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ISRN Pathology
Volume 2012 (2012), Article ID 691430, 7 pages
http://dx.doi.org/10.5402/2012/691430
Research Article

Cyclin A2 Protein Overexpression Is Not Caused by Gene Amplification in Colon Cancer

1Quality and Research Department, Ostfold Hospital Trust, Jernbanegaten 11, 2. Et, Postboks 16, 1603 Fredrikstad, Norway
2Institute of Clinical Epidemiology and Molecular Biology (EpiGen), Akershus University Hospital, 1478 Lørenskog, Norway
3Department of Pathology, Oslo University Hospital Rikshospitalet, 0027 Oslo, Norway
4Department of Pathology, Akershus University Hospital, 1478 Lørenskog, Norway
5Institute of Clinical Medicine, University of Oslo, 0316 Oslo, Norway
6Department of Surgery, Akershus University Hospital, 1478 Lørenskog, Norway
7Department of Health Promotion, Akershus University Hospital, 1478 Lørenskog, Norway
8Department of Chemistry, Biotechnology and Food Science, Norwegian University of Life Sciences, 1432 Ås, Norway

Received 8 June 2012; Accepted 19 July 2012

Academic Editors: C. E. Bacchi and M. Yamakawa

Copyright © 2012 Lise Aagaard Sørby et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Increased expression of cyclin A2 protein has been detected in different types of cancers. However, its prognostic importance appears to differ between tumours. The significance and precise mechanisms behind cyclin A2 overexpression remain to be elucidated. We used real-time PCR to examine CCNA2 amplification in tumour cells isolated by laser microdissection and in total tumour tissue in colon cancer patients in which overexpression of cyclin A2 protein had been revealed by immunohistochemistry ( š¯‘› = 2 2 patients). The results were verified by FISH. CCNA2 amplification was not detected in either the isolated tumour cells or the total tumour tissue. We verified our methods by demonstrating amplification of CCNA2 by real-time PCR in three out of eight breast tumours that overexpressed cyclin A2 protein (this frequency is consistent with the findings of others). However, FISH did not reveal any CCNA2 amplification in the breast tumours, but it did reveal polysomy of chromosome 4 or segments of chromosome 4 in three tumour tissue samples, indicating the importance of verifying the real-time PCR results with another method. To conclude, the increased cyclin A2 protein expression in these patients could not be explained by CCNA2 amplification in isolated colonic tumour cells.