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.

CaseTumour typeHistological gradeFold 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

1Ductal32.112.702.1/2.21.7/1.8
2Ductal31.832.042.0/2.21.7/1.8
3Ductal21.042.141.5/1.61.7/1.8
4Ductal31.651.813.4/3.71.7/1.8
5Ductal21.371.991.8/1.71.8/1.9
6Ductal30.390.60
7Ductal30.881.79
8Ductal30.670.99

a 2 Δ Δ C t , where ΔΔCt = ( C t 𝐶 𝐶 𝑁 𝐴 2 − Ctendogenouscontrols) 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 − Ctendogenouscontrols) 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 are indicated both in tumour and normal tissue.