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. Author manuscript; available in PMC: 2021 Apr 17.
Published in final edited form as: Nat Neurosci. 2019 Apr 8;22(5):729–740. doi: 10.1038/s41593-019-0370-y

Fig. 6 |. Association of AHR transcriptional response to clinical outcome in GBM.

Fig. 6 |

a, Left: representative immunofluorescence images of tissue array with non-tumor (n = 3) and human gliomas of different grades (n = 40) stained for KYN (green) and nuclei (blue). Scale bars, 20 μm. Right: quantification of KYN+ cells in non-tumor brain (n = 3) and tumors of grade 1 (n = 9), grade 2 (n = 16), grade 3 (n = 11) and grade 4 (n = 4). b, Heatmap of gene expression in GBM (n = 151) and lower-grade glioma (LGG, n = 527) samples generated using data shown in Supplementary Table 2 and arranged in the following order: group: GBM, LGG; grade: G2, G3 (LGG), G4 (GBM); LGG subclass: anaplastic astrocytoma, anaplastic oligoastrocytoma, astrocytoma, oligoastrocytoma, oligodendroglioma; GBM subclass: classical, G-CIMP, mesenchymal, neural, proneural; IDH mutant: no, yes. NA, not applicable or missing data. c, CCR2 and CCL2 mRNA RNA sequencing by expectation maximization (RSEM) from GBM patients with proneural (n = 29), neural (n = 26) or mesenchymal (n = 49) types using TCGA data (Supplementary Table 3). For a and c, each symbol represents one individual, and data are shown as mean ± s.e.m. P values were determined by one-way ANOVA.