Figure 1.
Comparison of cCGH (A, C) and arrayCGH (B, D) results from chromosome 9 of CWR22 and chromosome 14 of DU145-MN1.
A small region of gain on 9p close to the centromer (B, arrowhead) and a small deletion on 14q (D, arrowhead) are only detected by arrayCGH.
Table 1.
Overview of detected chromosomal aberrations by cCGH and aCGH
Figure 2.
Whole genome plot of gained (A) and lost (B) chromosomal regions of 11 prostate cancer cell lines, as detected with aCGH.
Numbers above the plot indicate chromosome numbers and vertical lines boundaries between chromosomes.
Figure 3.
Validation of amplicons by FISH analysis on cell lines.
Identification of increased copies of signals of the BAC clone RP11-165H19 mapped to 9p13.3 amplicon in cell line CWR22 and CWR22-Rv1 (A and B). C Optimal signal and lack of cross hybridization was verified using normal metaphase spreads showing two signals for each probe. BAC clone RP11-165H19 signals are green; red signals indicate chromosome 9 centromere (D9Z1).
Figure 4.
DNA copy number quantification of DCTN3 and IL11-RA genes in prostate cancer cell lines and 20 primary prostate carcinoma samples using quantitative real time PCR.
IL-11RA showed a significant increase in gene copy number above normal in CWR22, CWR22-Rv1, DU145HOM and DU145-MN1 and in 15 out of the 20 (75%) prostate cancer samples. For DCTN3, no copy number gain was detected in any cell line and in only 2 out of the 20 (10%) prostate cancer samples. Values above cut off line being assigned as increased gene copy number compared to normal.