FRA3B常见脆性区域的序列：对FHIT基因缺失机制的启示
Sequence of the FRA3B common fragile region: implications for the mechanism of FHIT deletion.
作者信息
Inoue H, Ishii H, Alder H, Snyder E, Druck T, Huebner K, Croce C M
机构信息
Kimmel Cancer Institute, Jefferson Medical College, Philadelphia, PA 19107, USA.
出版信息
Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14584-9. doi: 10.1073/pnas.94.26.14584.
Abstract
The hypothesis that chromosomal fragile sites may be "weak links" that result in hot spots for cancer-specific chromosome rearrangements was supported by the discovery that numerous cancer cell homozygous deletions and a familial translocation map within the FHIT gene, which encompasses the common fragile site, FRA3B. Sequence analysis of 276 kb of the FRA3B/FHIT locus and 22 associated cancer cell deletion endpoints shows that this locus is a frequent target of homologous recombination between long interspersed nuclear element sequences resulting in FHIT gene internal deletions, probably as a result of carcinogen-induced damage at FRA3B fragile sites.
摘要
染色体易碎位点可能是导致癌症特异性染色体重排热点的“薄弱环节”这一假说，得到了以下发现的支持：许多癌细胞纯合缺失以及一个家族性易位定位于FHIT基因内，该基因包含常见易碎位点FRA3B。对FRA3B/FHIT基因座的276 kb以及22个相关癌细胞缺失端点进行序列分析表明，该基因座是长散在核元件序列之间同源重组的常见靶点，导致FHIT基因内部缺失，这可能是致癌物诱导FRA3B易碎位点损伤的结果。
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