Journal
BREAST CANCER RESEARCH
Volume 6, Issue 5, Pages 188-191Publisher
BMC
DOI: 10.1186/bcr905
Keywords
antiestrogen resistance; breast cancer; genomic instability; low-molecular-weight cyclin E; prognostic marker
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Funding
- NCI NIH HHS [R01 CA087548, P50 CA091846, P30 CA016672, P50 CA91846, R01-CA87548, P30-CA16672] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [P50CA091846, P30CA016672, R01CA087548] Funding Source: NIH RePORTER
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Cyclin E, a key mediator of transition during the G(1)/S cellular division phase, is deregulated in a wide variety of human cancers. Our group recently reported that overexpression and generation of low-molecular-weight (LMW) isoforms of cyclin E were associated with poor clinical outcome among breast cancer patients. However, the link between LMW cyclin E biology in mediating a tumorigenic phenotype and clinical outcome is unknown. To address this gap in knowledge, we assessed the role of LMW isoforms in breast cancer cells; we found that these forms of cyclin E induced genomic instability and resistance to p21, p27, and antiestrogens in breast cancer. These findings suggest that high levels of LMW isoforms of cyclin E not only can predict failure to endocrine therapy but also are true prognostic indicators because of their influence on cell proliferation and genetic instability.
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