Skip to main content
. Author manuscript; available in PMC: 2014 Sep 9.
Published in final edited form as: Cancer Cell. 2013 Aug 29;24(3):10.1016/j.ccr.2013.08.001. doi: 10.1016/j.ccr.2013.08.001

Figure 2. GSCs Differ in the Transcriptome and Epigenetic Profiles When Compared to the Originating Tumor.

Figure 2

(A) Heatmap of the predominant signature of initiating GBM, derived GSC, and xenograft for fourteen samples is shown. A PN and MES qRT-PCR based metagene was calculated for each sample and then compared to each other after Z-score correction. Green shades represent a predominantly PN signature, red a MES one, and black a relatively balanced expression of both, as indicated in the figure. (B) IHC analysis of Nestin, OLIG2 and YKL40 expression in patient matched GBM and xenografts of GSCs. Scale Bar: 50 μm. (C) Methylight profiling of GBMs and their derivative GSCs for G-CIMP status. Eleven markers were tested for presence of methylation on their promoters and coded as red if methylated and green if unmethylated. Samples were deduced as G-CIMP if >50% of the loci showed methylation. A GBM and an anaplastic oligodendroglioma (AOD) sample were used as negative and positive controls respectively. The IDH1 and G-CIMP status of all samples is shown below. (D) Heatmap shows the unsupervised clustering of 2612 G-CIMP signature methylation probes based on p values for the indicated cell types. (E) Venn diagram showing the number of hypermethylated probes (β-values of >0.5) in GSCs 11, 23 and TCGA G-CIMP+ tumors. See also Figure S2.