Figure 4.
Upregulated genes in the TP53 immune gene classifier correlate with immune infiltration in TCGA-AML cases. (A) Heatmap of immune-cell-type–specific scores and biological activity scores (unsupervised hierarchical clustering; Euclidean distance; complete linkage) in TCGA-AML cases with (n = 93) or without (n = 54) abnormalities in the DE genes (TP53 immune classifier) between patients with TP53-mutated (n = 42) and TP53-WT AML (n = 22). Abnormalities were defined as mRNA upregulation, gene amplification, deep deletion, and missense mutations relative to the gene’s expression distribution in all profiled AML samples. Abnormalities in only 1 gene used in the cBioPortal query (by default, nonsynonymous mutations, fusions, amplifications, and deep deletions) were sufficient to define that particular patient sample as “altered." (B) Expression of IFN-γ signaling molecules, immune checkpoints, and markers of T-cell infiltration in TCGA-AML cases with or without abnormalities in the TP53 classifier genes. Bars denote median values. (C) Abnormalities in the 18 upregulated immune genes in the TP53 classifier in pretreatment BM samples from TCGA-AML cases. Data were retrieved, analyzed, and visualized using cBioPortal.34 The Kaplan-Meier method was used to generate survival curves, which were compared using a log-rank test.

Upregulated genes in the TP53 immune gene classifier correlate with immune infiltration in TCGA-AML cases. (A) Heatmap of immune-cell-type–specific scores and biological activity scores (unsupervised hierarchical clustering; Euclidean distance; complete linkage) in TCGA-AML cases with (n = 93) or without (n = 54) abnormalities in the DE genes (TP53 immune classifier) between patients with TP53-mutated (n = 42) and TP53-WT AML (n = 22). Abnormalities were defined as mRNA upregulation, gene amplification, deep deletion, and missense mutations relative to the gene’s expression distribution in all profiled AML samples. Abnormalities in only 1 gene used in the cBioPortal query (by default, nonsynonymous mutations, fusions, amplifications, and deep deletions) were sufficient to define that particular patient sample as “altered." (B) Expression of IFN-γ signaling molecules, immune checkpoints, and markers of T-cell infiltration in TCGA-AML cases with or without abnormalities in the TP53 classifier genes. Bars denote median values. (C) Abnormalities in the 18 upregulated immune genes in the TP53 classifier in pretreatment BM samples from TCGA-AML cases. Data were retrieved, analyzed, and visualized using cBioPortal.34  The Kaplan-Meier method was used to generate survival curves, which were compared using a log-rank test.

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