Genotine-wide analysis of epigenetics in cancer

被引:14
作者
Lee, MP [1 ]
机构
[1] NCI, Lab Populat Genet, Bethesda, MD 20892 USA
来源
EPIGENETICS IN CANCER PREVENTION: EARLY DETECTION AND RISK ASSESSMENT | 2003年 / 983卷
关键词
genomics; bioinformatics; cancer; epigenetics; genomic imprinting;
D O I
10.1111/j.1749-6632.2003.tb05965.x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Human cancers are caused by multiple mechanisms. Research in the last 30 years has firmly established the roles of a group of genes including oncogenes, tumor suppressor genes, and DNA repair genes in human cancers. The activation and inactivation of these cancer genes can be caused by genetic mutations or epigenetic alterations. The epigenetic changes in cancers include methylation of CpG islands, loss of imprinting, and chromatin modification. The completion of the genome sequences of many organisms including the human has transformed the traditional approach to molecular biology research into an era of functional genome research. Traditional research usually involves the study of one or a few genes (proteins) in a particular biological process in normal physiology or disease. Functional genome research takes advantage of newly available genome sequences and high-throughput genome technologies to study genes and/or proteins to inform the perspective of entire biological processes. I will focus on recent progress in the identification of imprinted genes and methylation of CpG islands through genome-wide analysis.
引用
收藏
页码:101 / 109
页数:9
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