Article Figures & Data
Figures
- FIGURE 1.
Regions of chromosome amplification and deletion detected using DNAcopy package and CGHAnalytics software for (in order from left to right) A172, Hs683, T98G, U251, and U87 glioma cell lines across all chromosomes. Red, amplifications; green, deletions.
- FIGURE 2.
Regions of loss of heterozygosity detected according to the genotype calls from GDAS software with a threshold of 6% for the probability of being homozygous for a given region for (in order from left to right) A172, Hs683, T98G, U251, and U87 glioma cell lines across all chromosomes. Green, loss of heterozygosity regions.
- FIGURE 3.
Differences in genomic alterations and transcriptomic profiles between established cell lines and tumor samples. A. The spectrum of genomic aberrations found in a consensus (10% or more) of 83 glioblastoma samples, in 5 glioma cell lines, and in 10 nonglioma tumor cell lines. Red, amplifications; green, deletions. Chromosome labels are indicated using two shades of gray bars on the top of A for 100K SNP arrays and on the bottom of A for 10K SNP arrays. Eclipse, alterations commonly present in both glioma cell lines and in tumor samples; rectangular shape, unique alterations present only in cell lines or only in tumor samples. B. PCA of glioblastoma, established glioma cell lines, and nonglioma tumor cell lines. C. HC of glioblastoma, established glioma cell lines, and nonglioma tumor cell lines. GBM, primary gliomas; GCL, glioma cell lines (in vitro cultured); GCL_in vivo, U87 and U251 intracranial xenografts; NGTCL, nonglioma tumor cell lines.
- FIGURE 4.
Results of GSEA for the phenotypes of glioblastomas and cell lines. A. Genes in significantly up-regulated gene sets in cell lines (red) in all data (gray). B. Genes in significantly up-regulated gene sets in glioblastoma (green) in all data (gray). C. Genes in significantly up-regulated gene sets in glioma representative pathways (yellow) in all data (gray). Data are transformed to reflect the expression value differences. D. Running enrichment scores for proteasome pathway in cell lines, the genes in the set as “hits” against the ranked list of genes (bottom) in the expression data set. E. Running enrichment scores for par1 signaling pathway in glioblastoma, the genes in the set as hits against the ranked list of genes (bottom) in the expression data set.
Tables
- Table 1.
Summary of GSEA of Glioblastomas Compared with Established Cell Lines
Gene sets Genes All cell lines Glioma cell lines In vivo In vitro ES Nom p ES Nom p Nom p Nom p BioCarta fatty_acid_metabolism 25 −0.586 0.008* −0.568 0.013* No† 0.724 badPathway 22 −0.496 0.019‡ −0.458 0.034‡ No† 0.933 dcPathway 20 −0.525 0.028‡ −0.474 0.095 No† 0.505 par1Pathway 18 −0.530 0.106 −0.620 0.011* 0.766 calcineurinPathway 18 −0.539 0.047‡ −0.493 0.145 No† 0.337 nfatPathway 52 −0.397 0.048‡ −0.358 0.144 No† 0.490 Gene Ontology GPCRs_Class_B_Secretin-like 24 −0.467 0.026‡ −0.480 0.016‡ 0.027‡ No Exp. sig. cell_adhesion Exp. sig. −0.436 0.002* −0.385 0.009* 0.042‡ No ANTI_CD44_up 23 −0.483 0.049‡ −0.353 0.397 0.023‡ No STKE and others ST_adrenergic 31 −0.447 0.068 −0.458 0.034‡ No† 0.21 SIG_PIP3_signaling_in_B_lymphocytes 35 −0.491 0.037‡ −0.428 0.1371 No† 0.133 - Table 2.
Summary of GSEA of Established Cell Lines Compared with Glioblastomas
Gene sets Sources Genes All cell lines Glioma cell lines ES Nom p ES Nom p Proteasome activities Proteasome_Degradation BioCarta 31 0.787 0* 0.787 0* proteasomePathway BioCarta 21 0.902 0* 0.863 0.002† Cell cycle activities CR_cell_cycle Exp. sig. 77 0.562 0.002† 0.510 0.051‡ Cell_cycle na 77 0.615 0* 0.523 0.091 cellcyclePathway na 21 0.560 0.011† 0.413 0.283 Purine_metabolism GenMapp 81 0.477 0* 0.414 0.029‡ HTERT_up Exp. sig. 98 0.563 0.017‡ 0.558 0.036‡ Mitochondrial activities PGC Exp. sig. 339 0.427 0.037‡ 0.413 0.052‡ Mitochondrial Exp. sig. 397 0.456 0.054‡ 0.402 0.141 Others RAP_down Exp. sig. 187 0.606 0.015‡ 0.570 0.05‡ LEU_down Exp. sig. 138 0.609 0.016‡ 0.532 0.105 GLUT_down Exp. sig. 249 0.595 0.01† 0.542 0.078
Supplementary Data, Li, et al.
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