Patients with AML with WT TP53 but defective TP53-mediated apoptosis have a dismal survival.

In the sensitive cases, we detected highly significant enrichments for oxidative phosphoryation (OXPHOS), Myc targets, fatty-acid metabolism, and DNA repair ( Figure 2B and Supplemental Figure 2 ), while in the resistant cases, we detected a profound enrichment for inflammatory pathways and mediators, including TNFA, IFNG, IFNA, multiple JAK/STAT signaling pathways, and K-RAS signaling.

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