Abstract
Cyclin E, a key mediator of transition during the G1/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.
Original language | English (US) |
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Pages (from-to) | 188-191 |
Number of pages | 4 |
Journal | Breast Cancer Research |
Volume | 6 |
Issue number | 5 |
DOIs |
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State | Published - Sep 2004 |
Keywords
- Antiestrogen resistance
- Breast cancer
- Genomic instability
- Low-molecular-weight cyclin E
- Prognostic marker
ASJC Scopus subject areas
- Oncology
- Cancer Research