FigureĀ 1.
Genomic profiling predicts the AML ontogeny. (A) Oncoplot of AML subtypes (de novo AML, t-AML, MR-Hx, and MR-CG). NGS panels are indicated as platforms (RDTS, RDTB, and IMPACT-heme). Genes not covered by RDTS are indicated in gray. The ELN2017 and ELN2022 risk groups are listed. EVI1 indicates EVI1 rearrangements. MLL indicates MLL rearrangements. (B) Bar plots of genomic aberrations for each AML subtype. Proportions are shown. The MR/RUNX1 genes are bolded. (C) Association between individual gene mutations and AML ontogeny. Odds ratio was depicted on a log10 scale. The comparison is between MR-Hx and de novo AML.

Genomic profiling predicts the AML ontogeny. (A) Oncoplot of AML subtypes (de novo AML, t-AML, MR-Hx, and MR-CG). NGS panels are indicated as platforms (RDTS, RDTB, and IMPACT-heme). Genes not covered by RDTS are indicated in gray. The ELN2017 and ELN2022 risk groups are listed. EVI1 indicates EVI1 rearrangements. MLL indicates MLL rearrangements. (B) Bar plots of genomic aberrations for each AML subtype. Proportions are shown. The MR/RUNX1 genes are bolded. (C) Association between individual gene mutations and AML ontogeny. Odds ratio was depicted on a log10 scale. The comparison is between MR-Hx and de novo AML.

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