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Background  We used bioinformatic tools to dichotomize 157 non-M3 AML patients from the TCGA dataset based on the presence or absence of  TP53  mutations, and screened out a key gene related to  TP53  mutation for future analysis.    Methods  DEGs were analyzed by R package “DESeq2” and then run GSEA, GO enrichment, KEGG pathway and PPI network. Hub genes were selected out according to MCC. Log-rank (Mantel–Cox) test was used for survival analysis. Mann–Whitney U’s nonparametric t test and Fisher’s exact test was used for continuous and categorical variables respectively.  p  value< 0.05 was considered to be statistical significance.    Results   TNFRSF4  was final screened out as a key gene. Besides  TP53  mutation ( p  = 0.0118), high  TNFRSF4  was also associated with  FLT3  mutation ( p  = 0.0102) and  NPM1  mutation ( p  = 0.0024). Elevated  TNFRSF4  was significantly related with intermediate ( p  = 0.0004) and poor ( p  = 0.0011) risk stratification as well as relapse statute ( p  = 0.0099). Patients with elevated  TNFRSF4  expression had significantly shorter overall survival (median survival: 2.35 months vs. 21 months,  p  < 0.0001). Based on our clinical center data,  TNFRSF4  expression was significantly higher in non-M3 AML patients than HDs ( p  = 0.0377) and MDS patients (EB-1, 2;  p  = 0.0017).    Conclusions  Elevated  TNFRSF4  expression was associated with  TP53 ,  FLT3 and NPM1  mutation as well as poor clinical outcome.  TNFRSF4  expression was significantly higher in non-M3 AML patients than HDs and MDS (EB-1, 2) patients.  TNFRSF4  is need for future functional and mechanistic studies to investigate the role in non-M3 AML.

Elevated TNFRSF4 gene expression is a predictor of poor prognosis in non-M3 acute myeloid leukemia