Journal
ONCOGENE
Volume 25, Issue 11, Pages 1620-1628Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1209371
Keywords
cell cycle; cyclin-dependent kinase; alternative splicing; nuclear localization; retinoblastoma tumor suppressor
Funding
- NCI NIH HHS [1R01CA111360, R01-CA099996] Funding Source: Medline
- NIEHS NIH HHS [U01-ES011038] Funding Source: Medline
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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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