Aurora-A over-expression in high-grade PIN lesions and prostate cancer.

Abstract

BACKGROUND:

Over-expression of Aurora-A (Aurora 2 kinase, STK-15), a protein found in centrosomes thought to be associated with genetic instability, has been previously documented in prostate cancer [Pihan et al.: Cancer Res 61(5):2212-2219, 2001]. It is unknown if this protein is also over-expressed in high-grade prostatic intraepithelial neoplasia (PIN) lesions.

METHODS:

PIN lesions were examined for increased Aurora-A using immunohistochemical staining on archival paraffin embedded prostatectomy tissue. Aurora-A expression was scored using size, number, and staining intensity. Protein expression was examined and compared between stromal cells, normal glands, high-grade PIN lesions, and invasive cancer.

RESULTS:

Immunohistochemistry shows an increased expression of Aurora-A in 96% of high-grade PIN cases, and 98% in cancer lesions. Twenty-nine percent of cases of normal glands from cancerous prostates also showed increased Aurora-A expression.

CONCLUSIONS:

Over-expression of Aurora-A is present in some normal and the majority of high-grade PIN lesions indicating that this may be an early event that leads to the genetic instability seen in prostate carcinogenesis.

• Authors: Holly McKlveen Buschhorn, Robert R Klein, Susan M Chambers, Margaret C Hardy, Sylvan Green, David Bearss, Raymond B Nagle
• Journal: The Prostate (Prostate) Vol. 64 Issue 4 Pg. 341-6 (Sep 01 2005) ISSN: 0270-4137 [Print] United States
• PMID: 15754349 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
• Copyright: Copyright 2005 Wiley-Liss, Inc.

Chemical References

• Cell Cycle Proteins
• Xenopus Proteins
• Protein Kinases
• AURKA protein, Xenopus
• Aurora Kinases
• Protein Serine-Threonine Kinases

Topics

• Aurora Kinases
• Cell Cycle Proteins (metabolism)
• Humans
• Immunohistochemistry
• Male
• Prostate (enzymology, pathology)
• Prostatic Intraepithelial Neoplasia (metabolism, pathology)
• Prostatic Neoplasms (metabolism, pathology)
• Protein Kinases (metabolism)
• Protein Serine-Threonine Kinases
• Xenopus Proteins (metabolism)