Cyclin D1: polymorphism, aberrant splicing and cancer risk

被引:325
作者
Knudsen, KE
Diehl, JA
Haiman, CA
Knudsen, ES
机构
[1] Univ Cincinnati, Ctr Canc, Ctr Environm Genet, Dept Cell Biol, Cincinnati, OH 45267 USA
[2] Univ Penn, Abramson Family Canc Res Inst, Ctr Canc, Philadelphia, PA 19104 USA
[3] Univ So Calif, Keck Sch Med, Dept Prevent Med, Los Angeles, CA USA
关键词
cell cycle; cyclin-dependent kinase; alternative splicing; nuclear localization; retinoblastoma tumor suppressor;
D O I
10.1038/sj.onc.1209371
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
The cyclin D1 proto-oncogene exercises powerful control over the mechanisms that regulate the mitotic cell cycle, and excessive cyclin D1 expression and/or activity is common in human cancers. Although somatic mutations of the cyclin D1 locus are rarely observed, mounting evidence demonstrates that a specific polymorphism of cyclin D1 (G/A870) and a protein product of a potentially related alternate splicing event (cyclin D1b) may influence cancer risk and outcome. Herein, we review the epidemiological and functional literatures that link these alterations of cyclin D1 to human tumor development and progression.
引用
收藏
页码:1620 / 1628
页数:9
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