Double-strand breaks and translocations in cancer

被引：123

作者：

Elliott, B

Jasin, M

机构：

[1] Mem Sloan Kettering Canc Ctr, Cell Biol Program, New York, NY 10021 USA

[2] Cornell Univ, Grad Sch Med Sci, New York, NY 10021 USA

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2002年 / 59卷 / 02期

关键词：

translocations; double-strand breaks; DNA repair pathways; cancer; recombination;

D O I：

10.1007/s00018-002-8429-3

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：

The correct repair of double-strand breaks (DSBs) is essential for the genomic integrity of a cell, as inappropriate repair can lead to chromosomal rearrangements such as translocations. In many hematologic cancers and sarcomas, translocations are the etiological factor in tumorigenesis, resulting in either the deregulation of a proto-oncogene or the expression of a fusion protein with transforming properties. Mammalian cells are able to repair DSBs by pathways involving homologous recombination and nonhomologous end-joining. The analysis of translocation breakpoints in a number of cancers and the development of model translocation systems are beginning to shed light on specific DSB repair pathway(s) responsible for the improper repair of broken chromosomes.

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页码：373 / 385

页数：13

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