Figure 5.
Kaplan-Meier analysis of patients with NPM1-mutated AML with different blast phenotypes who received standard induction chemotherapy. All analyses included patients who received standard induction chemotherapy (n = 172 in total). (A-B) Patients with a DN blast phenotype (n = 44) showed significantly prolonged RFS (64.7 months) (A) and OS (66.5 months) (B). Patients in the myeloid group (n = 55) showed significantly shortened RFS (8.4 months) and OS (20.2 months), with patients with a monocytic phenotype (n = 77) showing intermediate RFS (20.6 months; P < .0001 comparing all 3 groups) and OS (44.3 months; P = .01 comparing all 3 groups). (C-D) Looking specifically at patients harboring TET2 or IDH1/2 comutations, patients with a DN blast phenotype (n = 42) showed significantly prolonged RFS (64.7 vs 11.0 months; P = .0004) (C) and OS (66.5 vs 21.3 months; P = .01) (D), compared with patients lacking a DN phenotype (n = 54).

Kaplan-Meier analysis of patients with NPM1-mutated AML with different blast phenotypes who received standard induction chemotherapy. All analyses included patients who received standard induction chemotherapy (n = 172 in total). (A-B) Patients with a DN blast phenotype (n = 44) showed significantly prolonged RFS (64.7 months) (A) and OS (66.5 months) (B). Patients in the myeloid group (n = 55) showed significantly shortened RFS (8.4 months) and OS (20.2 months), with patients with a monocytic phenotype (n = 77) showing intermediate RFS (20.6 months; P < .0001 comparing all 3 groups) and OS (44.3 months; P = .01 comparing all 3 groups). (C-D) Looking specifically at patients harboring TET2 or IDH1/2 comutations, patients with a DN blast phenotype (n = 42) showed significantly prolonged RFS (64.7 vs 11.0 months; P = .0004) (C) and OS (66.5 vs 21.3 months; P = .01) (D), compared with patients lacking a DN phenotype (n = 54).

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