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Cyclin D1: polymorphism, aberrant splicing and cancer risk

期刊

ONCOGENE
卷 25, 期 11, 页码 1620-1628

出版社

NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1209371

关键词

cell cycle; cyclin-dependent kinase; alternative splicing; nuclear localization; retinoblastoma tumor suppressor

资金

  1. NCI NIH HHS [1R01CA111360, R01-CA099996] Funding Source: Medline
  2. NIEHS NIH HHS [U01-ES011038] Funding Source: Medline

向作者/读者索取更多资源

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.

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