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

Table 2

CCNA2 amplification in tumour cells and in total tumour in breast cancer tissue compared to normal tissue, as well as fluorescence in situ hybridization data in tumour tissue and in normal tissue.

Case	Tumour type	Histological grade	Fold change in isolated tumour cells^a	Fold change in total tumour^a	Tumour tissue: cyclin A2 pr nucleus/ centromere 4 pr nucleus^b	Normal tissue: cyclin A2 pr nucleus/ centromere 4 pr nucleus^b
1	Ductal	3	2.11	2.70	2.1/2.2	1.7/1.8
2	Ductal	3	1.83	2.04	2.0/2.2	1.7/1.8
3	Ductal	2	1.04	2.14	1.5/1.6	1.7/1.8
4	Ductal	3	1.65	1.81	3.4/3.7	1.7/1.8
5	Ductal	2	1.37	1.99	1.8/1.7	1.8/1.9
6	Ductal	3	0.39	0.60	—	—
7	Ductal	3	0.88	1.79	—	—
8	Ductal	3	0.67	0.99	—	—

^a2^−ΔΔCt, where ΔΔCt = (Ct_{𝐶𝐶𝑁𝐴2} − Ct_{endogenous controls})Tumourcells/Totaltumour − (Ct_{𝐶𝐶𝑁𝐴2} − Ct_{endogenous controls})Normal.
^bChromosome aberration was measured by fluorescence in situ hybridization counting cyclin A2 and centromere 4 signals in nuclei within tumour areas and normal mucosa. The average number of cyclin A2 and centromere 4 signals per nucleus are indicated both in tumour and normal tissue.