Transcriptional Characterization of Glioma Neural Stem Cells Diva ...

6.3 Copy Number Aberrations Results
Figure 6.6: Correlations for all combinations of cell lines: any GNS/GNS and
NS/NS cell lines.
and gains of DNA) and alterations in transcriptional regulation and mRNA
degradation, we analysed array comparative genomic hybridization (aCGH)
data for G144, G166 and G179 [404]. The candidate did not perform this
analysis but the results will be shown nonetheless to give the reader a clearer
understanding of the genomic identity of these cell lines. The aCGH method
reveals net gains and losses in a cell population over the average ploidy. Previ-
ous analysis of chromosomal alterations in G144, G179 and G166 by SKY and
CGH detected several alterations, mostly whole-chromosome gains and losses,
and found that the lines do not show gross chromosomal instability when cul-
tured. Specifically, the CGH data for G144 revealed the deletion of PTEN on
chromosome 10 [404].
These findings were confirmed by our analysis of the aCGH data (Fig 6.7).
We identified aberrations known to be common in glioblastoma, including
gain of chromosome 7 (EGFR, which is over-expressed in 40% of glioblas-
tomas [154,262], lies on chromosome 7) and losses of large parts of chromosomes
10, 13, 14 and 19 in more than one GNS line, as well as focal gain of CDK4
in G144 (arrow, chromosome 12 in figure 6.7) and focal loss of the CDKN2A-
CDKN2B locus in G179 (arrow, chromosome 9 in figure 6.7) [52,326]. We
found that both G166 and G179 had low copy numbers of chromosome 10, but
could not establish a focal PTEN loss as we did for CDK4.
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