instability and ectopically activating gene expression. Lesser known are the causes of aberrant DNA methylation. Recent studies have pointed out that intrinsic gene susceptibility to DNA methylation, environmental factors and gene function all have an intertwined participation in this process. Overall, these data support a deterministic rather than a stochastic mechanism for de novo DNA methylation in cancer. In this review article, we discuss the technologies available to study DNA methylation and the endogenous and exogenous factors that influence the onset of de novo methylation in cancer. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：2078 / 2086

页数：9

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