The DOI matches its Crossref record; 71 of the 71 references it cites were found in a registry or an index.
Aurora Kinases as Anticancer Drug Targets
Abstract
The human aurora family of serine-threonine kinases comprises three members, which act in concert with many other proteins to control chromosome assembly and segregation during mitosis. Aurora dysfunction can cause aneuploidy, mitotic arrest, and cell death. Aurora kinases are strongly expressed in a broad range of cancer types. Aurora A expression in tumors is often associated with gene amplification, genetic instability, poor histologic differentiation, and poor prognosis. Aurora B is frequently expressed at high levels in a variety of tumors, often coincidently with aurora A, and expression level has also been associated with increased genetic instability and clinical outcome. Further, aurora kinase gene polymorphisms are associated with increased risk or early onset of cancer. The expression of aurora C in cancer is less well studied. In recent years, several small-molecule aurora kinase inhibitors have been developed that exhibit preclinical activity against a wide range of solid tumors. Preliminary clinical data from phase I trials have largely been consistent with cytostatic effects, with disease stabilization as the best response achieved in solid tumors. Objective responses have been noted in leukemia patients, although this might conceivably be due to inhibition of the Abl kinase. Current challenges include the optimization of drug administration, the identification of potential biomarkers of tumor sensitivity, and combination studies with cytotoxic drugs. Here, we summarize the most recent preclinical and clinical data and discuss new directions in the development of aurora kinase inhibitors as antineoplastic agents.
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Cites
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A homologue of Drosophila aurora kinase is oncogenic and amplified in human colorectal cancers
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Bast, R. C., Hennessy, B., & Mills, G. B. (2009) · Nature Reviews Cancer · doi:10.1038/nrc2644 · Cited by 1,358
Cell cycle kinases as therapeutic targets for cancer
Lapenna, S., & Giordano, A. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2907 · Cited by 905
Radiation-induced cell death mechanisms
Eriksson, D., & Stigbrand, T. (2010) · Tumor Biology · doi:10.1007/s13277-010-0042-8 · Cited by 666
Proteasome Inhibitors in Cancer Therapy: Lessons from the First Decade
Orlowski, R. Z., & Kuhn, D. J. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-07-2218 · Cited by 578
Aurora A kinase (AURKA) in normal and pathological cell division
Nikonova, A. S., Astsaturov, I., Serebriiskii, I. G., Dunbrack, R. L., & Golemis, E. A. (2013) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-012-1073-7 · Cited by 448
Metadata
- Authors
- Gautschi, O., Heighway, J., Mack, P. C., Purnell, P. R., Lara, P. N., & Gandara, D. R.
- Venue
- Clinical Cancer Research
- Published
- 2008-03-15
- Volume
- 14
- Issue
- 6
- Pages
- 1639-1648
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W2160475600
- Cited by
- 386
- References
- 71
- FWCI
- 20.63
- Type
- journal article
- Language
- en
- Open access
- closed
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