Figure 5.
Expression of FOXO-repressed metabolic genes predicts poor survival in patients with MM. (A) Kaplan-Meier univariate analysis for the OS of k-means clustering–defined groups of patients with MM (776 patients in total). Patients were clustered based on the FOXO-regulated LE gene sets; LE glycolysis, LE TCA cycle, or LE OXPHOS, which were derived by combining the LE genes from GSEAs performed for several glycolysis, TCA cycle, or OXPHOS gene sets (Supplemental Table 1). Groups were defined as ‘high’ (red lines) or ‘low’ (blue lines) expressing groups. Numbers of patients at risk are tabulated below. (B) GSEA enrichment plots show enrichment of the FOXO-regulated LE glycolysis, LE TCA cycle, and LE OXPHOS gene sets (supplemental Table 1) in MM plasma cells from newly diagnosed patients (MMPCs, n = 75) compared with plasma cells from healthy donors (n = 15). FDR, ES, NES, and P-value are depicted in the plots.

Expression of FOXO-repressed metabolic genes predicts poor survival in patients with MM. (A) Kaplan-Meier univariate analysis for the OS of k-means clustering–defined groups of patients with MM (776 patients in total). Patients were clustered based on the FOXO-regulated LE gene sets; LE glycolysis, LE TCA cycle, or LE OXPHOS, which were derived by combining the LE genes from GSEAs performed for several glycolysis, TCA cycle, or OXPHOS gene sets (Supplemental Table 1). Groups were defined as ‘high’ (red lines) or ‘low’ (blue lines) expressing groups. Numbers of patients at risk are tabulated below. (B) GSEA enrichment plots show enrichment of the FOXO-regulated LE glycolysis, LE TCA cycle, and LE OXPHOS gene sets (supplemental Table 1) in MM plasma cells from newly diagnosed patients (MMPCs, n = 75) compared with plasma cells from healthy donors (n = 15). FDR, ES, NES, and P-value are depicted in the plots.

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