TABLE 2.
Risk stratification by DNMT3A R882 mutation/NPM1 mutation/FLT3‐ITD allelic ratio genotypes
| NPM1 mutation a | DNMT3A R882 mutation | FLT3‐ITD | Patient number (HSCT at 1st CR) | 2‐year OS | 2‐year OS censored at HSCT | 2‐year EFS | ELN 2017 | GS‐JAML (2022) |
|---|---|---|---|---|---|---|---|---|
| Positive | Negative | Negative | 73 (4) | 78.7% | 76.0% | 44.8% | Favorable | Favorable |
| Low AR | 21 (10) | 67.4% | 42.8% | 53.6% | Favorable | Favorable b | ||
| High AR | 29 (13) | 60.9% | 44.8% | 34.3% | Intermediate | Intermediate | ||
| Positive | Negative | 23 (4) | 78.2% | 60.4% | 20.5% | Favorable | Intermediate | |
| Low AR | 6 (2) | 25.0% | 16.7% | 0.0% | Favorable | Adverse | ||
| High AR | 19 (4) | 24.3% | 0.0% | 0.0% | Intermediate | Adverse |
TP53 mutation was detected in one patient with normal karyotype/NPM1 mutation positive/FLT3‐ITD negative/DNMT3A R882 mutation positive and in one patient with normal karyotype/NPM1 mutation positive/FLT3‐ITD negative/DNMT3A mutation negative. Furthermore, a complex karyotype was detected in one patient with NPM1 mutation positive/FLT3‐ITD high‐AR/DNMT3A mutation negative. These patients are included in the NPM1 mutation‐positive AML analysis data.
The NPM1 mutation positive/DNMT3A R882 negative/FLT3‐ITD low‐AR group exhibited a short survival in the analysis of OS censored at HSCT, and allogeneic HSCT should be actively indicated when FLT3 inhibitors are not used.