Genetic alterations in cancer as a result of breakage at fragile sites

被引：90

作者：

Popescu, NC ^{[1
]}

机构：

[1] NCI, Mol Cytogenet Sect, Expt Carcinogenesis Lab, Ctr Canc Res, Bethesda, MD 20814 USA

来源：

CANCER LETTERS | 2003年 / 192卷 / 01期

关键词：

fragile site; DNA replication; genomic DNA; oncogenic virus; gene alteration; oncogenes; tumor suppressor gene; chromosome translocations;

D O I：

10.1016/S0304-3835(02)00596-7

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The organization and replication of DNA render fragile sites (FSs) prone to breakage, recombination as well as becoming preferential targets for mutagens-carcinogens and integration. of oncogenic viruses. For many years, attempts to link FSs and cancer generated mostly circumstantial evidence. The discoveries that chromosome translocations, amplification of protooncogenes, deletion of tumor suppressor. genes, and integration of oncogenic viruses all result from the specific breakage of genomic DNA at FSs, however, have provided compelling support for such a link, further suggesting a causative role for FSs in cancer. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：1 / 17

页数：17

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