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• W1824134613 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." @default.
• W1824134613 created "2016-06-24" @default.
• W1824134613 creator A5042960706 @default.
• W1824134613 creator A5062594396 @default.
• W1824134613 date "2004-07-07" @default.
• W1824134613 modified "2023-10-06" @default.
• W1824134613 title "Low-molecular-weight cyclin E: the missing link between biology and clinical outcome" @default.
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• W1824134613 doi "https://doi.org/10.1186/bcr905" @default.
• W1824134613 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/549170" @default.
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• W1824134613 hasPublicationYear "2004" @default.
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