Aurora B expression correlates with aggressive behaviour in glioblastoma multiforme. Issue 2 (30th January 2007)

• Record Type: Journal Article
• Authors: Zeng, Weifen F; Navaratne, Kapila; Prayson, Richard A; Weil, Robert J
• Is Part Of: Journal of clinical pathology. Volume 60:Issue 2(2007)
• Page Start: 218
• Page End: 221
• Publication Date: 2007-01-30
• Subjects: FISH, fluorescence in situ hybridisation -- GBM, glioblastoma -- IHC, immunohistochemistry -- LTS, long-term survivor -- STS, short-term survivor; Pathology -- Periodicals; Pathology, Molecular -- Periodicals; 616.0705
• DOI: 10.1136/jcp.2006.036806
• Languages: English
• ISSNs: 0021-9746

Abstract

Abstract : Chromosomal abnormalities and genomic instability are common features of, and possible driving forces in, tumorigenesis. Recently, several mitotic proteins that are critical to proper chromosome segregation have been identified. Members of the Aurora kinase family have been identified as having important roles in mitosis; overexpression induces multicellularity and fosters polyploidy. As aneuploidy is a common feature of malignant gliomas, particularly glioblastomas (GBMs), we examined 25 prospectively collected GBMs to assess the role that overexpression of one member of this family, Aurora B, might have in the clinical behaviour of GBMs. Aurora B expression levels were markedly correlated with a shortened survival. Aurora B expression was not directly related to age, tumour proliferation status or to several common molecular changes found in GBMs. These results suggest that Aurora B may be a prognostic feature of impaired survival and a novel therapeutic target in some patients.