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Clinical Pharmacology |
aDivision of Clinical Pharmacology, Department of Medical Oncology, The Netherlands Cancer Institute, Amsterdam, The Netherlands; bUtrecht University, Faculty of Science, Department of Pharmaceutical Sciences, Section of Biomedical Analysis, Division of Drug Toxicology, Utrecht, The Netherlands; cDepartment of Pharmacy and Pharmacology, Slotervaart Hospital, Amsterdam, The Netherlands
Key Words. Aurora kinase • Mitosis • Targeted therapy • Drug development • Clinical trial
Correspondence: Jan H.M. Schellens, M.D., Ph.D., The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands. Telephone: 31-20-512-2569; Fax: 31-20-512-2572; e-mail: jhm{at}nki.nl
Received February 1, 2009; accepted for publication July 6, 2009; first published online in THE ONCOLOGIST Express on August 14, 2009.
Disclosures: David S. Boss: None; Jos H. Beijnen: None; Jan H.M. Schellens: Consultant/advisory role: AstraZeneca; Research funding/contracted research: AstraZeneca.
The content of this article has been reviewed by independent peer reviewers to ensure that it is balanced, objective, and free from commercial bias. No financial relationships relevant to the content of this article have been disclosed by the independent peer reviewers.
The aurora kinase family of serine/threonine kinases comprises three members, designated auroras A, B, and C. Auroras A and B are essential components of the mitotic pathway, ensuring proper chromosome assembly, formation of the mitotic spindle, and cytokinesis. The role of aurora C is less clear. Overexpression of aurora A and B has been observed in several tumor types, and has been linked with a poor prognosis of cancer patients. Several small molecules targeting aurora kinases A and B or both have been evaluated preclinically and in early phase I trials. In this review we aim to summarize the most recent advances in the development of aurora kinase inhibitors, with a focus on the clinical data.
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