Figure 4.
AML ontogeny determines the outcome of AML with MR/RUNX1 gene mutations. (A) Kaplan-Meier curves of OS of AML with MR/RUNX1 gene mutations divided by ontogeny. (B) AML ontogeny–related risk was evaluated in multivariable Cox-regression models adjusting for age (modeled by cubic spline), allogenic transplant (modeled as time-dependent variable), NRAS/KRAS mutations, and CG risks in patients with AML with MR/RUNX1 mutations uniformly treated with 7+3 induction therapy. (C) Kaplan-Meier curves of patients with AML were divided into ELN2022 risk groups. De novo AML with MR/RUNX1 gene mutations separated from the ELN2022 adverse group show an outcome falling in between the favorable and intermediate-risk groups.

AML ontogeny determines the outcome of AML with MR/RUNX1 gene mutations. (A) Kaplan-Meier curves of OS of AML with MR/RUNX1 gene mutations divided by ontogeny. (B) AML ontogeny–related risk was evaluated in multivariable Cox-regression models adjusting for age (modeled by cubic spline), allogenic transplant (modeled as time-dependent variable), NRAS/KRAS mutations, and CG risks in patients with AML with MR/RUNX1 mutations uniformly treated with 7+3 induction therapy. (C) Kaplan-Meier curves of patients with AML were divided into ELN2022 risk groups. De novo AML with MR/RUNX1 gene mutations separated from the ELN2022 adverse group show an outcome falling in between the favorable and intermediate-risk groups.

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