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First published online July 22, 2009
doi: 10.1242/10.1242/jcs.039719

Journal of Cell Science 122, 2579-2585 (2009)
Published by The Company of Biologists 2009
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Commentary

How do anti-mitotic drugs kill cancer cells?

Karen E. Gascoigne* and Stephen S. Taylor{ddagger}

Faculty of Life Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK

{ddagger} Author for correspondence (e-mail: stephen.taylor{at}manchester.ac.uk)

In 2007, over 12-million people were diagnosed with cancer. According to the American Cancer Society, at least one third of these individuals are not expected to survive the disease, making cancer the second most prevalent cause of death worldwide. Systemic chemotherapy forms the mainstay of cancer treatment, and agents that disrupt mitotic spindle assembly – so called `anti-mitotics' – are commonly used to treat a wide variety of cancers. Traditional anti-mitotic agents include the microtubule toxins such as taxol, other taxanes and the vinca alkaloids, all of which have proven successful in the clinic. However, patient response remains highly unpredictable, and drug resistance is common. In addition, toxicity is a problem. To address these limitations, a new generation of anti-mitotic drugs is being developed. As the first wave of these new agents enters clinical trails, much hope rests on their outcome. Meanwhile, significant attention is being focused on trying to predict which tumour types are likely to respond. In this Commentary, we outline recent advances in our understanding of how cancer cells respond to anti-mitotic drugs, and discuss the relevance of these studies to their use in the clinic.

Key words: Taxol, Paclitaxel, Spindle checkpoint


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© The Company of Biologists Ltd 2009