Cyclin A2 Protein Overexpression Is Not Caused by Gene Amplification in Colon Cancer
Table 1
No CCNA2 amplification was detected in either the isolated tumour cells or the total tumour in the colon cancer patients. Fluorescence in situ hybridization data in tumour tissue and in normal tissue confirm this.
Normal tissue: cyclin A2 pr nucleus/centromere 4 pr nucleusb
1
0.77
1.09
2
0.59
0.65
1.5/2.0
1.3/1.6
3
0.80
1.16
4
1.18
1.14
5
0.68
0.91
2.0/2.0
—
6
0.89
1.07
7
1.17
1.32
8
1.46
1.22
9
1.23
1.85
10
0.66
0.58
11
1.08
1.50
12
0.38
0.80
13
0.72
0.77
14
1.25
0.97
15
1.06
1.17
16
1.07
1.24
1.9/1.9
—
17
0.50
0.84
18
0.82
0.91
1.4/1.8
1.5/1.6
19
0.66
0.86
20
1.02
0.92
21
0.77
0.85
22
0.67
0.64
1.7/1.8
1.2/1.4
, where Ct = ( − )− ( − ).
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 is indicated both in tumour and normal tissue.
