Molecular characterization of common fragile sites as a strategy to discover cancer susceptibility genes

被引：14

作者：

Savelyeva, Larissa ^{[1
]}

Brueckner, Lena M. ^{[1
]}

机构：

[1] German Canc Res Ctr, D-69120 Heidelberg, Germany

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2014年 / 71卷 / 23期

关键词：

Fragile sites; Molecular mapping; Fragilome; cFS genes; NBEA; SPIDR; DPYD; COPY NUMBER CHANGES; HUMAN-CHROMOSOME; 7; HUMAN GENOME; DNA-DAMAGE; PREFERENTIAL INTEGRATION; REPLICATION DYNAMICS; VIRAL INTEGRATION; MULTIPLE-MYELOMA; TUMOR-SUPPRESSOR; BROAD REGION;

D O I：

10.1007/s00018-014-1723-z

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 cytogenetic hypothesis that common fragile sites (cFSs) are hotspots of cancer breakpoints is increasingly supported by recent data from whole-genome profiles of different cancers. cFSs are components of the normal chromosome structure that are particularly prone to breakage under conditions of replication stress. In recent years, cFSs have become of increasing interest in cancer research, as they not only appear to be frequent targets of genomic alterations in progressive tumors, but also already in precancerous lesions. Despite growing evidence of their importance in disease development, most cFSs have not been investigated at the molecular level and most cFS genes have not been identified. In this review, we summarize the current data on molecularly characterized cFSs, their genetic and epigenetic characteristics, and put emphasis on less-studied cFS genes as potential contributors to cancer development.

引用

页码：4561 / 4575

页数：15

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