Figure 3
Figure 3. Outcome by KIT and RTK gene mutations. (A) At 36 months, CIR was estimated at 44% (95% CI, 24-70) and 34% (95% CI, 18-59) in patients with exon 8 and exon 17 KIT-mutated gene, respectively, as compared with 30% (95% CI, 23-39) in those with wild-type KIT gene (SHR= 1.78 [95% CI, 0.98-3.24] for KIT-mutated AML patients; P = .057 by cause-specific hazard Cox model). (B-C) RTK (KIT and/or FLT3-ITD/TKD) gene mutations. (B) At 36 months, CIR was estimated at 42% (95% CI, 30-56) in patients with RTK-mutated genes, as compared with 27% (95% CI, 20-36) in those with wild-type RTK genes (SHR= 1.89 [95% CI, 1.11-3.22] for RTK-mutated AML patients; P = .019 by cause-specific hazard Cox model). (C) At 36 months, RFS was estimated at 53% (95% CI, 39-65) in patients with RTK-mutated genes, as compared with 69% (95% CI, 59-77) in those with wild-type RTK genes (HR= 1.80 [95% CI, 1.09-2.96] for RTK-mutated AML patients; P = .019 by the log-rank test).

Outcome by KIT and RTK gene mutations. (A) At 36 months, CIR was estimated at 44% (95% CI, 24-70) and 34% (95% CI, 18-59) in patients with exon 8 and exon 17 KIT-mutated gene, respectively, as compared with 30% (95% CI, 23-39) in those with wild-type KIT gene (SHR= 1.78 [95% CI, 0.98-3.24] for KIT-mutated AML patients; P = .057 by cause-specific hazard Cox model). (B-C) RTK (KIT and/or FLT3-ITD/TKD) gene mutations. (B) At 36 months, CIR was estimated at 42% (95% CI, 30-56) in patients with RTK-mutated genes, as compared with 27% (95% CI, 20-36) in those with wild-type RTK genes (SHR= 1.89 [95% CI, 1.11-3.22] for RTK-mutated AML patients; P = .019 by cause-specific hazard Cox model). (C) At 36 months, RFS was estimated at 53% (95% CI, 39-65) in patients with RTK-mutated genes, as compared with 69% (95% CI, 59-77) in those with wild-type RTK genes (HR= 1.80 [95% CI, 1.09-2.96] for RTK-mutated AML patients; P = .019 by the log-rank test).

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