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. Author manuscript; available in PMC: 2017 Nov 15.
Published in final edited form as: Cancer Res. 2016 Oct 6;76(22):6680–6689. doi: 10.1158/0008-5472.CAN-16-0696

Figure 2.

Figure 2

(A) Western blot analysis of histone H3K 4,9, and 27 methylation in E6E7 empty vector (lane 1), E6E7 IDH1WT (lane 2), E6E7 IDH1mut pre-crisis (lane 3), and E6E7 IDH1mut post-crisis (lane 4) cells. Values were derived from 3 independent experiments, *, p<.05. (B) Hierarchical clustering of the methylation array data from the cell lines used in this study (far left lanes) with that of G-CIMP negative/IDH WT (blue lanes) and G-CIMP positive/IDH1mut (red lanes) TCGA tumors. (C) Fluorescence in situ hybridization of E6E7 IDH1mut pre- (top) or post (bottom) -crisis cells using probes specific for centrosomal regions on chromosome 3, 10, or 11. (D) LOH plot of NHA, E6E7, E6E7 IDH1mut pre-crisis, and three independent E6E7 IDH1mut post-crisis clonal cultures. (E) A phylogenetic tree depicts the patterns of clonal evolution of E6E7 IDH1mut post-crisis clonal populations inferred from the pattern of somatic mutations.