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.

CaseFold change in isolated tumour cellsaFold change in total tumouraTumour tissue:
cyclin A2 pr
nucleus/centromere 4 pr nucleusb
Normal tissue:
cyclin A2 pr
nucleus/centromere 4 pr nucleusb

10.771.09
20.590.651.5/2.01.3/1.6
30.801.16
41.181.14
50.680.912.0/2.0
60.891.07
71.171.32
81.461.22
91.231.85
100.660.58
111.081.50
120.380.80
130.720.77
141.250.97
151.061.17
161.071.241.9/1.9
170.500.84
180.820.911.4/1.81.5/1.6
190.660.86
201.020.92
210.770.85
220.670.641.7/1.81.2/1.4

a 2 Δ Δ C t , where Δ Δ Ct = ( C t 𝐶 𝐶 𝑁 𝐴 2 C t e n d o g e n o u s c o n t r o l s ) T u m o u r c e l l s / T o t a l t u m o u r − ( C t 𝐶 𝐶 𝑁 𝐴 2 C t e n d o g e n o u s c o n t r o l s ) N o r m a l .
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.